Alcohol (ethanol) is consumed on a daily basis by a large fraction of the population, and in many countries, light-to-moderate alcohol consumption is considered as an integral part of the diet. Although the relationship between alcohol intake and obesity is controversial, regular consumption of alcohol, through its effects in suppressing fat oxidation, is regarded as a risk factor for weight gain, increased abdominal obesity and hypertriglyceridemia. Indeed, alcohol taken with a meal leads to an increase in postprandial lipemia—an effect on postprandial metabolism that is opposite to that observed with exercise. Furthermore, although regular exercise training and/or a preprandial exercise session reduce postprandial lipemia independently of alcohol ingestion, the exercise-induced reduction in postprandial lipemia is nonetheless less pronounced when alcohol is also consumed with the meal. Whether or not alcohol influences exercise and sport performance remains contradictory. It is believed that alcohol has deleterious effects on the performance, although it may contribute to reduce pain and anxiety. The alcohol effects on sports performance depend on the type and dosage of alcohol, acute vs chronic administration, the alcohol elimination rate as well as the type of exercise.
Alcohol is consumed on a daily basis by a major fraction of the population, but whether moderate amounts of alcohol represent a risk factor for weight gain and chronic metabolic diseases is still uncertain. For example, light-to-moderate alcohol consumption has long been associated with diminished cardiovascular morbidity and mortality, but several recent studies have reported that alcohol consumption worsens the cardiovascular risk factor profile, and hence questions the role of alcohol in cardioprotection.1, 2 By contrast, the health benefits of exercise and physical activity are well established, and physical activity represents a key component of all the guidelines for primary and secondary prevention of cardiovascular disease. As alcoholic beverages are often consumed before, during or after exercise sessions (for a variety of reasons that include ergogenic, thirst quenching, rehydration or for social reasons), the following questions arise: (i) is alcohol a usable source of energy during exercise and (ii) does alcohol as a fuel substrate during exercise offer any advantage or disadvantage over other energy substrates. In addressing these questions, this paper first reviews the effects of alcohol consumption during exercise on postprandial metabolism, and subsequently the effect of alcohol consumption on exercise performance.
Alcohol and postprandial metabolism
In the moderate alcohol consumer (who typically has 1–2 drinks containing 10 g of alcohol per day), the energy derived from alcohol is a usable source for ATP production.3 The metabolism of alcohol—through the alcohol dehydrogenase pathway or the microsomal ethanol oxidizing system—generates acetate, which, to a great extent, is metabolized to CO2 and H2O. Thus, only a small fraction of alcohol (<5% of a 20-g alcohol load) is used for de novo lipogenesis, whereas the largest fraction of alcohol carbons are shuttled in the form of acetate to the peripheral tissues where they are utilized as a source of energy.4, 5 On account of such peripheral utilization of acetate as a substrate energy occurs at the expense of fat oxidation,6 the ingestion of alcohol—through its effects in suppressing fat oxidation—is regarded as a risk factor for weight gain, increased abdominal obesity, type 2 diabetes and hypertriglyceridemia7 in regular alcohol consumers.
Many factors modulate postprandial lipemia, in particular the frequency of eating, diet composition and physical activity.8, 9, 10, 11, 12 These lifestyle factors might determine whether one has a normal postprandial metabolism or a postprandial dysmetabolism. To achieve the cardiovascular protection, lifestyle changes have to be implemented sustainably. This is also the case for the modulation of the postprandial lipemia by exercise. In a recent study, Hardman et al.12 showed that frequent physical activity is needed to counteract an exaggerated postprandial metabolic response. Obviously, a minimal level of activity is needed, and there is a relationship between the level of the exercise load and the postprandial metabolic response pattern. Exercise reduces the adverse effects of meals high in energy—high in simple carbohydrates or high in fat8—on the postprandial lipemia and dysmetabolism.13 By contrast, alcohol ingestion leads to an increased and prolonged postprandial lipemia.14 As shown in Figure 1 (left panel), there is an exaggerated postprandial triglyceride response after a meal when ingested with alcohol (compared with the same amount of water) in untrained individuals, in moderately trained (middle panel) and six highly trained (right panel) individuals.14 In the latter study,14 the participants received either 0.5 g of alcohol per kilogram body weight or the equal amount of water with a test meal containing 1 g of fat per kilogram body weight. Thus, although the impact of the training status on postprandial lipemia can be easily recognized in Figure 1, it is also clear that alcohol ingestion was associated with an increased postprandial triglyceride response independently of the level of training. The key question is whether these metabolic phenomena could be of advantage for exercise performance and metabolism during exercise?
Effect of alcohol on exercise performance
The advice given by the American College of Sport Medicine15 on alcohol and athletic performance is to refrain from alcohol consumption, in particular immediately before the exercise event. The professional association clearly emphasizes not only the lack of benefit of alcohol for an athlete but also highlights the adverse effects on performance and the possible detrimental effect to the athletes. Alcohol may decrease performance because of its metabolic and cardiovascular effects. Nevertheless, there are anecdotal reports that some athletes consume alcohol before training sessions or competitions. Excess alcohol consumption and binge drinking seem to be as prevalent in male and female athletic communities, as it is in the general population. Dietary surveys have shown that alcoholic drinks contribute up to 5% of the total daily energy intake of athletes16 and this amount is not lower than the general non-athlete population.17
Since the publication of ‘The use of alcohol in sports: position stand of American College of Sport Medicine’ a quarter of century ago,15 some inconsistent results about the influence of alcohol on performance have appeared in the literature—as pointed out by more recent comprehensive reviews on the topic.18 How alcohol consumption affects an individual's performance depends on several factors: (i) the amount and types of alcohol consumed, (ii) endogenous factors such as interindividual differences in tolerance and (iii) exogenous factors (mainly environmental). One must also differentiate between the acute vs chronic effects of alcohol on physical performance, leading to different effects. Only the acute effects of alcohol on human exercise and sport performance will be briefly considered here, with emphasis on the metabolic and physiologic functions.
Why and how could performance be affected by alcohol consumption?
It is well known that alcohol exerts effect on the central nervous system, muscle energy stores and the cardiovascular system.18 Alcohol is not used by the muscle as a source of energy; it is the liver, which is the main site of alcohol oxidation. So exercise does not increase alcohol metabolism, as generally believed by lay people! Overall alcohol is thought to impair muscular work capacity and to result in a decrease in overall performance levels (such as slower running and cycling times), to impair temperature regulation during exercise, and to increase the onset of fatigue during high-intensity exercise. Alcohol influences carbohydrate and fat metabolism partly by displacing these two macronutrients as energy sources. In addition, alcohol consumption has also been shown to inhibit liver glucose output during exercise,19 to blunt the uptake of gluconeogenic precursors, such as lactate and glycerol20 resulting in an impaired hepatic gluconeogenesis and ultimately precipitating hypoglycemia.21 Acute alcohol ingestion may compromise an adequate supply of fuel for normal aerobic energy production by lowering muscle glycogen and decreasing leg-muscle glucose uptake,20 thereby modifying the pattern of muscle glycogen degradation.21
A variety of psychomotor skills, such as impaired balance, reaction time and coordination are also altered.17, 22 Acutely, alcohol has deleterious effects on psychomotor skills, but again this depends on the dosage: low amounts of alcohol (producing low blood alcohol concentration, up to 0.05 g per 100 ml) result in decreased hand tremors, slowed reaction time and decreased eye–hand coordination. Moderate amounts of alcohol (blood alcohol concentration of 0.06–0.10 g per 100 ml) further amplify these factors and also decrease accuracy and balance and impair tracking, visual search, recognition and response skills.
However, it is not only negative side effects that are observed with alcohol consumption. In moderate dosage, alcohol may have some advantages through psychobiological mechanisms. For example, a decrease of pain and anxiety might be beneficial to performance in certain sports.22 Alcohol may also positively modulate the ratings of perceived exertion. A schematic view of the effect of alcohol on physical performance through physiological and psychological factors is presented in Figure 2.
Acute alcohol consumption on athletic performance
Earlier studies on the effects of acute alcohol consumption on athletic performance show conflicting results. Some studies have shown that alcohol negatively influences middle distance running23 and endurance performance,24 whereas other studies did not show any effect of alcohol on athletic performance25, 26 and on some metabolic parameters associated with exercise performance, such as blood lactate, heart rate, rates of perceived exertion, pulmonary ventilation and oxygen consumption. These discrepancies in the literature can be explained on several grounds: (i) differences in the experimental design, (ii) the type of exercise performed, (iii) the absolute and relative intensity of exercise used, as well as its duration, (iv) the nature of performance measured, (v) the training level (for both exercise and alcohol consumption!) and (vi) methodological issues.
Whether an acute low dose of alcohol would impair the endurance performance of trained amateur cyclists during 1-h time trials at high-intensity levels is still unknown. Through its deleterious effect on carbohydrate metabolism, an acute low dose of alcohol may affect endurance performance, even at low dosage. A recent well-controlled experiment performed in a respiratory chamber in which room air temperature and humidity were controlled, attempted to answer this question (V Lecoultre and Y Schutz, unpublished data). Most of the conditions of the study mimicked those encountered in real-life racing, except confinement: usual bicycle of athletes utilized, no mouthpiece or face mask used with indirect calorimetry (thus avoiding the increased resistance when breathing in and out), continuous energy expenditure measurements in a whole-body respiration chamber (rather than intermittent expenditure measurements), simulation of wind by a fan for increasing convection on the face of the individual and finally the use of low ‘physiological’ dosage of alcohol integrated into a normal habitual drink. It should also be pointed out that, unlike running, information on the effect of acute alcohol consumption on performance during cycling is very scanty.24
The aim of the study was to investigate the effect of an acute alcohol dose in a moderate amount on the endurance performance and metabolic response of 13 well-trained male cyclists. A 60-min time trial, at a work intensity corresponding to more than 80% of VO2 max, was performed after drinking alcohol or a non-alcohol control drink. Individuals ingested in a blind manner and wearing nose clips a solution containing either 0.5 ml of ethanol+0.5 g of carbohydrate (grapefruit juice) per kilogram fat-free mass or an isovolumetric control solution containing the same amount of carbohydrate, in a random manner. Blood alcohol levels remained low, reaching 18 mg per 100 ml at the start of exercise. Twenty minutes after the onset of exercise, it reached a maximum value of 20 mg per 100 ml, less than half of the Swiss legal value for driving a car.
Overall, alcohol induced a small but significant decrease in average cycling power, averaging 4% (Figure 3). The time course of mechanical power was interesting, as alcohol consumption induced a significant decrease in power in the early phase of the time trial. On account of the maintenance of a lower power output throughout the trial, oxygen consumption, carbon dioxide production and energy expenditure were, as expected, significantly lower with alcohol as compared with the non-alcohol situation. Similarly, total glucose oxidation was significantly lower, consecutive to alcohol consumption. There was no influence of alcohol on the pattern of glycemia during the trial. Similarly, the pattern of blood lactate plasma concentration was not influenced by alcohol (in both conditions lactate was above the 4 mmol anaerobic threshold). The small doses of alcohol used in this study and exogenous carbohydrate intake probably prevented an influence on hepatic glucose production and hepatic gluconeogenesis. No significant difference in heart rate response was found between the two conditions. However, when heart rate was normalized to effective cycling power output, it was significantly more elevated in the group drinking alcohol. Overall, this study showed that an acute low dose of alcohol has a negative effect on a 1-h high-intensity cycling performance.
These results are consistent with earlier studies on running.23, 24 A decrease in the performance of runners after ingestion of different alcohol doses inducing blood alcohol concentrations similar to those measured in this study has been reported earlier, and a significant negative effect of alcohol on the ability of well-trained runners to complete a 60-min running event has been shown.24 The mechanism responsible for this slight drop in performance is unknown but it may involve cardiovascular and psychobiological factors. Running may be considered as a complex motor skill, and the decrease in performance during running under the influence of alcohol may be partially attributed to an alteration of coordination skills and balance.23 In contrast, ‘static’ cycling on an ergometer may not require high psychomotor or coordination skills. Network efficiency did not decrease with alcohol consumption, which means that the main gross motor skill of cycling performance on a stationary bicycle (pedaling technique) was not altered. We concluded from this study that acute low doses of alcohol can be considered as deleterious to endurance performance, although the effect appears to be modest for amateur (non-elite) racing.
In practice, and as stated earlier,15 athletes are advised to abstain from drinking alcohol before intense exercise, in a training session or competition. For athletes who cannot refrain from consuming alcohol and deliberately choose to drink, the American College of Sport Medicine15 recommends for pre-event to avoid alcohol beyond a modest amount of social drinking for at least 48 h before the event. In the post-exercise recovery period, they suggest to rehydrate first with water and consume food before drinking to slow down the alcohol absorption.
Sung K-C, Kim SH, Reaven GM . Relationship among alcohol, body weight, and cardiovascular risk factors in 27 030 Korean men 10.2337/dc07-0315. Diabetes Care 2007; 30: 2690–2694.
Kloner RA, Rezkalla SH . To drink or not to drink? That is the Question Circulation 2007; 116: 1306–1317.
Lieber CS . Metabolism of ethanol. In: Lieber CS (ed). Medical and Nutritional Complications of Alcoholism. Plenum Publishing Corporation: New York, NY, 1992, 1–35.
Siler SQ, Neese RA, Parks EJ, Hellerstein MK . VLDL-triglyceride production after alcohol ingestion, studied using [2-13C1] glycerol. J Lipid Res 1998; 39: 2319–2328.
Siler SQ, Neese RA, Hellerstein MK . De novo lipogenesis, lipid kinetics, and whole-body lipid balances in humans after acute alcohol consumption. Am J Clin Nutr 1999; 70: 928–936.
Suter PM . Effect of alcohol on body weight. Nutr Clin Care 2000; 3: 102–108.
Yuan G, Al-Shali KZ, Hegele RA . Hypertriglyceridemia: its etiology, effects and treatment. CMAJ 2007; 176: 1113–1120.
Dubois C, Beaumier G, Juhel C, Armand M, Portugal H, Pauli AM et al. Effects of graded amounts (0–50 g) of dietary fat on postprandial lipemia and lipoproteins in normolipidemic adults. Am J Clin Nutr 1998; 67: 31–38.
Zilversmit DB . Atherosclerosis: a postprandial phenomenon. Circulation 1979; 60: 473–485.
Nitenberg A, Cosson E, Pham I . Postprandial endothelial dysfunction: role of glucose, lipids and insulin. Diabetes Metab 2006; 32: 2S28–2S33.
O'Keefe JH, Bell DS . Postprandial hyperglycemia/hyperlipidemia (postprandial dysmetabolism) is a cardiovascular risk factor. Am J Cardiol 2007; 100: 899–904.
Hardman AE, Lawrence JEM, Herd SL . Postprandial lipemia in endurance-trained people during a short interruption to training. J Appl Physiol 1998; 84: 1895–1901.
Koutsari C, Karpe F, Humphreys SM, Frayn KN, Hardman AE . Exercise prevents the accumulation of triglyceride-rich lipoproteins and their remnants seen when changing to a high-carbohydrate diet. Arterioscler Thromb Vasc Biol 2001; 21: 1520–1525.
Suter PM, Gerritsen Zehnder M, Häsler E, Gürtler M, Vetter W, Hänseler E . Effect of alcohol on postprandial lipemia with and without preprandial exercise. J Am Coll Nutr 2001; 20: 58–64.
Anonymous. The use of alcohol in sports: position stand of American College of Sport Medicine. MSSE 1982; 14: pp ix–xi.
Maughan RJ, Burke LM . Alcohol and sport. In: Maughan RJ, Burke LM (eds). Sports Nutrition. Blackwell Science: Malden, 2002, pp 64–70.
Burke LM, Maughan RJ . Alcohol in sport. In: Maughan RJ (ed). Nutrition in Sport. Blackwell Science: Oxford, 2000, pp 405–414.
Gutgesell M, Canterbury R . Alcohol usage in sport and exercise. Addict Biol 1999; 4: 373–390.
Heikkonen E, Ylikahri R, Roine R, Välimäki M, Härkönen M, Salaspuro M . Effect of alcohol on exercise-induced changes in serum glucose and serum free fatty acids. Alcohol Clin Exp Res 1998; 22: 437–443.
Jorfeldt L, Juhlin-Dannfelt A . The influence of ethanol on splanchnic and skeletal muscle metabolism in man. Metabolism 1978; 27: 97–106.
Juhlin-Dannfelt A, Jorfeldt L, Hagenfeldt L, Hulten B . Influence of ethanol on non-esterified fatty acid and carbohydrate metabolism during exercise in man. Clin Sci Mol Med 1977; 53: 205–214.
Williams MH . Alcohol, marijuana and beta blockers. In: Lamb DR, Williams MH (eds). Perspectives in Exercise Science and Sports Medicine. Cooper Publishing Group: Carmel, 1991, pp 331–369.
McNaughton L, Preece D . Alcohol and its effects on sprint and middle distance running. Br J Sports Med 1986; 20: 56–59.
Kendrick ZV, Affrime MB, Lowenthal DT . Effect of ethanol on metabolic responses to treadmill running in well-trained men. J Clin Pharmacol 1993; 33: 136–139.
Bond V, Franks BD, Howley ET . Effects of small and moderate doses of alcohol on submaximal cardiorespiratory function, perceived exertion and endurance performance in abstainers and moderate drinkers. J Sports Med Phys Fitness 1983; 23: 221–228.
Houmard JA, Langenfeld ME, Wiley RL, Siefert J . Effects of the acute ingestion of small amounts of alcohol upon 5-mile run times. J Sports Med Phys Fitness 1987; 27: 253–257.
We are indebted to V Lecoultre for his interest and outstanding help in performing the study on alcohol and cycling performance. This study was partly supported by the Swiss Foundation for Nutrition Research.
Conflict of interest
The authors have declared no financial interests.
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Suter, P., Schutz, Y. The effect of exercise, alcohol or both combined on health and physical performance. Int J Obes 32, S48–S52 (2008). https://doi.org/10.1038/ijo.2008.206
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Nutrition & Metabolism (2014)