International Journal of Sport Nutrition and Exercise Metabolism, 2008, 18, 19-36 © 2008 Human Kinetics, Inc.
Effect of Glycine Propionyl-L-Carnitine
on Aerobic and Anaerobic Exercise
Performance
Webb A. Smith, Andrew C. Fry, Lesley C. Tschume,
and Richard J. Bloomer
The purpose of this study was to evaluate the effect of glycine propionyl-Lcarnitine (GPLC) supplementation and endurance training for 8 wk on aerobicand anaerobic-exercise performance in healthy men and women (age 18–44 yr).
Participants were randomly assigned to 1 of 3 groups: placebo (n = 9), 1 g/d GPLC
(n = 11), or 3 g/d GPLC (n = 12), in a double-blind fashion. Muscle carnitine
(vastus lateralis), VO2peak, exercise time to fatigue, anaerobic threshold, anaerobic
power, and total work were measured at baseline and after an 8-wk aerobic-training
program. There were no statistical differences (p > .05) between or within the 3
groups for any performance-related variable or muscle carnitine concentrations
after 8 wk of supplementation and training. These results suggest that up to 3 g/d
GPLC for 8 wk in conjunction with aerobic-exercise training is ineffective for
increasing muscle carnitine content and has no significant effects on aerobic- or
anaerobic-exercise performance.
Keywords: skeletal muscle, dietary supplements, GXT, Wingate
The benefits of aerobic exercise for the cardiorespiratory system are well documented. It has been shown to increase VO2max and aerobic endurance (American College of Sports Medicine [ACSM], 2005; Callister, Shealy, Fleck, & Dudley, 1988;
Demarle et al., 2001; Fritz, 1979) in both trained and untrained populations, with
the largest improvements reported for sedentary individuals because of their low
initial level of fitness. Improvements in VO2peak of 10–30% have been traditionally
reported in untrained individuals (ACSM); however, the Family Heritage Study has
reported changes in VO2peak ranging from 0 to 53% after a 20-week aerobic-training
program (Bouchard et al., 1999). In addition, in populations in which low initial
fitness has been noted, minor improvements in anaerobic power have been observed
(Gaiga & Docherty, 1995; Rotstein, Dotan, Bar-Or, & Tenenbaum, 1986).
The dietary nutrient L-carnitine (LC) has also been used as an aid to improve
aerobic-exercise capacity (i.e., increase VO2peak, endurance time, and free-fattyacid use), with positive findings reported in some studies using healthy individuals
The authors are with the Dept. of Health and Sport Sciences, University of Memphis, Memphis, TN
38152.
19
20 Smith et al.
(Dragan, Vasiliu, Eremia, & Georgescu, 1987; Gorostiaga, Maurer, & Echlache,
1989; Marconi, Sassi, Carpinelli, & Cerretelli, 1985; Muller, Seim, Kiess, Loster, &
Richter, 2002; Vecchiet et al., 1990; Wutzke, & Lorenz, 2004), as well as a number
of studies that used patients with cardiovascular diseases (Bremer, 1983; Cacciatore
et al., 1991; Campos et al., 1993; Kamikawa et al., 1984; Siliprandi, Di Lisa, &
Menabo, 1990). The mechanisms of action that might explain improvements in
aerobic performance after LC supplementation have not been clearly identified but
might be contingent on increasing lipid metabolism. In order for fatty acids to be
metabolized they first must enter the inner mitochondrial matrix. Fatty acids by
themselves cannot penetrate the membranes of the mitochondria. They must have a
carrier that can penetrate both the outer and inner mitochondrial membranes. These
carriers are carnitine acyl transferase enzymes, which can move freely through the
membranes. There are two specific enzymes that work in this way. Carnitine acyl
transferase 1 acts to convert the fatty acid to a fatty acyl carnitine that can advance
through the outer membrane. Once it is through the outer membrane, carnitine
transferase 2 reverses the action and reforms the fatty acid. Once the fatty acid
is reformed by the carnitine transferase 2 enzyme, it can undergo beta oxidation
and be used for energy production. Studies measuring substrate utilization during
exercise have noted mixed results, however, with minimal increase in fatty-acid
oxidation (Heinonen, 1996; Heinonen, Takala, & Kvist, 1992; Vukovich, Costill,
& Fink, 1994; Wyss, Ganzit, & Rienzi, 1990).
More specific forms of LC, including propionyl-L-carnitine (PLC), a pharmaceutical agent used specifically to treat circulatory diseases such as peripheral artery
disease, also appear to be associated with improvements in circulation and blood
perfusion beyond those observed with LC supplementation alone (Brevetti, Diehm,
& Lambert, 1999; Ferrari, Ceconi, Curello, Pasini, & Visioli, 1989). Although PLC
has been used with success in patients with cardiovascular-related diseases (Loffredo et al., 2007), no investigations using healthy individuals have been conducted.
Moreover, few investigations (Arenas et al., 1991, 1994; Huertas et al., 1992; Lee,
Lee, & Park, 2007) have studied the combined effect of aerobic-exercise training
and LC supplementation on aerobic-exercise performance, and, in those studies,
the effect of LC supplementation on aerobic-exercise performance was either not
reported (Arenas et al., 1991, 1994; Huertas et al.) or not well explained (Lee et
al.). For example, in a recent study, Lee et al. reported no improvement in VO2max
after LC supplementation but failed to report the actual data or methods of data
collection for this variable.
A novel nutrient that mimics the action of PLC but also contains the amino
acid glycine in a molecularly bonded form has recently been developed (glycine
propionyl-L-carnitine [GPLC]). Glycine is a precursor to carnitine biosynthesis
and has been suggested to increase nitric oxide concentrations (Hafidi, Perez, &
Banos, 2006), which might positively influence physical performance. No studies, however, have investigated the effects of GPLC supplementation on muscle
carnitine concentrations or exercise performance in healthy or diseased populations. Theoretically, combining GPLC with aerobic-exercise training could have an
additive effect on exercise performance compared with training alone. Therefore,
the purpose of this investigation was to evaluate the efficacy of GPLC and aerobic
training for 8 weeks on improving aerobic- and anaerobic-exercise performance
in healthy men and women.
Carnitine, Exercise, and Exercise Performance 21
Methods
Participants
Forty-three untrained men and women between the ages of 18 and 44 years were
recruited to participate in the study. Participants could not be current smokers, be
using nutritional supplements, or have any cardiovascular, metabolic, or orthopedic problems that might affect their ability to perform submaximal and maximal
exercise. Health history, drug and nutritional-supplement use, and physical activity
questionnaires were completed by all participants to determine eligibility. Before
the study, each participant was informed of all procedures and potential risks and
benefits associated with the study through both verbal and written form in accordance with procedures approved by the university institutional review board for
human-subjects research.
Baseline Testing
During the initial visit to the laboratory, height, weight, waist and hip circumference, and body fat (seven skinfold sites) were measured. Heart rate (HR) and blood
pressure were recorded after a 10-min period of quiet rest in an isolated room, via
60-s palpation and standard auscultation procedures using a mercury manometer.
Participants were familiarized with the graded exercise test (GXT) while walking
on the treadmill for 4 min (2 min at each of the first two stages of the GXT) while
wearing the face mask used for gas collection. They were familiarized with the
anaerobic-power test by performing a similar cycle sprint test.
Graded Exercise Testing
A maximal GXT using the Bruce protocol was conducted using a motorized treadmill while expired gases were collected via face mask and analyzed (SensorMedics
Vmax 229 metabolic system, Viasys Healthcare, Yorba Linda, CA) for determination
of VO2peak and anaerobic threshold, and data needed to design the individualized
exercise prescriptions for study participants were obtained. The GXT was conducted in the morning (7–10 a.m.) after an overnight fast (minimum of 8 hr), and
participants were asked to avoid strenuous physical tasks during the 48-hr period
preceding it. In all cases, the test continued until volitional fatigue, and the highest
mean 1-min averaged VO2 value obtained during testing, used to represent VO2peak
and total exercise time (in seconds), was also recorded. The anaerobic threshold
was obtained using the V-slope method (plot of CO2 output [VCO2] as a function
of oxygen uptake) as described by Beaver, Wasserman, and Whipp (1986), using
software available with the metabolic system. Data were filtered and analyzed by
the same investigator for all tests.
During the GXT, HR was continuously monitored via electrocardiograph
tracings (SensorMedics Max-1 ECG unit, Viasys Healthcare, Yorba Linda, CA),
and expired gas was continuously monitored via breath-by-breath samples to
determine VO2 and respiratory-exchange ratio. Blood pressure was monitored at
rest and during testing, and the Borg rating of perceived exertion was used by the
participants to indicate their level of perceived effort. Specifically, data on HR,
respiratory-exchange ratio, and rating of perceived exertion were recorded at the
22 Smith et al.
end of each 3-min stage of the GXT for comparison between pre- and postintervention and between groups. The resting HR and blood-pressure values before
the GXT were used for comparisons between pre- and postintervention. After the
test, participants were allowed a passive cool-down until their HR fell below 120
beats/min or stabilized.
Anaerobic-Power Testing
On a separate day from the GXT, participants completed a 30-s test of anaerobic
power on a Lode Excalibur Sport cycle ergometer (Lode B.V. Medical Technology, Groningen, The Netherlands) interfaced with a computer. The force (N) that
participants pedaled against was determined based on their lean body mass and
equal to lean body mass (kg) × 0.7. Before performing the 30-s sprint, participants
underwent a 5-min warm-up using a low intensity (75 W), in which they performed a
3- to 5-s sprint at the top of each minute to familiarize themselves with the protocol.
The peak and mean power relative to lean body mass, fatigue rate, and total work
relative to lean body mass were recorded. All testing (including aerobic-exercise
training) was supervised by a clinical exercise physiologist, and all procedures were
performed in accordance with the established guidelines of the ACSM. Using the
same procedures described here for each test, these same variables were measured
after the 8-week intervention.
Supplementation
After the conclusion of all preintervention tests, participants were provided with
study instructions and were randomized in a double-blind manner to one of the
following three conditions plus aerobic exercise: 1 g cellulose (placebo, n = 9),
348 mg glycine + PLC at 1 g/day (GPLC-1, n = 11), or 1,044 mg glycine + PLC
at 3 g/day (GPLC-3, n = 12). Capsules were provided to participants in unlabeled
bottles every 2 weeks and were identical in appearance. In all conditions participants
ingested three capsules twice daily (morning and evening) to allow for the described
dosages. The GPLC consisted of a molecularly bonded form of PLC and the amino
acid glycine (GlycoCarn, Sigma-tau HealthScience S.p.A, Rome, Italy). This is a
USP-grade nutritional supplement. The actual dose of PLC was provided at either
1 or 3 g/day (~166 or 500 mg PLC per capsule, respectively), whereas the glycine
content was equal to 348 mg in the 1-g/day treatment and 1,044 mg in the 3-g/day
treatment. For ease of reporting throughout this article, we refer to the two dosages
as simply 1 and 3 g/day to reference the actual PLC content. After randomization
all participants began the aerobic-exercise program.
Aerobic-Exercise Training
All participants performed 8 weeks of supervised aerobic exercise consisting of
stationary cycling and walking/jogging (on an outdoor track or indoor treadmill).
The training intensity and duration began at the lower limit of the ACSM recommendations (55–60% HR reserve for 30 min) and progressed to higher levels over
the 8-week period (to 75–85% HR reserve for 45 min; Week 1 = 55–65%, Week 2
= 65–75%, Week 3 = 70–80%, and Weeks 4–8 = 75–85%). The training intensity
Carnitine, Exercise, and Exercise Performance 23
was prescribed in the form of a “target” HR range. HR (via Polar monitors) and
rating of perceived exertion were recorded at three equally spaced times during
each exercise session to ensure that participants were training at the appropriate
intensity, and all exercise logs were maintained by research assistants.
Muscle Biopsies
In a subset of the participant population (n = 18, 6 participants from each group),
a biopsy of the vastus lateralis muscle was taken before and after all testing was
completed, as previously described (Schilling, Fry, Chiu, & Weiss, 2005). Tissue
samples (~30–40 mg) were quick-frozen in isopentane cooled in liquid nitrogen
and immediately stored at –80 °C. Samples were assayed for total, free, and acyl
carnitine (combined short- and long-chain acyl carnitines) using ion-exchange/
reversed-phase HPLC. This procedure has four distinct phases. The first phase
involves isolating carnitine and acyl carnitines by protein precipitation/desalting
and silica-gel cation exchange. The second phase involves derivatization of carnitine
and acyl carnitines with the reagent pentafluorophenacyl trifluoromethane-sulfonate.
The third phase consists of sequential ion-exchange/reversed-phase chromatography of carnitine and acyl carnitine esters. After this, carnitine is detected by mass
spectrometry and tandem mass spectrometry. This multicomponent protocol has
been previously described in detail by Minkler, Ingalls, and Hoppel (2005).
Dietary Records
All participants were instructed to maintain their normal diets during the study
period. Participants completed 7-day food records at Week 1 and Week 8 of the
intervention and were given specific instructions regarding how to record portion
sizes and quantities, in addition to viewing food models to enhance precision.
Records were analyzed for total kilocalories, protein, carbohydrate, fat, and vitamins
C, E, and A using Diet Analysis Plus (ESHA Research, Salem, OR).
Statistical Analysis
Differences between and within groups were analyzed via a 3 (group) × 2 (session—pre- and postintervention) mixed factorial analysis of variance (ANOVA)
using SPSS statistical software (v. 14.0, SPSS, Chicago). When appropriate,
significant interactions (p ≤ 0.05) and main effects were further analyzed using
Tukey’s post hoc tests. Effect-size calculations were performed using Cohen’s d,
and all descriptive data are presented as M ± SD.
Results
Of the 43 participants who were enrolled in the program, only 32 successfully
completed all aspects of the program and were therefore included in the statistical analysis (placebo group = 4 men, 5 women; GPLC-1 = 5 men, 6 women; and
GPLC-3 = 0 men, 12 women). The other 11 participants voluntarily withdrew (n
= 8) or failed to complete the entire program (n = 3).
24 Smith et al.
Compliance
Supplement compliance was measured every 2 weeks via capsule counts on bottle
return and was greater than 95% in all three groups, with no statistical difference
between groups. No adverse side effects of supplementation were reported by
participants. There were no statistical differences between groups for percentage of
exercise sessions completed (placebo 84.3% ± 9.4%, GPLC-1 90.8% ± 7.5%, and
GPLC-3 88.8% ± 10.3%) or percentage of target HR obtained during exercise (placebo 91.3% ± 12.6%, GPLC-1 93.9% ± 7.6%, and GPLC-3 90.5% ± 17.9%).
Descriptive and Dietary Variables
No statistical interaction (p ≤ .05) effect or main effect was noted for age, height,
weight, body-fat percentage, body-mass index, waist-to-hip ratio, resting HR, resting
systolic blood pressure, or resting diastolic blood pressure (Table 1). In addition,
no interaction effect or main effects were noted for total kilocalories, total grams
of protein, percentage of protein, total carbohydrate, percentage of carbohydrate,
total fat, percentage of fat, or vitamin C, vitamin E, and vitamin A intake (Table 2).
Treatment main effects were noted for vitamin E intake (p = .027), with the placebo
group having lower vitamin E intake than the GPLC-1 at baseline (Table 2).
Muscle Carnitine and Performance Variables
No significant interaction or main effects were observed for total muscle carnitine,
free muscle carnitine, or acyl carnitine concentrations from pre- to postsupplementation (Table 3). The results for exercise performance also showed no significant
interactions or main effects for absolute or change values for VO2peak or total exercise
time during the GXT. The percent changes in VO2peak and time to exhaustion during
the GXT were 5.1% (placebo), 9.4% (GPLC-1), and 6.5% (GPLC-3) and 1.0% (placebo), 4.3% (GPLC-1), and 0.91% (GPLC-3), respectively (p ≤ .05; Table 4).
No interaction or main effect for time was found for anaerobic threshold. There
was, however, a significant (p = .036) treatment main effect for anaerobic threshold,
with GPLC-1 demonstrating a higher anaerobic threshold (64.5% ± 8.2%) than
the placebo group (56.0% ± 7.4%). In addition, the difference in percent change
for anaerobic threshold from pre- to postintervention between the placebo group
(3.5%) and the two GPLC groups (GPLC-1 = 10.3% and GPLC-3 = 8.8%) was not
statistically significant but approached significance (p = .09; Table 4).
Values for HR, respiratory-exchange ratio, and rating of perceived exertion
collected at the end of the first three stages of the GXT were generally lower for all
groups postintervention than preintervention. There were no statistically significant
differences, however, within or between groups (p > .05) during any stage of the
GXT (Table 5).
No significant interaction or main effects were noted within or between groups
for total work, peak power, or mean power when expressed as absolute values or
relative to lean body mass (p > .05). In addition, there were no significant differences in percent change from pre- to postintervention for total work, peak power,
and mean power between groups (Table 4).
Calculations for effect size from pre- to postintervention for all performancerelated variables are presented in Table 6. The effect sizes were small with the
25
24.7 ± 4.2
Body fat (%)
71 ± 11.3
Resting diastolic blood pressure (mm Hg)
69 ± 13.2
112 ± 13.0
64 ± 11.4
0.77 ± 0.07
27 ± 5.5
23.9 ± 3.1
78.6 ± 21.6
168.5 ± 8.1
27 ± 5.5
Post
76 ± 10.3
116 ± 11.6
70 ± 6.8
0.77 ± 0.07
28 ± 5.9
26.6 ± 8.3
81.8 ± 20.3
169.5 ± 11.6
26 ± 6.4
Pre
26 ± 6.4
Post
70 ± 8.5
112 ± 9.2
68 ± 10.9
0.78 ± 0.08
28 ± 6.0
24.2 ± 7.9
81.0 ± 20.2
169.5 ± 11.6
GPLC-1
69 ± 7.7
112 ± 6.1
69 ± 8.0
0.76 ± 0.04
24 ± 5.0
27.4 ± 7.0
68.6 ± 16.1
167.2 ± 7.1
27 ± 4.5
Pre
27 ± 4.4
Post
72 ± 7.5
109 ± 8.9
67 ± 9.8
0.76 ± 0.04
24 ± 4.4
25.9 ± 5.8
68.1 ± 14.8
167.2 ± 7.1
GPLC-3
Note. Data are presented as M ± SD. GPLC = glycine propionyl-L-carnitine. No interaction effects, time main effect, or treatment main effects were noted for any
descriptive variable (p > .05).
65 ± 7.0
115 ± 9.3
Resting systolic blood pressure (mm Hg)
0.78 ± 0.07
Resting heart rate (beats/min)
Waist-to-hip ratio
27 ± 5.4
78.3 ± 21.2
Weight (kg)
Body-mass index (kg/m )
168.5 ± 8.1
Height (cm)
2
27 ± 5.5
Age (years)
Pre
Placebo
Table 1 Descriptive Characteristics of Participants Before and After an 8-Week Intervention of Aerobic
Exercise and Placebo or GPLC Supplementation
26
865.9 ± 317.4
Vitamin A (RE)
872.4 ± 503.8
6.5 ± 2.6
61.4 ± 49.7
34 ± 5
79.8 ± 17.2
47 ± 7
252.8 ± 71.0
16 ± 3
85.9 ± 31.8
2159.2 ± 525.1
Post
872.4 ± 503.8
6.5 ± 2.6
61.4 ± 49.7
34 ± 5
79.8 ± 17.2
47 ± 7
252.8 ± 71.0
16 ± 3
85.9 ± 31.8
2159.2 ± 525.1
Pre
Post
811.6 ± 341.7
3.4 ± 1.7
52.3 ± 50.1
31 ± 9
67.1 ± 27.1
47 ± 17
242.9 ± 140.0
16 ± 3
81.57 ± 32.4
1988.7 ± 713.4
GPLC-1
921.0 ± 304.7
5.6 ± 2.9
48.0 ± 29.2
37 ± 7
75.1 ± 29.1
53 ± 13
232.7 ± 56.7
17 ± 6
76.7 ± 29.6
1800.7 ± 479.5
Pre
Post
614.6 ± 249.9
3.7 ± 1.3
81.7 ± 60.9
34 ± 6
62.1 ± 19.9
49 ± 7
202.5 ± 60.5
17 ± 4
69.0 ± 15.5
1643.1 ± 378.9
GPLC-3
Note. Data are presented as M ± SD. GPLC = glycine propionyl-L-carnitine. No interaction effects, time main effect, or treatment main effects were noted for any
descriptive variable (p > .05), with the following exception: Treatment main effects were noted for vitamin E intake (p = .027), with the PL group having lower vitamin
E intake than GPLC-1.
4.2 ± 2.6
Vitamin E (mg)
33 ± 9
85.4 ± 81.0
% fat
Vitamin C (mg)
66.9 ± 21.4
Fat (g)
50 ± 10
% carbohydrate
16 ± 3
222.7 ± 60.3
% protein
Carbohydrate (g)
74.6 ± 23.2
1800.6 ± 361.9
Protein (g)
Kcal
Pre
Placebo
Table 2 Dietary Data of Participants During Weeks 1 and 8 of an 8-Week Intervention of Aerobic Exercise and
Placebo or GPLC Supplementation
27
–4.0
Post
%∆
Pre
Post
GPLC-3
%∆
750.6 ± 492.4
511.0 ± 153.6 –31.9
2,951.1 ± 818.7 2,836.8 ± 687.6 –4.0
554.8 ± 412.8
758.5 ± 265.6 36.7
2,833.0 ± 722.1 2,593.25 ± 465.0 –8.5
3,702.0 ± 895.9 3,347.6 ± 654.8 –9.5 3,388.25 ± 659.3 3,352.0 ± 371.8 –1.1
Pre
GPLC-1
Note. Data are presented as M ± SD. GPLC = glycine propionyl-L-carnitine. No interaction effects, time main effect, or treatment main effects were noted for tissue
carnitine content (p > .05).
636.5 ± 262.3 608.75 ± 359.8 3,317.3 ± 376.6 2,763.8 ± 599.9 –16.7
Acyl carnitine
(nmol/g wet weight)
3,953.8 ± 510.4 3,372.5 ± 434.8 –14.7
%∆
Free carnitine
(nmol/g wet weight)
Post
Total carnitine
(nmol/g wet weight)
Pre
Placebo
Table 3 Muscle-Tissue Carnitine Content of Participants Before and After an 8-Week Intervention of Aerobic
Exercise and Placebo or GPLC Supplementation
28
219.0 ± 46.3
189.3–278.7
201.5 ± 48.8
171.8–231.8
12.7–19.5
10.1–17.9
6.3–8.3
14.8 ± 6.3
14.1 ± 6.0
8.7
4.9
8.9
4.4
3.5
5.1
1.0
%∆
152.3–203.7
178.0 ± 53.3
12.5–19.3
15.9 ± 7.2
5.1–6.8
5.9 ± 1.8
10.3–12.6
11.4 ± 2.8
54.2–65.6
59.9 ± 9.1
25.6–34.2
29.9 ± 9.6
553.6–659.9
606.8 ± 123.3
Pre
166.4–217.8
192.1 ± 43.6
12.7–19.5
16.1 ± 7.9
5.5–7.3
6.4 ± 1.5
10.6–12.9
11.7 ± 2.6
60.1–69.4
64.5 ± 8.2
28.1–36.7
32.4 ± 9.5
576.8–683.2
630.0 ± 121.5
Post
GPLC-1
7.9
1.3
8.5
2.6
10.3
9.4
4.3
%∆
138.9–192.6
165.8 ± 38.3
7.0–14.1
10.5 ± 2.6
4.7–6.5
5.6 ± 1.3
8.9–11.3
10.10 ± 0.7
52.9–62.7
58.0 ± 6.8
23.9–32.9
28.4 ± 6.8
516.8–627.9
572.4 ± 71.3
Pre
161.2–214.8
188.0 ± 34.1
7.3–14.4
10.8 ± 2.7
5.4–7.2
6.3 ± 1.1
9.7–12.1
10.93 ± 0.9
57.9–67.7
62.0 ± 8.5
25.7–34.7
30.2 ± 6.8
522.5–633.5
578.0 ± 79.0
Post
GPLC-3
13.4
2.9
12.5
8.2
8.8
6.5
1.0
%∆
Note. Data are presented as M ± SD and range. GPLC = glycine propionyl-L-carnitine. No interaction effects, time main effect, or treatment main effects were noted
for VO2peak, exercise treadmill time, mean power, peak power, and total work (p > .05). A treatment main effect was noted with the GPLC-1 group having a statistically
higher anaerobic threshold than the placebo group and higher percent fatigue than the GPLC-3 group (p < .05).
Total work (kJ)
Percent fatigue
5.7–7.7
10.5–13.2
9.9–15.6
7.3 ± 1.5
11.8 ± 1.9
11.3 ± 1.8
Peak power (W)
6.7 ± 1.6
50.6–61.4
Mean power (W/s)
56.0 ± 7.4
48.7–59.5
28.0–38.0
26.7–36.6
54.1 ± 7.1
33.0 ± 4.0
567.6–690.4
562.8–685.6
31.7 ± 4.6
629.0 ± 59.0
624.2 ± 50.2
Post
Anaerobic threshold
(% VO2peak)
VO2peak
(mL · kg–1 · min–1)
Exercise time (s)
Pre
Placebo
Table 4 VO2peak, Exercise-Treadmill Time, Anaerobic Threshold, Mean Power, Peak Power, Total Work Relative
to Lean Body Mass, and Percent Fatigue of Participants Before and After an 8-Week Intervention of Aerobic
Exercise and Placebo or GPLC Supplementation
29
7.8 ± 0.8
11.0 ± 0.9
15.0 ± 1.5
10.4 ± 1.7
13.9 ± 1.6
2
3
1.19 ± 0.10
1.22 ± 0.08
3
8.3 ± 1.5
0.98 ± 0.07
0.99 ± 0.04
2
1
0.82 ± 0.04
179 ± 10.9
182 ± 9.7
3
0.85 ± 0.04
144 ± 12.4
149 ± 13.1
2
1
115 ± 14.1
119 ± 14.3
Post
1
Pre
15.0 ± 2.3
11.3 ± 2.1
8.3 ± 1.7
1.20 ± 0.10
0.98 ± .06
0.83 ± 0.05
181 ± 10.8
146 ± 14.8
119 ± 13.3
Pre
Post
15.2 ± 1.8
12.0 ± 1.2
8.8 ± 1.3
1.15 ± 0.11
0.95 ± 0.05
0.81 ± 0.05
181 ± 15.1
155 ± 15.6
121 ± 18.9
GPLC-1
17.1 ± 2.2
12.1 ± 1.4
8.8 ± 1.5
1.22 ± 0.13
0.99 ± 0.07
0.82 ± 0.04
185 ± 13.4
153 ± 12.7
121 ± 9.2
Pre
Post
16.3 ± 1.9
11.3 ± 1.8
8.1 ± 1.5
1.18 ± 0.11
0.95 ± 0.08
0.79 ± 0.07
184.1 ± 17.5
151 ± 20.0
123 ± 12.1
GPLC-3
Note. Data are presented as M ± SD. GPLC = glycine propionyl-L-carnitine. No statistically significant differences were noted in these variables from pre- to postintervention or between groups during any stage of the graded exercise test (p > .05).
Rating of perceived exertion
Respiratory-exchange ratio
Heart rate (beats/min)
Stage
Placebo
Table 5 Heart Rate, Respiratory-Exchange Ratio, and Rating of Perceived Exertion of Participants During
Graded Exercise Testing Before and After an 8-Week Intervention of Aerobic Exercise and Placebo or GPLC
Supplementation
30 Smith et al.
Table 6 Effect-Size Calculations From Pre- to Postintervention
Using Cohen’s d
Variable
Main effect
Placebo
GPLC-1
GPLC-3
VO2peak
0.2564
0.1799
0.3341
0.3185
Time to exhaustion
0.1304
0.0519
0.2527
0.0600
Anaerobic threshold
0.4404
0.2401
0.5801*
0.5006*
Peak power
0.2891
0.2972
0.1537
0.4131
Mean power
0.3839
0.3899
0.3151
0.4418
% fatigue
0.0627
0.1265
0.0255
0.0510
Total work
0.4031
0.3929
0.3165
0.4997*
Note. GPLC = glycine propionyl-L-carnitine. *Considered moderate effect size.
exception of GPLC-1 and GPLC-3 on anaerobic threshold, which showed a moderate effect (d = 0.58 and 0.50, respectively).
Discussion
The findings of the current investigation indicate that 1 or 3 g/day of GPLC supplementation for 8 weeks in combination with aerobic training does not improve
aerobic- or anaerobic-exercise performance variables more than aerobic exercise
alone. There was excellent, and similar, compliance to supplementation between
groups, as well as similar compliance to aerobic training. Thus, we do not believe
that our lack of finding for a benefit of GPLC is the result of poor supplement or
training compliance. Dietary records were also similar between all three groups
over time, with the exception of a slightly greater vitamin E intake in the GPLC-1
group than in the placebo group. Nonetheless, the difference in vitamin E intake
is so small that it likely had no influence on the results, because previous literature suggests that vitamin E does not improve exercise performance, even with a
supplemented dosage of 100–200 mg daily (Dunford, 2006).
The aerobic-performance variables including VO2peak and time to exhaustion
have been shown to improve with aerobic training (ACSM, 2005; Bouchard et
al., 1999) and with carnitine supplementation (Dragan et al., 1987; Marconi et
al., 1985; Vecchiet et al., 1990) independently. The training protocol used in the
current investigation did result in a modest, albeit nonsignificant, improvement in
VO2peak and time to exhaustion, which was similar in all three groups and indicates
that GPLC offers no additional benefit for improving exercise performance above
aerobic training alone in healthy individuals. The traditional reported values of
VO2peak improvements from aerobic training alone are 10–30% (ACSM). The
Family Heritage Study, however, has noted changes in VO2peak ranging from 0 to
53% after a 20-week aerobic training program (Bouchard et al.). Based on these
observations, our observed increases in VO2peak appear normal, although falling in
the lower end of the range.
Our finding of no statistically significant increases in aerobic performance with
GPLC supplementation is somewhat unexpected and is contradictory to the find-
Carnitine, Exercise, and Exercise Performance 31
ings of other studies that examined the effect of LC in healthy adults. For example,
Vecchiet et al. (1990) used 2 weeks of oral LC supplementation at a dose of 2 g/day
in 10 moderately trained young men and reported a 6.9% improvement in VO2max
above that observed for placebo. Marconi et al. (1985) noted similar findings (6.0%
increase) for VO2max in competitive long-distance walkers provided 4 g/day of LC
for 2 weeks. In addition, Dragan et al. (1987) reported a predicted increase in VO2max
after intravenous LC supplementation of 3 g/day in elite athletes.
Not all the studies that have examined the effect of LC supplementation on
exercise performance have reported significant findings, however. Colombani et al.
(1996) reported no change in well-trained endurance athletes’ marathon run time (or
predicted VO2max) when participants received 2 g of LC 2 hr before the race. Wyss
et al. (1990) noted no change in aerobic performance in healthy men as measured
by VO2max and exercise endurance after the administration of 1 g/day of LC for 7
days. In two separate but related studies, Greig et al. (1987) and Onyono-Enguelle
et al. (1988) showed no changes in VO2max after supplementation of 2 g/day of LC
for 28 days.
The findings of the cited studies (Colombani et al., 1996; Greig et al., 1987;
Onyono-Enguelle et al., 1988; Wyss et al., 1990) are in agreement with those of the
current study. To our knowledge this is the first study to use healthy participants
to examine the effect of GPLC supplementation for up to 8 weeks in combination
with an aerobic-exercise training program. Although some previous studies demonstrated an improvement in VO2max after LC supplementation (Dragan et al., 1987;
Marconi et al., 1985; Vecchiet et al., 1990), the overall percent changes in VO2max
were similar to those found in the current study. Because of the higher variability
among our participants, however, group differences were not detected. Perhaps a
more homogeneous sample of participants would be needed in future studies to
maximize the ability to detect differences across time and between groups. Related
to this, previous studies demonstrating an improvement in exercise performance
using older, diseased participants likely report such findings based on the very low
level of physical conditioning of these participants at study entry. Aside from the
need to maintain a homogeneous sample, future studies should strive to include
larger sample sizes than have been used in previous work, including the current
study. Small sample sizes paired with high variability results in nonsignificant findings. Further research using these suggestions might provide additional insight into
the efficacy of various forms of LC in improving exercise performance.
With regard to exercise time to exhaustion, it is possible that a longer duration
exercise or a time trial at a submaximal workload would better detect the potential
benefits of GPLC, because longer duration bouts might function to deplete muscle
glycogen stores and result in greater reliance on fatty acids for energy production.
Because carnitine is an intermediate in lipid metabolism and has been suggested
to be the rate-limiting step in this process (Bremer, 1983; Fritz, 1979), increased
availability of carnitine might allow for greater fat utilization during longer duration
exercise bouts. Further research on the role of carnitine and the limiting steps of
lipid utilization is needed to address this proposed hypothesis. In addition, the type
of carnitine might have an impact, with PLC being considered the most specific to
skeletal muscle, potentially leading to a greater influence on lipid metabolism.
There was no statistically significant effect for anaerobic threshold, although
moderate effect sizes were noted for the GPLC-1 (d = 0.58) and GPLC-3 (d = 0.50)
32 Smith et al.
groups (Table 6). No previous study to our knowledge has reported on anaerobic
threshold after LC supplementation. At least two previous studies (Gorostiaga et
al., 1989; Oyono-Enguelle et al., 1988), however, have reported mixed findings in
response to aerobic-exercise training and carnitine supplementation with regard
to substrate utilization. Oyono-Enguelle et al., using 10 untrained men given
2 g/day of LC orally for 28 days, reported no change in respiratory-exchange
ratio after or during a GXT. Participants were measured during fixed-workload
exercise for 60 min followed by 120 min of rest on the 10th, 20th, and 28th day
of supplementation and again between the 72nd and 86th day from the start of
supplementation. Gorostiaga et al. had 10 participants perform 45 min of cycling
at 66% of VO2max after 2 g/day of oral LC for 28 days and reported a significant
decrease in respiratory-exchange ratio, suggestive of greater fatty-acid utilization. Although carnitine is necessary for oxidation of fatty acids, and LC might
decrease the use of carbohydrate metabolism during exercise with greater reliance
on lipids, we failed to note any difference in either respiratory-exchange ratio
(Table 5) or anaerobic threshold. Based on our effect-size calculations, however,
it is possible that we were underpowered to detect statistical significance in
anaerobic threshold. Future studies using larger sample sizes might be needed
to further evaluate the role of GPLC in increasing the anaerobic threshold in
otherwise healthy individuals.
Although there were no statistically significant improvements in anaerobic
performance, all three groups showed modest improvements in peak power, mean
power, and total work (Table 4). These findings support those of Trappe, Costill,
Goodpaster, Vukovich, and Fink (1994), who reported no further improvement in
anaerobic work (five 100-yd sprints with 2-min rest intervals in an Olympic size
pool) after supplementation of 2 g/day of oral LC for 7 days in college swimmers.
In further agreement, Ransone and Lefavi (1997) provided supplementation of 2
g/day of oral LC for 21 days and noted no effect on anaerobic performance in elite
runners after a high-intensity run/sprint protocol. In contrast, other studies using
patients with mitochondrial myopathies (Campos et al., 1993) and peripheral artery
disease (Colombani et al., 1996) have reported significant increases in muscle
strength after LC supplementation for up to 11 months. Therefore, carnitine might
be more effective at increasing muscle strength and other indices of anaerobicexercise performance in diseased populations than in healthy adults.
Although not including measures of anaerobic-exercise performance directly,
data from Kraemer et al. (2006) and Volek et al. (2002) indicate positive hormonal
adaptations and decreased markers of exercise stress, respectively, after 2 g/day of
oral LC supplementation for 3 weeks. These data are in reference to young, otherwise healthy men. They indicate that it is possible that carnitine supplementation
favorably affects variables not measured in the current investigation. Future studies
are needed to confirm the findings of Kraemer et al. and Volek et al.
In addition, the muscle carnitine concentrations did not improve significantly
(Table 3). Although both the placebo and GPLC-1 groups experienced a decrease
in muscle carnitine from pre- to postintervention, a finding that has previously been
observed after intense aerobic training (Arenas et al., 1991, 1994; Huertas et al.,
1992; Lee et al., 2007), total carnitine was decreased to a lesser degree with GPLC3, and acyl carnitine was increased but in a nonsignificant manner. These findings
have also been previously observed in studies (Arenas et al., 1991, 1994; Huertas
Carnitine, Exercise, and Exercise Performance 33
et al.; Lee et al.) in which participants received carnitine in doses from 1 (Arenas et
al., 1991) to 4 (Lee et al.) g/day for periods of 4 weeks to 6 months. Not all studies
have shown increases in muscle carnitine after LC supplementation. In very similar
protocols, researchers found no significant increase in muscle carnitine after either
14 days (Barnett et al., 1994) or 3 months (Watcher et al., 2002) of supplementation with 4 g/day in healthy men. Recent work by Stephens, Constantin-Teodosiu,
Laithwaite, Simpson, and Greenhaff (2006) demonstrates that insulin can augment
skeletal-muscle carnitine transport, leading to increased muscle-tissue carnitine content. In addition, an acute state of hyperinsulinemia induced via high-carbohydrate
feeding, in conjunction with carnitine supplementation to induce hypercarnitinemia,
might promote more favorable retention of carnitine in skeletal muscle (Stephens,
Evans, Constantin-Teodosiu, & Greenhaff, 2007). Although it seems reasonable
to hypothesize that increased carnitine tissue content might lead to greater energy
production via fatty-acid metabolism and, hence, improved exercise performance,
the supplementation protocol used here did not increase muscle carnitine concentrations. Without a significant increase in muscle carnitine content, it follows that other
dependent measures might not be favorably affected. Based on the recent findings
of Stephens (2006, 2007), future studies might consider carnitine administration
along with carbohydrate-rich feedings to induce hyperinsulinemia in an attempt
to increase skeletal-muscle carnitine content.
Some potential limitations of the current research need to be presented. First,
the precision of maximal exercise testing using the GXT with gas collection might
not be adequate to assess small changes in aerobic performance. Hence, although
participants might have improved their aerobic capacity, our testing methods might
not have been able to detect small differences. This is especially true considering
the potential learning curve involved with maximal stress testing when collecting
expired gases. We attempted to control for this by allowing all participants a familiarization trial before they performed the GXT. Nonetheless, this familiarization
trial was not a complete GXT, and perhaps that would have been most appropriate.
In relation to this, individual response to training interventions is also an issue, and
we made every attempt to address this by providing consistent interaction with all
participants throughout the training period.
Second, we noted a high degree of variability in participants’ response to the
intervention. This, coupled with our relatively small sample size, decreased our
statistical power and might have made it difficult to observe group differences. A
final limitation associated with our work is the lack of gender matching among the
groups. This is in part because of gender differences in drop-out or withdrawal. That
is, each group started with approximately one third men and two thirds women.
Unfortunately, by chance alone we lost 4 men from the GPLC-3 group and ended
up with no men in that condition. Although we do not believe that the unequal
gender balance significantly influenced the results, we do concede that there might
be gender differences in response to aerobic training (Tarnopolsky, 2000). We
performed further analysis, however, to investigate the influence of gender on our
dependent variables and noted no statistical differences between genders for any
variable (Gender × Time). If focused on healthy participants, future studies using
larger, more homogeneous samples, possibly including longer duration exercise
tests as dependent variables, are necessary to gain a better understanding of the
effect of GPLC on aerobic- and anaerobic-exercise performance.
34 Smith et al.
To our knowledge, the current investigation is the first to use a combination of
LC supplementation, in the form of GPLC, and aerobic exercise in an attempt to
improve markers of exercise performance. Supplementation was well tolerated by all
participants, with no reports of adverse side effects during the 8-week intervention
period. We noted no additional benefits of GPLC beyond aerobic exercise alone,
however, in improving any measure of aerobic- or anaerobic-exercise performance
or muscle carnitine concentrations. Our data are in reference to a sample of younger,
healthy participants. Future studies might use metabolically or cardiovascularly
compromised participants, populations that likely are more responsive to carnitine
supplementation.
Acknowledgments
This work was supported in part by Sigma-tau HealthSciences, The National Strength and
Conditioning Association (GNC Graduate Student Research Grant), and the Gatorade
Sport Science Institute (Graduate Student Research Grant).
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