Lack of β2AR improves exercise capacity and skeletal muscle oxidative phenotype in mice

Vanessa Azevedo Voltarelli1, Aline V. N. Bacurau1, Luiz R. G. Bechara1, Carlos Roberto Bueno Júnior2, Luiz H. M. Bozi1, Katt Coelho Mattos1, Vera Maria Cury Salemi3, Patrı́cia C. Brum1
1School of Physical Education and Sport, University of São Paulo, São Paulo, Brazil
2Human Genome Research Center, Biosciences Institute, University of São Paulo, São Paulo, Brazil
3Cardiomyopathy Unit Heart Institute (InCor) University of São Paulo School of Medicine São Paulo Brazil

Tóm tắt

β2‐adrenergic receptor (β2AR) 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 β2AR activation are highly recognized, less is known about the impact of β2AR in endurance capacity. We presently used mice lacking β2AR2‐knockout (β2 KO)] to investigate the role of β2AR 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 β2AR improves oxidative metabolism in skeletal muscle of β2 KO mice and this is associated with increased exercise capacity.

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