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

• DOI: 10.1007/s00421-016-3530-8
• Publication Date: 2017-01-25T05:14:11Z
• Authors: William J. Smiles; Miguel S. Conceição; Guilherme D. Telles; Mara P. T. Chacon...; Cláudia R. Cavagl...; Felipe C. Vechin; Cleiton A. Libardi; John A. Hawley; Donny M. Camera
• Keywords: Cycling; Endurance Training; Exercise intensity; Exercise physiology; Hypoxia

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 × 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 ULK1Ser757 phosphorylation above rest and BFR (~37 to 51%, P < 0.05). Following REX, there were significant elevations compared to rest (~348%) and BFR (~973%) for p38γ MAPKThr180/Tyr182 phosphorylation (P < 0.05). Parkin content was lower following BFR cycling compared to REX (~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 (~143 to 338%) and BFR cycling (~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.