European Journal of Applied Physiology

, Volume 117, Issue 2, pp 345–358

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

  • William J. Smiles
  • Miguel S. Conceição
  • Guilherme D. Telles
  • Mara P. T. Chacon-Mikahil
  • Cláudia R. Cavaglieri
  • Felipe C. Vechin
  • Cleiton A. Libardi
  • John A. Hawley
  • Donny M. Camera
Original Article

DOI: 10.1007/s00421-016-3530-8

Cite this article as:
Smiles, W.J., Conceição, M.S., Telles, G.D. et al. Eur J Appl Physiol (2017) 117: 345. doi:10.1007/s00421-016-3530-8

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.

Keywords

Blood-flow restrictionExerciseAutophagyMitophagy

Abbreviations

AMPK

AMP-activated protein kinase

ANOVA

Analysis of variance

Atg

Autophagy-related gene

BFR

Blood-flow restriction

BM

Body mass

BNIP3

Bcl-2/adenovirus E1B 19 kDa-interacting protein-3

eIF2α

Eukaryotic initiation factor 2α

eIF2Bε

Eukaryotic initiation factor 2Bε

END

Endurance exercise

ERK1/2

Extracellular signal-regulated kinase 1/2

ES

Effect size

GLUT4

Glucose transporter 4

GS

Glycogen synthase

GSK3β

Glycogen synthase kinase 3β

HK

Hexokinase

LC3b

Microtubule-associated protein-1 light chain 3 beta

MAPK

Mitogen-activated protein kinase

mTORC1

Mechanistic target of rapamycin complex 1

PDK4

Pyruvate dehydrogenase kinase 4

PGC-1α

PPARγ-coactivator-1α

REX

Resistance exercise

RM

Repetition maximum

SQSTM1

p62/sequestosome-1

ULK1

Unc-51-like kinase 1

VO2peak

Peak oxygen uptake

W

Watts

Copyright information

© Springer-Verlag Berlin Heidelberg 2017

Authors and Affiliations

  • William J. Smiles
    • 1
  • Miguel S. Conceição
    • 2
  • Guilherme D. Telles
    • 2
  • Mara P. T. Chacon-Mikahil
    • 2
  • Cláudia R. Cavaglieri
    • 2
  • Felipe C. Vechin
    • 3
  • Cleiton A. Libardi
    • 4
  • John A. Hawley
    • 1
    • 5
  • Donny M. Camera
    • 1
  1. 1.Mary MacKillop Institute for Health ResearchCentre for Exercise and Nutrition, Australian Catholic UniversityMelbourneAustralia
  2. 2.Faculty of Physical EducationUniversity of CampinasCampinasBrazil
  3. 3.School of Physical Education and SportUniversity of São PauloSão PauloBrazil
  4. 4.Laboratory of Neuromuscular Adaptations to Resistance Training, Department of Physical EducationFederal University of São CarlosSão CarlosBrazil
  5. 5.Research Institute for Sport and Exercise SciencesLiverpool John Moores UniversityLiverpoolUK