Premium
Inhibition of Glycolysis and mTORC1 activation in Human Skeletal Muscle with Blood Flow Restriction Exercise
Author(s) -
Gundermann David M,
Dickinson Jared M,
Fry Christopher S,
Walker Dillon K,
Volpi Elena,
Rasmussen Blake B
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1076.3
Subject(s) - glycolysis , mtorc1 , medicine , endocrinology , glycogen , skeletal muscle , incremental exercise , anabolism , chemistry , lactic acidosis , phosphorylation , biology , metabolism , biochemistry , heart rate , protein kinase b , blood pressure
Low‐intensity resistance exercise (RE) coupled with blood flow restriction (BFR) stimulates an increase in muscle size and strength, however the mechanisms contributing to the anabolic effects of BFR exercise are not well understood. One potential mechanism includes the acidosis‐induced inhibition of glycolysis leading to an accumulation of glycolytic intermediates known to stimulate mTORC1 signaling. The aim of this preliminary study was to compare glycolytic flux from BFR exercise and traditional RE. Young men were divided into two groups. One group performed leg extensions at 70% 1RM (traditional RE). A second group performed leg extensions at 20% 1RM coupled with BFR. The number of repetitions was similar between groups. Phosphorylation of mTOR and muscle protein synthesis in the vastus lateralis was increased to a similar extent in both groups following exercise. Muscle glycogen decreased 37% after traditional RE, whereas it was unchanged following BFR exercise. Lactate production increased in both groups but did not disperse during BFR until after the release of the cuff. The maintenance of muscle glycogen levels in concert with increased lactate production following BFR exercise is in agreement with a proposed mechanism in which accumulated glycolytic intermediates may contribute to increased mTORC1 signaling following BFR exercise. Funded by: NIAMS R01AR049877, NIA P30AG024832, NIH T32HD07539