Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise

David M. Gundermann, Christopher Fry, Jared M. Dickinson, Dillon K. Walker, Kyle L. Timmerman, Micah J. Drummond, Elena Volpi, Blake Rasmussen

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Blood flow restriction (BFR) to contracting skeletal muscle during low-intensity resistance exercise training increases muscle strength and size in humans. However, the mechanism(s) underlying these effects are largely unknown. We have previously shown that mammalian target of rapamycin complex 1 (mTORC1) signaling and muscle protein synthesis (MPS) are stimulated following an acute bout of BFR exercise. The purpose of this study was to test the hypothesis that reactive hyperemia is the mechanism responsible for stimulating mTORC1 signaling and MPS following BFR exercise. Six young men (24 ± 2 yr) were used in a randomized crossover study consisting of two exercise trials: low-intensity resistance exercise with BFR (BFR trial) and low-intensity resistance exercise with sodium nitroprusside (SNP), a pharmacological vasodilator infusion into the femoral artery immediately after exercise to simulate the reactive hyperemia response after BFR exercise (SNP trial). Postexercise mixed-muscle fractional synthetic rate from the vastus lateralis increased by 49% in the BFR trial (P < 0.05) with no change in the SNP trial (P > 0.05). BFR exercise increased the phosphorylation of mTOR, S6 kinase 1, ribosomal protein S6, ERK1/2, and Mnk1- interacting kinase 1 (P < 0.05) with no changes in mTORC1 signaling in the SNP trial (P > 0.05). We conclude that reactive hyperemia is not a primary mechanism for BFR exercise-induced mTORC1 signaling and MPS. Further research is necessary to elucidate the cellular mechanism(s) responsible for the increase in mTOR signaling, MPS, and hypertrophy following acute and chronic BFR exercise.

Original languageEnglish (US)
Pages (from-to)1520-1528
Number of pages9
JournalJournal of Applied Physiology
Volume112
Issue number9
DOIs
StatePublished - May 1 2012

Fingerprint

Muscle Proteins
Hyperemia
Exercise
Ribosomal Protein S6 Kinases
Nitroprusside
Resistance Training
Quadriceps Muscle
Muscle Strength
Femoral Artery
Vasodilator Agents
Cross-Over Studies
Hypertrophy
Skeletal Muscle
Phosphotransferases
Phosphorylation
Pharmacology

Keywords

  • BFR
  • Fractional synthetic rate
  • KAATSU
  • Resistance exercise
  • Vascular occlusion training

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise. / Gundermann, David M.; Fry, Christopher; Dickinson, Jared M.; Walker, Dillon K.; Timmerman, Kyle L.; Drummond, Micah J.; Volpi, Elena; Rasmussen, Blake.

In: Journal of Applied Physiology, Vol. 112, No. 9, 01.05.2012, p. 1520-1528.

Research output: Contribution to journalArticle

Gundermann, David M. ; Fry, Christopher ; Dickinson, Jared M. ; Walker, Dillon K. ; Timmerman, Kyle L. ; Drummond, Micah J. ; Volpi, Elena ; Rasmussen, Blake. / Reactive hyperemia is not responsible for stimulating muscle protein synthesis following blood flow restriction exercise. In: Journal of Applied Physiology. 2012 ; Vol. 112, No. 9. pp. 1520-1528.
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