Abstract
Several performance-enhancing or ergogenic drugs have been linked to both significant adverse cardiovascular effects and increased cardiovascular risk. Even with increased scrutiny on the governance of performance-enhancing drugs (PEDs) in professional sport and heightened awareness of the associated cardiovascular risk, there are some who are prepared to risk their use to gain competitive advantage. Caffeine is the most commonly consumed drug in the world and its ergogenic properties have been reported for decades. Thus, the removal of caffeine from the World Anti-Doping Agency (WADA) list of banned substances, in 2004, has naturally led to an exponential rise in its use amongst athletes. The response to caffeine is complex and influenced by both genetic and environmental factors. Whilst the evidence may be equivocal, the ability of an athlete to train longer or at a greater power output cannot be overlooked. Furthermore, its impact on the myocardium remains unanswered. In contrast, anabolic androgenic steroids are recognised PEDs that improve athletic performance, increase muscle growth and suppress fatigue. Their use, however, comes at a cost, afflicting the individual with several side effects, including those that are detrimental to the cardiovascular system. This review addresses the effects of the two commonest PEDs, one legal, the other prohibited, and their respective effects on the heart, as well as the challenge in defining its long-term implications.
Highlights
Caffeine (1,3,7-Trimethylxanthine) is a popular workplace substance that has been well-researched, with its ergogenic effects being known for centuries [1]
Its use has become highly prevalent amongst athletes, especially after 2004, when it was removed from the World Anti-Doping Agency (WADA) list of banned substances; it was, unsurprising when a study reported that 74% of urine samples from athletes, between 2004 to 2008, demonstrated measurable levels [1]
Left ventricular hypertrophy and fibrosis have both been identified as risk factors to Sudden cardiac death (SCD) [64,65], and may be argued to be the sequelae of ongoing anabolic androgenic steroids (AASs) use that results in the terminal event
Summary
Caffeine (1,3,7-Trimethylxanthine) is a popular workplace substance that has been well-researched, with its ergogenic effects being known for centuries [1]. Its use has become highly prevalent amongst athletes, especially after 2004, when it was removed from the World Anti-Doping Agency (WADA) list of banned substances; it was, unsurprising when a study reported that 74% of urine samples from athletes, between 2004 to 2008, demonstrated measurable levels [1]. Common physiological effects of caffeine on the body include an increase in heart rate, catecholamine levels, blood lactate, free fatty acids and glycerol [4]. Its use has illustrated benefits in both endurancebased and high-intensity exercise, permitting the athlete to train longer and at a greater intensity. It is recommended that ingestion of 3–9 mg/kg approximately 60 min prior to exercise may provide the extra competitive advantage for the athlete [1]. The response to caffeine is multifaceted, influenced by both genetic and non-genetic predilections, with there being inter-subject variation in response to caffeine consumption, and this heterogeneous response makes it difficult to extrapolate the objective impact of caffeine as a vital ingredient to athletic prowess
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