Acute low-intensity cycling with blood-flow restriction has no effect on metabolic signaling in human skeletal muscle compared to traditional exercise

Author(s)

Smiles, William J. ; Conceicao, Miguel S. ; Telles, Guilherme D. ; Chacon-Mikahil, Mara P. T. ; Cavaglieri, Claudia R. ; Vechin, Felipe C. ; Libardi, Cleiton A. ; Hawley, John A. ; Camera, Donny M.

• Document type: Journal article
• Source: EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY; v. 117, n. 2, p. 345-358, FEB 2017.
• Web of Science Citations: 4

Abstract

Autophagy is an intracellular degradative system sensitive to hypoxia and exercise-induced perturbations to cellular bioenergetics. We determined the effects of low-intensity endurance-based exercise performed with blood-flow restriction (BFR) on cell signaling adaptive responses regulating autophagy and substrate metabolism in human skeletal muscle. In a randomized cross-over design, nine young, healthy but physically inactive males completed three experimental trials separated by 1 week of recovery consisting of either a resistance exercise bout (REX: 4 x 10 leg press repetitions, 70% 1-RM), endurance exercise (END: 30 min cycling, 70% VO2peak), or low-intensity cycling with BFR (15 min, 40% VO2peak). A resting muscle biopsy was obtained from the vastus lateralis 2 weeks prior to the first exercise trial and 3 h after each exercise bout. END increased ULK1(Ser757) phosphorylation above rest and BFR (similar to 37 to 51%, P < 0.05). Following REX, there were significant elevations compared to rest (similar to 348%) and BFR (similar to 973%) for p38 gamma MAPK(Thr180/Tyr182) phosphorylation (P < 0.05). Parkin content was lower following BFR cycling compared to REX (similar to 20%, P < 0.05). There were no exercise-induced changes in select markers of autophagy following BFR. Genes implicated in substrate metabolism (HK2 and PDK4) were increased above rest (similar to 143 to 338%) and BFR cycling (similar to 212 to 517%) with END (P < 0.001). A single bout of low-intensity cycling with BFR is insufficient to induce intracellular ``stress{''} responses (e.g., high rates of substrate turnover and local hypoxia) necessary to activate skeletal muscle autophagy signaling. (AU)

• FAPESP's process: 14/00985-0 - Effect of 12 weeks of concurrent training in the molecular signaling responses in older subjects
• Grantee: Miguel Soares Conceição
• Support Opportunities: Scholarships abroad - Research Internship - Doctorate