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1Sports Science and Sports Medicine, Australian Institute of Sport, Belconnen, Australian Capital Territory 2616; 2School of Health Sciences, Deakin University, Waurn Ponds, Victoria 3217; and 3School of Health Sciences, Deakin University, Burwood, Victoria, 3125, Australia
Submitted 3 February 2003 ; accepted in final form 16 April 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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ethanol; glycogen resynthesis
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 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.
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METHODS |
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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·min-1·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·min-1·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 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 · kg-1 · 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 ·
kg-1 · 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 · kg-1 · 24
h-1 (1.1 g · kg-1 ·
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.
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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 high-glycemic-index CHO-rich foods, identical to the first two meals in the 24-h trial. Total CHO intake = 3.5 g/kg (1.75 g · kg-1 · 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 ·
kg-1 · 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 · kg-1
· 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 (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 705-0013, 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).
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).
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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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).
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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-displacement 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).
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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 concentrations was greater with control than both alcohol-displacement 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.
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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.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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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 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 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 fiber-specific reduction in activation of glycogen synthase in association with the ethanol infusion (32). However, there is the potential for a range of defects in insulin-stimulated glucose metabolism in response to large amounts of ethanol, including membrane-associated impairments in insulin signaling and glucose transport (32).
In the present studies, postexercise muscle glycogen storage in human subjects was impaired when alcohol was used for isoenergetic displacement of CHO intake from the recovery diet. Reduced levels of glycogen restoration were seen at 8 h of recovery and after 24 h on the alcohol-displacement diet and may simply reflect the reduced intake of dietary CHO. Therefore, hepatic metabolism of ethanol to acetaldehyde and acetate neither provided a substrate for glycogen synthesis nor spared the coingested CHO for a nonoxidative (glycogen storage) fate in the muscle, even when the total energy intake was increased by the addition of the alcohol to the control (high-CHO) recovery diet.
We saw a trend to reduced muscle glycogen storage at 8 h of recovery when alcohol was consumed in addition to the high-CHO recovery diet, associated with increased variability in muscle glycogen storage. It is possible that we were unable to detect a true impairment of glycogen storage after large amounts of alcohol because of individual responses in difference subjects or because the fiber-type specificity of response was masked in a mixed muscle sample, as seen in rat studies (8). Further studies are needed to investigate the possibility of direct effects of alcohol on glycogen synthesis in individual subjects or specific muscle fibers. Nevertheless, by 24 h of recovery and after the full metabolism of the alcohol, differences in muscle glycogen recovery between the CHO (control) and alcohol + CHO trials were trivial. It is likely that, if glycogen recovery was impaired during the early phases of recovery, this was followed by a period of "catch up" (35) in the presence of adequate dietary CHO.
In summary, the intake of large amounts of alcohol immediately after prolonged exercise was associated with impairments of CHO and lipid metabolism. Evidence for a direct effect of elevated blood alcohol concentrations on muscle glycogen synthesis was unclear, but it appears that, if an early impairment of glycogen synthesis exists, it may be compensated by adequate CHO intake and longer recovery time. The most important effects of alcohol intake on glycogen resynthesis are likely to be indirect, by interfering with the athlete's ability or interest to achieve the recommended amounts of CHO required for optimal glycogen restoration. Athletes are therefore guided to follow the guidelines for sensible use of alcohol in sport (5), in conjunction with the well-supported recommendations for recovery eating.
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DISCLOSURES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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ACKNOWLEDGMENTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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