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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 exercise
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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 exercise
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Journal Article
Acute low-intensity cycling with blood-flow restriction has no effect on metabolic signaling in human skeletal muscle compared to traditional exercise
2017
Overview
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%
V
O
2peak
), or low-intensity cycling with BFR (15 min, 40%
V
O
2peak
). 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 ULK1
Ser757
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 MAPK
Thr180/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.
Publisher
Springer Berlin Heidelberg,Springer Nature B.V
Subject
/ Adult
/ Biomedical and Life Sciences
/ Energy Metabolism - physiology
/ Exercise
/ Humans
/ Hypoxia
/ Kinases
/ Male
/ Muscle, Skeletal - physiology
/ Occupational Medicine/Industrial Medicine
/ Proteins
/ Regional Blood Flow - physiology
/ Resistance Training - methods
