J Appl Physiol 95: 983–990, 2003.
First published May 9, 2003; 10.1152/japplphysiol.00115.2003.
Effect of alcohol intake on muscle glycogen
storage after prolonged exercise
Louise M. Burke,1 Greg R. Collier,2 Elizabeth M. Broad,1 Peter G. Davis,1
David T. Martin,1 Andrew J. Sanigorski,2 and Mark Hargreaves3
1
Sports Science and Sports Medicine, Australian Institute of Sport, Belconnen, Australian Capital
Territory 2616; 2School of Health Sciences, Deakin University, Waurn Ponds, Victoria 3217; and
3
School of Health Sciences, Deakin University, Burwood, Victoria, 3125, Australia
Submitted 3 February 2003; accepted in final form 16 April 2003
ethanol; glycogen resynthesis
to undertake prolonged moderate- to high-intensity training or competition sessions within 8–24 h of their previous exercise
bout. Restoration of muscle glycogen levels is a key
issue in recovery between exercise sessions; enhanced
muscle fuel stores may improve endurance capacity
and performance during subsequent exercise trials (for
review, see Ref. 14). Dietary factors that promote muscle glycogen storage in exercise-depleted muscles include early intake of carbohydrate (CHO) (15), adequate amounts of total CHO (10, 16), and the choice of
CHO-rich foods and beverages with a high glycemic
ATHLETES ARE COMMONLY REQUIRED
Address for reprint requests and other correspondence: L. M. Burke,
Dept. of Sports Nutrition, Australian Institute of Sport, P.O. Box 176,
Belconnen, ACT, Australia 2616 (E-mail: [email protected]).
http://www.jap.org
index (3). Other factors in postexercise nutrition such
as the spacing of meals and snacks (2, 10), the coingestion of other macronutrients (1, 7, 29), and hydration
status (20) do not appear to affect muscle glycogen
storage, as long as total CHO requirements are met.
One postexercise nutritional practice to receive little
scientific attention is the consumption of alcohol. The
alcohol intake practices of athletes are poorly described
in the scientific literature; however, there is anecdotal
evidence that some athletes consume large amounts of
alcohol in the postexercise period, particularly in team
sports in which a weekly competition is undertaken.
Indeed, a dietary survey of elite Australian Rules football players revealed that large amounts of alcohol
were consumed postgame; these self-reported practices
were confirmed by the high prevalence of positive blood
alcohol readings when blood samples were collected
from these players at a training session on the morning
after a match (6). Although one might expect athletes
to consume less alcohol than their sedentary counterparts as part of a “healthy lifestyle,” in fact, some
surveys of athletes have found great self-reported intakes of alcohol compared with control sedentary populations, both as a daily mean intake of alcohol (31) as
well as a greater prevalence of binge drinking (19).
Alcohol intake practices appear to vary according to
the level of participation (13) as well as the type of
sport. Dietary surveys have commented on a higher
self-reported intake of alcohol in team sports than in
endurance-, power-, or skill-based sports (4, 30) or
individual sports (31).
The acute intake of alcohol has significant effects on
CHO metabolism in the liver and muscle (for review,
see Ref. 22). In humans, ingestion of alcohol has been
shown to inhibit glucose uptake into skeletal muscle
(17), decrease the stimulatory effect of exercise on
muscle glucose uptake (18), and impair glucose utilization (25). Rat studies have shown that intragastric
administration of alcohol interferes with glycogen synthesis in the liver (8) and oxidative skeletal muscle
fibers (32, 34) in response to glucose refeeding after
The costs of publication of this article were defrayed in part by the
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8750-7587/03 $5.00 Copyright © 2003 the American Physiological Society
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Burke, Louise M., Greg R. Collier, Elizabeth M.
Broad, Peter G. Davis, David T. Martin, Andrew J.
Sanigorski, and Mark Hargreaves. Effect of alcohol intake on muscle glycogen storage after prolonged exercise. J
Appl Physiol 95: 983–990, 2003. First published May 9, 2003;
10.1152/japplphysiol.00115.2003.—We studied the effects of
alcohol intake on postexercise muscle glycogen restoration
with samples from vastus lateralis being collected immediately after glycogen-depleting cycling and after a set recovery
period. Six well-trained cyclists undertook a study of 8-h
recovery (2 meals), and another nine cyclists undertook a
separate 24-h protocol (4 meals). In each study, subjects
completed three trials in crossover order: control (C) diet
[meals providing carbohydrate (CHO) of 1.75 g/kg]; alcoholdisplacement (A) diet (1.5 g/kg alcohol displacing CHO energy from C) and alcohol ⫹ CHO (AC) diet (C ⫹ 1.5 g/kg
alcohol). Alcohol intake reduced postmeal glycemia especially
in A trial and 24-h study, although insulin responses were
maintained. Alcohol intake increased serum triglycerides,
particularly in the 24-h study and AC trial. Glycogen storage
was decreased in A diets compared with C at 8 h (24.4 ⫾ 7 vs.
44.6 ⫾ 6 mmol/kg wet wt, means ⫾ SE, P ⬍ 0.05) and 24 h
(68 ⫾ 5 vs. 82 ⫾ 5 mmol/kg wet wt, P ⬍ 0.05). There was a
trend to reduced glycogen storage with AC in 8 h (36.2 ⫾ 8
mmol/kg wet wt, P ⫽ 0.1) but no difference in 24 h (85 ⫾ 9
mmol/kg wet wt). We conclude that 1) the direct effect of
alcohol on postexercise glycogen synthesis is unclear, and 2)
the main effect of alcohol intake is indirect, by displacing
CHO intake from optimal recovery nutrition practices.
984
ALCOHOL AND POSTEXERCISE RECOVERY
METHODS
Subjects
Two separate investigations, an 8-h study and a 24-h study,
were undertaken in our research protocol, which was approved
by the Human Ethics Committee of the Australian Institute of
Sport. Nine subjects (28.7 ⫾ 2.2 yr; 73.2 ⫾ 3.1 kg; 60.0 ⫾ 1.8
ml䡠min⫺1 䡠kg⫺1, means ⫾ SE) recruited from a local pool of
well-trained cyclists completed the 24-h study, and an additional six subjects (28.4 ⫾ 1.7 yr; 70.7 ⫾ 1.7 kg; 60.2 ⫾ 2.0
ml䡠min⫺1 䡠kg⫺1) completed the 8-h study. All subjects were
informed of the risks associated with participation in the study
before providing written consent. Criteria for exclusion as a
subject included past or current history of heavy alcohol intake
(⬎50 g/day), history of gastrointestinal pathology such as ulcers, and current use of any medications. All subjects described
themselves as light drinkers, consuming ⬍20 g/day of alcohol.
Initially, 12 subjects were recruited for the first (24 h) trial;
however, three subjects withdrew from the study because of
side effects (vomiting) of excessive alcohol consumption. These
incidences occurred at almost identical times in the recovery
protocol (after ⬃3 h) but were not linked to each other because
they took place on separate days. These three subjects are not
included in any further discussion in this paper; however, it is
noted that all vomited while undertaking the alcohol-displacement diet and that, because of the randomization of diets, two of
these subjects had previously completed, without incident, the
alcohol and carbohydrate diet, which provided an identical
amount of alcohol.
Study Protocol
Each study involved three trials, which subjects undertook
on separate occasions in a randomized allocation, each 1 wk
apart. On each occasion, subjects reported to the laboratory
in the morning after an overnight fast. Each subject had been
instructed verbally and in writing to undertake a standard
preparation before each treatment: no strenuous exercise
was to be undertaken for the previous 36 h, and a standardized diet containing at least 300 g/day of CHO was to be
consumed during the 48 h before each treatment. To facilitate compliance, subjects kept a food and activity diary before
the first treatment and were required to replicate these
J Appl Physiol • VOL
practices before the other treatments. Food and exercise
diaries were checked on arrival at the laboratory before the
start of each treatment. Once correct study preparation was
determined, a catheter was placed in a forearm vein for blood
sampling and was kept patent by periodic flushing with 0.9%
saline containing a small amount of heparin (10 U/ml). Subjects then undertook an exercise bout to deplete muscle
glycogen levels: riding for 2 h, either on their own cycle
mounted on a wind-trainer or a cycle ergometer, with a heart
rate equivalent to 75% of maximal O2 uptake, followed by
four 30-s “all-out” sprints with a 2-min recovery between
bouts. The exercise bout was standardized over the three
treatments for each subject, with heart rates being continuously monitored to ensure this and to provide feedback to
subjects. Within 5–10 min of cessation of exercise, a muscle
sample was obtained from the vastus lateralis by use of the
percutaneous biopsy technique with suction (12) and was
immediately frozen in liquid nitrogen.
Twenty-four-hour study. For 24 h after each exercise bout,
the subjects rested and were assigned to the following diets
in randomized order.
The control diet was composed exclusively of high glycemic
index CHO-rich foods. CHO intake ⫽ 7 g 䡠 kg⫺1 䡠 24 h⫺1 divided equally into four meals (1.75 g/kg), providing ⬃77% of
total energy intake.
The alcohol ⫹ CHO diet consisted of the 24-h control diet ⫹
1.5 g/kg of alcohol consumed as vodka (divided into 6 equal
doses and consumed every 30 min during the first 3 h of
recovery). Total CHO intake ⫽ 7 g 䡠 kg⫺1 䡠 24 h⫺1, providing
⬃49% of total energy intake; alcohol ⫽ 18% of total energy
intake.
The alcohol-displacement diet was 1.5 g/kg of alcohol as in
the alcohol ⫹ CHO diet. The energy equivalent of this alcohol
was displaced from the control diet by removing an equal
amount of CHO from each of the meals. Thus total CHO
intake ⫽ 4.4 g 䡠 kg⫺1 䡠 24 h⫺1 (1.1 g 䡠 kg⫺1 䡠 meal⫺1), providing
⬃37% of total energy; alcohol ⫽ 22% of total energy intake.
In all the diets, meals were consumed at t ⫽ 0 h (immediately after the biopsy) and at 3, 8, and 21 h. A full description
of diets is provided in Table 1.
Venous blood samples were obtained from fasting subjects
before the start of the exercise; immediately before each
meal; and at 30, 60, 90, and 120 min after each meal. Care
was taken to use non-alcohol-containing swabs in all blood
collection procedures. Blood samples (5 ml) were collected in
tubes containing fluoride heparin and were spun, and the
plasma was stored at ⫺20°C until determination of plasma
glucose, insulin, and triglyceride levels was undertaken. Further blood samples (3 ml) were taken after the first biopsy
(t ⫽ 0) and at t ⫽ 1, 2, 3, 4, 6, 8, 10, and 21 h and collected in
well-sealed fluoride oxalate tubes for immediate determination of BAL. Twenty-four hours after the recovery commenced, a second biopsy was taken from the vastus lateralis
at least 3 cm distal to the first biopsy site (9) and frozen.
Eight-hour study. An identical exercise and recovery protocol was used to the 24-h trial, except that the trial was
terminated with a second biopsy after 8 h. Two meals were
fed in each treatment, at t ⫽ 0 and 3 h. Blood samples were
taken at identical time points to the first trial until 8 h.
Because the same amount of alcohol was consumed during
the first 3 h of the trial, and the alcohol-displacement diet
was required to be isocaloric with the control diet, greater
amounts of CHO were removed from the alcohol-displacement diet. A summary of dietary treatments is as follows (see
also Table 1).
The control diet consisted of two meals composed of highglycemic-index CHO-rich foods, identical to the first two
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starvation. Glycogen storage during 30 min of recovery
from high-intensity exercise was also impaired in oxidative but not nonoxidative fibers of rat skeletal muscle by alcohol administration (24). These effects have
not been investigated in a human model.
Because of the potential for impaired glycogen restoration and the relevance to the real-life practices of
some athletes, we decided to study the effect of acute
ingestion of large amounts of alcohol on postmeal metabolism and glycogen storage after prolonged moderate- to high-intensity exercise. Separate studies were
undertaken to investigate muscle glycogen storage after 8 and 24 h of recovery in exercise-depleted muscles
when alcohol was consumed immediately after the
work bout. These periods, representing common intervals between training sessions, examined glycogen restoration while blood alcohol levels (BAL) were substantial (8 h) and after the metabolism of alcohol (24 h). The
study was designed to test the direct effect of alcohol
added to a high-CHO recovery diet, as well as its indirect
effect in displacing CHO from the postexercise diet.
ALCOHOL AND POSTEXERCISE RECOVERY
Table 1. Description of dietary treatments
Total Diet
Meals
8-h study
Control
CHO
Alcohol
Protein
Fat
Energy
Alcohol displacement
CHO
Alcohol
Protein
Fat
Energy
Alcohol ⫹ CHO
CHO
Alcohol
Protein
Fat
Energy
3.5 g/kg (60% of energy)
0
1 g/kg (17% of energy)
0.6 g/kg (23% of energy)
23.5 kcal/kg
1.75 g/kg
0
0.5 g/kg
0.3 g/kg
0.9 g/kg (15% of energy)
1.5 g/kg (45% of energy)
1 g/kg (17% of energy)
0.6 g/kg (23% of energy)
23.5 kcal/kg
0.45 g/kg
6 ⫻ 0.25 g/kg
0.5 g/kg
0.3 g/kg
3.5 g/kg (41% of energy)
1.5 g/kg (31% of energy)
1 g/kg (12% of energy)
0.6 g/kg (16% of energy)
34 kcal/kg
1.75 g/kg
6 ⫻ 0.25 g/kg
0.5 g/kg
0.3 g/kg
Control
CHO
Alcohol
Protein
Fat
Energy
Alcohol displacement
CHO
Alcohol
Protein
Fat
Energy
Alcohol ⫹ CHO
CHO
Alcohol
Protein
Fat
Energy
7 g/kg (60% of energy)
0
2 g/kg (17% of energy)
1.2 g/kg (23% of energy)
47 kcal/kg
1.75 g/kg
0
0.5 g/kg
0.3 g/kg
4.4 g/kg (37% of energy)
1.5 g/kg (22% of energy)
2 g/kg (18% of energy)
1.2 g/kg (23% of energy)
47 kcal/kg
1.1 g/kg
6 ⫻ 0.25 g/kg
0.5 g/kg
0.3 g/kg
7 g/kg (49% of energy)
1.5 g/kg (18% of energy)
2 g/kg (14% of energy)
1.2 g/kg (19% of energy)
57 kcal/kg
1.75 g/kg
6 ⫻ 0.25 g/kg
0.5 g/kg
0.3 g/kg
Statistical Analyses
The metabolic profiles from the three trials in each study
were compared by repeated-measures analysis of variance.
Contrast analysis was used to compare individual time
points, with Scheffé’s post hoc test being used to locate
specific differences. Areas under the curves (AUC) were also
compared by repeated-measures analysis of variance, with
the individual diets being compared by use of multiple-comparison and least significant difference post hoc tests. Glycogen storage during recovery was calculated as the difference
between postexercise and postrecovery levels, and the differences between storage with each dietary treatment were
compared by using a two-tailed t-test with a Bonferroni
correction. All data are reported as means ⫾ SE, and significance was accepted when P ⬍ 0.05. The statistical analyses
were undertaken with the use of Statistica software for
Windows (StatSoft, version 5.1, 1997, Tulsa, OK).
RESULTS
Dietary treatments were provided to subjects on the basis of their
body mass (kg). Meals were given at 0 and 3 h in the 8-h study and
at 0, 3, 8, and 21 h in the 24-h study. Diets provided in the Control
and Alcohol Displacement trials were isoenergetic. The percentage of
energy provided by the macronutrients in each diet was calculated
by use of the following estimations of energy content: carbohydrate
(CHO) ⫽ 4 kcal/g; alcohol ⫽ 7 kcal/g; protein ⫽ 4 kcal/g; and fat ⫽ 9
kcal/kg.
meals in the 24-h trial. Total CHO intake ⫽ 3.5 g/kg (1.75
g 䡠 kg⫺1 䡠 meal⫺1), CHO intake providing 60% of total energy
intake.
The alcohol ⫹ CHO diet consisted of the control diet ⫹ 1.5
g/kg of alcohol in the form of vodka (divided into 6 equal doses
and consumed every 30 min during the first 3 h of recovery).
Total CHO intake ⫽ 1.75 g 䡠 kg⫺1 䡠 meal⫺1, providing ⬃41% of
total energy intake; alcohol ⫽ 31% of total energy intake.
The alcohol-displacement diet included 1.5 g/kg of alcohol
as in the alcohol ⫹ CHO diet. The energy equivalent of the
alcohol was displaced from the control diet by removing an
equal amount of CHO from each of the meals. Total CHO
intake ⫽ 0.9 g/kg (0.45 g 䡠 kg⫺1 䡠 meal⫺1), providing ⬃15% of
total energy; alcohol ⫽ 45% of total energy intake.
Analytical Methods
Plasma glucose was measured with an automatic analyzer
(model 705-0013, Hitachi) by using an enzymatic method
J Appl Physiol • VOL
(Boehringer Mannheim, Mannheim, Germany). Plasma insulin levels were measured by use of a commercially available
double-antibody radioimmunoassay (Phadeseph insulin RIA,
Pharmacia Diagnostic, Uppsala, Sweden). Plasma triglycerides were determined on an automatic analyzer (model 7050013, Hitachi) by using a colorimetric method (Boehringer
Mannheim). Twenty-four-hour and 8-h profiles were drawn
for each of these variables, and the postprandial incremental
area was calculated by using the trapezoid rule, taking the
value immediately before each meal as baseline and including all time points. Total incremental areas for each variable
were calculated from the sum of individual postprandial
incremental areas in each trial.
BAL were measured via a radiative energy attenuation
assay, using a TDxFLx analyzer and reagent kit (Abbot
Diagnostics, Abbot Park, IL). Muscle glycogen content of
muscle samples was measured by use of an enzymatic, fluorometric technique (23).
BAL achieved during the alcohol-displacement and
alcohol ⫹ CHO diets are summarized in Fig. 1, A (8-h
study) and B (24-h study). There was a main effect of
time in both studies, with blood alcohol concentrations
rising from zero levels in the fasting sample to a mean
peak of ⬃0.12 g/100 ml at ⬃4 h of recovery. BAL were
still substantial (⬃0.06–0.07 g/100 ml) after 8 h of
recovery, but alcohol was largely cleared from the blood
by 24 h of recovery. There were no overall differences in
BAL between dietary treatments in either study (not
significant).
Figure 2 summarizes blood metabolite data from the
8-h study, with concentrations of plasma glucose (A),
insulin (B), and triglyceride (C) after an overnight fast
and in response to the two meals eaten at t ⫽ 0 and 3 h
of recovery from prolonged exercise. There was a main
effect of dietary treatment for plasma glucose concentrations, with lower concentrations being seen in the
alcohol-displacement diet than in the control or alcohol ⫹ CHO diet (P ⬍ 0.05). This finding was confirmed
by a lower AUC from plasma glucose responses to
meals with alcohol-displacement treatment compared
with control and alcohol ⫹ CHO diets (P ⬍ 0.05). There
was an also an interaction of diet and time, with
plasma glucose levels being lower in alcohol-displace-
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24-h study
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ALCOHOL AND POSTEXERCISE RECOVERY
ment treatment at various time points after meals
than in the other two diets (Fig. 2A; P ⬍ 0.05). Plasma
insulin concentrations mirrored the results seen for
blood glucose; there was a main dietary effect and
differences in the total postmeal AUC response such
that insulin concentrations were lower with the alcohol-displacement diet than with the control or alcohol ⫹ CHO treatments (P ⬍ 0.05). Time points at
which there was a diet-time interaction for plasma
insulin concentrations are shown in Fig. 2B. There
were no differences in the glucose and insulin responses to the control and alcohol ⫹ CHO diets. There
was a significant interaction of diet and time on plasma
triglyceride concentrations, with triglyceride levels on
the alcohol-displacement and alcohol ⫹ CHO diets rising above those of the control diet at various time
points after 3 h (Fig. 2C; P ⬍ 0.05). The total AUC for
postmeal triglyceride concentrations was significantly
greater with the alcohol ⫹ CHO diet than control diet
(P ⬍ 0.05).
Figure 3 summarizes blood metabolite results from
the 24-h study, with concentrations of plasma glucose
(A), insulin (B), and triglyceride (C) after an overnight
fast, and in response to the meals eaten at t ⫽ 0 and 3,
8, and 21 h of recovery from prolonged exercise. Overall, plasma glucose concentrations were higher with
the control diet than alcohol-displacement diet (P ⬍
0.05), and the sum of AUC for postmeal glucose conJ Appl Physiol • VOL
DISCUSSION
We investigated the effects of the intake of substantial amounts of alcohol on postexercise recovery of
muscle glycogen stores in well-trained subjects. On the
basis of the comparison of trials in which alcohol was
added to a control (high-CHO diet), we failed to find
clear evidence that alcohol directly inhibits glycogen
storage in mixed human muscle. Although we saw a
trend for lower glycogen storage despite equal dietary
carbohydrate intake during the period in which blood
alcohol concentrations were elevated (8 h study), after
24 h and the complete metabolism of the alcohol there
were no differences in muscle glycogen stores. The
main finding of our investigations is that, because
alcohol does not provide a substrate for glycogen formation per se, alcohol intake can have an indirect
effect on postexercise glycogen resynthesis if it displaces the consumption of adequate amounts of CHO.
This is an important practical finding, because in real
life it is unlikely that athletes will follow guidelines for
postexercise intake of CHO when they indulge in excessive intake of alcohol, either during the binge drinking episode or in the period immediately afterward
(“hangover”).
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Fig. 1. Blood alcohol levels (BAL) after alcohol intake (1.5 g/kg body
mass) during the first 3 h of recovery from glycogen-depleting exercise in separate studies after 8 h (n ⫽ 6 subjects; A) and 24 h (n ⫽ 9
subjects; B) of recovery. 8-A and 24-A, trials in which alcohol displaced the carbohydrate (CHO) content of a control (C) diet in the 8and 24-h studies, respectively; 8-AC and 24-AC, diets in which
alcohol was consumed in addition to the control diet. There were no
differences in BAL between A and AC trials. Data are means ⫾ SE.
centrations was greater with control than both alcoholdisplacement and alcohol ⫹ CHO treatments (P ⬍
0.05). The diet-time interaction showed greater blood
glucose concentrations with control than alcohol-displacement and alcohol ⫹ CHO treatments at numerous
postmeal time points (see Fig. 3A, P ⬍ 0.05) and several time points at which blood glucose concentrations
were lower with alcohol-displacement than alcohol ⫹
CHO treatment (see Fig. 3A, P ⬍ 0.05). The total AUC
for postmeal plasma insulin concentrations was
greater for control treatment than alcohol displacement (P ⬍ 0.05), and the diet and time interaction
revealed several time points at which insulin concentrations were higher with control than alcohol-displacement (see Fig. 3B, P ⬍ 0.05). Plasma triglyceride
concentrations rose over time with the alcohol ⫹ CHO
diet and remained elevated above corresponding values for control and alcohol-displacement until 10 h of
recovery (see Fig. 3C, P ⬍ 0.05). The total AUC for
postmeal triglyceride concentrations was greater with
alcohol ⫹ CHO than alcohol-displacement and control.
Muscle glycogen concentrations in postexercise and
postrecovery samples are summarized in Table 2, together with a calculation of glycogen storage during
the recovery period. The exercise depletion protocol
reduced muscle glycogen stores to similarly low values
in all trials. In the 8-h study, glycogen storage was
reduced in the alcohol-depletion trial compared with
control (P ⬍ 0.05), and there was a trend to lower
glycogen storage in the alcohol ⫹ CHO trial (P ⬍ 0.1).
Glycogen storage was also lower with alcohol-displacement compared with control trial in the 24-h study
(P ⬍ 0.05). There was no difference in glycogen storage
after 24 h of recovery between alcohol ⫹ CHO and
control.
ALCOHOL AND POSTEXERCISE RECOVERY
987
Fig. 2. Blood metabolites [plasma glucose (A), insulin
(B), and triglyceride (C)] after an overnight fast (F) and
in response to 2 meals eaten at t ⫽ 0 and 3 h of recovery
(M1 and M2, respectively) from glycogen-depleting exercise with the 8-h control (8-C) diet and when alcohol
(1.5 g/kg body mass) is consumed during the first 3 h
under the 8-A and 8-AC protocols. AUC, area under the
curve. Data are means ⫾ SE for 6 subjects. * A ⬍ C, AC
(P ⬍ 0.05); #C ⬍ A, AC (P ⬍ 0.05).
J Appl Physiol • VOL
was largely metabolized and cleared from the blood.
The lack of overall differences in BAL between the two
alcohol trials in each study (i.e., alcohol-displacement
diet and alcohol ⫹ CHO diet) suggests that the intake
of greater amounts of food and CHO energy did not
have a substantial impact on the rate of absorption or
metabolism of the alcohol.
Our studies showed evidence of alterations in CHO
and lipid metabolism in response to the intake of large
amounts of alcohol, particularly in the 24-h study.
Plasma glucose concentrations and the overall glycemic response to CHO-rich meals over 24 h were reduced when large amounts of alcohol were consumed in
conjunction with the control diet (Fig. 3A). Despite
lower plasma glucose levels compared with the control
trial, the insulinemic response to the alcohol-CHO diet
was not substantially reduced. In sedentary subjects,
alcohol infusion has been shown to have no net effect
on plasma glucose levels after glucose infusion as a
result of equal declines in the rates of glucose appearance and disappearance; however, there was an increase in plasma insulin concentrations and insulin
resistance (25). Alcohol intake was associated with an
increase in triglyceride concentrations above the control trial, especially in the 24-h study and in the case of
the higher energy CHO diet in which plasma triglyceride did not return to fasting levels until the alcohol
was fully metabolized and cleared from the blood. Hypertriglyceridemia is a well-known outcome of the
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In our studies, well-trained athletes were required to
consume alcoholic spirits providing 1.5 g/kg of ethanol,
equivalent to ⬃11 “standard drinks” (each ⬃10 g alcohol) for a typical subject, during the first 3 h of recovery
from prolonged exercise. Such an intake is well above
the level of drinking considered “safe and healthy” by
various health bodies and was the maximum intake of
alcohol that our Human Ethics Committee would allow
us to provide to subjects. However, it represents only
the mean intake reported in two studies of the binge
drinking practices of competitive sports people [viz.,
⬃120 g, (range ⫽ 27–368 g), with alcohol providing a
mean contribution of 19% of total energy intake on
match day (range ⫽ 3–43% of total energy intake); Ref.
6) and ⬃130 g (range ⫽ 1–38 standard alcoholic
drinks); Ref. 21]. Although such official reports of
drinking patterns by athletes are limited and are susceptible to the challenges of poor reliability and accuracy, the lay press regularly provides anecdotal evidence of binge drinking episodes by some athletes,
particularly in the immediate celebration or commiseration of their competition performances. The alcohol
consumption protocol used in the present studies
caused a rise in BAL to a mean peak of 0.12 mg/100 ml
after 4 h of recovery. After 8 h of recovery, BAL were
still substantially raised (⬃0.06–0.07 g/100 ml), compared with the BAL of 0.05 g/100 ml, which is the legal
limit for the driving of a motor vehicle by fully licensed
drivers in Australia. By 24 h of recovery, the alcohol
988
ALCOHOL AND POSTEXERCISE RECOVERY
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Fig. 3. Blood metabolites [plasma glucose
(A), insulin (B), and triglyceride (C)] after
an overnight fast (F) and in response to 4
meals eaten at t ⫽ 0, 3, 8, and 21 h of
recovery (M1, M2, M3, and M4, respectively) from glycogen-depleting exercise
when alcohol (1.5 g/kg body mass) is consumed under the 24-A and 24-AC protocols. Data are means ⫾ SE for 9 subjects.
* C ⬍ A, AC (P ⬍ 0.05); #AC ⬍ A (P ⬍
0.05); @C ⬎ A (P ⬍ 0.05); $AC ⬎ C, A (P ⬍
0.05).
acute and chronic consumption of moderate to large
intakes of ethanol (11, 26–28), even in physically active
populations (28) and after an acute bout of exercise (11,
28), with a variety of proposed mechanisms involving
increased production or decreased clearance of VLDL
triglyceride.
Rat studies have shown that the infusion of ethanol
causes the impairment of glycogen deposition in the
liver and selective muscle fiber types during CHO
feeding of previously starved animals (8, 32–34) and
during the immediate recovery from high-intensity exercise associated with high muscle and plasma lactate
levels (24). These effects of ethanol have been reported
in oxidative but not nonoxidative fiber types (32–34)
but were not observed in mixed muscle samples (8).
One observed mechanism to explain the impairment of
glycogen synthesis in oxidative muscle types was a
J Appl Physiol • VOL
Table 2. Muscle glycogen concentrations after exercise
depletion and after a recovery period with different
dietary interventions
Postexercise
Postrecovery
Net Storage
(Postrecovery
minus
postexercise)
11.5 ⫾ 2.8
15.8 ⫾ 6.9
16.2 ⫾ 5.3
56.0 ⫾ 3.6
40.2 ⫾ 2.8
52.5 ⫾ 6.6
44.6 ⫾ 6
24.4 ⫾ 7*
36.2 ⫾ 8
20.8 ⫾ 5.5
19.9 ⫾ 4.2
21.8 ⫾ 5.1
102.5 ⫾ 8.8
88.2 ⫾ 5.8
106.9 ⫾ 10.0
81.7 ⫾ 5
68.4 ⫾ 5*
85.1 ⫾ 9
8-h Recovery study
Control
Alcohol displacement
Alcohol ⫹ CHO
24-h Recovery study
Control
Alcohol displacement
Alcohol ⫹ CHO
Values are means ⫾ SE for 6 subjects in the 8-h study and 9
subjects in the 24-h study, * alcohol displacement ⬍ control and
alcohol ⫹ CHO (P ⬍ 0.05).
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ALCOHOL AND POSTEXERCISE RECOVERY
We thank Professor Peter Fricker and Susan Beasley for assistance with the muscle biopsy procedure, and Mark Collins for help
with the statistical analyses.
J Appl Physiol • VOL
DISCLOSURES
The study was funded by an internal research grant from the
Sports Science Sports Medicine Centre of the Australian Institute of
Sport.
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