Weight reduction, body composition, thyroid hormones and basal metabolic rate in elite athletes 2 Effects of weight reduction rate on body composition, thyroid hormones and basal metabolic rate in elite athletes A randomized controlled clinical trial Anu Koivisto Master thesis in Clinical Nutrition Medical Faculty, Department of Nutrition UNIVERSITY OF OSLO 20th of April 2009 Master thesis in Clinical Nutrition, Anu Koivisto 2009 3 Abbreviations BMD Bone Mineral Density BMR Basal Metabolic Rate BW Body Weight BCOAD Branched- Chain 2-Oxo Acid Dehydrogenase CR Calorie Restriction DEXA Dual Energy X-ray Absorptiometry EE Energy Expenditure FAST Weight reduction of 1.4% of body weight/week FFM Fat Free Mass FM fat mass LBM Lean Body Mass LCD Low Calorie Diet NBAL Nitrogen Balance NEAT Non-Exercise Activity Thermogenesis NREE Non-Resting Energy Expenditure RMR Resting Metabolic Rate SLOW Weight reduction of 0.7% of body weight/week SPA Spontaneous Physical Activity TEE Total Energy Expenditure VLCD Very Low Calorie Diet WL Weight Loss Master thesis in Clinical Nutrition, Anu Koivisto 2009 4 Abstract Background: Optimal body composition and body weight (BW) are important performance factors in sports that emphasize aesthetics and high power to weight ratio. Weight reduction guidelines for athletes per date suggest a weekly weight loss of 0.51.0 kg which corresponds to 0.7% and 1.4% of BW in a 70-kg athlete. Weight reduction may lead to loss of lean body mass (LBM) and changed thyroid hormone (TH) profile and thereby reduced basal metabolic rate (BMR). Combining energy restriction with resistance training may inhibit loss of LBM in obese subjects. Little is known about these changes and their effect on metabolism (BMR, TH) in athletes. Purpose: To compare changes in body composition, TH and BMR in two different weight-loss interventions promoting loss of 0.7% versus 1.4% of BW per week in elite athletes. Methods: 30 male and female elite athletes were randomized into slow weight reduction [“SLOW”, n=14, 23.5 (3.3) y, 72.1 (12.2) kg] and fast weight reduction [“FAST”, n=16, 22.3 (4.7) y, 72.2 (11.3) kg]. Both intervention groups included energy restricted diets and resistance training regimen for 4-12 weeks. The duration of the intervention was dependent on the desired weight loss and the type of intervention group the participant was allocated to. Diets were recorded at baseline by 4-day weighed food records which were used to design individual intervention diets promoting weekly BW loss of 0.7% or 1.4%. Four weekly resistance training sessions were added to the usual training regimen to stimulate muscle hypertrophy. The following measurements were taken at baseline and post intervention: BW, LBM, fat mass (FM) with dual energy x-ray absorptiometry (DEXA), serum thyroid stimulating hormone(s-THS) and free thyroxine (s-free T4) and BMR with indirect calorimeter. Results: There were no significant differences between the groups in any variables at the baseline. BW was reduced by 5.6 (3.0) % [mean(SD)], p<0.001 and 5.4 (2.3%), p<0.001) for SLOW- and FAST weight reduction group, respectively. The changes were not significantly different between the intervention groups (p=0.8). LBM was significantly increased for SLOW [2.0 (1.3) %, p<0.001] but not for FAST [1.1 (3.0) %, p=0.3]. There was a significant difference in FM reduction obtained during weight loss between the intervention groups SLOW -31 (2.9) %, p<0.001) and FAST -23.4 Master thesis in Clinical Nutrition, Anu Koivisto 2009 5 (13.8) %, p<0.001 (p=0.04). Free T4 reduction during the intervention was significant in FAST [-11.2 (7.6) %, p=0.001] but not in SLOW. These changes were significantly different between the groups (p<0.001). BMR was reduced significantly for both SLOW [12.3 (11.4) %, p=0.036] and FAST [9.8 (6.5) %, p=0.018], but the changes did not differ between the intervention groups (p=0.9). Changes in LBM were associated with baseline LBM (r=0.49, p=0.006) but not with weight reduction rate. Changes in free T4 or LBM were not associated with changes in BMR. Conclusion: Body composition changes were different between the groups; LBM increased only in the SLOW group who also obtained a larger FM reduction than the FAST group, thus body composition changes were more beneficial in SLOW weight loss intervention. Only FAST weight reduction had an impact on thyroid hormones, producing a larger decline in free-T4 but not in TSH compared with SLOW intervention. BMR reductions did not differ between the interventions. Thus for optimal body composition changes in athletes a moderate energy restriction combined with resistance training leading to a weekly weight loss of 0.7% seems preferable. Despite maintained or increased LBM, and maintained free T4 athletes experienced reductions in BMR. Master thesis in Clinical Nutrition, Anu Koivisto 2009 6 Acknowledgements First I would like to thank my supervisors who gave me irreplaceable feedback and guidance during the whole study. Ina Garthe at Norwegian School of Sports Sciences –Thank you for including me in this project, being always available and patiently answering the endless flow of questions! Thank you for being an excellent supervisor by directing my focus to the essentials! Lene Frost Andersen at the Department of Nutrition, University of Oslo –Thank you for posing many important critical questions! Jorunn Sundgot-Borgen at Norwegian School of Sports Sciences -Thank you for keeping me on track and giving me support and encouragement! I would also like to acknowledge Per-Egil Refsnes and Sindre Madsgaard (Norwegian Olympic Sports Centre) for their contribution in the strength training part of the study. Thanks to Monica Viker Brekke (Norwegian Olympic Sports Centre) for making blood sampling and testing logistics run smoothly. Big thanks to Nils Kvamme and Truls Raastad (Norwegian School of Sports Sciences) for being so flexible with a short notice and helping me with BMR data collection and analysis. Thanks to all athletes who participated in this study – May all of you reach your athletic goals! Special thanks go to Børge, Kia and Alexis for their unconditional love! Master thesis in Clinical Nutrition, Anu Koivisto 2009 7 Table of contents ABBREVIATIONS .............................................................................................................................. 3 ABSTRACT.......................................................................................................................................... 4 ACKNOWLEDGEMENTS................................................................................................................. 6 TABLE OF CONTENTS..................................................................................................................... 7 1. INTRODUCTION ................................................................................................................... 10 2. THEORY.................................................................................................................................. 11 2.1 WEIGHT REDUCTION AND ATHLETES ................................................................................. 11 2.2 WEIGHT REDUCTION AND DIET .......................................................................................... 12 2.2.1 Energy metabolism during weight loss......................................................................... 12 2.2.2 Composition of energy restricted diet for athletes ....................................................... 16 2.3 WEIGHT REDUCTION AND STRENGHT TRAINING ................................................................. 19 2.4 WEIGHT REDUCTION AND BODY COMPOSITION .................................................................. 20 2.5 WEIGHT REDUCTION AND THYROID HORMONES................................................................. 23 2.6 WEIGHT REDUCTION AND BASAL METABOLIC RATE ........................................................... 25 2.7 POTENTIAL ADVERSE EFFECTS OF WEIGHT REDUCTION ...................................................... 27 2.8 WEIGHT REDUCTION RATE ................................................................................................. 29 2.9 AIM OF THE STUDY ............................................................................................................ 29 3. SUBJECTS AND METHODS ................................................................................................ 31 3.1 SUBJECTS ........................................................................................................................... 31 3.1.1 Inclusion and exclusion criteria ................................................................................... 31 3.2 PROCEDURE ....................................................................................................................... 32 3.3 DESIGN .............................................................................................................................. 33 3.3.1 Recruitment .................................................................................................................. 33 3.3.2 Randomization.............................................................................................................. 33 Master thesis in Clinical Nutrition, Anu Koivisto 2009 8 3.3.3 3.4 MEASUREMENTS ................................................................................................................ 38 3.4.1 Dietary registration...................................................................................................... 38 3.4.2 Diet analysis................................................................................................................. 39 3.4.3 Body composition ......................................................................................................... 40 3.4.4 Thyroid hormones ........................................................................................................ 41 3.4.5 Indirect calorimetry...................................................................................................... 42 3.5 4. Intervention .................................................................................................................. 34 STATISTICAL ANALYSIS ..................................................................................................... 43 3.5.1 Sample size estimation ................................................................................................. 43 3.5.2 Missing data ................................................................................................................. 44 RESULTS ................................................................................................................................. 45 4.1 SUBJECTS ........................................................................................................................... 45 4.2 DIET................................................................................................................................... 46 4.3 BODY COMPOSITION .......................................................................................................... 47 4.3.1 Body weight.................................................................................................................. 47 4.3.2 Fat mass and body fat percent ..................................................................................... 47 4.3.3 Lean body mass ............................................................................................................ 48 4.3.4 Bone mineral density (BMD)........................................................................................ 49 4.4 THYROID HORMONES ......................................................................................................... 50 4.5 BASAL METABOLIC RATE ................................................................................................... 51 4.6 COMPLIANCE ..................................................................................................................... 53 5. DISCUSSION........................................................................................................................... 55 5.1 SUBJECTS ........................................................................................................................... 55 5.1.1 Gender and age ............................................................................................................ 55 Master thesis in Clinical Nutrition, Anu Koivisto 2009 9 5.1.2 Compliance .................................................................................................................. 56 5.1.3 Training hours and types of sports............................................................................... 57 5.1.4 Previous weight reduction............................................................................................ 57 5.2 METHODS .......................................................................................................................... 58 5.2.1 Design .......................................................................................................................... 58 5.2.2 Diet............................................................................................................................... 58 5.2.3 DEXA ........................................................................................................................... 60 5.2.4 Indirect calorimeter...................................................................................................... 60 5.3 5.4 6. RESULT INTERPRETATIONS ................................................................................................ 61 5.3.1 Body composition ......................................................................................................... 61 5.3.2 Thyroid hormones ........................................................................................................ 63 5.3.3 BMR ............................................................................................................................. 65 STRENGTHS AND WEAKNESSES OF THE STUDY ................................................................... 67 CONCLUSION ........................................................................................................................ 68 PRACTICAL IMPLICATIONS....................................................................................................... 69 REFERENCES.....................................................................................................................................70 LIST OF APPENDICES......................................................................................................................84 Master thesis in Clinical Nutrition, Anu Koivisto 2009 10 1. Introduction Body composition and body weight are two of many factors influencing athletic performance. Athlete’s ability to sustain power and overcome resistance (drag) is closely related to body composition.2 In most sports the typical elite athlete is expected to be well trained, lean and toned due to hours of training combined with a proper diet. It is generally believed that athletes’ weight and body composition are easily regulated, but their body size and shape vary and many athletes experience difficulties obtaining optimal body weight and/or composition.3;4 The weight loss methods used by athletes are often counterproductive and may cause loss of lean body mass (LBM), and impair performance and health.5;6;6-8 Furthermore energy restriction seems to reduce basal metabolic rate (BMR) but it is still unresolved whether it is caused by changes in LBM, thyroid hormones or other factors 9. Weight loss literature represents mostly overweight and obese population thus specific research in athletes is required. Per date recommended weekly weight loss for athletes is 0.5-1 kg10 but no study has evaluated the extremes of these guidelines in athletes. This study aims to determine the effect and potential difference of these guidelines on body composition, thyroid hormones and LBM in elite athletes. Master thesis in Clinical Nutrition, Anu Koivisto 2009 11 2. Theory 2.1 Weight reduction and athletes There are several reasons for weight regulation in sports. For most athletes it is desirable to have a solid lean body mass and a low body fat percentage since this gives an advantageous power to weight ratio.11 There are sports that require vertical (long distance running, long jump) or horizontal (high jump) movements of the body where excessive fat mass is considered as “dead weight”. High FM has also shown to increase energy demands and therefore could affect performance negatively.12 Furthermore in sports where aerodynamics and reduced resistance or drag is important (cycling, swimming) body composition plays an important role. Low body fat % can also be desirable in sports for aesthetics reasons (figure skating, gymnastics, bodybuilding/fitness and diving). And finally there are sports with weight categories where athletes wish to get an advantage over their rivals by obtaining lowest possible body weight with greatest reach and strength thus they often compete in weight class under their natural body weight.7 When athletes with a relatively low body fat% wish to reduce their body weight it needs to be planned carefully, since a desire to increase LBM and reduce body fat % can lead to unhealthy training regimen and disordered eating.13 A thorough evaluation of athletes’ physical and mental health, training regimen and athletic goals is required. Especially in sports with weight categories there has been an unhealthy tradition to reduce body weight rapidly during the last few days before a weigh-in.7;14;15 Gradual weight loss is recommended and additional dehydration up to 2% of body weight is acceptable.10;15 Larger dehydration and/or use of laxatives and/or total food restriction should and could be avoided by providing athletes and their coaches up to date information and guidance in optimal weight regulation. Master thesis in Clinical Nutrition, Anu Koivisto 2009 12 2.2 Weight reduction and diet It is well documented that weight loss requires a negative energy balance. Though dehydration can create a rapid transient weight loss it does not reduce fat mass or fat free mass at the tissue level. Furthermore dehydration may cause adverse effects for both health and performance.8;16 Negative energy balance by restricted energy intake leads to a weight loss as long as physical activity is maintained. But the optimal macronutrient composition of the calorie restricted diet and type of physical activity for maximal FM and minimal LBM loss are still discussed.9 2.2.1 Energy metabolism during weight loss The body can utilize energy from several sources during exercise (figure 2.1.1). The type of training, intensity and duration together with athlete’s diet (energy and macronutrient content), training status and training environment (altitude, temperature) determine the amount and type of substrates oxidised. Figure 2.2.1. Size of energy stores and rates of utilization (Coyle et al 1997).17 During energy restriction carbohydrate (CHO) stores can easily become reduced if not enough CHO is consumed. The total muscle glycogen store is around 350-400g depending on athlete’s body size and body composition, and can provide substrate for exercise at 65%VO2max up to 90min.18 Most athletes’ CHO intake during weight Master thesis in Clinical Nutrition, Anu Koivisto 2009 13 reduction is 2-4g/kg body weight19-21 which is well below the specific recommendations for optimal glycogen restoration in athletes (5-12g/kg BW dependent of type of sport)22, thus athletes’ glycogen stores may be suboptimal during the whole weight loss period. This might have a negative impact on athletes’ performance especially at intensities above 60% VO2max when most of the energy is provided by CHO (figure 2.1.2).23 It has been shown previously that large glycogen stores improve performance in some sports.24;25 Thus not surprisingly reduced power output and impaired anaerobic performance has been reported in athletes with low CHO weight loss diets.26;27 Inadequate CHO intake between training sessions compromises glycogen store refilling and can have a negative impact also on recovery and the immune system.28 Furthermore when CHO availability is not sufficient to maintain high exercise intensity alternative substrates are oxidised and/or exercise intensity is reduced.29 Body fat and protein from skeletal muscle become the main fuelling substrates under these circumstances. It follows that FA oxidation is increased during energy restriction30 and becomes the major source of fuel. Fat contributes to energy metabolism at all intensities but comprises most of the energy at intensities below 65%VO2max,23 when lipolysis sufficiently supply muscles with fatty acids. As exercise intensity increases lipolysis is markedly suppressed, fatty acid availability is reduced and not enough ATP is produced at high enough rate.18 There are two main explanations for that31: 1) Fatty acid availability in muscle is reduced during intense exercise because of reduced blood flow to fat tissue and following decline in fatty acid release from FM. 2) Increased rate of glycogenolysis during intense exercise may lead to accumulation of acetyl-CoA and a following flux to malonyl-CoA that inhibits the entry of LCFA into the mitochondria for oxidation. Thus FA can not provide energy for skeletal muscles at high enough rate during high-intensity muscle work, something that most likely will impair performance. Low CHO diets for athletes complicates high-intensity performance and Master thesis in Clinical Nutrition, Anu Koivisto 2009 14 may put the athletes at increased risk for injury and infections.32 Glykogen Intramuscular triglycerides Plasma free fatty acids Plasma glucose Figure 2.2.2.Utilization of substrates during exercise at different intensities (Romjin et al).23 Proteins contribute usually very little to total energy expenditure when subjects are in energy balance. During exercise amino acid oxidation is increased accompanied with reduction in whole body protein synthesis and protein breakdown. During exercise at 65-75% VO2max proteins can provide 1-6% of energy.33;34 Though skeletal muscle can oxidise certain amino acids for energy it is counterproductive since they serve either as structural or functional role in the body. Proteins that are preferable oxidised by muscle during exercise include branched-chain amino acids especially leucine. The enzyme oxidising these amino acids, branched chain oxo-acid dehydrogenize (BCOAD), is relatively inactive during rest but is activated during exercise by glycogen depletion, increased ADP/ATP ratio and decreased pH34. Furthermore some but not all studies have shown that glycogen concentration is inversely related to branched chain 2-oxo-acid dehydrogenase (BCOAD) activation during exercise.35;36 This enzyme oxidises branched chain amino acids (BCAA) that are the preferable amino acids oxidised during exercise. Thus strategies to ensure CHO availability may spare oxidation of BCAA. Therefore not only dietary protein but also CHO intake needs to be optimised. Master thesis in Clinical Nutrition, Anu Koivisto 2009 15 Also catabolic hormone profile during exercise in energy restriction can negatively affect muscle protein breakdown. Glycogen depletion makes the muscle rely more on blood sugar for energy/glucose supply leading to reductions in serum glucose concentration.29 Hypoglycemia markedly stimulates epinephrine release in an attempt to increase liver glucose output (gluconeogenesis) and attenuate blood sugar levels. Glycogen depletion is also associated with elevation of plasma cortisol. These stress hormones induce the proteolysis and muscle protein breakdown often seen in physiological stress situations.37 During fasting gluconeogenesis provides glucose for glucose dependent tissue thus mobilising amino acids from the skeletal muscle, mainly alanine, which can be converted to glucose in liver (figure 1.2.2). This results in muscle breakdown and loss of LBM. Figure 2.2.3. Illustration of alanine-glucose cycle. 1 Roemmich et al21 detected reduced serum prealbumin in wrestlers that was strongly associated with FFM loss. These athletes diets provided 0.9g protein/kg BW and 3.4g/kg BW CHO. Reduced prealbumin is an early sign of malnutrition and an Master thesis in Clinical Nutrition, Anu Koivisto 2009 16 inadequate protein intake, thus 0.9g/kg BW protein for these athletes on a weight loss diet (<125kJ/kg BW) was not adequate. Also Walberg et al38 studied the effect of weight loss diet on body composition and performance in athletes. They showed that only high (1.6g/kg BW) protein intake produced positive nitrogen balance though it did not have a superior effect on LBM changes compared with moderate protein intake (0.8g/kg BW). Tarnopolsky et al34 concluded in a review that most athletes achieve the daily dietary protein intake of 1.0-1.6g/kg BW which is sufficient for endurance athletes in energy balance. But athletes with low energy and CHO intake may require assistance in optimising their protein intake. Although exercise increases protein oxidation it also results in a more efficient protein metabolism (amino acid re-use) and improved protein net balance39 thus protein needs in athletes in general are not increased as much as expected. But as described a low energy and/or carbohydrate intake will increase amino acid oxidation and total protein requirements since protein metabolism during exercise is closely linked to the regulation of fuel metabolism.34 Taken all this together, energy restriction and suboptimal carbohydrate and protein intake during weight loss can affect LBM and performance negatively and attention needs to be paid to the macronutrient composition of the weight loss diet. 2.2.2 Composition of energy restricted diet for athletes Existing literature suggests that energy restricted diets with higher than average protein content may offer some benefit in terms of promoting fat mass loss and maintaining LBM9;40. High protein content may also assist with satiety and increase the thermic effect of food. 41;42 Since more protein is oxidised for energy during weight reduction protein requirements are increased.11 In order to maintain LBM the body needs to be in nitrogen balance (NBAL). This means that all sources of nitrogen intake has to equal nitrogen output (urine, faeces, sweat and miscellaneous). CHO and total energy intake can positively affect NBAL. But provision of dietary protein at levels above requirements results in increased protein oxidation or energy storage as fat.43 Protein intake per se does not have an anabolic effect.33 Master thesis in Clinical Nutrition, Anu Koivisto 2009 17 Hypo caloric diet with varying macronutrient composition has been studied extensively in overweight and obese subjects but relatively few studies are conducted on athletes. Baba et al44 showed a significantly larger decrease in RMR with a high CHO diet (-17.4%) compared with high protein diet (-5.9%). Torbay et al found similar changes in BMR with identical diet composition (30E% fat, 45E% protein, 25E% CHO). Dietary protein recommendation for athletes is 1.2g/kg body weight during weight loss10. It is important that the protein quality (content of essential amino acids and bioavailability) of weight loss diet is high. The amount of protein that contributes to total energy intake varies according to the amount of CHO and fat in the diet. Athletes’ CHO intake should be as high as possible within other dietary goals during weight reduction since CHO play an important role in optimal performance and has a net positive effect on nitrogen balance. Studies have shown the importance of carbohydrates during weight reduction for maintenance of high-power performance where high carbohydrate diet (66-70 E%) but not lower CHO diet (41-55 E%) was required for wrestlers to perform at their best.27;45 To secure the minimum carbohydrate and protein intake fat content needs to be substantially reduced but is not recommended to be below 20E% for not to compromise essential fatty acid intake. There are many fad diets promising superior weight reduction results. Low carbohydrate, low GI, high protein, high fat, low fat and very low fat diets alone or in combinations with each other are probably the most common strategies. Low CHO diets have been reported to result in lower lactate threshold which is unfortunate for elite athletes’ performance.32 There is also some evidence that the nutritional adequacy of such a diet may be suboptimal (low in fibre, vitamins and minerals).46 Furthermore low CHO diets result in glycogen depletion and a following fatigue, delayed recovery and possibly a reduction in immune function. Depletion of carbohydrate stores has also shown to result in increased s-cortisol which might affect LBM negatively.47 Though in a review from 2007 the authors (reviewed only 5 small clinical performance studies) concluded that low FAT and low CHO diets appear indifferent relative to performance (no change or improved time to exhaustion at 60-80%VO2max) in endurance athletes and that low CHO diets seem to induce larger weight and FM Master thesis in Clinical Nutrition, Anu Koivisto 2009 18 reductions in athletes32. However, Walberg et al38 revealed that although high proteinlow CHO hypocaloric diet resulted in positive nitrogen balance and maintained LBM in weightlifters muscular endurance was significantly better with isocaloric high CHO diet. The mechanisms are somewhat unclear but some studies have reported reduced anaerobic performance with low CHO weight loss diets.27;48 Theoretically this could be due to elevated free fatty acids’ glycolysis inhibiting function. Greenhaff et al suggested that low CHO diet may diminish the buffering capacity of the blood.49 Meal frequency seems to play an important role in stimulating muscular hypertrophy and therefore might contribute to maintenance of LBM during weight reduction.20;50 Iwao et al compared the effect of 2 meals versus 6 meals on weight loss among wrestlers and demonstrated that high meal frequency is to prefer during weight reduction in order to reduce loss of LBM20. Especially timing of carbohydrate and protein intake after work-outs is important. The highest rate of muscle glycogen storage occurs during the first hour after exercise due to activation of glycogen synthase, increased insulin sensitivity and permeability of glucose over the cell membrane.51-53 It is important that fuel is provided during this period so advantage can be taken from the chemical state of the cell. It seems that the type of carbohydrate consumed after exercise should preferably have a moderate to high glycaemic index in order to enhance the post-exercise refuelling54. Low GI foods may contain considerable amount of CHO that is malabsorbed and so less CHO is available for rapid glycogen resynthesis.55 Post exercise CHO intake has a protein sparing effect since it reduces cortisol secretion and increases insulin secretion thus switching the body from catabolic state to anabolic state.56 Co-ingestion of protein with carbohydrate in ratio 1:3-4 (PRO:CHO) has shown to increase the glycogen synthesis in the early recovery phase.57;58 Proteins provide substrate for increased net muscle protein synthesis post exercise.59,60 Also pre exercise protein intake has shown to be important for optimal protein synthesis.61 Athletes’ diets during weight loss may be low in nutrients (thiamine, magnesium and zinc).14 Though blood levels of these micronutrients remained stable during 3-week weight loss longer-term energy restriction could deplete the vitamin stores if not Master thesis in Clinical Nutrition, Anu Koivisto 2009 19 counterbalanced with increased intake or supplementation. Furthermore weight loss diets may be low in iron and fat (including omega 3 fatty acids) and fat soluble vitamins48 and could theoretically affect the immune system and performance negatively.62 To summarize, weight loss diets in athletes should provide adequate amounts of protein and as much as possible carbohydrate without compromising intake of other nutrients and reduced amount of fat in order to induce negative energy balance. The diet should be nutrient dense, have a lot of variation and contain adequate amount of fibre. Total daily food intake should be divided in frequent small meals. And careful planning of meal composition around the work-outs is required. Table 2.2.4. Summary of current recommendations for minimum energy and macronutrient composition of the weight reduction diet for athletes.11 Nutrient Energi, kJ Carbohydrate, g/kg BW Protein, g/kg BW Fat, E% Minimum recommended intake 6280 5 1.2 20 2.3 Weight reduction and strenght training Strength training has shown to enhance LBM preservation in overweight populations during weight loss63;64;65. But only one study has investigated this in athletes66. Garthe et al reported though no difference in LBM changes between13 weight class athletes who were allocated to either ordinary training group or strength training group during a weight loss. Maintenance of LBM is desirable because of its effect on metabolism (discussed in 1.4 and 1.6). Stiegler et al9 reviewed effects of different types and intensities of exercise on weight loss in overweight subjects. They concluded that high intensity exercise seems to be the preferred weight loss strategy but resistance training (RT) may give the most beneficial body composition changes. Geliebter et al67 Master thesis in Clinical Nutrition, Anu Koivisto 2009 20 reported that despite the type of exercise (strength training versus aerobic training) declines in RMR could not be prevented during 8-week weight loss, but the literature is still inconclusive.9 Exercise alone often fails in BW reduction but combining resistance training with energy restriction might be the best way to maintain LBM while reducing BW and FM.68 2.4 Weight reduction and body composition The main components of human body on tissue level are fat free mass (FFM) and fat mass (FM). FFM is defined as all fat-free chemicals and tissue including water, muscle, bone, connective tissue and organs. Very often FFM and lean body mass (LBM) are used interchangeably. The only difference is that LBM includes in addition to FFM also fat in cell membranes (~10% of FM).69 FFM consist of highly metabolically active tissue and tissue with lower metabolic rate like bone and connective tissue. High lean to fat mass ratio is advantageous for athletes and therefore ideally a body composition change would lead to loss of FM and maintenance or even increased LBM. But a simultaneous increase in LBM and a decrease in body fat % is difficult to achieve since reduction in FM requires a negative energy balance whereas LBM increase is stimulated by a positive energy balance.70 Restricted energy intake and following weight loss in athletes and non-athletes is unfortunately often accompanied with reductions in LBM.68;71 Koutedakis et al72 reported that 50% of weight loss in elite rowers consisted of LBM. The rowers reduced their body weight by 6-7% during a 2 or 4 months pre-season period. It seems that the larger the weight reductions the larger loss of LBM both in athletes and non-athletes according to several studies.71;73 Muscular hypertrophy during energy restriction has been detected only among rats. Goldberg et al reported decades ago muscular hypertrophy in rats during energy restriction.74 Lately results from clinical trials has strengthened the positive effect of resistance training under weight reduction for the maintenance of LBM64;65;75;76, and one study has shown an increase in LBM during a 12-week weight loss.75 But all these studies are conducted on overweight/obese subjects thus the results cannot be Master thesis in Clinical Nutrition, Anu Koivisto 2009 21 extrapolated to elite athletes. Forbes et al demonstrated that LBM loss is related to initial body fat content, indicating that lean subjects will lose larger proportion of FFM during weigh loss than subjects with higher % body fat.70 Figure 2.4.1. Anatomic skeletal muscle components at the first four body composition levels.77 FM loss during weight reduction seems to affect several other aspects than sole body composition. FM loss has been linked to reduced serum leptin.78 Leptin is a signal substance released from adipose tissue (adipokine) reflecting the state of the fat stores. It acts as a long-term satiety signal in the hypothalamus satiety centre. Low plasma leptin signals to hypothalamus of reduced energy stores (FM) and thus promotes hunger and suppresses satiety. As fat stores decline during weight loss leptin release is reduced which might have an affect on BMR as reported by Dionne et al79. Furthermore reduced energy availability but not the exercise stress seems to suppress leptin.80 Thus exercise does not induce hunger to same extent than energy restriction does, emphasizing the importance of exercise in weight loss regimen in improving satiety and perhaps adherence to the regimen. Also athletes with low energy intakes have shown to have low serum leptin indicating low fat stores and low energy availability.81 But there are no studies looking at changes in leptin as a result of weight loss intervention. Interestingly leptin may execute its effect on thermogenesis via thyroid hormones (see 1.5). Doucet et al82 showed that leptin could explain 28% of Master thesis in Clinical Nutrition, Anu Koivisto 2009 22 variance RMR changes during weight loss in overweight subjects, association being stronger for males than for females. Figure 2.4.2. Main components of human body. Probably the most challenging part of weight reduction is the maintenance of the new body weight. Many studies have reported weight regain within a year after weight reduction.83;84 The main explaining variables for weight regain are the loss of LBM and following reduction in BMR in addition to behavioural changes.85 It is debated though, whether or not the decrease in total energy expenditure is proportional to the loss of metabolic tissue and what are the possible other factors that influence weight regain.86 Reduced physical activity especially non-exercise activity and changes in thyroid hormones may explain some of it 87(see 2.4). The association between weight reduction and BMR is discussed later in the thesis (see 2.5). Master thesis in Clinical Nutrition, Anu Koivisto 2009 23 2.5 Weight reduction and thyroid hormones Thyroid hormone is the primary determinant of body’s overall metabolic rate. They control body’s basal metabolism and heat production furthermore thyroid hormones are important for growth, and development and function of the nerve system.88 They execute their effects by different mechanisms either by direct stimulation of mitochondria activity (inducing enzymes production) or via symphatetic nerve system activation (increasing responsiveness to catecholamines). About 90% of the secreted thyroid hormone is thyroxin (T4) and the rest is triidothyronine (T3), the biologically active form of thyroid hormone. First outside the thyroid gland T4 is converted to T3 which binds to thyroid receptors inside the target cells. This conversion happens by enzymatic cleavage of one of T4’s iodine molecules by deiodinase (DI 1 and 2). Thyroid hormone secretion is under strict regulation by feed-back mechanisms to both pituitary gland and hypothalamus (see figure 2.5.1). - Hypothalamus - TRH - Pituitary gland TSH TSH Thyroidea - Growth - CNS development T4 (T3) T3 D1, D2 Target T3T cells 3 - Metabolic rate (BMR) - Heat production - Sympathetic activity Figure 2.5.1. Negative feedback control of thyroid hormone secretion, their activation and their central effects in human body. Master thesis in Clinical Nutrition, Anu Koivisto 2009 24 Serum thyroid hormone concentrations seem to reflect energy status in humans89;90 Reinehr et al investigated serum T3 and T4 concentrations in obese children and adolescents before and after a weight loss and reported that T3 and T4 were increased in overweight subjects but the hormone concentrations decreased as a result of weight loss.89 Thompson et al showed that male athletes whose caloric consumption was not adequate were prone to hypothyroidism.90 Also in anorexic athletes T3 is substantially reduced due to energy deprivation and increases as a result of weight gain91. Furthermore it has been reported that plasma T3 concentrations can predict weight change in euthyroid subjects.92 During weight loss decreased serum T3 and T4 concentrations signal for a need to spare energy. Welle et al93 showed that reductions in serum T3 and T4 partly explained reductions in BMR (a mechanism for energy sparing) during weight loss. They administered T3 and T4 to obese subjects who were on a very low energy diet and that normalised their reduced BMR almost completely. But recently Araujo et al94 pointed out the negative aspect of replacing reduced T4 during weight loss. Although administering T4 restored RMR, loss of muscle protein was increased. They suggested that reduction in serum T4 concentration could be a protective mechanism to avoid body protein loss. As much as 20-25% of resting energy expenditure is thyroid-hormone dependent and even small changes in thyroid hormone levels have a significant effect on resting energy expenditure95. Al-Adsani et al showed that small increases in thyroid stimulating hormone (TSH) (0.1-1mU/l) reduce resting energy expenditure (REE) in a manner that is physiologically relevant (REE reduced by 17%) and can thus complicate weight maintenance96. Furthermore Kozlowska et al78 found out that during weight loss T3/T4 ratio decreased significantly in a stepwise manner dependent on the degree of calorie restriction reflecting energy deficiency’s effect on deiodinase activity (conversion of T4 to T3). They suggested that smaller energy deficits might be preferably in obesity treatment since larger energy deficiencies seem to affect negatively the deiodination of T4 thus less biologically active T3 is available. There exists some evidence that reduced T4 during energy restriction might have a muscle protein sparing function.94 Low replacement dose of T4 restored deiodinase Master thesis in Clinical Nutrition, Anu Koivisto 2009 25 activity and RMR in rats during calorie restriction but increased body protein loss. This illustrates that decline in T4 during energy deprivation is an important survival mechanism since body proteins due to their structural and functional role are the last resort to meet other energy needs. 2.6 Weight reduction and basal metabolic rate Basal metabolic rate (BMR) is the energy expended by cells to maintain normal body functions at rest. BMR stands for approximately 60-70% of total daily energy expenditure. Other components of the total energy expenditure are diet induced thermogenesis (also called thermic effect of food) and activity thermogenesis, both non-exercise and exercise energy expenditure (figure 1.6.1). Per date following factors are considered to have an impact on BMR: age, gender, height, growth, genetics, LBM, disease (fever), diet (over/underfeeding), environmental temperature, altitude, stress hormones, pre menstrual hormone profile and thyroid hormones.97-99 There is evidence that weight loss induced with calorie restriction leads to reduced BMR.86 Maintenance of new body weight is complicated by reduced energy expenditure which favours weight regain.100;101 Reduced BMR as a result of weight reduction has been proposed as one of the main factors for poor long term weight maintenance. Some studies102;103, but not all63;104, have reported larger BMR losses than predicted from changes in LBM. Suggesting that 1) there must be other important factors affecting changes in BMR during acute weight reduction 2) there is great inter-individual variability in metabolic reactions to energy restriction. Several studies have reported that weight loss induced reduction in energy expenditure persists long after the actual weight loss when the new body weight is maintained, a sort of metabolic adaptation occurs.105;106 Whereas other studies have shown that reduced energy expenditure is a transient response to low energy availability and is normalised simultaneously with stabilization of body weight.107 The reduced energy expenditure after weight loss seems to result from reduced sleeping metabolic rate, reduced plasma concentration of thyroid hormones, hypoleptinemia, reduced spontaneous activity and increased skeletal muscle work-efficiency.105 Rosenbaum et Master thesis in Clinical Nutrition, Anu Koivisto 2009 26 al showed that increased exercise efficiency is not due simply to moving a lower mass during exercise after weight loss. In their study 10% weight loss resulted in significant reductions in RMR, FFM, FM and DIT whereas the cost of low-level skeletal muscle work was reduced, measured with graded cycle ergometry and muscle ATP flux. There exists no similar data of athletes. But Melby et al108 reported that RMR does not differ between weight cycling athletes and non weight cycling athletes when the athletes are at their natural (off-season) body weight, even though BMR is lower after weight loss prior to tournaments. Athletes’ physical activity during weight reduction remains usually unchanged since they follow a strict training regimen, but theoretically, as observed in overweight/obese subjects, the amount of energy used for non exercise activity may be reduced. Furthermore reduced body weight itself reduces the cost of weight bearing activities. Also reduced food intake itself results in lower thermic effect of the food and lower total energy expenditure. Physical activity Thermic effect of food Exercise BM R 30 % Age Non-exercise avtivity thermogenesis (NEAT) Spntneous physical ativity (SPA) Gender LBM Hormones Diet, etc CHO 5-10% 60 % Fat 0-5% Protein 15-20% 10 % Figure 2.6.1. Components of total energy expenditure (basal metabolic rate, physical activity and thermic effect of food) and the main factors affecting them modified from Manore et al.109 Several studies have shown that subjects exposed to weight gain have relatively low BMR and high respiratory quotient (RQ) i.e. a low fat to carbohydrate oxidation rate.85;110 Other factors shown to predict weight gain in non-athletes are low plasma Master thesis in Clinical Nutrition, Anu Koivisto 2009 27 leptin, low physical activity and low insulin sensitivity.111 It appears that weight loss regimen with very low calorie diet especially when no programme for physical activity is included leads to larger BMR reductions.9 Taken all this together attenuating the decline in BMR under weight reduction is desirable for successful weight maintenance. And the mechanisms for maintaining BMR under these circumstances need further studying. 2.7 Potential adverse effects of weight reduction There are potential metabolic, physical and mental adverse effects with energy restriction and weight regulation. Metabolically reduced carbohydrate intake and depletion of glycogen stores during weight loss may lead to increased cortisol release during strenuous exercise.47 This can lead to loss of LBM as often seen during weight loss and thus contribute to reduced metabolic rate. It can also compromise immune system by inhibiting the innate immune system.112 Athletes undergoing weight reduction are recognised as being more prone to infection. Kowatari et al showed that neutrophil function was reduced following a 20-day weight reduction in judoists.6 Also Imai et al showed impaired immune function as a result of 4% body weight loss.113 Inadequate protein and micronutrient intake as well will affect the immune system negatively47 pointing out the importance of well planned, balanced weight loss diet. Dehydration as a weight loss method commonly used in weight class sports leads to plasma volume loss, reduces the body’s ability to produce sweat and increases susceptibility to heat illness.10 Dehydration may have severe outcomes as demonstrated by the deaths of three American collegiate wrestlers in 1998 who had used extreme dehydration methods for making weight prior to competition.16 Cognitive function in dieting athletes has been assessed by Choma et al.8 A reduced short-term memory and transient mood reduction was observed as a result of rapid weight loss in 14 collegiate wrestlers. Also Horswill et al reported changes in mood in athletes during a 4-day weight loss. Energy restriction regardless of diet resulted in elevated tension, anger, depression and fatigue measured with the profile of mood Master thesis in Clinical Nutrition, Anu Koivisto 2009 28 states (POMS)26. Filaire et al reported similar findings during a 7-day weight loss in judoists.48 Energy restriction has an impact on bone mineral density as it decreases bone formation.114 Energy deficiency’s effect on BMD has been studied in female athletes with menstrual disturbances (the female athlete triad).115;116 Energy deficiency and following hypo estrogenism is associated with suppressed bone formation and increased bone repression and thus bone mass loss. Recent review by Voskowi et al concluded that the most successful and indeed essential strategy for improving BMD in females with amenorrhea is to increase caloric intake such that body mass is increased and there is a resumption of menses. This is important to keep in mind when working with young athletes since BMD reaches its peak at the age of 20-30.117;118 Adequate amounts of micronutrients important for bone mass (calcium, vitamin D and K) need to be included in weight reduction diets for athletes. Increased focus on body composition and body weight might theoretically increase the prevalence of disordered eating (DE).119 DE is not uncommon in sports where body weight control is considered important. Prevalence of eating disorders(DE) in female elite athletes in leanness sports has been reported to be 46.7% respectively.120 Sundgot-Borgen et al suggested that dieting and frequent weight cycling are important risk factors for the development of eating disorders in athletes.121 Screening for ED or potential disordered eating is an important part of evaluating whether an athlete should be allowed to undergo a weight reduction. Furthermore weight loss may lead to impaired performance in athletes10 either due to reduced strength and sprint abilities,21;26;122 dehydration or LBM loss or impairment of cognitive function as discussed earlier. Roemmich et al showed in a prospective study of wrestlers that body weight, FM and strength decreased during the competitive season. Long-tem adverse effects of weight reduction are not well established, but Saarni et al123 showed that athletes with repeated weight gains and reductions defined as weight Master thesis in Clinical Nutrition, Anu Koivisto 2009 29 cyclers had significantly higher BMI increase from their twenties until reached middle age than their controls. The amount of obese subjects was significantly higher among the weight cyclers, thus past weight cycling had made them more prone for obesity. To avoid these potential adverse effects athletes and coaches need clear guidelines about the optimal weight loss methods. It should be emphasized also that thorough medical and psychological screening of the athlete is required prior to weight reduction. 2.8 Weight reduction rate There exist no studies comparing the effects of two different weight reduction rates on body composition, thyroid hormones or BMR. Some studies have compared small versus large weight reduction or rapid versus slow weight reduction and looked at body composition, performance, immunological and psychological parameters in addition to metabolic changes (see summary of weight loss studies with athletes in appendix 1). Only a few studies have included a dietary intervention for the weight loss, most of the studies are observational studies where weight class athletes have used their own weight loss methods. In most studies dietary composition and the energy content of the diets has been analysed after the study has been conducted. The small number of studies might be due to the difficulty in reaching a specific weight reduction rate because of the large inter-individual variation in response to calorie restriction and following problems in compliance, and secondly because of the invasive nature of such a study. Undoubtedly, information about weight reduction’s effects for athletes’ body composition and metabolism is important for fine-tuning the weight loss recommendations for this special population. 2.9 Aim of the study The aim of the study was to determine whether weight reduction at the extremes of the current recommendations for athletes (0.7%BW/week versus 1.4%BW/week) (SLOW Master thesis in Clinical Nutrition, Anu Koivisto 2009 30 versus FAST) affects body composition, thyroid hormones and BMR differently. We hypothesized following: 1. FAST weight reduction results in greater loss of LBM than SLOW weight reduction. 2. FAST weight reduction results in larger decline in thyroid hormones than SLOW weight reduction. 3. And thus FAST weight reduction results in larger BMR reduction than SLOW weight reduction. 4. We expect to find an association between changes in body composition, thyroid hormones and BMR. Master thesis in Clinical Nutrition, Anu Koivisto 2009 31 3. Subjects and methods 3.1 Subjects Thirty-six well trained Norwegian females (n=20) and males (n=17), junior and senior athletes aged 17-28 years were included in this study. All the athletes were national team members or students at the Norwegian elite athlete college (Norges Toppidrettsgymnas, Wang Toppidrettsgymnas). The following types of sports were represented in this study: technical, endurance, aesthetic, weight-class, ball game, power and anti-gravitation. The athletes obtained information about the study either from their sport federations where information bullets and invitation letters were sent to or when they contacted the department of sports nutrition at the Norwegian Olympic Sport Centre in order to get assistance in body weight regulation (appendix 4 and 5). 3.1.1 Inclusion and exclusion criteria Inclusion and exclusion criteria for the subjects in this study are shown in table 3.1.1. Master thesis in Clinical Nutrition, Anu Koivisto 2009 32 Table 3.1.1 Inclusion and exclusion criteria. Inclusion criteria 1) Member or recruit of the national team in any Norwegian Sports Federations (NIF) sports associations and/or a student at Norwegian sports college (NTG, Wang). 2) A wish to reduce body weight by at least 4%. 3) Body fat% no lower than 12% for females and 5% for males after accomplished intervention.1 4) Age 18-35 years 5) No serious illness or injury that compromise training- or dietary regimen. Exclusion criteria 1) Diagnosed with one or more triad components2 2) Disorders of metabolism (hyper- or hypothyroidism) 3) Medical examination contraindicating weight reduction. 4) Illness or injury that compromises training regimen. 5) Absence from training for more than a week. 6) Use of creatine during the last 6 weeks. 1 Calculated beforehand from baseline body fat% assuming only FM will be lost. Athlete triad components: eating disorder (anorexia nervosa, bulimia nervosa, eating disorder not otherwise specified), amenorrhea and/or low bone mineral density. 2 3.2 Procedure The study included in this thesis is part of a larger research project in cooperation with Norwegian Olympic Sports Centre and Norwegian School of Sports Sciences. Subjects participating in this study were insured by the Norwegian insurance policy. Participation in the study was voluntarily and the subjects could terminate the study at any moment without a reason. All subjects provided written informed consent before participation. Blood samples from the study are being stored in a bio bank for 10 years until destruction. This biological material and other confidential information was deleted if subjects who withdrew from the study required it. The study protocol was approved by the Regional Ethics Committee of Norway (appendix 2) and the Data Inspectorate (appendix 3). Master thesis in Clinical Nutrition, Anu Koivisto 2009 33 3.3 Design 3.3.1 Recruitment Athletes who contacted the department of sports nutrition at Norwegian Olympic Sports Centre (Olympiatoppen) or Norwegian School of Sports Sciences in order to get assistance in body weight reduction got verbal and written information about the research project (appendix 5). The same information was sent to several sports federations as to recruit subjects (appendix 4). Next the athletes who wished to participate were invited to a personal consultation where they were provided detailed information about the project in person. After this consultation the athletes were directed to a physician for a general medical examination. Their weight reduction goals were evaluated towards their health, medical history, age, body composition and athletic career goals. The athletes were also controlled for possible history and/or signs of eating disorders by means of an initial questionnaire including the eating Disorder Inventory (EDI)124 followed by a clinical interview. This interview was conducted by a sports scientist, specialized in eating disorders. The screening included mental and physical status, questions regarding menstrual history, oral contraceptive use and pregnancy, weight history, training history and present training volume, dietary history, possible eating disorders (ED), as well as illness and injury history (appendix 6). 3.3.2 Randomization The athletes who full filled the inclusion criteria were block randomized to either weight reduction group with slow weight reduction rate SLOW (weekly reduction of 0.7% of body weight) or to a weight reduction group with FAST weight reduction rate (weekly reduction of 1.4% of body weight). Master thesis in Clinical Nutrition, Anu Koivisto 2009 34 Included n=36 Randomization BMR, n=8 Intervention Intervention SLOW n=16 FAST n=20 4 drop-outs 2 drop-outs (12.5%) BMR data BMR, n=10 Accomplished Accomplished intervention n=14 intervention n= 16 compliance 88 % compliance 80 % (20%) n=6 BMR data n= 10 BMR = basal metabolic rate Figure 3.3.2. Flow chart of the study. SLOW weight reduction equals 0.7% of body weight/week and FAST weight reduction equals 1.4% of body weight/week. 3.3.3 Intervention Every athlete got an individual dietary plan that they were encouraged to follow in detail. In addition specially designed resistance training program for the intervention was handed out. The duration of the intervention period depended on the athlete’s weight reduction goal and the weight reduction rate. An athlete with bodyweight of 70kg set to reduce 5kg of his body weight would have either a 5-(FAST) or 10(SLOW) week intervention depending on which intervention group he would randomly be allocated to. During the intervention every subject had weekly follow-up consultations with the dietician and personal trainer where body weight, body composition, subjective experience of hunger; general well-being and athletic performance were registered. Eventual adjustments in the dietary plan or weight training regimen were evaluated and discussed. Athletes were informed at the first meeting that if they would have any need for medical or physical therapy during the Master thesis in Clinical Nutrition, Anu Koivisto 2009 35 intervention this would be provided by the medical staff at the Olympic Sports Centre. The day before the intervention start and on the day finishing the intervention subjects underwent the following tests. 1) Measuring the basal metabolic rate (BMR) with indirect calorimeter at 7am. The subjects spent the night at the Olympic Sports Centre hotel and were awakened carefully in the morning. The subjects were lying in their beds relaxed but awake. They were encouraged to avoid any large muscular movements during the gas sampling. 2) Fasting blood samples for analysis of thyroid stimulating hormone (TSH) and free thyroxin (f-T4) were collected at 8am. 3) Body composition with DEXA (Dual energy X-ray absorptiometry) was measured at 9am. The subjects were fasting prior to DEXA measurements. 4) Physical tests were conducted at 11am after the athletes had eaten a standardized breakfast. Athletes were encouraged to participate in the study long before the start of their competitive season to minimize the interference of the intervention with their competition schedule. Master thesis in Clinical Nutrition, Anu Koivisto 2009 36 Table 3.3.3. Timeline of the study. -1 week 0 week Pre intervention Pretest Inclusion BMR Weekly follow-up with dietitian BMR Randomization Blood samples and personal trainer Blood Standard medical DEXA monitoring weight, fat% and general samples examination Physical tests well being DEXA Screening for eating Handing out Eventual adjustments to the Physical disorders intervention diet intervention diet tests Intervention 4-12 weeks Post test Getting accustomized with Psychological strenght training program screening 4-day weighed dietary registration Dietary intervention In order to meet the desired weight reduction rate the diet plan for each athlete was energy restricted but at the same time as optimal as possible for both athletic performance and good health. The main focus in the dietary plan in general was to obtain high nutrient density. The plan was designed to provide enough protein and as much as possible carbohydrates while fat intake and total energy intake was reduced. The diet was designed to provide satiety, have variety and reduced amount of energy while still securing sufficient intake of micronutrients and essential fatty acids. The dietary plan was tailored to meet every athlete’s specific needs. An example of a meal plan is attached (appendix 9). Energy For SLOW group the energy intake was reduced to promote 0.7 % body weight (BW) reduction per week. The reduction rate for FAST group was 1.4 % BW per week. The energy content of the dietary plans was calculated knowing that 1 g of mixed tissue gives 29 kJ, and therefore reducing body weight by 1 g demands 29kJ negative energy balance. For example an athlete in SLOW group weighing 60 kg got a plan with reduced energy intake by 1740 kJ [(60000 g x 0.7%) / (7days x 29 kJ) = 1740 kJ/day] Master thesis in Clinical Nutrition, Anu Koivisto 2009 37 and would obtain a 420g-weight reduction per week. The lowest allowed energy intake per day in the dietary plans was set to 6300 kJ. Athletes with the energy intakes below 6700 kJ/day who struggled to meet their weight reduction rate were encouraged to jog 2-3x20 min/week in order to increase their energy expenditure. Macronutrients In addition to energy intake the macronutrient intake was carefully planned providing at least 1.2g protein/kg BW and as close to 5g carbohydrate/kg BW as possible while still providing the minimum of 20E% from fat. Micronutrients and supplements Also micronutrient and fibre intake was to meet the dietary recommendations for the age group. But a multi-vitamin-mineral supplement (Nycomed, Norwa) was prescribed to secure the micronutrient intake when energy intake was very low (< 6700kJ). Since the fat intake was relatively low every athlete was told to take cod liver oil (Møller’s cod liver oil, Norway) daily either as 2 capsules or 5ml liquid supplement to provide omega 3 supplements and A, D and E vitamins. Furthermore if the blood samples or DEXA measurements indicated any other specific micronutrient needs (iron, calcium) these vitamins were provided to the athletes and biochemical changes were monitored. Meal pattern A very important aspect in the dietary plan was meal pattern. The athletes were recommended to eat every 3rd hour and have 5-7 meals depending on how many daily work-outs they had. They ingested an recovery meal containing carbohydrates (26-35 g) and protein of high biological value (5-10 g) immediately after every work-out and were exhorted to eat a balanced meal within 2 hours to obtain the recommended amount of protein (6-12 g essential amino acids) and carbohydrate 1g/kg BW to promote post exercise recovery.28 As the athletes began to follow the dietary plan they were encouraged to use a kitchen scale to ensure correct portion sizes. Fluids and snacks They were persuaded to drink minimum 0.5L/hour of fluids during the work-outs and 2 litres of fluids otherwise during the day. Intake of low calorie beverages (non Master thesis in Clinical Nutrition, Anu Koivisto 2009 38 sugared tea, light soft drinks, artificially sweetened fluids) were not restricted but consumption was registered to avoid high (>1.5L) intakes. Artificially sweetened chewing gum and candy intake was not limited either though athletes were warned about the laxative effect of those products at high doses. If the athletes were unable to follow the dietary plan they were instructed to write down every deviation from the meal plan. The subjects had a possibility to snack vegetables in the evenings if they wished to. Resistance training intervention Participants performed strength training four days per week. The strength training program was designed to stimulate muscular hypertrophy and increase lean body mass (LBM) and power under the weight reduction period. The program was designed by an experienced strength training coach at the Norwegian Olympic Sports Centre (appendix 8). Before the intervention started, all athletes got an appointment with their personal trainer to go through the strength training program and the test exercises. The training program was periodized and added to subjects’ existing training regimen only replacing eventual strength training work-outs in their regular training regimen. One of the four weekly work-outs had to be carried out at the Norwegian Olympic Sports Centre under the supervision of a personal trainer working with the project. This weekly control had an injury preventive purpose. It also provided an opportunity to follow athletes’ progress closely and encourage them to follow the work-out plan. The strength training program was adjusted for participants with shorter than 8-week intervention so that they could complete the planned progression in the training program. 3.4 Measurements 3.4.1 Dietary registration During the last two weeks prior to intervention the athletes conducted a 4-day weighed dietary registration, where 3 of the 4 consecutive days were weekdays and one of them was either a Saturday or Sunday. Athletes received registration schemes (appendix 7), Master thesis in Clinical Nutrition, Anu Koivisto 2009 39 kitchen scales (Philips Essence HR-2393) with accuracy of 1g and thorough instructions from the dietician for conducting the registration as precisely as possible (attachment 4). Athletes were guided to continue with their regular eating and training habits during the whole registration period. They were told to weigh and write down everything they ate and drank including information about the brands and types of the food items consumed and the time of consumption. Athletes were also advised to write down recipes for mixed dishes they prepared themselves or knew the type and amount of the ingredients in. The kitchen scales had a reset function which made registration of mixed meals easier. If athletes dined in restaurants or cafeterias where they didn’t want to use the kitchen scale they were told to estimate the amount of foods with regular household devices. Athletes were encouraged to avoid travelling during the registration period to minimise consumption of dishes and food items with unknown nutritional content. Intakes of any supplements that could contain illegal substances or were in conflict with the guidelines provided by the nutrition department of the Norwegian Olympic Sports Centre were forbidden. 3.4.2 Diet analysis The dietary registrations were analysed with a computer program Mat på Data version 5.0.125 Mat på data is based on the Norwegian food composition table where the energy and nutrient content of food items and prepared food dishes are presented 126. All tabular values refer to content per 100g edible food i.e. without skin, shell, bone, peel, core or other parts which are not normally eaten. The protein content in the food composition table is calculated on the basis of the analysed content of nitrogen. The software gives also the amount of total fat and fatty acids (saturated, trans unsaturated, cis unsaturated and cis polyunsaturated) and cholesterol. Carbohydrates are divided into following subgroups; fibre, total carbohydrate, starch, mono- and disaccharides and added sugar. In our analysis we looked only at total carbohydrate and protein intake in grams and how much these macronutrients in addition to fat contributed to total energy intake. Based on the analysis of the dietary registration the same dietician then designed an individual dietary plan for each athlete. Body weight changes were Master thesis in Clinical Nutrition, Anu Koivisto 2009 40 controlled weekly during intervention and when weight reduction rate was not reached the individual dietary plan was adjusted. 3.4.3 Body composition Body composition measurements were done by dual energy x-ray absorptiometry (DEXA) (GE Medical Systems, Lunar). DEXA was used for measuring body composition before and after the intervention period. Harpenden caliper (Baty International) was implicated weekly as a part of the follow-up monitoring body composition changes during weight reduction, but caliper data is not shown in this thesis. During the weekly follow-up also body weight was registered. For that purpose athletes used their own regular scales at home. They were instructed to weigh themselves with empty bladder right after waking-up and before eating breakfast. Dual energy X-ray absorptiometry (DEXA) The amount of lean body mass (LBM) and fat mass (FM) as well as bone mineral density (BMD) and fat percentage were measured with DEXA (GE Medical Systems, Lunar) at the Volvat medical centre in Oslo. The DEXA machine sends a thin, invisible beam of low dose x-rays with two distinct energy peaks through the body parts being examined. One peak is absorbed mainly by the soft tissue and the other by bone. This makes it possible to distinguish between the different tissue types. During the measurement the patient is laying on his back with arms on the sides and palms facing down. Legs and feet are loosely strapped together and toes are pointing upward. The patient is directed to avoid any movement to minimize the motion artefacts. The x-ray source is mounted under the bench and the detector is placed above the bench. As the whole body scan takes only 20-30 minutes and the radiation dose is very low 15µSv (which is equivalent with 10 chest x-rays) DEXA scan is a very lucrative method for precise body composition measurements127. To obtain an accurate measurement the personnel at the Volvat medical centre calibrate the DEXA system daily. This method has been validated several times128;129;129-131. DEXA Lunar Prodigy Total body scan has a coefficient of variation (CV) of ~1% for bone mineral density (BMD) and ~1 % for total body, and up to 7% for regional measures132. Estimates of body fat with Master thesis in Clinical Nutrition, Anu Koivisto 2009 41 DEXA are within 1-3% from multi component analysis 133 dependent on the type of scanner. Thus for regional measures the margin of error is somewhat larger but in this study we looked only at total FM, LBM and BMD. Weyers et al134 and Gong et al135 have reported that DEXA is a sensitive method for measuring changes in body composition also during weight reduction. Figure 3.4.3. Dual energy x-ray absorptiometry (DEXA). 3.4.4 Thyroid hormones Subjects had been fasting at least 8 hours before the blood was sampled. The blood was collected by an experienced nurse at the Olympic sports Centre from peripheral vein into an EDTA treated glass. The samples were placed in room temperature for 20 minutes and thereafter centrifuged for 10 minutes at 30000 rpm. The samples were stored in +4°C until they were analyzed later the same day at Fürst medical laboratory in Oslo. Free thyroxin (FT4) and thyroid stimulating hormone (TSH) were analyzed by Chemiluminescent Microparticle Immunoassay (CMIA). In principle the sample is added an antibody for the hormone under detection, thereafter the sample is washed, labelled with acridinium and added Trigger solution. Finally the resulting chemiluminescent reaction is detected and measured in relative light units with an optical system (Architect, Abbott, Ireland). Master thesis in Clinical Nutrition, Anu Koivisto 2009 42 3.4.5 Indirect calorimetry For measuring basal metabolic rate we used Douglas bag. Douglas bag technique is highly operator dependent and under optimal conditions the margin of error is small <3%.128 It is an indirect calorimetry method that is used for examining energy expenditure and substrate oxidation in humans. It is an open-circuit calorimeter where the system’s both ends are open for atmospheric pressure and where the subject’s inhaled and exhales air is kept separate by means of a three-way respiratory valve. The expired gasses are collected to an air tight Douglas bag for analysis. When gas collections were made the subjects had been fasting for 12 hours and had restrained from hard physical activity 24 hours before. During the measurements the subjects were lying relaxed in the bed in a silent, dark and temperate environment (22-24°C) with the mouth piece correctly placed and a nose clip to avoid respiration through the nose. The pulse was monitored throughout the night and during gas collection with a pulse watch (Polar, RS400) as to see if subjects’ heart rate increased due to the procedure. The gas collection lasted 20-30 min and the gasses were collected in 2 separate bags with maximum volume of 100 litres. The collected gas volume (Flow turbine type K202, KL Engineering Madison, WI, USA) and gas concentration (oxygen analyser type S-3A; carbon dioxide analyser type CD-3A, Amatek Corporate, Paoli, PA, USA) of the bags were analysed within 15min after collection. The gas analysers were calibrated against certiWed gasses of known concentration prior to each test and the ventilation sensors were calibrated frequently with a 3l-syringe. The following formula was applied to calculate the daily basal metabolic rate (BMR) from the data obtained from gas analysis: VO2 (l) x [(1.1 x RQ1) + 3.9].136 The ratio between the gasses (respiratory quotient, RQ) tells which substrates (carbohydrate, fat, protein) the body is oxidising. Some equations require collection of diurnal urine for establishing nitrogen balance and estimating protein turnover in addition to BMR. We used Weir’s equation that doesn’t require urine collection to minimize the stress for subjects. Master thesis in Clinical Nutrition, Anu Koivisto 2009 43 Cunningham equation was also applied to estimate resting metabolic rate (RMR) in every subject [RMR = 500 + 22 (LBM)]137. Cunningham equation is based on LBM and is considered to be the best equation in predicting RMR values in athletes.138 3.5 Statistical analysis For all statistical analysis SPSS version 14.0 (SPSS Inc., Chicago, IL, USA) was applied. Distribution of data was analysed with Kolmogorov- Smirnov and ShapiroWilk tests. The changes in body weight, LBM, FM, fat%, TSH, f-T4 and BMR within the groups from baseline were analysed with paired samples t-test (for variables with normal distribution) or Wilcoxon ranked sign test (for variables that were not normally distributed). Whether the changes resulting from the interventions were statistically different between the groups was analysed by independent samples t-test or Mann Whitney’s test for nonparametric data. Correlation analysis was conducted either with Spearman (non parametric correlation) or Pearson’s method. To evaluate the linear relationship between two variables simple linear regression analysis were performed. For analysis of frequency tables Chi squared distribution was used. The significance level was set to p< 0.05 and all the tests were analysed two-sided. Trend is defined as p< 0.1. 3.5.1 Sample size estimation The sample size was estimated using Altman’s nomogram 139. The power of the study was set to 80% (1-ß=80) and the two-sided significance level to 0.05 (α=0.05). Standardised difference was calculated for f-T4 which was expected to require the greatest number of subjects. Clinically relevant difference (δ) for %change for f-T4 was set to 5% and standard deviation was estimated to be 8.5%. Standardised difference was calculated by the following formulae for paired data: 2δ/s= 1.18 and for two independent samples analysis δ/s=0.6. This equals a sample size of 23 and 85 subjects respectively. In our study due to ethical and economic reasons in addition to time pressure sample size was set to 30 subjects. This gives an appropriate power of Master thesis in Clinical Nutrition, Anu Koivisto 2009 44 the study for paired analysis but for the in between group comparisons the power is somewhat reduced. 3.5.2 Missing data In FAST weight reduction group one subject’s pre intervention blood sample analysis was lacking data of TSH and free T4. This missing data was replaced with the group mean of successfully analysed blood samples for TSH and free T4. Master thesis in Clinical Nutrition, Anu Koivisto 2009 45 4. Results 4.1 Subjects Anthropometric and biochemical data was collected from 30 subjects. Indirect calorimeter data was obtained only from 16 athletes due to late onset of data collection and time pressure. On average intervention lasted 9 weeks for subjects in the SLOW weight reduction group and 6 weeks for subjects in the FAST weight reduction group. Between intervention groups gender was equally spread, though fewer males than females accomplished the intervention, n=11 and n=19 respectively. The drop-out rates are presented in figure 1 on page 32. Reasons for withdrawal were as follows: lack of time (n=3), weight training program was not individualized enough (n=1) or retirement from sport (n=1). One athlete was excluded from the study because of suspected risk for developing an eating disorder. There were no statistically significant differences between the groups in any investigated variable at the baseline (table 4.1). Distribution of subjects with past weight reduction attempts were also similar between the groups, 57% and 50% for intervention SLOW and FAST respectively. Every subject self-reported being weight stable the last month prior to intervention. Table 4.1. Characteristics of the subjects at baseline presented as mean (SD). Gender, Age, yrs Height, cm Weight, kg LBM, kg FM, kg Fat% BMR, kJ 1 TSH, mU/L Hours of training/week, h Strenght training/week, h2 Strenght training history, yrs SLOW (n=14) Mean (SD) females n=8, males n=6 23.5 (3.3) 173 (10) 72.1 (12.2) 52.9 (11.2) 16.4 (6.0) 23.8 (8) FAST (n=16) Mean (SD) females n=10, males n=6 22.3 (4.7) 171 (8) 72.2 (11.3) 51.8 (10.9) 17.4 (5.8) 25.3 (7.9) 6807 (1053) 2.35 (0.7) 14.1 (4) 7112 (1156) 2.28 (1.4) 15 (3.2) 2.6 (1.6) 6.9 (4.1) 2.4 (1.5) 4.8 (4.3) 1 n=6(SLOW), n=10(FAST) 2 Average of the last year Master thesis in Clinical Nutrition, Anu Koivisto 2009 46 4.2 Diet The average energy intake was reduced from 9708 kJ to 7999 kJ in the SLOW weight reduction group and from 9788kJ to 7018 kJ in the FAST weight reduction group. The percentage change in energy intake was significantly greater for the FAST (p=0.02) than for the SLOW weight reduction group as planned. The intervention diet was not statistically different between the groups in any other parameter than energy intake. The energy and macronutrient content in gram per kg body weight of the 4 day weighed registration and intervention diets for the SLOW and the FAST weight reduction groups are presented in table 4.2, and the composition of the diets is shown in figure 4.3. Table 4.2. Energy, carbohydrate (CHO) and protein (PRO) intake. 4-d weighed Intervention registration Diet median (95% CI) median Energy, MJ SLOW1 9.7 (7.4 , 12.6) 8.0 FAST2 9.8 (8.1 , 11.5) 7.0 CHO, g/kg BW SLOW 3.9 (2.8 , 5.2) 3.5 FAST 4.0 (3.2 , 4.5) 3.2 PRO, g/kg BW SLOW 1.4 (1.1 , 1.7) 1.6 FAST 1.5 (1.0 , 1.7) 1.4 * Difference between 4-d weighed registration and intervention diet ** Between groups comparison, p <0.05 1 n=14 2 n=16 Nutrient 60 % Group p-value* 0.004 0.001 0.053 <0.001 0.025 0.297 56 % 60 % 54 % 51 % % Change median (95%CI) ** -20 % (-3 , -32) -31 %** (-21 , -37) -9 % (-21 , 11) -22 % (-28 , -3) 15 % (-7 , 33) -9 % (-22 , 20) (95% CI) (6.6 , 10.5) (6.4 , 7.4) (2.9 , 4.5) (2.6 , 3.6) (1.2 , 1.9 (1.2 , 1.5) 50 % 50 % 50 % 40 % 40 % 30 % 30 % 25 %25 % 21 % Dietary registration Intervention diet 31 % 30 % 20 % 20 % 20 % 10 % 10 % 0% 24 % 24 % 0% E%CHO E% PRO E%FAT E%CHO E% PRO Figure 4.3 Macronutrient composition of the 4-day dietary registrations and intervention diets. Master thesis in Clinical Nutrition, Anu Koivisto 2009 E%FAT 47 4.3 Body composition 4.3.1 Body weight Both interventions resulted in significant weight reductions, on average -5.6 (3.0) % mean (SD) p<0.01 and -5.4 (2.3) % p<0.001 for SLOW and FAST respectively (figure 4.3.1). In accordance with the aim of the study the average weekly weight reduction rate for the intervention groups were significantly different [0.7 % for SLOW and 1.0 % for FAST, (p= 0.02)], while the total amount of weight loss was not statistically different between groups (p= 0.661). 4 * 2 kg 0 -2 SLOW -4 FAST -6 -8 -10 * * Change in BW * C hange in LBM * Change in FM Figure 2.3.1. Changes (kg) mean (SD), in body weight, lean body mass (LBM) and fat mass (FM) for SLOW and FAST weight reduction groups presented as mean (SD). *Significant change from baseline, p<0.05. 4.3.2 Fat mass and body fat percent The body weight lost during the interventions was mostly fat tissue. The fat mass (FM) reduction was significant in both groups (table 4.3.2). The SLOW weight reduction group reduced FM by 31 (2.9) % mean (SD), p<0.001 and the FAST weight reduction group by 23 (13.8) %, p<0.001 respectively. The difference in the %FM lost between the groups was significant (p=0.043). Body fat percentage decreased by 6.2 (2.5) %, p<0.001 and 4.5 (2.6) %, p<0.001 for SLOW and FAST weight reduction groups respectively. There was a trend for difference between the groups (p=0.08) for body fat% change. Percentage change in body weight correlated with % change in FM and fat%. Master thesis in Clinical Nutrition, Anu Koivisto 2009 48 Table 4.3.2. Body composition pre and post intervention in SLOW and FAST weight reduction groups presented as mean (SD). Group SLOW N Weight, kg 14 Pre 72.1 (12.2) Post 68.0 (11.0)* FAST 16 Pre 72.2 (11.3) Post 68.3 (10.3)* *Significantly different from baseline p-value <0,001 LBM, kg 52.9 (11.2) 53.9 (11.2)* 51.8 (10.9) 52.2 (9.9) FM, kg 16.4 (6.0) 11.3 (4.4)* 17.4 (5.8) 13.7 (5.9)* Body fat % 23.8 (8.0) 17.6 (7.1)* 25.3 (7.9) 20.8 (8.1)* 4.3.3 Lean body mass The weight reduction interventions in this study did not result in lean body mass (LBM) losses (table 4.3.2). The SLOW weight reduction group had a significant increase in LBM [2.0 (1.3) % mean (SD), p < 0.001] during weight reduction, while the FAST intervention did not result in any significant changes in LBM [1.1 (3.0) %, p=0.3] from baseline. LBM changes did not differ significantly between the interventions. But when LBM changes were analysed by gender, males in the SLOW weight reduction had a significantly greater increase in LBM [1.8 (1.0) %, p=0.003] compared with the FAST weight loss [-2.0 (2.2) %, p=0.115], (p=0.004). Females in both SLOW and FAST weight reduction had significant increases in LBM (figure 4.3.3). But the changes between the groups did not differ significantly (p=0.7). Females obtained a larger %LBM gain than males (p=0.008) regardless of intervention. 3 Change in LBM, kg 2 * * * 1 0 SLOW -1 FAST -2 -3 -4 Males Females Figure 4.3.3.Change in LBM [mean(SD)] by gender in SLOW and FAST weight reduction. *Change from baseline, p<0.05 Master thesis in Clinical Nutrition, Anu Koivisto 2009 49 There was an inverse relationship between relative change in LBM and baseline LBM (r2=0.24, 95% CI (-0.002, 0.00), p=0.006) (figure 3.3.4.). There was also an association between subjects’ weight, but not FM, at the baseline and percentage change in LBM (r=0.431, p=0.018). 80.0 SLOW FAST LBM at baseline, kg 70.0 60.0 50.0 40.0 R Sq Linear = 0.24 -5.0 -2.5 0.0 2.5 5.0 7.5 % change in LBM Figure 3.3.4. Relationship between baseline LBM and %change in LBM with 95% CI for mean. Weekly weight reduction rate was not correlated with any body composition parameter. But there was a significant correlation between time in intervention and changes in LBM (r=0.4, p=0.045). 4.3.4 Bone mineral density (BMD) There were no statistical differences in BMD at the baseline between the groups. BMD did not change significantly for either SLOW (p= 0.657) or FAST (p=0.375) weight reduction group. Master thesis in Clinical Nutrition, Anu Koivisto 2009 50 4.4 Thyroid hormones SLOW weight reduction did not affect free T4 whereas FAST weight reduction resulted in a significant reduction of free T4 (figure 4.4), this change was significantly different between the intervention groups (p<0.001). No significant change in TSH was detected in SLOW or FAST weight reduction group (table 4.4). 60 40 Change (%) 20 0 -20 SLO W FAST * -40 -60 -80 -100 f-T4 TSH Figure 4.4. Percentage change in free T4 and TSH [median (SD)] in SLOW and FAST weight reduction group. * Change from baseline, p<0.001 Table 4.4. TSH and free T4 at the baseline and after intervention in SLOW and FAST weight reduction groups. Group SLOW Thyroid hormones TSH, mU/L Pre 2.3 (1.7 , 3.2) 12.9 (11.6 , 14.2) 2.1 (1.3 , 2.9) 12.9 (11.6 , 15.7) Median 95% CI free T4, pmol/L Median 95% CI FAST TSH, mU/L Median 95% CI free T4, pmol/L Median 95% CI *Change from baseline, p-value< 0.05 †Comparison of changes between the groups p-value<0.001 1 Fürst medical laboratorium, Oslo, Norway Master thesis in Clinical Nutrition, Anu Koivisto 2009 Post 2.3 (1.4 , 2.7) 12.9 (11.5 , 15.1) 1.9 (1.0 , 2.2) 11.6 *† (9.6 , 13.6) Reference value1 0.2 - 4.0 9.0 – 22.0 0.2 - 4.0 9.0 – 22.0 51 4.5 Basal metabolic rate Basal metabolic rate (BMR) was measured from 16 subjects, 6 of them were randomly assigned to SLOW group and 10 of them to FAST group. There were no statistically significant differences in any of the relevant detected variables (body composition, gender, age, thyroid hormones, amount of training, energy intake) affecting BMR between the groups at the baseline. BMR was reduced significantly for both SLOW (12.3± 11.4%, p=0.036) and FAST (-9.8± 6.5%, p=0.018) weight reduction groups measured with indirect calorimeter (table 4.5.1). These changes were not significantly different between the groups (p=0.941). Weight reduction rate was not associated with changes in BMR. Table 4.5.1. Basal metabolic rate in the SLOW and FAST weight reduction groups at the baseline and post intervention. Group SLOW N 6 Mean (SD) FAST 10 Mean (SD) * Change from baseline, p<0.05 Basal metabolic rate, MJ Pre 6.8 (1.1) 7.1 (1.2) Post 5.7* (1.3) 6.5* (0.8) We also calculated resting metabolic rates (RMR) for all subjects (pre and post intervention) with Cunningham equation. Applying Cunningham equation estimated RMR increased significantly as a result of intervention for SLOW group (p=0.005), but not for FAST group (figure 4.5.2). There were no significant differences in measured BMR or calculated RMR between the intervention groups. These methods correlated with each other prior to intervention (p <0.05), but after accomplished weight reductions measured BMR did not correlate with RMR estimates anymore. Master thesis in Clinical Nutrition, Anu Koivisto 2009 52 5 * % change 0 -5 SLOW n=6 -10 FAST n=10 -15 -20 * * -25 BMR, Douglas RMR, Cunningham Figure 4.5.2. Change in BMR/RMR in SLOW and FAST weight reduction group measured/estimated with Douglas bag and Cunningham equation. * Change from baseline, p<0.05 When BMR was adjusted for LBM the changes from baseline were significant (p<0.05). LBM correlated with BMR both at baseline and after weight reduction. The regression lines had similar slopes but intercepts were different (figure 2.4.1) indicating that changes in BMR could not be explained only by changes in LBM. Master thesis in Clinical Nutrition, Anu Koivisto 2009 53 10000 SLOW FAST At the baseline 9000 BMR, kJ/day Post intervention 8000 7000 6000 R Sq Linear = 0.29 R Sq Linear = 0.28 5000 4000 40.0 50.0 60.0 70.0 LBM, kg Figure 4.5.1. Linear relationship between basal metabolic rate (BMR) and lean body mass (LBM) at the baseline and after the interventions. We did not find any correlation between changes in body composition (weight, LBM, FM, fat%) and BMR (n=16) as was hypothesized. Changes in f-T4 did not correlate with changes in LBM or BMR either. 4.6 Compliance Compliance was defined as successfully obtained planned weight reduction rate. The average weight reduction rate for SLOW was 0.7%BW/week and 1.0%BW/week for FAST weight reduction. Nineteen % of the subjects in FAST weight reduction group obtained the planned weight reduction rate whereas 50% of the SLOW weight reduction group subjects reached their respective weight reduction rate. There was a trend for lower compliance in FAST weight reduction group (p= 0.08). Subjects with successful weight reduction rate (compliants) did not differ from their counterparts (non-compliants) in number of previous weight reduction attempts, baseline LBM, Master thesis in Clinical Nutrition, Anu Koivisto 2009 54 BMR or thyroid hormones. Neither were the %changes in body composition or metabolic parameters different. But there was a significant difference in hours of training (p=0.047) between the groups where subjects who managed their weight reduction rate trained less prior to intervention than the ones who did not reach the planned weight reduction rate (table 3.7). Also a trend for difference in body weight prior to intervention was detected (table 3.7). Table 3.7. Hours of training and body weight prior to intervention in compliants and non-compliants. Variable Hours of training, h Body weight, kg Compliants, n=10 mean (SD) 12.8 (2.1) 77.9 (9.6) Master thesis in Clinical Nutrition, Anu Koivisto 2009 Non compliants, n=20 mean (SD) 15.5 (3.8) 69.3 (11.5) p-value* 0.047 0.053 55 5. Discussion We studied the effect of two different weight reduction rates on body composition, thyroid hormones and basal metabolic rate. Both interventions resulted in significant reduction of body weight, FM, fat% and BMR. Only SLOW weight reduction resulted in significant increase of LBM. And only FAST weight reduction resulted in significant reduction of f-T4. The differences between the groups were significant only in %change in FM, LBM for males and f-T4. 5.1 Subjects There were 38 potential athletes of whom 36 were included in this study. Thirty athletes accomplished the study and 10 of them managed to obtain the planned weight reduction rate (see compliance 5.1.2). Athletes were highly motivated to participate in the project and were grateful for the help they received. Though weight reductions were seemingly easy to accomplish it is important to emphasize that athletes were followed up closely and the results need to be carefully interpreted because of the large inter individual variation. Furthermore since negative energy balance itself may be a key component in development of the female triad140 extra attention needs to be paid in athletes in weight conscious sports during weight reduction in order to capture any possible sign of disordered eating. We included EDI (eating disorder inventory)124 screening of all athletes before and after intervention for this purpose. One of the athletes was excluded because of suspected risk for developing an eating disorder. 5.1.1 Gender and age Eighteen females and 12 males accomplished the study and the gender was equally spread between the groups. Since males have a larger LBM and higher BMR we controlled for gender in these variables and found significantly differing results between males and females which are discussed later. Davidsen et al reviewed the role of menstrual cycle on weight loss attempts and concluded that it may play an Master thesis in Clinical Nutrition, Anu Koivisto 2009 56 important role in adherence to weight loss programs98. We could not find any significant difference in compliance between females and males. Furthermore sleeping metabolic rate (SMR) increases in luteal phase by 6-8% of the menstrual cycle and ideally BMR measurements should be taken at the same time in the cycle98. Because of the varying intervention length (5-12 weeks) in our study the pre and post tests would not necessarily collide with the same point of time in menstrual cycle thus this control was not included in our study. The average age of subjects was 23 which is reported by others as the average age of Norwegian elite athlete illustrating our population’s representativeness regarding age.141 5.1.2 Compliance Athletes met weekly for follow-up and were vigorously encouraged to follow the meal plans and training regimen to manage the weight reduction rate. Athletes’ self-reported adherence to intervention diet was very good. It might be due to inclusion of some of the athletes’ preferred food items in the meal plan, close follow-up and/or motivational factors. But anyhow some of the athletes did not obtain planned weight reduction rate despite following the meal plan in detail thus the energy content of their plans were adjusted or eventually extra low intensity endurance exercise (2 x 20min/week) was implemented (n=5). Weight reduction rates were 0.7% BW/week and 1.0% BW/week for SLOW and FAST weight reduction groups. Compared with the planned 0.7% BW/week and 1.4% BW/week it was apparently harder to obtain the faster weight reduction rate and analysis did show a trend in lower compliance in FAST intervention. We compared subjects who managed their weight reduction rate with those who did not. Earlier studies have reported that previous weight reduction attempts, baseline body weight, BMR and thyroid hormones could predict successful weight loss therefore these parameters were investigated78;92;142. Subjects with successful weight reduction rate did not differ from the subjects with unsuccessful weight reduction rate in any of the mentioned parameters. Thus, these factors could not explain the struggle some athletes experienced with obtaining weight reduction rate during the Master thesis in Clinical Nutrition, Anu Koivisto 2009 57 intervention. But interestingly we found a significant difference in baseline training hours and a trend in baseline body weight between the compliants and non-compliants, suggesting that athletes who trained the least and had the highest body weight prior to intervention were most likely to reach the assigned weight reduction rate. For athletes with good compliance additional training might have contributed more to total energy expenditure than for athletes who already had high training volumes. It has been reported previously that high baseline body weight is an important predictor of successful weight reduction in overweight subjects.142 5.1.3 Training hours and types of sports The subjects were recruited from several types of sports (combat sports, endurance, other) with different types of training regimen thus the study population is relatively heterogeneous. There were no significant differences between the groups in the amount of weekly training hours or strength training history. However results need to be interpreted with caution since type of sport could theoretically affect the body composition results. 5.1.4 Previous weight reduction The study population was composed of athletes who wished to reduce their body weight. Sixty percent of them had attempted weight reduction previously where weight-class sport athletes had the highest prevalence. Other studies have reported similar prevalence of weight reduction attempts among athletes illustrating just how common weight regulation is.4;119 Several studies have shown that a single weight reduction induced by calorie restriction can affect BMR.143;144 Repeated weight reductions’ negative effect on athletes’ BMR has also been shown.145 In our study athletes with previous weight reduction attempts were equally spread between the intervention groups, thus eventual effect on BMR would be similar for both groups. Master thesis in Clinical Nutrition, Anu Koivisto 2009 58 5.2 Methods 5.2.1 Design This was a prospective randomised clinical trial. We have experimented how two different levels of energy restriction effect athletes’ body composition, BMR and thyroid hormones. Energy content of the meal plans and the duration of intervention were the only differing variables between the groups. Other weight loss studies on athletes have for the most part looked at weight class athletes’ attempts to lose weight prior to competition (making weight). Those interventions have been either very short < 1 week (rapid weight loss) or relatively long >3 weeks (gradual weight loss)5;14 (see appendix 1). Our intervention lasted on average 9 weeks for SLOW and 6 weeks for FAST thus both categorised as gradual weight loss interventions. The inclusion of a control group was evaluated before start but since we analyse paired data and percentage change in the variables of interest subjects function as their own controls and therefore the control group was abandoned. In addition finding matching controls is extremely difficult due to limited number of athletes at this performance level. For paired data analysis our study has appropriate power ß>80 but for detection of differences between the groups the study population should preferably have been larger (n=85). This means that we can not be sure that differences between the interventions that we did not find do not exist in real life. 5.2.2 Diet 4-day weighed registration Information about subjects’ dietary habits before intervention start was collected with a 4-day weighed dietary registration. Earlier studies have shown that a 7-day registration period gives a precision (CV) between 20 and 26% for energy and macronutrient intake146 and this is the preferred duration of registration. A 3-day record is considered to be the minimum to indicate the usual intake of a group of athletes (data on group level) but the period needs to include both weekdays and weekends in order to avoid bias.147;148 We chose a 4-day weighed registration consisting of 3 weekdays and a weekend in order to minimize the burden and poor Master thesis in Clinical Nutrition, Anu Koivisto 2009 59 compliance. In addition athletes tendency to eat routinely and stick to stable training timetables may justify a shorter registration period. Furthermore weekly measurements of body weight and skin fold thickness (data not shown) enabled us to control for potential underreporting and adjust to the meal plan when weight reduction rate was not reached. Energy and macronutrient composition of the intervention diet The energy intake for the athletes was restricted on average by -18% for SLOW and 29% for FAST intervention group. Athletes’ diets were manipulated so that the amount of protein in the intervention diet was kept constant whereas the amount of fat was reduced and the amount of carbohydrate maintained whenever possible. Filaire et al48 demonstrated the need for dietary guidance for athletes during weight loss. In their post hoc diet analysis athletes’ diets (self chosen) included too little of carbohydrate 45E% and micronutrients, unnecessary large amount of fat 37E% but fortunately adequate amount of protein 1.2g/kg BW. Although fat content of the intervention diet in our study were kept above the recommended minimum (>20E%) for some athletes this reduction from their usual diet was very large. The absolute carbohydrate content had to be reduced for most of the athletes (n=22) in order to reduce energy intake and maintain adequate protein supply. But carbohydrates still provided 54-56% of the total energy intake as recommended by American College of Sports Medicine (ACSM)149. Energy derived from protein in the intervention diets was 24% and 25% for SLOW and FAST weight reduction groups respectively. Protein content in the meal was prioritized to ensure adequate amino acid supply to the muscles and possibly induce thermo genesis and satiety.42;150 It is important to point out that theoretical recommendations of optimal macronutrient composition for athletes’ in weight reduction are not always achievable in real life. To exemplify this; an athlete on a 6280 kJ/day meal plan (the lowest recommended energy intake for an athlete in weight reduction11) must weigh no more than 43 kg in order to achieve the recommended protein (1.2g/kg BW) and carbohydrate (5g/kg BW) intake while the fat content is no lower than 20E%. This illustrates the need for adjustments in macronutrient composition in some cases. Master thesis in Clinical Nutrition, Anu Koivisto 2009 60 The meal frequency for all subjects averaged at 6 meals per day (breakfast, recovery meal, lunch, snack, dinner and supper), providing energy and macronutrients in a manner that enables good quality work-outs and improves satiety. Several of the studies cited in this thesis have not declared their macronutrient composition or meal pattern of the calorie restricted diets complicating interpretations the effects of such interventions on body composition, especially LBM. 5.2.3 DEXA We chose DEXA for body composition measures because it is a precise and convenient method and gives information not just about FM and LBM but also about bone mineral density. There are three different DEXA softwares which might theoretically give varying results though they all are based on the same principles, thus using the same machine, software and technician in repetitive measures as performed in this thesis increases the reliability of the results. DEXA measurements assume that the hydration of FFM remains constant, but hydration of FFM in athletes can vary and increase the possibility of false result (dehydration underestimates LBM151). We did not control for hydration status in our athletes thus LBM might have been underestimated in some cases. Dehydration effects on body fat% estimates are relatively small; 5% dehydration results in changed fat% estimate by 1-2.5%133. This makes DEXA an excellent method for measuring body fat% in weight class sports where dehydration unfortunately often is used as a weight loss strategy. To avoid inaccuracies due to stomach contents (overestimated LBM151), all the DEXA measurements were done fasting and at the same time of the day. Although the radiation dose is relatively small corresponding to a transcontinental flight possible pregnancy in subjects was unravelled.127 5.2.4 Indirect calorimeter There are several indirect calorimeter methods with 2 main classifications; open circuit and closed circuit. We chose Douglas back, which is an open circuit method, because it is portable and convenient to use. We calibrated the gas analyser prior to each Master thesis in Clinical Nutrition, Anu Koivisto 2009 61 analysis in with atmospheric amounts of carbon dioxide (0.03%) and oxygen (20.93%) as required to ensure valid results.152 Furthermore the time from collection to analysis should be minimised to avoid loss of CO2 by molecular diffusion. All gas analysis in our study were performed within 15 minutes after collection, an approved time interval by Mills.153 Due to possible loss of carbon dioxide in large volume Douglas bags we chose 2 small volume bags (volume= 100 l) where the gas volumes never exceeded 85l. Weir’s equation that converts gasses to kJ assumes that the protein content of diet is constant (15 E%). The protein content in intervention diets and at the baseline was somewhat higher, but it did not differ between the groups. 5.3 Result interpretations 5.3.1 Body composition Both interventions resulted in significant weight losses. Despite the weight loss athletes in SLOW weight reduction group gained LBM during the intervention while their FM decreased by 31% improving their power to weight ratio. Our study is the first to report increased LBM during weight loss study in athletes. Even in FAST weight reduction group LBM was maintained despite the large calorie restriction (26%). Previous studies with similar calorie restrictions and/or body weight loss interventions in athletes have all resulted in LBM loss5;66;72 (see summary in appendix 1). There are several potential explanations for our findings. First, heavy resistance training was included in our study. Several studies have reported strength training’s beneficial effect on LBM maintenance.64;65 Whereas calorie restrictions without training regimen results in significant reduction of LBM.143 There are a few studies, although conducted on non athletes that have shown increases in LBM during weight reduction when strength training was included.75;154 Importantly, both of these studies resulted only in relatively small body weight reductions in contrary to other studies where larger weight reductions have caused loss of LBM. There is scarce data on resistance training’s effect on LBM during weight loss in athletes. Only one study has Master thesis in Clinical Nutrition, Anu Koivisto 2009 62 looked at the combinatory effect of energy restriction and resistance training on body composition in athletes. This 6-week weight loss study with additional resistance training in weight-class athletes gave no benefit regarding LBM changes compared with control group.66 There are also other potential factors that might have an impact on the maintenance of LBM during weight reduction. Chaston et al73 concluded in a review, where they identified LBM’s contribution of total body weight loss among overweight subjects, that the degree of calorie restriction, exercise and weight reduction rate seem to be the main factors predicting LBM loss during weight reduction. Also Umeda et al5 demonstrated that the degree of energy restriction is related to the decrease in FFM. They looked at judoists reducing BW either <4% or >4% during 20 days and showed larger FFM loss and increased blood nitrogen urea concentration in the large weight loss group compared with the moderate weight loss group, thus catabolism of muscle proteins was enhanced by the larger energy restriction. Though no LBM was lost in our study the finding that only SLOW weight loss group gained LBM confirms findings from earlier studies that the degree of weight reduction rate has a strong impact on LBM changes. Weight loss diets in our study provided adequate amounts of protein which probably has contributed to the maintenance of LBM. Several other weight loss studies on athletes have reported LBM losses with lower protein content of the energy restricted diets.38 Observational studies have reported that athletes often consume too little protein during weight loss periods5;21;155 and thus risk being in a negative nitrogen balance. Walberg et al38 tested the effect of high versus low protein hypocalorie diet on FFM. They found that only high protein diet produced positive protein balance though no difference in FFM changes between the groups was detected. Short duration of their study might explain that lack of difference in FFM between the groups. Other dietary factors may also play a role in LBM maintenance during weight loss in athletes (meal pattern, timing of meals around work-outs, snacking etc), but few studies have investigated them.20 Master thesis in Clinical Nutrition, Anu Koivisto 2009 63 We found an association between LBM gain and duration of the intervention. This is probably explained by the time aspect of muscular hypertrophy giving an advantage for the long intervention. Subjects with the longest interventions had smaller energy restriction which also could partly explain the finding. Contrary to our finding several studies on athletes have suggested that long/gradual weight reduction leads to larger LBM loss compared with rapid weight loss.14;71 Rapid weight loss in these studies refers to weight loss due to fasting and dehydration few days prior to weigh-in. In our study both weight reductions belong in gradual weight reduction category, but despite the relative long duration no LBM was lost. In our study females’ LBM increase was significantly greater than males regardless of strength training background. Since we did find a linear relationship between LBM at the baseline and change in LBM this gender difference might be due to females low baseline LBM compared with males and thus larger capacity to increase LBM. Theoretically it could also be due to weight loss induced reduction in testosterone as previously reported in male athletes during weight reduction.11 Thus our results suggest that males, especially with large LBM at the baseline, have limited possibility to increase LBM during weight reduction, whereas LBM increase for females during weight reduction appears to be easier independent of weight reduction rate. Furthermore a longer duration of energy restriction combined with muscular hypertrophy stimulating weight training seems to be the preferred weight reduction method for optimal body composition changes. Finally the maintenance of LBM is important for improving physical performance, thus not surprisingly several studies but not all30 have reported decreased performance associated with LBM loss in athletes.5;48;156 (Physical test data not shown in this thesis.) 5.3.2 Thyroid hormones We detected a significant reduction in f-T4 for FAST but not for SLOW weight reduction. Thus degree of calorie restriction seems to have an impact on thyroid hormones. Kozlowska et al detected a decline in T3/T4 ratio during weight loss Master thesis in Clinical Nutrition, Anu Koivisto 2009 64 correlating with the magnitude of energy restriction. Other studies have reported reductions in f-T4 as a result of low energy intake and weight reduction.87;90;143, while some have shown no difference in T4, only reduced T3.87 Since thyroxin needs to be activated by deiodination to the biologically active T3 a decrease in deiodinase activity may affect the T3 feedback mechanism so that TSH is increased simultaneously with T4, while T3 is decreased. This theory is supported by Ortega et al’s finding that only T3 was associated with sleeping metabolic rate and weight change.92 We did not find any association between T4 and TSH and unfortunately we have no data on T3. THS did not change in either of our intervention groups during energy restriction. It has been reported previously that athletes with low energy intakes were prone to hypothyroidism; a reduced metabolic state where TSH is increased.157,158 All the values for free T4 and TSH (except TSH for one athlete post intervention) in our study were within reference values and that raises a question whether these relatively small changes can affect metabolism (BMR) which we, due to low sample size, could not detect? Previous studies in non-athletes have reported that even small reduction in TSH has a significant impact on BMR.96 We could not detect an association between TSH and BMR in our subjects. Although thyroid hormones are the major endocrine regulators of metabolic rate (BMR),159 there are only a few studies that have investigated thyroid hormones and/or metabolic rate among healthy athletes as a result of weight reduction.143;144 These studies all report reduced metabolism. We observed significant reduction in T4 and BMR but could not find them to be associated as hypothesized. Araujo et al94 showed the that reductions in T4 during weight reduction (40% calorie restriction) seem to have a LBM protective role. We were not able to detect an association between T4 and changes in LBM. Master thesis in Clinical Nutrition, Anu Koivisto 2009 65 5.3.3 BMR BMR reduced for both groups but the changes did not differ between the interventions. Earlier studies have also reported that weight loss results in reduced BMR both in overweight subject and athletes.108;144 BMR is influenced by many factors such as age, gender, genetic factors, LBM and hormonal pattern.160 There is a strong correlation between LBM and BMR.161 Thus given that LBM is a key determinant of BMR it follows that lean body mass loss could predict reductions in BMR. In or study though changes in LBM could not predict changes in BMR. We detected reduced BMR but LBM was maintained or increased, and these changes were not correlated as hypothesized. BMR reductions in our study appear larger than expected when adjusted to body composition changes. Also Heilbronn et al demonstrated that calorie restriction resulted in a 6% larger RMR loss than could be explained by changes in metabolic tissue.102 Melby et al reported 12% reduction in LBM adjusted BMR. Since FM loss in our study was very large some of the decline in BMR could theoretically be explained by it regardless of the low metabolic activity of fat tissue. But we did not find an association between changes in FM and BMR as hypothesized. Thus as a result of calorie restriction metabolic changes seem to get more complicated and some sort of metabolic adaptation seems to appear. Some studies have shown significant reductions in BMR after weight loss but a relatively fast recovery back to baseline values when energy balance is established at the new body weight.107 In contrary some studies have reported that declines in energy expenditure (EE) persist well beyond the dynamic weight loss.105;106 Weinsier et al emphasizes the importance of taking metabolic measures after re-established energy balance since transient hypothyroid-hypometabolic state due to weight loss gives misleading impression that weight-reduced persons are energy conservative. We collected blood samples and measured BMR immediately after intervention, thus all the subjects were still in negative energy balance. Master thesis in Clinical Nutrition, Anu Koivisto 2009 66 Few studies have looked at long-term effects of intentional weight reduction on RMR in athletes.108;162 In one study athletes reduced their body weight repeatedly during the competitive season108. Both LBM and BMR were reduced after weight reduction periods but returned to baseline after season when the wrestlers’ body weight was normalised. McCargar et al162 reported no difference in RMR between weight-cyclers and non weight-cyclers before or during the competitive season, but they detected a trend for lower RMR in weight cyclers during off-season (5 months after last weight loss) when body weight was normalised. It remains to be determined whether BMR remains reduced and for how long after new lower body weight is established. Future research in this field should focus on investigating the duration of this hypometabolic state in athletes. In our study estimated RMR (Cunningham equation) did not correlate with measured BMR (indirect calorimeter) after weight loss. Cunningham equation is based on LBM and due to LBM gain in our study RMR was overestimated (by 784kJ). This information is of clinical importance since applying Cunningham equation for estimating energy needs for an athletes after weight loss will be incorrect (too high). The lack of difference in BMR changes between the intervention groups might be explained by the duration of the intervention. Since changes in BMR happen relatively slowly the duration of FAST weight reduction might have been too short for detecting a greater BMR fall that could have happened if the weight loss had lasted longer at the same rate. Anyhow we did not find a correlation between duration of intervention and changes in BMR. BMR can also be affected by heavy exercise up to 48 hours (extra post exercise oxygen consumption, EPOC).163 In our study heavy exercise was restricted 24 hours prior to BMR measures, thus real reductions in BMR could have been masked by metabolic after-effects of intense exercise. Though this effect would be similar for both interventions, and therefore can not explain the lack of difference in BMR between the groups. Master thesis in Clinical Nutrition, Anu Koivisto 2009 67 5.4 Strengths and weaknesses of the study Our study is the first experimental weight loss study to look at how specific weight reduction rates effect body composition, thyroid hormones and BMR. In our study weight loss diet was defined in detail and controlled through out the study thus confounding from dietary factors was minimised. The sample size in the study is adequate for paired analysis but lacks power for between group comparisons, especially for BMR (n=16) though compared with other weight loss studies in athletes our sample size is superior. Random allocation minimised systematic bias and the similarity of groups at the baseline reduced confounding. Though separate control group might have been ideal it is not needed when studying within subject changes from baseline. Athletes’ weight stability prior to the intervention was controlled only verbally which might not be adequate. Furthermore we probably should have collected diurnal urine, measured nitrogen content and established whether any of the athletes were in negative nitrogen balance. But it was considered to be too large a burden for the athletes. For detection of TEE and underreporting we should preferentially have used DLW but since the weekly follow-up allowed for adjustments, information from 4-day weighed food record and 1-day activity registration was considered adequate. Seasonal variation in BMR was not taken into consideration (impossible due to competitive season) and could theoretically impact BMR results though block allocation secured similar number of subjects in the interventions at any time thus the potential effect would be alike for both groups. We should have measured T3 or T3/T4 ratio since those parameters are affected by low energy availability into a larger extent than f-T4. Ideally the study should have been designed to allow control for menstrual cycle and it’s potential effect on BMR. Finally, drop-out rate in the study was very small. And there were no differences between the athletes who accomplished or aborted the study. Master thesis in Clinical Nutrition, Anu Koivisto 2009 68 6. Conclusion Despite the energy restriction and significant body weight reduction neither of the interventions resulted in LBM losses. Subjects in SLOW weight reduction group actually gained LBM. Free T4 plasma concentration decreased only in FAST weight reduction group suggesting that the faster weight reduction rate is more likely to initiate energy preserving mechanisms although we were not able to detect this in BMR changes. The basal metabolism reductions did not differ between the interventions. Changes in LBM, thyroid hormones or BMR were not associated as a result of weight reduction. Thus for optimal body composition changes in athletes a moderate energy restriction combined with resistance training leading to a weekly weight loss of 0.7% seems preferable and should be the recommended protocol. Despite maintained or increased LBM, athletes experienced reductions in BMR. Several weight loss studies combining energy restriction and strength training need to be conducted to better understand the mechanisms that lead to BMR reductions in athletes. Also the duration of the weight loss induced hypo-metabolic state in athletes needs to be established. Master thesis in Clinical Nutrition, Anu Koivisto 2009 69 Practical Implications Based on existing literature and findings from our study the following guidelines for weight loss in athletes are suggested. • Careful evaluation of athletes’ medical, anthropometric, nutritional and psychological status together with an assessment of their performance goals is required prior to weight reduction. • Weight reduction needs to be planned in advance and timed to avoid interference with sports specific goals and competitions. • It is not recommended that athletes reduce body weight on their own. Regular follow-up with nutritionist is recommended. • Energy restriction should be combined with strength training to avoid some of the detrimental effects of weight reduction on LBM. • The recommended weight loss rate is 0.7% of body weight per week. • Weight loss diet should contain minimum 1.2g protein/kg body weight and as much carbohydrate as possible while fat content is reduced, but to no lower than 20E%. • The diet should be nutrient rich and high in fibre. Eventual supplementing with a multivitamin-mineral and essential fatty acids should be considered with low energy intakes (<8000kJ). • Total daily energy intake should be divided in frequent small meals that match athletes’ work-out schedule and provide fuel and satiety throughout the day. Master thesis in Clinical Nutrition, Anu Koivisto 2009 70 Reference List (1) http://chem.csusb.edu/ . 2009. Ref Type: Online Source (2) Benardot D. Body composition and weight. Advanced sports nutrition. Champaign, IL: Human Kinetics; 2006;209-232. (3) Davis C, Cowles M. A comparison of weight and diet concerns and personality factors among female athletes and non-athletes. J Psychosom Res 1989;33:527-536. (4) Fogelholm M, Hiilloskorpi H. Weight and diet concerns in Finnish female and male athletes. Med Sci Sports Exerc 1999;31:229-235. (5) Umeda T, Nakaji S, Shimoyama T, Yamamoto Y, Totsuka M, Sugawara K. Adverse effects of energy restriction on myogenic enzymes in judoists. J Sports Sci 2004;22:329-338. (6) Kowatari K, Umeda T, Shimoyama T, Nakaji S, Yamamoto Y, Sugawara K. Exercise training and energy restriction decrease neutrophil phagocytic activity in judoists. Med Sci Sports Exerc 2001;33:519-524. (7) Steen SN, Brownell KD. Patterns of weight loss and regain in wrestlers: has the tradition changed? Med Sci Sports Exerc 1990;22:762-768. (8) Choma CW, Sforzo GA, Keller BA. Impact of rapid weight loss on cognitive function in collegiate wrestlers. Med Sci Sports Exerc 1998;30:746-749. (9) Stiegler P, Cunliffe A. The role of diet and exercise for the maintenance of fat-free mass and resting metabolic rate during weight loss. Sports Med 2006;36:239-262. (10) Rankin JW. Making weight in sports. In: Burke L, Deakin V, eds. Clinical sports nutrition. 3rd edition ed. Australia: McGraw-Hill Australia Pty Ltd; 2006;175-200. (11) O'Connor H, Caterson I. Weight loss and the athlete. In: Burke L, Deakin V, eds. Clinical sports nutrition. 3rd edition ed. McGraw-Hill; 2006;135-174. Master thesis in Clinical Nutrition, Anu Koivisto 2009 71 (12) Olds TS, Norton KI, Craig NP. Mathematical model of cycling performance. J Appl Physiol 1993;75:730-737. (13) Rankin JW. Weight loss and gain in athletes. Curr Sports Med Rep 2002;1:208-213. (14) Fogelholm GM, Koskinen R, Laakso J, Rankinen T, Ruokonen I. Gradual and rapid weight loss: effects on nutrition and performance in male athletes. Med Sci Sports Exerc 1993;25:371-377. (15) Garthe I. Vektregulering blant landslagsutøvere i vektklasseidretter i Norgeen undersøkelse gjort av Olympiatoppen for å kartlegge vektreduksjonsmetoder og rutiner hos norske vektklasseutøvere. Olympiatoppen., editor. 2005. Ref Type: Report (16) From the Centers for Disease Control and Prevention. Hyperthermia and dehydration-related deaths associated with intentional rapid weight loss in three collegiate wrestlers--North Carolina, Wisconsin, and Michigan, November-December 1997. JAMA 1998;279:824-825. (17) Coyle EF. Fuels for sports performance. Perspectives in exercise science and sports medicine. Indiana: Cooper publishing group; 1997;95-129. (18) Hawley J, Burke L. Nutritional strategies to enhance fat oxidation. In: Burke L, Deakin V, eds. Clinical sports nutrition. 3rd edition ed. Australia: McGraw-Hill; 2006;455-483. (19) Rankin JW, Ocel JV, Craft LL. Effect of weight loss and refeeding diet composition on anaerobic performance in wrestlers. Med Sci Sports Exerc 1996;28:1292-1299. (20) Iwao S, Mori K, Sato Y. Effects of meal frequency on body composition during weight control in boxers. Scand J Med Sci Sports 1996;6:265-272. (21) Roemmich JN, Sinning WE. Weight loss and wrestling training: effects on nutrition, growth, maturation, body composition, and strength. J Appl Physiol 1997;82:1751-1759. (22) Burke LM, Cox GR, Culmmings NK, Desbrow B. Guidelines for daily carbohydrate intake: do athletes achieve them? Sports Med 2001;31:267-299. Master thesis in Clinical Nutrition, Anu Koivisto 2009 72 (23) Romijn JA, Coyle EF, Sidossis LS et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol 1993;265:E380-E391. (24) Bangsbo J, Norregaard L, Thorsoe F. The effect of carbohydrate diet on intermittent exercise performance. Int J Sports Med 1992;13:152-157. (25) Hawley JA, Schabort EJ, Noakes TD, Dennis SC. Carbohydrate-loading and exercise performance. An update. Sports Med 1997;24:73-81. (26) Horswill CA, Hickner RC, Scott JR, Costill DL, Gould D. Weight loss, dietary carbohydrate modifications, and high intensity physical activity [abstract]Horswill CA, Hickner RC, Scott JR, Costill DL, Gould D. Med Sci Sports Exerc 1990;22:470-477 (27) McMurray RG, Proctor CR, Wilson WL. Effect of caloric deficit and dietary manipulation on aerobic and anaerobic exercise. Int J Sports Med 1991;12:167-172. (28) Burke L. Nutrition for recovery after training and competition. In: Burke L, Deakin V, eds. Clinical sports nutrition. 3rd edition ed. Australia: McGrawHill; 2006;415-453. (29) Coyle EF. Physical activity as a metabolic stressor. Am J Clin Nutr 2000;72:512S-520S. (30) Parkes SC, Belcastro AN, McCargar LJ, McKenzie D. Effect of energy restriction on muscle function and calcium stimulated protease activity in recreationally active women. Can J Appl Physiol 1998;23:279-292. (31) Frayn K. Metabolic regulation: a human perspective. 2nd edition ed. Portland: Blakcwell Science, 2003. (32) Cook CM, Haub MD. Low-carbohydrate diets and performance. Curr Sports Med Rep 2007;6:225-229. (33) Tarnopolsky MA. Protein and amino acid needs for training and bulking up. Clinical sports nutrition. 3rd edition ed. Australia: McGraw-Hill; 2006;73111. (34) Tarnopolsky M. Protein requirements for endurance athletes. Nutrition 2004;20:662-668. Master thesis in Clinical Nutrition, Anu Koivisto 2009 73 (35) Wagenmakers AJ, Beckers EJ, Brouns F et al. Carbohydrate supplementation, glycogen depletion, and amino acid metabolism during exercise. Am J Physiol 1991;260:E883-E890. (36) Jackman ML, Gibala MJ, Hultman E, Graham TE. Nutritional status affects branched-chain oxoacid dehydrogenase activity during exercise in humans. Am J Physiol 1997;272:E233-E238. (37) Wolfe RR. Control of muscle protein breakdown: effects of activity and nutritional states. Int J Sport Nutr Exerc Metab 2001;11 Suppl:S164-S169. (38) Walberg JL, Leidy MK, Sturgill DJ, Hinkle DE, Ritchey SJ, Sebolt DR. Macronutrient content of a hypoenergy diet affects nitrogen retention and muscle function in weight lifters. Int J Sports Med 1988;9:261-266. (39) Rennie MJ, Bohe J, Smith K, Wackerhage H, Greenhaff P. Branched-chain amino acids as fuels and anabolic signals in human muscle. J Nutr 2006;136:264S-268S. (40) Phillips SM. Dietary protein for athletes: from requirements to metabolic advantage. Appl Physiol Nutr Metab 2006;31:647-654. (41) Potier M, Darcel N, Tome D. Protein, amino acids and the control of food intake. Curr Opin Clin Nutr Metab Care 2009;12:54-58. (42) Halton TL, Hu FB. The effects of high protein diets on thermogenesis, satiety and weight loss: a critical review. J Am Coll Nutr 2004;23:373-385. (43) Tarnopolsky MA, Atkinson SA, MacDougall JD, Chesley A, Phillips S, Schwarcz HP. Evaluation of protein requirements for trained strength athletes. J Appl Physiol 1992;73:1986-1995. (44) Baba NH, Sawaya S, Torbay N, Habbal Z, Azar S, Hashim SA. High protein vs high carbohydrate hypoenergetic diet for the treatment of obese hyperinsulinemic subjects. Int J Obes Relat Metab Disord 1999;23:12021206. (45) Horswill CA. Weight loss and weight cycling in amateur wrestlers: implications for performance and resting metabolic rate. Int J Sport Nutr 1993;3:245-260. (46) Williams L, Williams P. Evaluation of a tool for rating popular diet books [abstract]Williams L, Williams P. Nutr Diet 2003;60:185-197 Master thesis in Clinical Nutrition, Anu Koivisto 2009 74 (47) Gleeson M. Can nutrition limit exercise-induced immunodepression? Nutr Rev 2006;64:119-131. (48) Filaire E, Maso F, Degoutte F, Jouanel P, Lac G. Food restriction, performance, psychological state and lipid values in judo athletes. Int J Sports Med 2001;22:454-459. (49) Greenhaff PL, Gleeson M, Maughan RJ. The effects of diet on muscle pH and metabolism during high intensity exercise. Eur J Appl Physiol Occup Physiol 1988;57:531-539. (50) Hulmi JJ, Volek JS, Selanne H, Mero AA. Protein ingestion prior to strength exercise affects blood hormones and metabolism. Med Sci Sports Exerc 2005;37:1990-1997. (51) Ivy JL, Katz AL, Cutler CL, Sherman WM, Coyle EF. Muscle glycogen synthesis after exercise: effect of time of carbohydrate ingestion. J Appl Physiol 1988;64:1480-1485. (52) Richter EA, Mikines KJ, Galbo H, Kiens B. Effect of exercise on insulin action in human skeletal muscle. J Appl Physiol 1989;66:876-885. (53) Wojtaszewski JF, Nielsen P, Kiens B, Richter EA. Regulation of glycogen synthase kinase-3 in human skeletal muscle: effects of food intake and bicycle exercise. Diabetes 2001;50:265-269. (54) Burke LM, Collier GR, Hargreaves M. Muscle glycogen storage after prolonged exercise: effect of the glycemic index of carbohydrate feedings. J Appl Physiol 1993;75:1019-1023. (55) Jozsi AC, Trappe TA, Starling RD et al. The influence of starch structure on glycogen resynthesis and subsequent cycling performance. Int J Sports Med 1996;17:373-378. (56) Biolo G, Williams BD, Fleming RY, Wolfe RR. Insulin action on muscle protein kinetics and amino acid transport during recovery after resistance exercise. Diabetes 1999;48:949-957. (57) Ivy JL, Goforth HW, Jr., Damon BM, McCauley TR, Parsons EC, Price TB. Early postexercise muscle glycogen recovery is enhanced with a carbohydrate-protein supplement. J Appl Physiol 2002;93:1337-1344. (58) Kerksick C, Harvey T, Stout J et al. International Society of Sports Nutrition position stand: Nutrient timing. J Int Soc Sports Nutr 2008;5:17. Master thesis in Clinical Nutrition, Anu Koivisto 2009 75 (59) Tipton KD, Rasmussen BB, Miller SL et al. Timing of amino acidcarbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol Endocrinol Metab 2001;281:E197-E206. (60) Ivy JL, Ding Z, Hwang H, Cialdella-Kam LC, Morrison PJ. Post exercise carbohydrate-protein supplementation: phosphorylation of muscle proteins involved in glycogen synthesis and protein translation. Amino Acids 2008;35:89-97. (61) Wolfe RR. Effects of amino acid intake on anabolic processes. Can J Appl Physiol 2001;26 Suppl:S220-S227. (62) Pedersen BK, Bruunsgaard H, Jensen M, Toft AD, Hansen H, Ostrowski K. Exercise and the immune system--influence of nutrition and ageing. J Sci Med Sport 1999;2:234-252. (63) Bryner RW, Ullrich IH, Sauers J et al. Effects of resistance vs. aerobic training combined with an 800 calorie liquid diet on lean body mass and resting metabolic rate. J Am Coll Nutr 1999;18:115-121. (64) Ballor DL, Katch VL, Becque MD, Marks CR. Resistance weight training during caloric restriction enhances lean body weight maintenance. Am J Clin Nutr 1988;47:19-25. (65) Ballor DL, Poehlman ET. Exercise-training enhances fat-free mass preservation during diet-induced weight loss: a meta-analytical finding. Int J Obes Relat Metab Disord 1994;18:35-40. (66) Garthe I. Betydningen av styrketrening i en vektreduksjonsperiode hos toppidrettsutøvere i vektklasseidretter [ Norges Idrettshøgskole; 2002. (67) Geliebter A, Maher MM, Gerace L, Gutin B, Heymsfield SB, Hashim SA. Effects of strength or aerobic training on body composition, resting metabolic rate, and peak oxygen consumption in obese dieting subjects. Am J Clin Nutr 1997;66:557-563. (68) Tsai AC, Sandretto A, Chung YC. Dieting is more effective in reducing weight but exercise is more effective in reducing fat during the early phase of a weight-reducing program in healthy humans. J Nutr Biochem 2003;14:541549. (69) Heyward VH, Wagner DR. Applied body composition. 2nd edition ed. Champaign, Illinois: Human Kinetics, 2004. Master thesis in Clinical Nutrition, Anu Koivisto 2009 76 (70) Forbes GB. Body fat content influences the body composition response to nutrition and exercise. Ann N Y Acad Sci 2000;904:359-365. (71) Slater GJ, Rice AJ, Jenkins D, Gulbin J, Hahn AG. Preparation of former heavyweight oarsmen to compete as lightweight rowers over 16 weeks: three case studies. Int J Sport Nutr Exerc Metab 2006;16:108-121. (72) Koutedakis Y, Pacy PJ, Quevedo RM et al. The effects of two different periods of weight-reduction on selected performance parameters in elite lightweight oarswomen. Int J Sports Med 1994;15:472-477. (73) Chaston TB, Dixon JB, O'Brien PE. Changes in fat-free mass during significant weight loss: a systematic review. Int J Obes (Lond) 2007;31:743750. (74) Goldberg AL, Etlinger JD, Goldspink DF, Jablecki C. Mechanism of workinduced hypertrophy of skeletal muscle. Med Sci Sports 1975;7:185-198. (75) Demling RH, DeSanti L. Effect of a hypocaloric diet, increased protein intake and resistance training on lean mass gains and fat mass loss in overweight police officers. Ann Nutr Metab 2000;44:21-29. (76) Weiss EP, Racette SB, Villareal DT et al. Lower extremity muscle size and strength and aerobic capacity decrease with caloric restriction but not with exercise-induced weight loss. J Appl Physiol 2007;102:634-640. (77) Committee on military nutrition research, Committee on body composition nah, Board institute of medicine. The role of protein and amino acids in sustaining and enhancing performance. 1999. Washington, National academy press. Ref Type: Report (78) Kozlowska L, Rosolowska-Huszcz D. Leptin, thyrotropin, and thyroid hormones in obese/overweight women before and after two levels of energy deficit. Endocrine 2004;24:147-153. (79) Dionne I, Despres JP, Bouchard C, Tremblay A. Gender difference in the effect of body composition on energy metabolism. Int J Obes Relat Metab Disord 1999;23:312-319. (80) Hilton LK, Loucks AB. Low energy availability, not exercise stress, suppresses the diurnal rhythm of leptin in healthy young women. Am J Physiol Endocrinol Metab 2000;278:E43-E49. Master thesis in Clinical Nutrition, Anu Koivisto 2009 77 (81) Saris WH. The concept of energy homeostasis for optimal health during training. Can J Appl Physiol 2001;26 Suppl:S167-S175. (82) Doucet E, St PS, Almeras N, Mauriege P, Richard D, Tremblay A. Changes in energy expenditure and substrate oxidation resulting from weight loss in obese men and women: is there an important contribution of leptin? J Clin Endocrinol Metab 2000;85:1550-1556. (83) Ayyad C, Andersen T. Long-term efficacy of dietary treatment of obesity: a systematic review of studies published between 1931 and 1999. Obes Rev 2000;1:113-119. (84) Glenny AM, O'Meara S, Melville A, Sheldon TA, Wilson C. The treatment and prevention of obesity: a systematic review of the literature. Int J Obes Relat Metab Disord 1997;21:715-737. (85) Filozof C, Gonzalez C. Predictors of weight gain: the biological-behavioural debate. Obes Rev 2000;1:21-26. (86) Martin CK, Heilbronn LK, de JL et al. Effect of calorie restriction on resting metabolic rate and spontaneous physical activity. Obesity (Silver Spring) 2007;15:2964-2973. (87) Rosenbaum M, Hirsch J, Murphy E, Leibel RL. Effects of changes in body weight on carbohydrate metabolism, catecholamine excretion, and thyroid function. Am J Clin Nutr 2000;71:1421-1432. (88) Sherwood L. The peripheral endocrine glands. Human physiology - from cells to systems. 3rd edition ed. Belmont, CA: West Publishing Company; 2009;654-699. (89) Reinehr T, Andler W. Thyroid hormones before and after weight loss in obesity. Arch Dis Child 2002;87:320-323. (90) Thompson JL, Manore MM, Skinner JS, Ravussin E, Spraul M. Daily energy expenditure in male endurance athletes with differing energy intakes. Med Sci Sports Exerc 1995;27:347-354. (91) Reinehr T, Isa A, de SG, Dieffenbach R, Andler W. Thyroid hormones and their relation to weight status. Horm Res 2008;70:51-57. (92) Ortega E, Pannacciulli N, Bogardus C, Krakoff J. Plasma concentrations of free triiodothyronine predict weight change in euthyroid persons. Am J Clin Nutr 2007;85:440-445. Master thesis in Clinical Nutrition, Anu Koivisto 2009 78 (93) Welle SL, Campbell RG. Decrease in resting metabolic rate during rapid weight loss is reversed by low dose thyroid hormone treatment. Metabolism 1986;35:289-291. (94) Araujo RL, de Andrade BM, de Figueiredo AS et al. Low replacement doses of thyroxine during food restriction restores type 1 deiodinase activity in rats and promotes body protein loss. J Endocrinol 2008;198:119-125. (95) Douyon L, Schteingart DE. Effect of obesity and starvation on thyroid hormone, growth hormone, and cortisol secretion. Endocrinol Metab Clin North Am 2002;31:173-189. (96) al-Adsani H, Hoffer LJ, Silva JE. Resting energy expenditure is sensitive to small dose changes in patients on chronic thyroid hormone replacement. J Clin Endocrinol Metab 1997;82:1118-1125. (97) Poehlman E, Horton E. Energy needs:assessment and requirements in humans. Modern nutrition in health and disease. 9th edition ed. Baltimore: Lippincott Williams & Wilkins; 1999;95-104. (98) Davidsen L, Vistisen B, Astrup A. Impact of the menstrual cycle on determinants of energy balance: a putative role in weight loss attempts. Int J Obes (Lond) 2007;31:1777-1785. (99) Butterfield GE, Gates J, Fleming S, Brooks GA, Sutton JR, Reeves JT. Increased energy intake minimizes weight loss in men at high altitude. J Appl Physiol 1992;72:1741-1748. (100) Lazzer S, Boirie Y, Montaurier C, Vernet J, Meyer M, Vermorel M. A weight reduction program preserves fat-free mass but not metabolic rate in obese adolescents. Obes Res 2004;12:233-240. (101) Menozzi R, Bondi M, Baldini A, Venneri MG, Velardo A, Del RG. Resting metabolic rate, fat-free mass and catecholamine excretion during weight loss in female obese patients. Br J Nutr 2000;84:515-520. (102) Heilbronn LK, de JL, Frisard MI et al. Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial. JAMA 2006;295:15391548. (103) Byrne HK, Wilmore JH. The effects of a 20-week exercise training program on resting metabolic rate in previously sedentary, moderately obese women. Int J Sport Nutr Exerc Metab 2001;11:15-31. Master thesis in Clinical Nutrition, Anu Koivisto 2009 79 (104) Carey DG, Pliego GJ, Raymond RL. Body composition and metabolic changes following bariatric surgery: effects on fat mass, lean mass and basal metabolic rate: six months to one-year follow-up. Obes Surg 2006;16:16021608. (105) Rosenbaum M, Hirsch J, Gallagher DA, Leibel RL. Long-term persistence of adaptive thermogenesis in subjects who have maintained a reduced body weight. Am J Clin Nutr 2008;88:906-912. (106) Weyer C, Walford RL, Harper IT et al. Energy metabolism after 2 y of energy restriction: the biosphere 2 experiment. Am J Clin Nutr 2000;72:946-953. (107) Weinsier RL, Nagy TR, Hunter GR, Darnell BE, Hensrud DD, Weiss HL. Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory. Am J Clin Nutr 2000;72:1088-1094. (108) Melby CL, Schmidt WD, Corrigan D. Resting metabolic rate in weightcycling collegiate wrestlers compared with physically active, noncycling control subjects. Am J Clin Nutr 1990;52:409-414. (109) Manore MM, Thompson JL. Energy requirements of the athlete: assessment and evidence of energy efficiency. Clinical sports nutrition. 3rd edition ed. Ausralia: McGraw-Hill; 2006;113-134. (110) Seidell JC, Muller DC, Sorkin JD, Andres R. Fasting respiratory exchange ratio and resting metabolic rate as predictors of weight gain: the Baltimore Longitudinal Study on Aging. Int J Obes Relat Metab Disord 1992;16:667674. (111) Ravussin E, Gautier JF. Metabolic predictors of weight gain. Int J Obes Relat Metab Disord 1999;23 Suppl 1:37-41. (112) Venkatraman JT, Pendergast DR. Effect of dietary intake on immune function in athletes. Sports Med 2002;32:323-337. (113) Imai T, Seki S, Dobashi H, Ohkawa T, Habu Y, Hiraide H. Effect of weight loss on T-cell receptor-mediated T-cell function in elite athletes. Med Sci Sports Exerc 2002;34:245-250. (114) Talbott SM, Shapses SA. Fasting and energy intake influence bone turnover in lightweight male rowers. Int J Sport Nutr 1998;8:377-387. Master thesis in Clinical Nutrition, Anu Koivisto 2009 80 (115) De Souza MJ, West SL, Jamal SA, Hawker GA, Gundberg CM, Williams NI. The presence of both an energy deficiency and estrogen deficiency exacerbate alterations of bone metabolism in exercising women. Bone 2008;43:140-148. (116) Nattiv A, Loucks AB, Manore MM, Sanborn CF, Sundgot-Borgen J, Warren MP. American College of Sports Medicine position stand. The female athlete triad. Med Sci Sports Exerc 2007;39:1867-1882. (117) Torres-Mejia G, Guzman PR, Tellez-Rojo MM, Lazcano-Ponce E. Peak bone mass and bone mineral density correlates for 9 to 24 year-old Mexican women, using corrected BMD. Salud Publica Mex 2009;51 Suppl 1:S84-S92. (118) Khan AA, Brown JP, Kendler DL et al. The 2002 Canadian bone densitometry recommendations: take-home messages. CMAJ 2002;167:11411145. (119) Torstveit MK, Sundgot-Borgen J. The female athlete triad: are elite athletes at increased risk? Med Sci Sports Exerc 2005;37:184-193. (120) Torstveit MK, Rosenvinge JH, Sundgot-Borgen J. Prevalence of eating disorders and the predictive power of risk models in female elite athletes: a controlled study. Scand J Med Sci Sports 2008;18:108-118. (121) Sundgot-Borgen J. Risk and trigger factors for the development of eating disorders in female elite athletes. Med Sci Sports Exerc 1994;26:414-419. (122) Buford TW, Rossi SJ, Smith DB, O'Brien MS, Pickering C. The effect of a competitive wrestling season on body weight, hydration, and muscular performance in collegiate wrestlers. J Strength Cond Res 2006;20:689-692. (123) Saarni SE, Rissanen A, Sarna S, Koskenvuo M, Kaprio J. Weight cycling of athletes and subsequent weight gain in middleage. Int J Obes (Lond) 2006;30:1639-1644. (124) Garner DM, Olmsted MP, Polivy J. Manual of eating disorder inventory [abstract]Garner DM, Olmsted MP, Polivy J. Psychological assesments resources 1984;1-19 (125) Mattilsynet, Sosial -og helsedirektoratet, Universitet i Oslo. Mat på data 5.0. 2006. Oslo. Ref Type: Report Master thesis in Clinical Nutrition, Anu Koivisto 2009 81 (126) Statens råd for ernæring og fysisk aktivitet, Satens næringsmiddeltilsyn, Institutt for ernæringsforskning U. Den store matvaretabellen. 2 ed. Oslo: Gyldendal Undervisning, 2001. (127) Lewis MK, Blake GM, Fogelman I. Patient dose in dual x-ray absorptiometry. Osteoporos Int 1994;4:11-15. (128) Levine JA, Abboud L, Barry M, Reed JE, Sheedy PF, Jensen MD. Measuring leg muscle and fat mass in humans: comparison of CT and dual-energy X-ray absorptiometry. J Appl Physiol 2000;88:452-456. (129) Visser M, Fuerst T, Lang T, Salamone L, Harris TB. Validity of fan-beam dual-energy X-ray absorptiometry for measuring fat-free mass and leg muscle mass. Health, Aging, and Body Composition Study--Dual-Energy X-ray Absorptiometry and Body Composition Working Group. J Appl Physiol 1999;87:1513-1520. (130) Mazess RB, Barden HS, Bisek JP, Hanson J. Dual-energy x-ray absorptiometry for total-body and regional bone-mineral and soft-tissue composition. Am J Clin Nutr 1990;51:1106-1112. (131) Bolanowski M, Nilsson BE. Assessment of human body composition using dual-energy x-ray absorptiometry and bioelectrical impedance analysis. Med Sci Monit 2001;7:1029-1033. (132) Margulies L, Horlick M, Thornton JC, Wang J, Ioannidou E, Heymsfield SB. Reproducibility of pediatric whole body bone and body composition measures by dual-energy X-ray absorptiometry using the GE Lunar Prodigy. J Clin Densitom 2005;8:298-304. (133) Lohman TG, Harris M, Teixeira PJ, Weiss L. Assessing body composition and changes in body composition. Another look at dual-energy X-ray absorptiometry. Ann N Y Acad Sci 2000;904:45-54. (134) Weyers AM, Mazzetti SA, Love DM, Gomez AL, Kraemer WJ, Volek JS. Comparison of methods for assessing body composition changes during weight loss. Med Sci Sports Exerc 2002;34:497-502. (135) Going SB, Massett MP, Hall MC et al. Detection of small changes in body composition by dual-energy x-ray absorptiometry. Am J Clin Nutr 1993;57:845-850. (136) WEIR JB. New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol 1949;109:1-9. Master thesis in Clinical Nutrition, Anu Koivisto 2009 82 (137) Cunningham JJ. A reanalysis of the factors influencing basal metabolic rate in normal adults. Am J Clin Nutr 1980;33:2372-2374. (138) Thompson J, Manore MM. Predicted and measured resting metabolic rate of male and female endurance athletes. J Am Diet Assoc 1996;96:30-34. (139) Altman DG. Clinical Trials: Sample size. Practical Statistics for Medical Research. USA: Chapman and Hall/CRC; 1991;455-460. (140) Manore MM. Dietary recommendations and athletic menstrual dysfunction. Sports Med 2002;32:887-901. (141) Sundgot-Borgen J, Berglund B, Torstveit MK. Nutritional supplements in Norwegian elite athletes--impact of international ranking and advisors. Scand J Med Sci Sports 2003;13:138-144. (142) Teixeira PJ, Going SB, Sardinha LB, Lohman TG. A review of psychosocial pre-treatment predictors of weight control. Obes Rev 2005;6:43-65. (143) Kajioka T, Tsuzuku S, Shimokata H, Sato Y. Effects of intentional weight cycling on non-obese young women. Metabolism 2002;51:149-154. (144) Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med 1995;332:621-628. (145) Steen SN, Oppliger RA, Brownell KD. Metabolic effects of repeated weight loss and regain in adolescent wrestlers. JAMA 1988;260:47-50. (146) Black AE. Dietary assessment for sports dietetics [abstract]Black AE. British Nutrition Bulletin 2001;26:29-42 (147) Magkos F, Yannakoulia M. Methodology of dietary assessment in athletes: concepts and pitfalls. Curr Opin Clin Nutr Metab Care 2003;6:539-549. (148) Deakin V. Measuring nutritional status of athletes. In: Burke L, Deakin V, eds. Clinical sports nutrition. 3rd edition ed. Australia: McGraw-Hill; 2006;21-51. (149) Oppliger RA, Case HS, Horswill CA, Landry GL, Shelter AC. American College of Sports Medicine position stand. Weight loss in wrestlers. Med Sci Sports Exerc 1996;28:ix-xii. Master thesis in Clinical Nutrition, Anu Koivisto 2009 83 (150) Brehm BJ, D'Alessio DA. Benefits of high-protein weight loss diets: enough evidence for practice? Curr Opin Endocrinol Diabetes Obes 2008;15:416421. (151) Horber FF, Thomi F, Casez JP, Fonteille J, Jaeger P. Impact of hydration status on body composition as measured by dual energy X-ray absorptiometry in normal volunteers and patients on haemodialysis. Br J Radiol 1992;65:895900. (152) SHEPHARD RJ. A critical examination of the Douglas bag technique. J Physiol 1955;127:515-524. (153) Mills J. The use of an infra red analyser in testing properties of Douglas bag [abstract]Mills J. J Physiol 1951;116:22-23 (154) Ryan AS, Pratley RE, Elahi D, Goldberg AP. Resistive training increases fatfree mass and maintains RMR despite weight loss in postmenopausal women. J Appl Physiol 1995;79:818-823. (155) Finaud J, Degoutte F, Scislowski V, Rouveix M, Durand D, Filaire E. Competition and food restriction effects on oxidative stress in judo. Int J Sports Med 2006;27:834-841. (156) Koral J, Dosseville F. Combination of gradual and rapid weight loss: Effects on physical performance and psychological state of elite judo athletes. J Sports Sci 2009;27:115-120. (157) Ciloglu F, Peker I, Pehlivan A et al. Exercise intensity and its effects on thyroid hormones. Neuro Endocrinol Lett 2005;26:830-834. (158) Fatourechi V. Subclinical hypothyroidism: an update for primary care physicians. Mayo Clin Proc 2009;84:65-71. (159) Luke A, Schoeller DA. Basal metabolic rate, fat-free mass, and body cell mass during energy restriction. Metabolism 1992;41:450-456. (160) Ravussin E, Bogardus C. A brief overview of human energy metabolism and its relationship to essential obesity. Am J Clin Nutr 1992;55:242S-245S. (161) Cunningham JJ. Body composition as a determinant of energy expenditure: a synthetic review and a proposed general prediction equation. Am J Clin Nutr 1991;54:963-969. Master thesis in Clinical Nutrition, Anu Koivisto 2009 84 (162) McCargar LJ, Simmons D, Craton N, Taunton JE, Birmingham CL. Physiological effects of weight cycling in female lightweight rowers. Can J Appl Physiol 1993;18:291-303. (163) Speakman JR, Selman C. Physical activity and resting metabolic rate. Proc Nutr Soc 2003;62:621-634. Master thesis in Clinical Nutrition, Anu Koivisto 2009 85 List of appendices Appendix 1: Summary of weight loss studies with athletes Appendix 2: Approval from Regional Ethics Committee of Norway Appendix 3: Approval from Appendix 4: Information letter to sport federations Appendix 5: Information letter to participants Appendix 6: Dietary registration scheme Appendix 7: Screening questionnaire Appendix 8: Strength training programme Appendix 9: Example meal plan Master thesis in Clinical Nutrition, Anu Koivisto 2009 Study Population N Duration 19 1 week Design Results Walberg et al weight RCT BW -4.9%(MP) -4.6% (HP), FFM -3.7%(MP) -2%(HP) 1988 lifters Energy restriction (75kJ/kg per day) No difference in FM, FFM changes between the groups. M Moderate (0.8g/kg BW) vs high protein (1.6g/kg BW) Only high protein produced positive protein balance. Horsewill et al athletes 12 4 days RCT, cross-over BW -6% energy restriction high CHO vs low CHO Sprint work was higher in low CHO than high CHO diet. Energy restriction (<30kcal/kg BW) BW -6.8%(WC), FFM -5.4% Clinical trial, preseason-post season RMR/LBM – 12% weight cyclers (WC) vs non-weight cyclers (NWC) No changes in any variable among NWC. Clinical trial, energy restriction 92kJ/FFM/day No significant differences in aerobic performance. Normal CHO versus high CHO diet Power output reduced in normal but not in high CHO group. 2.4 days/ RCT BW -5% 3 weeks Rapid (2.4day) and gradual (3 week) weight Increased jump height in gradual WL. reduction by energy restriction and dehydration Low micronutrient intake. Reduced s-magnesium in gradual WL Part I: 2month weight loss with energy restriction BW -6-7% (50%FFM) for part I and part II 1990 Appendix 1 Master thesis in Clinical Nutrition, Anu Koivisto 2009 Table 2.6. Summary of weight reduction studies on athletes from 1988*. Elevated tension, anger, confusion and fatigue in both groups. Melby et al wrestlers 1990 M McMurray et al wrestlers 25 12 4-6 month 7 days 1991 Fogelholm et al judoists 1993 wrestlers 10 M Koutedakis et al rowers W 1994 F Iwao et al boxers 1996 F,M Morris et al rowers 1996 F,M 6 2months/ 4 months 12 2 weeks 18 Rankin et al wrestlers 1996 M 12 Roemmich et al wrestlers 1997 M Choma et al wrestlers 14 Parkes et al endurance 14 1998 athletes 3 days 9 Reduced anaerobic treshold and strenght (Part I) Part II: 4month weight loss with energy restriction Improved anaerobic treshold (Part II) Clinical trial, 2 vs 6 meals per day BW -8%, larger LBM decrease (6.9%) and myoprotein Energy restriction (5.2MJ/day) catabolism (3Me/Cr) in 2 meal group. RQ decreased for both. Observational study BW -6-7% Weight loss during pre season and season by No change in LBM exercise and reduced fat and total energy intake FM (F) -12% FM(M) -23% Clinical trial BW -3.3% Energy restriction (75kJ/kg per day), 60E% CHO Reduced work and power during high-intensity exercise. Clinical trial BW -4%, LBM -2% weight loss during season (pre-post) Reduced s-prealbumin. rapid weight loss and dehydration Reduced BW, short-term memory, plasma glucose RCT BW reduced 2.6%, body fat% reduced by 2.9% energy restriction (75% kJ) Fat oxidation increased 1998 and volume 86 F 12 days No change in estimated LBM. No change in muscle function Continued on next page Master thesis in Clinical Nutrition, Anu Koivisto 2009 Table 2.6 Continued Study Population Kowatari et al judoists 2001 M Filaire et al judoists 2001 M N Duration 18 20 days 11 Clinical trial. Very low energy intake (VLE) versus BW -4%, LBM reduced only for VLE (-3.2%). No difference in low energ intake (LE) leukocytt count, but reduced phagocytic activty in VLE. Clinical trial BW - 4.9%, FFM – 3.7% Energy restriction (by own choice of means) Decreased performance (jump and strenght) Post hoc analysis: 30% CR, 1.2g protein /kg/d Elevated anger and fatigue. Low CHO and micronutrient intake. RCT BW -3.7%, no diference in WL.Larger FFM reduction (-2.4%) in resistance 2001 trainers Energy restriction combined with placebo group, but urinary nitrogen losses were similar. M creatine supplementation or placebo Trend for higher total work in sprint in creatine group Clinical trial, energy restrction BW -4% Streght training and diet vs diet alone Total LBM -2.8%, no difference between groups. Clinical trial, <4%WL vs >4% WL No body composition data. Energy restriction No difference in leukocytt counts between the groups. weight 2002 class Imai et al wrestlers 2002 M Umeda et al judoists 2004 M 13 4 days Results Rockwell et al Garthe 16 7 days Design 6 weeks athletes, M No difference in performance between the groups 18 1 month Reduced responsiveness to CD3 stimulation in >4% WL. 27 20 days Clinical trial, <4%WL vs >4% WL FFM reduced 2.4-3.3%, no difference between groups Energy restriction by own choice of means Maximal power reduced for high WL group Post hoc analysis: 42-48 %CR, ~0.9g protein/kg/d Finaud et al judoists 2006 M Slater et al rowers 2006 M Koral et al judoists 2009 F,M 20 3 20 7 days RCT BW -5% , LBM -3.6% Energy restriction (by own choice of means) Antioxidant status; no difference Post hoc analysis: 33% CR, 0.8g PRO/kg BW between weight loss and control group 16 weeks 3 case studies BW, LBM, FM reduced for all. RMR reduced most for the case Energy restriction with largest BW and LBM loss and lowest baseline body fat %. 4 weeks Prospective controlled study BW -3.9%, body fat -1.7%. Energy restriction (4MJ) and additional No difference in jump, power or sprint, but reduced 30 second dehydration during the last 6 days exercise performance. Increased confuion and reduced vigour. calorie restriction or weight regulation. BW= body weight, FFM= fat free mass, LBM= lean body mass, FM= fat mass, F=females, M=males, WL= weight loss, RCT= randomised controlled trial, nd= no data 87 *Clinical trials and randomised controlled trials from Pubmed. Search words; athlete and one of the following: weight loss, weight reduction, energy restriction, 88 Appendix 2 Master thesis in Clinical Nutrition, Anu Koivisto 2009 89 Master thesis in Clinical Nutrition, Anu Koivisto 2009 90 Appendix3 Master thesis in Clinical Nutrition, Anu Koivisto 2009 91 Master thesis in Clinical Nutrition, Anu Koivisto 2009 92 Appendix 4 Informasjon til særforbund om deltakelse i forskningsprosjekt for Idrettsutøvere Vi henvender oss til idrettstøvere i utvalgte særforbund for å spør om de kan tenke seg å være med på en studie i regi av Norges Idrettshøgskole og Olympiatoppen. Hensikten med forskningsprosjektet er å se hvordan den veiledningen som gis på Olympiatoppen når det gjelder ernæring, vektregulering og forstyrret spiseatferd virker. Bakgrunn Idrettsutøvere har et økt behov for energi og næringsstoffer. Valg av matvarer, måltidsfrekvens, timing av måltider og restitusjon er viktige faktorer i et treningsregime for å få maksimalt utbytte av utøvers potensial. Dette kan by på flere utfordringer for noen utøvere: energiinntak (kaloriinntak) i forhold til forbruk, tilstrekkelig inntak av makro- og mikronæringsstoffer og planlegging og tilrettelegging av måltider. Ernæringsavdelingen, treningsavdelingen og helseavdelingen på Olympiatoppen har i de siste årene tilbudt veiledning på styrketrening, vektregulering og behandling av utøvere med forstyrret spiseatferd/spiseforstyrrelser. Vi ønsker nå å teste ut effekten av de veiledningsregimene vi tilbyr. Regimene inkluderer kost- og treningsveiledning og vil bli tilrettelagt din idrett i samarbeid med deg og evt. din trener. Formål Formålet med denne studien er følgende: 1) Se på effekten av en 24 ukers behandling/veiledning av utøvere med forstyrret spiseatferd/spiseforstyrrelse, menstruasjonsforstyrrelser og redusert beinmasse 2) Se på effekten av 6-12 ukers veiledning på vektreduksjon 3) Se på effekten av 6-12 ukers veiledning på vektøkning Metode Utøvere som henvender seg til Olympiatoppens helseavdeling og ernæringsavdeling vil få avtale om tid for en samtale med Professor Jorunn Sundgot-Borgen. I forbindelse med denne samtalen vil det bli klargjort hvilke behov utøveren har og hva han/hun ønsker hjelp til, og utøverne blir således delt inn i: triade, vektreduksjon og vektøkning.Utøverne blir så randomisert inn i to grupper, veiledning I og veiledning II, der vi ønsker å se på effekten av de ulike veiledningsregimene. Hvem blir forespurt om å delta? Juniorer og seniorer (landslagsutøvere – A, B og rekrutter) i utvalgte særforbund som er Master thesis in Clinical Nutrition, Anu Koivisto 2009 93 medlem av Norges Idrettsforbund, samt elever/utøvere ved Norges Toppidrettsgymnas, Wang Toppidrettsgymnas. Primært vil det være utøvere som henvender seg til Olympiatoppens helseavdeling, ernæringsavdeling eller treningsavdeling for følgende veiledning: 1) 2) 3) Vektøkning (vektøkning i form av økt muskelmasse) Vektreduksjon (vektreduksjon i form av tap av fettmasse) Veiledning i forhold til forstyrret spiseadferd/spiseforstyrrelser, menstruasjonsforstyrrelser eller påvist tap av beinmasse Hva skal du gjøre dersom du blir med? • • En samtale med Jorunn Sundgot-Borgen Fylle ut spørreskjema Målinger som blir gjort i forbindelse med studien • • • • • • Måle kroppssammensetning (DXA og kaliper) Blodprøve: Østradiol, progesteron, LH, FSH, DHEA, testosteron, kortisol, T3, T4, TSH, IGF-1, jern, B12, kolesterol, HDL, LDL, triglyserider, albumin, kalsium. Styrketester 4 dagers veid kostregistrering Mat og treningsdagbok Mental evaluering: EDE, EDI, Contingent self-esteem Scale. De involverte i prosjektet er underlagt taushetsplikt og prosjektet er meldt til personvernombudet for forskning. Blodprøvene vil bli oppbevart i en biobank uten kommersielle interesser (vurdert av Regional Etisk Komité). Prøvene vil bli lagret i inntil 10 år. Andre forskningsdata vil bli anonymisert i utgangen av 2016. Ansvarlig for biobanken er Professor Jorunn Sundgot-Borgen ved NIH. Dersom utøver/foreldre ønsker å tilbakekalle samtykket, kan dere kreve det biologiske materialet destruert og innsamlede helse- og personopplysninger slettet eller utlevert. Vi startet undersøkelsen i januar 2006 og regner med å avslutte desember 2008. Det er selvfølgelig frivillig å delta i undersøkelsen og om du ønsker det, kan du trekke seg fra studien uten grunn når du vil. Dersom du vil være med på studien, ber vi deg skrive under på en samtykkeerklæring på neste side. Dersom du er under 18 år skal dine foreldre informeres om studien. De har således mulighet til å nekte deltakelse på vegne av deg (se vedlagt skriv). Dersom du er under 16 år må vi ha dine forelders skriftlige godkjennelse (se vedlagt skriv). Vi vil samarbeide med trenere og ledere slik at forsøket legges til rette med tanke på å forstyrre sesongen minst mulig. Du vil få mulighet til å gå igjennom en del tester som en vanligvis ikke får anledning til, og det er ikke knyttet risiko eller smerte til noen av testene. Du vil også få en profesjonell vurdering av kostholdet, og nøye oppfølging gjennom den perioden du er med på undersøkelsen. Som forsøksperson er du forsikret gjennom forsøket, slik at de er sikret økonomisk kompensasjon for eventuelle skader eller komplikasjoner. Olympiatoppens helseavdeling, ernæringsavdeling og treningsavdeling er med i teamet. Prosjektleder for studien er Professor Jorunn Sundgot-Borgen og dr.grad stipendiat Ina Garthe (som for tiden er erstattet av Anu Koivisto) . Medisinsk ansvarlig er Olympiatoppens sjefslege Professor Lars Engebretsen. Master thesis in Clinical Nutrition, Anu Koivisto 2009 94 For spørsmål, kontakt Anu eller Ina: Anu Koivisto: [email protected] / 45465743 Ina Garthe: [email protected] Med vennlig hilsen Jorunn Sundgot-Borgen (sign.) Ina Garthe (sign.) Jarle Aambø (sign.) Professor dr.grad stipendiat Toppidrettssjef Norges idrettshøgskole Norges idrettshøgskole Olympiatoppen Olympiatoppen Olympiatoppen Master thesis in Clinical Nutrition, Anu Koivisto 2009 95 Appendix 5 Forespørsel om deltakelse i forskningsprosjekt for Idrettsutøvere Vi henvender oss til deg som utøver og spør om du kan tenke deg å være med på en studie i regi av Norges Idrettshøgskole og Olympiatoppen. Hensikten med forskningsprosjektet er å se hvordan den veiledningen som gis på Olympiatoppen når det gjelder ernæring, vektregulering og forstyrret spiseatferd virker. Bakgrunn Idrettsutøvere har et økt behov for energi og næringsstoffer. Valg av matvarer, måltidsfrekvens, timing av måltider og restitusjon er viktige faktorer i et treningsregime for å få maksimalt utbytte av utøvers potensial. Dette kan by på flere utfordringer for noen utøvere: energiinntak (kaloriinntak) i forhold til forbruk, tilstrekkelig inntak av makro- og mikronæringsstoffer og planlegging og tilrettelegging av måltider. Ernæringsavdelingen og helseavdelingen på Olympiatoppen har i de siste årene tilbudt veiledning på vektregulering og behandling av utøvere med forstyrret spiseatferd/spiseforstyrrelser. Vi ønsker nå å teste ut effekten av de veiledningsregimene vi tilbyr. Formål Formålet med denne studien er følgende: 4) Se på effekten av en 24 ukers behandling/veiledning av utøvere med forstyrret spiseatferd/spiseforstyrrelse, menstruasjonsforstyrrelser og redusert beinmasse 5) Se på effekten av 6-12 ukers veiledning på vektregulering (vektøkning, vektreduksjon) 6) Se på effekten av kostoptimalisering Metode Utøvere som henvender seg til Olympiatoppens helseavdeling og ernæringsavdeling vil få avtale om tid for en samtale med Professor Jorunn Sundgot-Borgen. I forbindelse med denne samtalen vil det bli klargjort hvilke behov utøveren har og hva han/hun ønsker hjelp til, og utøverne blir således delt inn i: triade, vektreduksjon, vektøkning og kostoptimalisering. Utøverne blir så randomisert inn i to grupper, veiledning I og veiledning II, der vi ønsker å se på effekten av de ulike veiledningsregimene. Hvem blir forespurt om å delta? Master thesis in Clinical Nutrition, Anu Koivisto 2009 96 Juniorer og seniorer (landslagsutøvere – A, B og rekrutter) i utvalgte særforbund som er medlem av Norges Idrettsforbund, samt elever/utøvere ved Norges Toppidrettsgymnas, Wang Toppidrettsgymnas. Primært vil det være utøvere som henvender seg til Olympiatoppens helseavdeling, ernæringsavdeling eller treningsavdeling for følgende veiledning: 1) 2) 3) 4) kostoptimalisering (optimalisering av kostholdet i forhold til din idrett) Vektøkning (vektøkning i form av økt muskelmasse) Vektreduksjon (vektreduksjon i form av tap av fettmasse) Veiledning i forhold til forstyrret spiseadferd/spiseforstyrrelser, menstruasjonsforstyrrelser eller påvist tap av beinmasse Hva skal du gjøre dersom du blir med? • • En samtale med Jorunn Sundgot-Borgen Fylle ut et spørreskjema Målinger som blir gjort i forbindelse med studien • • • • • • Måle kroppssammensetning (DXA og kaliper) Blodprøve: Østradiol, progesteron, LH, FSH, DHEA, testosteron, leptin, kortisol, T3, T4, TSH, IGF-1, jern, B12, kolesterol, HDL, LDL, triglyserider, albumin, kalsium. Styrketester 4 dagers veid kostregistrering Mat og treningsdagbok Mental evaluering: EDE, EDI, Contingent self-esteem Scale. De involverte i prosjektet er underlagt taushetsplikt og prosjektet er meldt til personvernombudet for forskning. Blodprøvene vil bli oppbevart i en biobank uten kommersielle interesser (vurdert av Regional Etisk Komite). Prøvene vil bli lagret i inntil 10 år. Andre forskningsdata vil bli anonymisert i utgangen av 2016. Ansvarlig for biobanken er Professor Jorunn Sundgot-Borgen ved NIH. Dersom utøver/foreldre ønsker å tilbakekalle samtykket, kan dere kreve det biologiske materialet destruert og innsamlede helse- og personopplysninger slettet eller utlevert. Vi starter undersøkelsen i løpet av januar 2006. Det er selvfølgelig frivillig å delta i undersøkelsen og om du ønsker det, kan du trekke seg fra studien uten grunn når du vil. Dersom du vil være med på studien, ber vi deg skrive under på en samtykkeerklæring på neste side. Dersom du er under 18 år skal dine foreldre informeres om studien. De har således mulighet til å nekte deltakelse på vegne av deg (se vedlagt skriv). Dersom du er under 16 år må vi ha dine forelders skriftlige godkjennelse (se vedlagt skriv). Vi vil samarbeide med trenere og ledere slik at forsøket legges til rette med tanke på å forstyrre sesongen minst mulig. Du vil få mulighet til å gå igjennom en del tester som en vanligvis ikke får anledning til, og det er ikke knyttet risiko eller smerte til noen av testene. Du vil også få en profesjonell vurdering av kostholdet, og nøye oppfølging gjennom den perioden du er med på undersøkelsen. Som forsøksperson er du forsikret gjennom forsøket, slik at de er sikret økonomisk kompensasjon for eventuelle skader eller komplikasjoner. Master thesis in Clinical Nutrition, Anu Koivisto 2009 97 Olympiatoppens helseavdeling, ernæringsavdeling og treningsavdeling er med i teamet. Prosjektleder for studien er Professor Jorunn Sundgot-Borgen og stipendiat er Cand.Scient Ina Garthe. Medisinsk ansvarlig er Olympiatoppens sjefslege Professor Lars Engebretsen. Jorunn Sundgot-Borgen: 23262335 [email protected] Ina Garthe: 2300000/99003916 [email protected] Anu Koivisto:45465743 [email protected] Med vennlig hilsen Jorunn Sundgot-Borgen Ina Garthe Jarle Aambø Professor Cand.Scient Toppidrettssjef Norges idrettshøgskole Norges idrettshøgskole Olympiatoppen Olympiatoppen Olympiatoppen Master thesis in Clinical Nutrition, Anu Koivisto 2009 98 Samtykkeerklæring for utøver Ja, jeg har lest informasjonsskrivet og blitt muntlig informert om studien og vet hva inklusjonen innebærer. Jeg vet at jeg kan trekke meg når som helst underveis, uten grunn. Jeg samtykker herved å delta i studien. Dato:………….. Sted:………………. Underskrift utøver:…………………………………………………………………………… Samtykkeerklæring for foresatte dersom utøver er under 16 år Ja, jeg har lest informasjonsskrivet og sier meg enig i at min sønn/datter kan delta i studien. Dato:………….. Sted:………………. Underskrift foresatt:……………………………………………………………………… Master thesis in Clinical Nutrition, Anu Koivisto 2009 99 Appendix 6 4-DAGERS KOSTREGISTRERING FOR IDRETTSUTØVERE Navn: …………………………………………………………………….. Adresse: …………………………………………………………………….. Telefon: …………………………………………………………………….. E-mail: …………………………………………………………………….. Idrett: …………………………………………………………………….. Dato (fra-til): …………………………………………………………………….. Alder:……… Høyde:…..…… Vekt::……… Veiledning for kostregistreringen • Du skal registrere kostholdet ditt i 4 dager (3 ukedager + 1 lørdag) • Prøv å unngå at kostregistreringen forandrer matvanene dine - spis slik du vanligvis gjør! • Skriv ned alt du spiser og drikker, også evt. kosttilskudd • Skriv ned evt. væskeinntak og matinntak under trening på sidene for treningsregistreringen • Start med det første måltidet den dagen registreringen begynner. Fyll inn de hoved- og mellommåltidene du spiser. For hvert måltid skal følgende skrives ned: 1) Klokkeslett 2) Navnet på matvaren eller retten → gi flest mulig opplysninger - Birkebeinerbrød, Norvegia ost F45, Nora jordbærsyltetøy, lett melk, 5 kr Freia melkesjokolade - oppskrift på hjemmelagete retter (skriv oppskriften bak på arket) - evt. hvordan retten er tilberedt (kokt, stekt) 3) Mengde av matvaren eller retten → oppgi mengde i gram hvis du har vekt Master thesis in Clinical Nutrition, Anu Koivisto 2009 100 → oppgi mengde i husholdningsmål hvis du ikke har vekt - antall, stykker, spiseskje, teskje, glass, kopp, dl • Ring mg hvis du har noen spørsmål: # 45465743 eller mail: [email protected] • Send eller e-mail registreringen på Toppidrettsenteret så snart du er ferdig Toppidrettssenteret /Anu Koivisto Postboks 4004 Ullevål Stadion N-0806 Oslo Lykke til! Hilsen Anu Koivisto Master thesis in Clinical Nutrition, Anu Koivisto 2009 101 Dag 1 Måltid 1 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 2 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 3 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 4 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 5 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 6 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Master thesis in Clinical Nutrition, Anu Koivisto 2009 Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. 102 TRENINGSREGISTRERING Dag 1 NB! Skriv ned væskeinntak og matinntak (mengde og type) hvis du bruker det under trening DAG 1 Økt 1 Kl. ………..…….. Type trening og intensitet ……………………………………………………………..…. ……………………………………………………………..…. Type væske-mat inntak ……………………………………………………………..…. Økt 2 Varighet ……………………. ……………………. Mengde ……………………. Kl. ………..…….. Type trening og intensitet Varighet ……………………………………………………………..…. ……………………. ……………………………………………………………..…. ……………………. Type væske-mat inntak Mengde ……………………………………………………………..…. ……………………. Kommentarer til kostregistrering/treningsregistrering: ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ……………………………………………………………………………………………… Master thesis in Clinical Nutrition, Anu Koivisto 2009 103 Dag 2 Måltid 1 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 2 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 3 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 4 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 5 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 6 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Master thesis in Clinical Nutrition, Anu Koivisto 2009 Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. 104 TRENINGSREGISTRERING Dag 2 NB! Skriv ned væskeinntak og matinntak (mengde og type) hvis du bruker det under trening DAG 1 Økt 1 Kl. ………..…….. Type trening og intensitet ……………………………………………………………..…. ……………………………………………………………..…. Type væske-mat inntak ……………………………………………………………..…. Økt 2 Varighet ……………………. ……………………. Mengde ……………………. Kl. ………..…….. Type trening og intensitet Varighet ……………………………………………………………..…. ……………………. ……………………………………………………………..…. ……………………. Type væske-mat inntak Mengde ……………………………………………………………..…. ……………………. Kommentarer til kostregistrering/treningsregistrering: ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… Master thesis in Clinical Nutrition, Anu Koivisto 2009 105 Dag 3 Måltid 1 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 2 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 3 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 4 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 5 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 6 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Master thesis in Clinical Nutrition, Anu Koivisto 2009 Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. …………. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. 106 TRENINGSREGISTRERING Dag 3 NB! Skriv ned væskeinntak og matinntak (mengde og type) hvis du bruker det under trening DAG 1 Økt 1 Kl. ………..…….. Type trening og intensitet ……………………………………………………………..…. ……………………………………………………………..…. Type væske-mat inntak ……………………………………………………………..…. Økt 2 Varighet ……………………. ……………………. Mengde ……………………. Kl. ………..…….. Type trening og intensitet Varighet ……………………………………………………………..…. ……………………. ……………………………………………………………..…. ……………………. Type væske-mat inntak Mengde ……………………………………………………………..…. ……………………. Kommentarer til kostregistrering/treningsregistrering: ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… Master thesis in Clinical Nutrition, Anu Koivisto 2009 107 Dag 4 Måltid 1 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 2 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 3 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 4 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 5 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Måltid 6 Matvarer/retter …………………………………………………………. …………………………………………………………. …………………………………………………………. …………………………………………………………. Master thesis in Clinical Nutrition, Anu Koivisto 2009 Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………... Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. Kl. ………….. Mengde ……………………………. ……………………………. ……………………………. ……………………………. 108 TRENINGSREGISTRERING Dag 4 NB! Skriv ned væskeinntak og matinntak (mengde og type) hvis du bruker det under trening DAG 1 Økt 1 Kl. ………..…….. Type trening og intensitet ……………………………………………………………..…. ……………………………………………………………..…. Type væske-mat inntak ……………………………………………………………..…. Økt 2 Varighet ……………………. ……………………. Mengde ……………………. Kl. ………..…….. Type trening og intensitet Varighet ……………………………………………………………..…. ……………………. ……………………………………………………………..…. ……………………. Type væske-mat inntak Mengde ……………………………………………………………..…. ……………………. Kommentarer til kostregistrering/treningsregistrering: ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… ………………………………………………………………………………………………………… Master thesis in Clinical Nutrition, Anu Koivisto 2009 109 Appendix 7 Master thesis in Clinical Nutrition, Anu Koivisto 2009 110 Master thesis in Clinical Nutrition, Anu Koivisto 2009 111 Master thesis in Clinical Nutrition, Anu Koivisto 2009 112 Appendix 8 TRENINGSPROGRAM FOR Å ØKE MUSKELSTØRRELSE Ma Ti To Fr Benkpress Liggende roing Chins evt. nedtr. nakke Pec deck Stående opptrekk Deltaraise Sidel. kroppshev Rygg-ups rett rygg Styrkevending Svikthopp med 0-40 kg Knebøy Markløft Leg extension Leg curl Dips Bicepscurl manual Bjørndalen Rotary torso Benkpress Liggende roing Nedtrekk mot bryst Flies i kabelapparat Stående opptrekk Shoulderpress Sidel. Kroppshev Rygg-ups rull opp Styrkevending Knebøy 90 grader Knebøy Markløft Hack-lift Strak mark Triceps pushdown Bicepscurl Z-stang Brutalbenk Stå buk rot skive Master thesis in Clinical Nutrition, Anu Koivisto 2009 Uke 1-3 1 x 12.10.8 1 x 12.10.8 3 x maks 3 x 12 3 x 12 3 x 12 3 x 12 3 x 15 2x5 2x5 1 x 12.10.8 3 x 10 3 x 12 3 x 12 3 x maks 3 x 12 3 x 15 3 x 12 1 x 12.10.8 1 x 12.10.8 3 x 12 3 x 12 3 x 12 3 x 12 3 x 12 3 x 15 2x5 2x6 1 x 12.10.8 3 x 10 3 x 12 3 x 12 3 x 12 3 x 12 3 x maks 3 x 12 Uke 4-8 1 x 12.10.8.6 1 x 12.10.8.6 4 x maks 4 x 10 4 x 10 4 x 10 3 x 10 3 x 12 3x4 3x4 1 x 12.10.8.6 4x8 4 x 10 4 x 10 4 x maks 4 x 10 3 x 12 3 x 10 1 x 12.10.8.6 1 x 12.10.8.6 4 x 10 4 x 10 4 x 10 4 x 10 3 x 10 3 x 12 3x4 3x6 1 x 12.10.8.6 4x8 4 x 10 4 x 10 4 x 10 4 x 10 3 x maks 3 x 12 Uke 9-12 1 x 10.8.6.6.6 1 x 10.8.6.6.6 5 x maks 5x8 5x8 5x8 3x8 3 x 10 4x4 4x4 1 x 10.8.6.6.6 5x5 5x8 5x8 5 x maks 5x8 3 x 10 3x8 1 x 10.8.6.6.6 1 x 10.8.6.6.6 5x8 5x8 5x8 5x8 3x8 3 x 10 4x4 4x6 1 x 10.8.6.6.6 5x5 5x8 5x8 5x8 5x8 3 x maks 3 x 12 113 Appendix 9 Forslag til dagsmeny for ... Du plasserer måltidene slik det passer som avtalt (prøv å variere pålegg og middag), men det er tre ting som er viktig i forhold til å opprettholde forbrenningen og få best utbytte av treningen: 1) det skal ikke gå mer enn 3 timer mellom hvert måltid 2) du skal aldri begynne treningen på tom mage/sulten 3) du skal alltid ha et inntak av karbohydrat og protein rett etter treningen Ca 07.30 frokost 2 grove brødskiver med pålegg (alternativer til pålegg: lett ost, kokt skinke, cottage cheese, makrell i tomat, lett leverpostei, ev syltetøy) 1 glass appelsinjuice Tran (enten 2 kapsler eller 1 barneskje flytende tran) TRENING Rett etter trening (ca kl 10): 2 dl lett yoghurt/drikkeyoghurt/smoothie med yoghurt og 1 frukt Ca 12.00 lunsj 2 grove brødskiver med pålegg (alternativer til pålegg: kokt egg, makrell i tomat, hvit ost, leverpostei -Husk ekstra grønnsaker på brødskivene!) Ca. 15.30 middag (1) Ca 130g kyllingfilet (alternativer: filet av svin/okse/lam/fisk (evt. tunfisk på boks)) 200 g grønnsaker (salat, stekt, woket, frossenblanding eller dampkokt) ca 1 dl kokt natur ris (fullkornpasta, poteter) Liker du å bruke dressing velg en fettredusert variant eller oljebasert (fransk dressing/olje/balsamico). Du kan spise MYE grønnsaker hvis du er sulten. TRENING Rett etter trening: 3dl sjokolademelk eller Recovery drink Ca. 20.00 kveldsmat 2 grove knekkebrød med cottage cheese, kokt skinke, lett ost eller tunfisk med paprika 1 frukt (eple, appelsin osv) Husk å drikke minst 2L liter vann utenom treningene og 0,5-1/t i løpet av treningsøktene! Master thesis in Clinical Nutrition, Anu Koivisto 2009
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