Among athletes, this is high considering the WHO’s 25% worldwide estimate of smoking prevalence. It can be hypothesized that the metabolites stem mostly from smokeless tobacco due to the adverse effects of conventional cigarettes for athletes, which most severely affects athletes engaging in endurance type sports. Further, a large number of human and animal studies have found nicotine-induced improvements in several aspects of cognitive function, including learning and memory, reaction time and fine motor abilities . Studies addressing the question of a direct performance enhancing effect of nicotine are rare but will be summarized here. Sports most affected include ice hockey, skiing, biathlon, bobsleigh, skating, football, basketball, volleyball, rugby, American football, wrestling and gymnastics. These sports seem to gain performance benefits from the stimulating effect of nicotine as evident from the use of other prohibited stimulants according to the Anti-Doping Database. Muendel et al. found a 17% improvement in time to exhaustion after nicotine patch application compared to a placebo without affecting cardiovascular and respiratory parameters or substrate metabolism. In this sense, nicotine seems to exert similar effects as caffeine by delaying the development of central fatigue as impaired central drive is an important factor contributing to fatigue during exercise. To date, no improvement on anaerobic performance has been reported . It is important to note that, compared to rest, exercise can lead to increased drug absorption from transdermal nicotine patches, possibly due to exercise-induced increase in peripheral blood flow at the site of the transdermal patch. Lenz et al. report increased plasma nicotine levels and toxicity due to increased drug absorption during physical exercise. To prevent undesirable side effects, health professionals,4×8 grow table with wheels trainers and coaches should therefore be aware of proper transdermal patch use, particularly while exercising. Athletes are encouraged to inform their physician about their exercise routine before beginning transdermal patch use. Athletes should further be familiar with signs and symptoms of drug toxicity related to the medication contained in thetransdermal patch and consult their physician if signs or symptoms arise.
Reducing exercise intensity and duration for the first 1–2 weeks until potential side effects are known might also help to minimize toxicity. To reduce increased exercise-induced drug absorption, athletes are encouraged to avoid exercising in extreme environmental and temperature conditions, wear appropriate breathable sports garments and drink plenty of fluids to prevent dehydration. Additionally, although nicotine may have ergogenic potential, it is also highly addictive, reportedly as addictive as heroin and cocaine. Therefore, detrimental effects on motor performance can be altered after a short abstinence duration. Burtscher et al. noted that motor performance declines in heavy smokers after a short period of abstinence appears, this decline being similar to the motor symptoms of Parkinsonism. The abstinence symptoms are ameliorated by cigarette smoking. It is important to consider the concerning addictive potential with following deterioration of motor performance upon abstinence. Interestingly, however, it was noted that moderate and vigorous exercise led to significant reductions of the desire to smoke among abstaining smokers, possibly via reductions in cortisol. A recent meta-analysis showed that exercise has the potential to acutely reduce cigarette cravings and could therefore be a promising strategy to attenuate withdrawal symptoms in smokers. It is also important to mention that the vasoconstriction mediated by nicotine could limit exercise performance in a hot environment. As skin blood flow increases during exercise to transfer heat impaired nicotine-induced skin blood flow may be ergolytic. A recent meta-analysis conducted by Heishman and colleagues clearly suggests significant effects of nicotine on fine motor abilities, including attention and memory. Participants of the studies included in the metaanalysis were mainly nonsmokers, therefore avoiding confounding of nicotine withdrawal. Considering the importance of cognition in sport, such an optimization of neurobiological function in our view seems to be beneficial for a variety of sports such as sport games or track and field. Finally, nicotine’s effect on increased pain tolerance might be of advantage in a wide variety of sports. More research will hopefully fill the gap to further evaluate nicotine’s effects on exercise performance.Based on observations of possible extensive smokeless nicotine consumption among certain athletes, a recent report by Marclay et al. from the Swiss Laboratory for Doping Analyses in Lausanne caught the interest of the sporting community and the WADA. Thereafter, discussions within WADA took place in the List Committee which is a subcommittee of the Health, Medical and Research Committee. Dr. Arne Ljungqvist, chairman of the Health, Medical and Research Committee, reports that WADA wants to know more about the use of nicotine in sports.
Once the prevalence is known, WADA will discuss a potential ban. Ljungqvist also reports that the IOC has already monitored nicotine as far back as 30 years ago in collaboration with the antidoping laboratory in Cologne, and did not report abusea. Since this time, smokeless tobacco and other nicotine delivery systems that might be appealing to the sporting community have entered the market. As a reaction, WADA has included nicotine, categorized as a stimulant and ‘in-competition only’ in its 2013 monitoring program. For this purpose, WADA reports: “WADA, in consultation with signatories and governments, shall establish a monitoring program regarding substances which are not on the Prohibited List, but which WADA wishes to monitor in order to detect patterns of misuse in sport”.In summary, nicotine seems to have ergogenic potential. Athletes appear to benefit from activation of the sympathoadrenal system with increased catecholamine release and subsequent increases in muscle blood flow and lipolysis. One component of nicotine action seems to act via a central mechanism . There is evidence for the abuse of nicotine by athletes. Although the sale of snus is illegal within the European Union, anecdotal observations by coaches and research from Scandinavia shows a high prevalence of snus use among athletes. It might therefore be reasonable to assume that smoking cigarettes will not be an issue for athletes. Instead, as there are several nicotine alternatives many of the negative effects of cigarettes can be circumvented.Alcohol is and has been one the most commonly consumed and abused drugs for a substantial period in human history. Alcohol is a dependence-producing drug which affects a host of organ systems and one that increases the risk of morbidity and mortality from different diseases when abused. Indeed, some authors have suggested that alcohol is harmful similar to drugs such as heroin or cocaine and that excessive alcohol consumption is a serious world-wide health risk. Although the detrimental effects of alcohol on human physiology are well known, even elite athletes consume alcohol. When looking at the effects of alcohol on overall health, it is, however, important to distinguish between chronic, moderate alcohol consumption versus alcohol abuse. Alcohol consumption and sport have been inextricably linked since ancient times when alcohol was considered the elixir of life. To some extent that may be true, given that a substantial body of epidemiological evidence shows that moderate ingestion of alcohol may reduce the risk of cardiovascular disease.
The link between alcohol consumption and mortality is subject to a J-shaped curve i.e. improved longevity with moderate consumption with increasing intake resulting in greater mortality risk. Indeed, dietary guidelines from the American Heart Association recommend moderation of alcohol intake as it has been associated with a lower risk of cardiovascular events. Alcohol use is fairly widespread among the athletic population with 88% of intercollegiate American athletes reporting the use of alcohol. It is also noteworthy that many athletes consume alcohol prior to sports events. However, it is important to note that scientific evidence suggests that the consumption of alcohol has some detrimental effects on exercise performance. It is fairly obvious that it is unlikely for competitive athletes to be alcohol abusers and most performance studies have focused on the acute ergolytic effects of EtOH consumption. The chronic studies merely reinforce the point that EtOH is profoundly ergolytic in the long term setting. They also serve to reinforce that chronic EtOH use can be toxic to cardiac and skeletal muscle.Chronic alcohol abuse has significant detrimental effects on the human cardiac muscle and one of the putative mechanisms via which alcohol may induce cardiac dysfunction is through the induction of increased oxidative stress. Interestingly, exercise training blunted the oxidative damage observed in a rat model of chronic alcohol consumption. The authors suggest that exercise training results in an up-regulation of cardiac antioxidants which may in turn reduce the deleterious effects of chronic alcohol induced oxidative stress. Acute alcohol use can also have effects on cardiovascular determinants of exercise performance. Lang et al. examined the effects of acute alcohol administration on left ventricular contractility using echocardiography and found that alcohol had a significant depressant effect on the myocardium. Specifically,grow tray stand acute alcohol consumption resulted in a decreased endsystolic pressure-dimension slope and reduced velocity of myocardial fiber shortening. Alcohol has significant effects on skeletal muscle substrate utilization during exercise. Specifically, it has been demonstrated that alcohol consumption decreases glucose and amino acid utilization, which can have adverse effects on energy supply to exercising muscle. Ethanol consumption induces hypoglycemia and decreases glucose appearance in plasma by decreasing hepatic gluconeogenesis. Ethanol administration has been shown to worsen skeletal muscle determinants of exercise performance such as muscle capillary density and muscle fiber cross-sectional area . It was shown in vitro that alcohol can inhibit sarcolemmal calcium channel actions thereby potentially impair excitationcontraction coupling and diminishing muscular performance.Greater capillary density also allows for a greater surface area for gas exchange and delivery of metabolic substrates. Long term alcohol consumption is associated with the development of alcoholic myopathy which is characterized by a reduction in skeletal muscle capillarity. Exercise training, however, appears to attenuate these adverse changes. Epidemiological data suggest that moderate alcohol consumption is associated with many salutary changes in blood coagulation and fibrinolysis. However, compelling experimental evidence is lacking and often conflicting. Alcohol can also lead to significant post-exercise perturbations in levels of clotting factors. Moderate postexercise alcohol consumption resulted in significantly elevated levels of Factor VIII at 5 and 22 hours during the post-exercise milieu.
Both circulating catecholamine and vasopressin levels have been implicated in upregulation of Factor VIII. These factors in turn, have been implicated in the pathogenesis of atherosclerosis in prospective studies. Alcohol and exercise may interact with each other to induce disorders in platelet aggregation which are associated with an elevated risk of cardiovascular and cerebrovascular events. Alcohol intoxication has been shown to be linked to cerebrovascular infarctions in a few casecontrol studies. However, the exact pathological mechanisms of the same are currently unknown. Alcohol consumption following athletic participation is commonly observed and may be associated with disorders in platelet aggregation. El-sayed et al. demonstrated that alcohol ingestion following exercise was associated with a marked increase in platelet count 1-hour following exercise. Platelet aggregation induced by adenosine diphosphate was found to be reduced when exercise was followed by alcohol consumption. Thus, it appears that ingestion of a moderate quantity of alcohol is associated with delayed recovery of platelet aggregation. It is important to note however, that the performance impact of ethanol consumption mediated post-exercise coagulopathy is unknown. Acute alcohol consumption is associated with the deterioration of psychomotor skills. A significant difference exists in injury rates between drinkers and non-drinkers in athletic populations. Athletes that consume alcohol at least once a week have almost a 2-fold higher risk of injury compared to non-drinkers and this elevated injury rate holds true for the majority of sports examined. The exact mechanisms that may be responsible for the elevated risk of injury are unknown. Alcohol may also interfere with the body’s ability to recover from injury. Barnes et al. examined the effects of 1 g/kg body weight alcohol consumption on recovery from eccentric exercise-induced muscle injury. The authors measured peak and average peak isokinetic and isometric torque produced by the quadriceps. Alcohol consumption was associated with significantly greater decreases in torque production 36 hours into recovery. The authors concluded that the consumption of a moderate amount of alcohol after damaging exercise magnified the loss of muscle force production potential. Finally, there is some evidence to suggest that chronic alcohol consumption may result in a positive energy balance and a potentially obesogenic state.