Athletes, like the rest of the population, consume alcohol. Sporting clubs and associations are frequently reported in the media to place bans or restrictions on the availability and consumption of alcohol by contracted athletes. Yet the same media organizations also report on alcohol-fuelled violence or misdemeanors perpetrated by these same athletes, suggesting anecdotally that athletes consume alcohol, occasionally to excess. This is quantitatively supported by dietary surveys of athletic populations that demonstrate self-reported alcohol intake constitutes up to 5% of the total daily energy intake in elite athletes [1]. However this is far from universal, as survey data reports either greater [2,3], or reduced [4,5] alcohol ingestion in athletic populations than the general community. This high variability in reported alcohol intake within athletic groups may in part be due to the characteristics of each sporting discipline. Alcohol intake appears to be positively associated with team sports where alcohol consumption is often encouraged as a component of team/group bonding and can be related to stress relief [6].

The detrimental effects of alcohol on human physiology have been well documented with acute alcohol ingestion affecting many aspects of metabolism, neural function, cardiovascular physiology, thermoregulation and skeletal muscle myopathy [7,8,9]. Yet the impact that alcohol ingestion has on exercise performance and more critically recovery has received less detailed scrutiny. This review aims to provide insights into the current knowledge around how alcohol acts to impair both exercise performance and the critical mechanisms by which alcohol acts at the cellular level to retard recovery following strenuous activity.

Alcohol consumption has a deleterious effect on a multitude of systems within the body and an in-depth analysis of each is beyond the scope of this review. However a brief insight into common symptoms linked to acute alcohol misuse will guide the following discussion on how alcohol influences human performance and recovery.

Given the numerous and complex mechanisms by which ethanol impacts on physiological systems it can be strongly hypothesized that elevated blood alcohol concentrations at the time of exercise will impair performance. Remarkably there are relatively few clinical trials that address this question.

Most of the studies examining alcohol and athlete recovery have focused predominately on functional measures of muscle performance and blood borne markers of cellular tissue damage. To date, these studies have produced inconclusive results that fail to demonstrate a dose-dependency or critical threshold above which muscular recovery is compromised. Creatine kinase (CK) is an intra-muscular enzyme which when present in the peripheral circulation is widely used as a measure of muscle damage. Despite the clinical association between chronic alcohol abuse and skeletal muscle myopathy, acute ingestion appears to have little impact on exercise-mediated muscular damage [13,16,18]. The lack of results may be attributable to the parameters measured within these above mentioned trials. CK is highly variable and may not provide the best measure of muscle damage [45,48]. More recently, circulating levels of pro-inflammatory cytokines, released from the musculature may provide alternative measures of muscular stress and damage [47]. Inflammatory processes appear to be variably modulated by chronic and acute alcohol use. Prolonged alcoholism is associated with high circulating levels of pro-inflammatory mediators [49], whilst conversely acute consumption has been shown to decrease production of TNF-α and (IL-1) in rodent studies [50,51,52] It has yet to be established if cytokine concentrations are altered by acute alcohol ingestion during or immediately following intense exercise.

Similarly to the analysis of markers of muscle damage, the intra-muscular consequences of acute alcohol ingestion on aspects metabolic pathways of recovery are also ambiguous in humans. Alcohol ingestion immediately following prolonged cycling exercise has a modest impact to impair glycogen re-synthesis [48]. This action is dependent in part on alcohol replacing carbohydrates in energy-matched meals. Although acute suppression of glycogen synthesis may have been evident, examination of glycogen repletion over 24 hours demonstrated no long term detrimental impact of alcohol ingestion on muscle glycogen stores.

Of particular relevance to the recovery of strength athletes is the enhanced protein synthesis that occurs post-exercise to facilitate repair and adaptive hypertrophy [53]. Acute alcohol ingestion decreases muscle protein synthesis in a dose- and time-dependent manner, in the absence of an exercise stimulus. Alcohol facilitates this firstly by suppressing the phosphorylation and activation of the mTOR pathways, the critical kinase cascade regulating translation initiation [54]. Complementing the decreased activation of the protein synthetic pathway, alcohol increases the expression of muscle specific E3 ligases; atrogin-1 and Muscle-specific RING finger 1 (MuRF1) [55]. These proteins are up regulated by conditions that promote skeletal muscle atrophy. Interestingly this was not associated with increased proteolysis, suggesting alcohol primarily impairs protein synthesis. It remains to be confirmed in rodents subjected either to muscle loading or resistance exercise that alcohol impairs protein synthesis. Subsequent clinical data is also lacking and this remains a critical absence in the scientific literature.

Functionally, the consumption of moderate amounts of alcohol augments the loss of force associated strenuous eccentric exercise [18,56]. To the researchers knowledge Barnes, Mündel and Stannard have produced the only research that has used functional measures of muscle performance to identify an interaction between post-exercise muscle damage and alcohol [18,56]. This research established a significant decrease in average peak isometric, concentric and eccentric torques at 36 hours post-exercise. This decrement appeared to be exacerbated across all three variables in the group that consumed 1g per kg of body weight immediately post-exercise. Whilst this research provides new insights into the effect of alcohol consumption on post-exercise muscle recovery, further research is required to ascertain how this relationship exists and establish the physiological mechanisms governing this response.

Both the affects of alcohol on human physiology and the parameters that determine athletic performance are multi-factorial and extremely complicated. A significant body of literature has established an array of adverse symptoms caused by acute alcohol ingestion. However the notion that alcohol consumption effects performance has not received enough consistent validation to advance beyond being anecdotal. Nevertheless, just because alcohol is not yet comprehensively shown to have a negative influence on performance, does not imply this review advocates its use prior to, or following competition. Indeed, the data demonstrates a severe lack of analysis on the possible detrimental action of alcohol in the recovering athlete. However, based on the available experimental evidence in cellular and rodent-models, athletes should remain wary of ingesting alcohol following intense exercise, focusing instead on effective dietary strategies proven to enhance recovery.