Lack of β2‐AR improves exercise capacity and skeletal muscle oxidative phenotype in mice

β₂‐adrenergic receptor (β₂‐AR) agonists have been used as ergogenics by athletes involved in training for strength and power in order to increase the muscle mass. Even though anabolic effects of β₂‐AR activation are highly recognized, less is known about the impact of β₂‐AR in endurance capacity. We presently used mice lacking β₂‐AR [β₂‐knockout (β₂ KO)] to investigate the role of β₂‐AR on exercise capacity and skeletal muscle metabolism and phenotype. β₂ KO mice and their wild‐type controls (WT) were studied. Exercise tolerance, skeletal muscle fiber typing, capillary‐to‐fiber ratio, citrate synthase activity and glycogen content were evaluated. When compared with WT, β₂ KO mice displayed increased exercise capacity (61%) associated with higher percentage of oxidative fibers (21% and 129% of increase in soleus and plantaris muscles, respectively) and capillarity (31% and 20% of increase in soleus and plantaris muscles, respectively). In addition, β₂ KO mice presented increased skeletal muscle citrate synthase activity (10%) and succinate dehydrogenase staining. Likewise, glycogen content (53%) and periodic acid‐Schiff staining (glycogen staining) were also increased in β₂ KO skeletal muscle. Altogether, these data provide evidence that disruption of β₂‐AR improves oxidative metabolism in skeletal muscle of β₂ KO mice and this is associated with increased exercise capacity.