Aerobic-interval exercise with blood flow restriction potentiates early markers of metabolic health in man.

Abstract

This study examined whether aerobic-interval exercise with blood flow restriction (BFR) potentiates early markers of metabolic health compared to exercise with systemic hypoxia or normoxia in man. In a randomized-crossover fashion, eight healthy men completed nine 2-minute running bouts at 105% of their lactate threshold on three occasions separated by one week, either with BFR (BFR-trial), systemic hypoxia (HYP-trial) or normoxia (control; CON-trial). Near-infrared spectroscopy was used to assess the muscle level of hypoxia. A muscle biopsy was collected at rest and 3hours after exercise to quantify genes involved in cholesterol synthesis (PGC-1α2), glucose disposal (GLUT4) and capillary growth (HIF-1α; VEGFA), as well as mitochondrial respiration (PGC-1α2/3), uncoupling (UCP3) and expansion (p53; COXIV-1/2; CS; AMPKα1/2). The muscle level of hypoxia was matched between the BFR-trial and HYP-trial (~90%; P>.05), which was greater than the CON-trial (~70%; P<.05). PGC-1α2 increased most in the BFR-trial (16-fold vs CON-trial; 11-fold vs HYP-trial; P<.05). GLUT4 and VEGFA selectively increased by 2.0 and 3.4-fold, respectively in BFR-trial (P<.05), which was greater than CON-trial (1.2 and 1.3 fold) and HYP-trial (1.2 and 1.8 fold; P<.05). UCP3 increased more in BFR-trial than the HYP-trial (4.3 vs 1.6 fold), but was not different between BFR-trial and CON-trial (2.1 fold) or between CON-trial and HYP-trial (P>.05). No trial differences were evident for other genes (P>.05). Independent of the muscle level of hypoxia, BFR-exercise potentiates early markers of metabolic health associated with the regulation of cholesterol production and glucose homeostasis in man.