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Smiles, WJ, Conceicao, MS, Telles, GD, Chacon-Mikahil, MPT, Cavaglieri, CR, Vechin, FC, Libardi, CA, Hawley, JA and Camera, DM (2017) Acute low-intensity cycling with blood-flow restriction has no effect on metabolic signaling in human skeletal muscle compared to traditional exercise. European Journal of Applied Physiology, 117 (2). pp. 345-358. ISSN 1439-6319
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Acute low-intensity cycling with blood-flow restriction has no effect on metabolic signaling in human skeletal muscle compared to traditional exerc.pdf - Accepted Version Download (489kB) | Preview |
Abstract
Purpose
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.
Methods
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.
Results
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).
Conclusion
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.
| Item Type: | Article |
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| Additional Information: | The final publication is available at Springer via http://dx.doi.org/10.1007/s00421-016-3530-8 |
| Uncontrolled Keywords: | 1106 Human Movement And Sports Science |
| Subjects: | R Medicine > RC Internal medicine > RC1200 Sports Medicine |
| Divisions: | Sport & Exercise Sciences |
| Publisher: | Springer |
| Related URLs: | |
| Date Deposited: | 24 Oct 2017 11:45 |
| Last Modified: | 04 Sep 2021 03:42 |
| DOI or ID number: | 10.1007/s00421-016-3530-8 |
| URI: | https://researchonline.ljmu.ac.uk/id/eprint/7417 |
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