Disruption and recovery of testicular function during and after androgen abuse: the HAARLEM study.

STUDY QUESTION: What is the speed and extent by which endogenous testosterone production and spermatogenesis recover after androgen abuse? SUMMARY ANSWER: Testosterone concentrations normalized within 3 months after discontinuation of androgen abuse in most subjects but recovery of spermatogenesis took longer-approximately 1 year. WHAT IS KNOWN ALREADY: An estimated 4-6% of amateur strength athletes use androgens. Abuse of supraphysiological doses of androgens completely suppresses endogenous testosterone production and spermatogenesis. STUDY DESIGN, SIZE, DURATION: Prospective and observational cohort study in which 100 male amateur athletes participated for 1 year. PARTICIPANTS/MATERIALS, SETTING, METHODS: Subjects (≥18 years) were included if they had not used androgens for at least 3 months and intended to start an androgen cycle within 2 weeks. Clinic visits took place before (T0), at the end (T1), and 3 months after the end of the cycle (T2), and 1 year after start of the cycle (T3), and included a blood test for gonadotrophins and sex hormones, and semen analysis. MAIN RESULTS AND THE ROLE OF CHANCE: During androgen abuse, 77% of subjects had a total sperm count (TSC) below 40 million. Three months after the end of the cycle (T2), total (-1.9 nmol/l, CI -12.2 to 8.33, P = 0.71) and free (-38.6 pmol/l, CI -476 to 399, P = 0.86) testosterone concentrations were not different compared to baseline, whereas mean TSC was 61.7 million (CI 33.7 to 90.0; P < 0.01) lower than baseline. At the end of follow-up (T3), there was no statistically significant difference for total (-0.82 nmol/l, CI -11.5 to 9.86, P = 0.88) and free (-25.8 pmol/l, CI -480 to 428, P = 0.91) testosterone compared to baseline, but there was for TSC (-29.7 million, CI -59.1 to -0.39, P = 0.05). In nine (11%) subjects, however, testosterone concentrations were below normal at the end of follow-up (T3), and 25 (34%) subjects still had a TSC below 40 million. LIMITATIONS, REASONS FOR CAUTION: The follow-up period (after the cycle) was relatively short, especially considering the long recovery time of spermatogenesis after discontinuation of androgens. WIDER IMPLICATIONS OF THE FINDINGS: Endogenous testosterone production and spermatogenesis recover following androgen abuse in the vast majority of users. Nevertheless, not all users achieve a normalized testicular function. This may especially be the case for athletes with a high past exposure to androgens. STUDY FUNDING/COMPETING INTEREST(S): There is no conflict of interest. The study was funded by the Spaarne Gasthuis academy. TRIAL REGISTRATION NUMBER: N/A.

Four weeks' corticosteroid inhalation does not augment maximal power output in endurance athletes.

OBJECTIVE: To assess possible ergogenic properties of corticosteroid administration. DESIGN: A balanced, double-blind, placebo-controlled design was used. PARTICIPANTS: 28 well-trained cyclists and rowers. INTERVENTION: 4 weeks' daily inhalation of 800 microg budesonide or placebo. MAIN OUTCOME MEASUREMENTS: The subjects performed three incremental cycle ergometer tests until exhaustion, before and after 2 and 4 weeks of placebo or budesonide administration, to measure maximal power output (W(max)). Once a week they filled in a profile of mood state (POMS) questionnaire. RESULTS: There was no significant difference in W(max) between the placebo (376 (SD 25) W) and the corticosteroid group (375 (36) W) during the preintervention test, and there were no significant changes in either group after 2 and 4 weeks of intervention. No effect of the intervention on mood state was found. CONCLUSION: 4 weeks of corticosteroid or placebo inhalation in healthy, well-trained athletes did not affect maximal power output or mood state. Hence no ergogenic properties of 4 weeks' corticosteroid administration could be demonstrated, which corroborates previous studies of short-term corticosteroid administration.

[Rhabdomyolysis in a bodybuilder using steroids]. / Rabdomyolyse bij een bodybuilder na gebruik van diverse dopingmiddelen.

A 34-year-old bodybuilder presented at the emergency room with fever, vomiting and muscle cramps that had started during a bodybuilding session. Several days before he started training he had used tablets and intramuscular injections containing the anabolic steroids: dehydro-chloro-methyltestosterone, boldenone and trenbolone. In addition, he had taken clenbuterol tablets, liothyronine tablets and subcutaneous injections of phosphatidylcholine. Laboratory investigations revealed massive rhabdomyolysis. The patient was treated with intravenous fluid replacement and sodium bicarbonate to alkalinize the urine. He recovered quickly and his renal function remained unaffected. 'Doping' among amateur athletes in the Netherlands occurs frequently. Apart from long term side-effects, doping can also cause acute health problems. Therefore it is important to ask about doping use during history taking in amateur athletes.

Gene doping.

Together with the rapidly increasing knowledge on genetic therapies as a promising new branch of regular medicine, the issue has arisen whether these techniques might be abused in the field of sports. Previous experiences have shown that drugs that are still in the experimental phases of research may find their way into the athletic world. Both the World Anti-Doping Agency (WADA) and the International Olympic Committee (IOC) have expressed concerns about this possibility. As a result, the method of gene doping has been included in the list of prohibited classes of substances and prohibited methods. This review addresses the possible ways in which knowledge gained in the field of genetic therapies may be misused in elite sports. Many genes are readily available which may potentially have an effect on athletic performance. The sporting world will eventually be faced with the phenomena of gene doping to improve athletic performance. A combination of developing detection methods based on gene arrays or proteomics and a clear education program on the associated risks seems to be the most promising preventive method to counteract the possible application of gene doping.

Inhaled salbutamol and endurance cycling performance in non-asthmatic athletes.

Beta(2)-adrenergic agonists are important therapeutic agents for the prevention and treatment of (exercise-induced) asthma in athletes, but may have ergogenic effects. In this study we investigated whether inhalation of a supra-therapeutic dose of 800 microg salbutamol before exercise affects endurance performance during a cycling trial in non-asthmatic athletes. In a double-blind, randomized cross-over study, 16 athletes performed two trials, where they had to perform a certain amount of work as fast as possible on a cycle ergometer, 30 minutes after inhalation of 800 micro g salbutamol or placebo. Peak expiratory flow (PEF), forced vital capacity (FVC), and forced expiratory volume in 1 second (FEV(1)) were measured before and after exercise and blood samples were obtained before and during exercise. Cycling performance time was 4010.2 +/- 327.7 s after placebo inhalation and 3927.6 +/- 231.3 s after inhalation salbutamol (p < 0.05). Although salbutamol inhalation increased plasma free fatty acids, glycerol and lactate concentrations and decreased plasma potassium concentrations at rest, no differences between placebo and salbutamol in these variables were found during exercise. PEF and FEV(1) were increased after salbutamol inhalation at rest compared with placebo, but the difference between placebo and salbutamol after exercise was no longer significant. Inhalation of a supratherapeutic dose of 800 micro g salbutamol improved endurance cycling performance by 1.9 +/- 1.8 % in non-asthmatic athletes, which indicates that this route of administration does not exclude the possibility of an ergogenic effect of beta(2)-adrenergic agents in athletes. The increase in performance was not explained by changes in plasma concentrations of free fatty acids, glycerol, lactate, and potassium during exercise or by changes in ventilatory parameters at rest and after exercise. Therefore, the mechanism of the increase in performance remains to be determined.