PubMed Health⌕ Search

PubMed · 15776342

The World Anti-Doping Code 2003--consequences for physicians associated with elite athletes.

Abstract

The purpose of the World Anti-Doping Code 2003 and the 2004 Prohibited List is to create a universal international standard to fight doping in competitive sports. The result of this is a whole series of changes for doctors with regard to their work with competitive athletes. The revised definition of doping now includes physicians in the group of persons who can fulfil the elements of a doping offence. Moreover, the mere possession of substances appearing on the Prohibited List represents a violation of anti-doping regulations. The 2004 Prohibited List includes several changes to the Olympic Movement List from 2003. Caffeine, for example, was removed from the list. Cannabinoids, on the other hand, are now prohibited in competition for all sports. The same is true for all forms of glucocorticosteroids. Therapeutic use exemptions in an abbreviated process are possible for the administration of glucocorticosteroids by non-systemic routes, as well as inhalative therapy with the beta-2-agonists formoterol, salbutamol, salmeterol, and termbutalin. In other cases, a therapeutic use exemption is possible using a standard application process. Further changes will become effective in the 2005 Prohibited List. In 2005, it is essential that beta-2-agonists are prohibited in and out of competition. HCG and LH are prohibited for all athletes. Dermatological preparations of glucocorticosteroids are no longer prohibited, and intravenous infusions will be a prohibited method in 2005, except as a legitimate acute medical treatment. In cases of violations of anti-doping regulations where it is permissible for the affected person to furnish proof of exoneration, the burden of proof is not higher than that required to prove the violation. The sanctions provided for in the World Anti-Doping Code follow a principle of rules and exceptions which at first glance seems difficult to understand. In the case of doping violations by physicians, the anti-doping code provides--as a general rule--for exclusion from sports associations for at least four years. Since several of the changes are questionable under constitutional aspects, it remains to be seen whether the World Anti-Doping Code 2003 will allow the achievement of a universal standard to combat doping.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

H Striegel, D Rössner, P Simon, A M Niess. 2005. The World Anti-Doping Code 2003--consequences for physicians associated with elite athletes.. https://doi.org/10.1055/s-2004-830545

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Orchidectomy increases beta-adrenoceptor activation-mediated neuronal nitric oxide and noradrenaline release in rat mesenteric artery.

BACKGROUND/AIMS: A previous study has demonstrated that endogenous male sex hormones do not alter neuronal nitric oxide (NO) release in rat mesenteric artery. However, the regulatory role of endogenous male sex hormones on noradrenaline (NA) release in rat mesenteric artery is not known. The present study was designed to analyze whether endogenous male sex hormones influence the NA release induced by electrical field stimulation (EFS), as well as the possible modification in NA and neuronal NO release by presynaptic beta-adrenoceptor activation. METHODS: For this purpose, mesenteric arteries from control and orchidectomized male Sprague-Dawley rats were used. Basal and EFS-induced neuronal NO and NA release, as well as the contractile effect induced by EFS, was measured. RESULTS: Basal and EFS-induced neuronal NO and NA release were similar in arteries from control and orchidectomized rats. The beta-adrenoceptor agonist clenbuterol did not modify EFS-induced neuronal NO and NA release in arteries from control rats. In contrast, in arteries from orchidectomized animals, clenbuterol increased both neuronal NO and NA release; this increase was prevented by incubation with the beta-adrenoceptor antagonist propranolol. However, the contractile response elicited by EFS was not modified by clenbuterol in either group of rats. CONCLUSIONS: These results show that orchidectomy does not alter the EFS-induced NA release. What is more, activation of presynaptic beta-adrenoceptors does not modify EFS-induced NA and neuronal NO release in arteries from control rats although it increases the release of both neurotransmitters in arteries from orchidectomized rats. Despite these modifications, the EFS-induced contractile response is preserved in arteries from orchidectomized rats.

Adrenergic beta-Agonists↗

Effect of formoterol and salmeterol on IL-6 and IL-8 release in airway epithelial cells.

Beta(2)-adrenoceptors are widely distributed and occur on airway epithelial cells. The aim of this study was to find out whether the two long-acting beta(2)-agonists formoterol and salmeterol influence interleukin-6 (IL-6) and -8 (IL-8) release from airway epithelial cells in vitro. A549 cells and primary bronchial epithelial cells (PBEC) were stimulated with organic dust from pig barns. Non-stimulated and dust-stimulated cells were incubated for 24h with formoterol or salmeterol (10(-13)-10(-6)M) and the release of IL-6 and IL-8 into the medium was assessed by ELISA technique. Propranolol (10(-5)M) or sotalol (10(-3)M) were used to block the beta(2)-agonist mediated effects. Formoterol and salmeterol both induced enhancement of IL-6 and IL-8 release and added to the effect of organic dust. This enhanced release was blocked by a beta-blocker in PBEC but not in A549 cells. To our knowledge, this is the first time beta(2)-agonists have been shown to stimulate IL-6 release from airway epithelial cells. The results indicate different mechanisms of beta(2)-agonist action in bronchial and alveolar epithelial cells. Furthermore, our results indicate that A549 cells do not possess functional beta(2)-adrenoceptors.

Adrenergic beta-Agonists↗