Blood Flow Restricted Exercise and Reduced Oxygen Tension Decrease Mitochondrial ROS Emission in Human Muscle

Abstract

Low volume blood flow restricted (BFR) training has been proposed to induce comparable adaptations to traditional resistance training, however the underlying mechanisms remain unknown. Despite the absence of direct support, a suggested mechanism of BFR is an increase in reactive oxygen species (ROS). PURPOSE: We aimed to determine if the rate of mitochondrial ROS emission was altered following an acute bout of occluded (BFR) or non-occluded resistance training (RT), and to mechanistically investigate the role of skeletal muscle O2 partial pressure (pO2) in this response. METHODS: Ten males (25±1yrs) performed 3 sets of single leg squats to failure at 30% 1RM, with either BFR (60-70% occlusion), or without occlusion (RT), while skeletal muscle tissue oxygenation was estimated using near-infrared spectroscopy. Muscle biopsies were obtained at rest and 2-hours post-exercise to determine mitochondrial respiration and ROS emission in permeabilized muscle fibers. In a separate cohort, muscle biopsies were obtained from six males (25±2yrs) to examine the effects of pO2 on in vitro mitochondrial bioenergetics. RESULTS: Resistance exercise, with or without BFR, did not alter maximal respiratory capacity or mitochondrial sensitivity to ADP. While maximal mitochondrial ROS emission was unchanged following RT, BFR decreased this response compared to rest (66.6 vs. 86.2 pmol min-1 mg dry wt-1, p<0.05). Skeletal muscle oxygenation was lower in the BFR compared to RT leg, both during (41.4% vs. 46.1% saturation respectively, p<0.01) and between (50.3% vs. 61.1% saturation respectively, p<0.01) exercise sets. Further evaluation of mitochondrial bioenergetics in vitro revealed that mild O2 restriction (50μM) dramatically attenuated maximal mitochondrial ROS emission (~4-fold), and fraction electron leak to ROS (~3-fold) compared to room air (200μM). This effect was especially evident in the presence of non-saturating ADP, as submaximal ROS emission was almost completely suppressed during O2 restriction, without a reduction in submaximal respiration. CONCLUSIONS: These data indicate that a reduction in skeletal muscle pO2 attenuates the propensity of mitochondria to produce ROS, a mechanism which may contribute to the acute responses to BFR training. This research is supported by NSERC funding.