An actual study from 2008:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2439523/
Conclusions
None of the drugs acting directly on β1-ARs are used to enhance performance in sport. Agonists acting at this subtype have the potential to cause cardiac damage, whereas β1-AR selective antagonists, although useful therapeutically as antihypertensives and in the treatment of cardiac failure, do not possess the ergogenic effects required. The major target for many illicitly used drugs in sport is the β2-AR that is found in the heart, lungs and skeletal muscle where it controls rate and force, relaxes tone and stimulates growth, respectively. β2-AR agonists are demonstrably powerful bronchodilators, anabolic agents and, in combination with corticosteroids, powerfully enhance their anti-inflammatory actions. However, there is little evidence from animal or human studies that these effects translate into an improvement in performance. Indeed, many of the drugs developed to treat asthma are partial agonists that may limit the effectiveness of adrenaline in producing cardiovascular and metabolic responses. There is the potential to cause cardiac arrhythmias and to exacerbate allergic reactions by improving the access of allergens to the lung. The anti-anxiety effects of β-AR antagonists may be potentially advantageous in some sports, but their negative effects on physical performance will be a handicap in endurance sports. Indirectly acting sympathomimetics will not only have similar actions to adrenaline and noradrenaline on the cardiovascular and metabolic systems but may also have psychostimulant effects that reduce fatigue and give an illusion of better performance. Again, the results of controlled trials reveal a disappointing lack of convincing improvement of trained athletes. There is also a real risk of cardiac damage associated with the prolonged use of these agents. Although β2-ARs are the most attractive drug target, they are also the most susceptible to downregulation. The effects of drugs would be expected to be transient in nature, and this is borne out in practice with many reports of loss of efficacy after a few weeks. There are also genetic variations in the receptors that influence their effectiveness and regulation on exposure to β2-AR agonists.