Titleβ-Adrenergic receptor blockade blunts postexercise skeletal muscle mitochondrial protein synthesis rates in humans.
Publication TypeJournal Article
Year of Publication2011
AuthorsRobinson, MM, Bell, C, Peelor, FF, Miller, BF
JournalAm J Physiol Regul Integr Comp Physiol
Date Published2011 Aug
KeywordsAdrenergic beta-Agonists, Adrenergic beta-Antagonists, Adult, Cross-Over Studies, Gene Expression Regulation, Humans, Isoproterenol, Male, Muscle Proteins, Muscle, Skeletal, Propranolol, Young Adult

β-Adrenergic receptor (AR) signaling is a regulator of skeletal muscle protein synthesis and mitochondrial biogenesis in mice. We hypothesized that β-AR blockade blunts postexercise skeletal muscle mitochondrial protein synthesis rates in adult humans. Six healthy men (mean ± SD: 26 ± 6 yr old, 39.9 ± 4.9 ml·kg(-1)·min(-1) peak O(2) uptake, 26.7 ± 2.0 kg/m(2) body mass index) performed 1 h of stationary cycle ergometer exercise (60% peak O(2) uptake) during 1) β-AR blockade (intravenous propranolol) and 2) administration of saline (control). Skeletal muscle mitochondrial, myofibrillar, and sarcoplasmic protein synthesis rates were assessed using [(2)H(5)]phenylalanine incorporation into skeletal muscle proteins after exercise. The mRNA content of signals for mitochondrial biogenesis was determined using real-time PCR. β-AR blockade decreased mitochondrial (from 0.217 ± 0.076 to 0.135 ± 0.031%/h, P < 0.05), but not myofibrillar or sarcoplasmic, protein synthesis rates. Peroxisome proliferator-activated receptor-γ coactivator-1α mRNA was increased ∼2.5-fold (P < 0.05) at 5 h compared with 1 h postexercise but was not influenced by β-AR blockade. We conclude that decreased β-AR signaling during cycling can blunt the postexercise increase in mitochondrial protein synthesis rates without affecting mRNA content.

Alternate JournalAm. J. Physiol. Regul. Integr. Comp. Physiol.
PubMed ID21613574
PubMed Central IDPMC3154708
Grant List1-K01-AG-031829-01A1 / AG / NIA NIH HHS / United States