beta2-Adrenergic receptor downregulation and performance decrements during high-intensity resistance exercise overtraining.

Previous research on overtraining due to excessive use of maximal resistance exercise loads [100% 1 repetition maximum (1 RM)] indicates that peripheral muscle maladaptation contributes to overtraining-induced performance decrements. This study examined the cellular and molecular responses of skeletal muscle to performance decrements due to high-relative-intensity (%1 RM) resistance exercise overtraining. Weight-trained men were divided into overtrained (OT, n = 8) and control (Con, n = 8) groups. The OT group performed 10 x 1 at 100% 1 RM daily for 2 wk, whereas the Con group performed normal training 2 days/wk. Muscle biopsies from the vastus lateralis muscle, voluntary static and dynamic muscle performances, and nocturnal urinary epinephrine were assessed before (pre) and after (post) overtraining. Overtraining occurred as indicated by a decrease in 1-RM strength for the OT group (mean +/- SE; OT pre = 159.3 +/- 10.1 kg, OT post = 151.4 +/- 9.9 kg, Con pre = 146.0 +/- 12.9 kg, Con post = 144.9 +/- 13.3 kg), as well as a 36.3% decrease in mean power at 100% 1-RM loads. Normal training could be resumed only after 2-8 wk of training cessation. Muscle beta(2)-adrenergic receptor (beta(2)-AR; fmol/mg protein) density significantly decreased by 37.0% for the OT group and was unchanged for the Con group (-1.8%). Nocturnal urinary epinephrine for the OT group increased by 49%, although this was not significant (effect size = 0.42). The ratio of nocturnal urinary epinephrine to beta(2)-AR density suggested a decreased beta(2)-AR sensitivity for the OT group (2.4-fold increase). Overtraining occurred based on decreased muscular force and power. Desensitization of the beta(2)-AR system suggests that this may be an important contributor to performance decrements due to excessive use of maximal resistance exercise loads.