The heavy-to-severe intensity exercise threshold (i.e. critical force) distinguishes between steady-state and progressive metabolic and neuromuscular responses to exercise. High-levels of skeletal muscle sensory feedback related to peripheral fatigue development are thought to restrict motor-unit activation and limit exercise tolerance. Utilizing limb blood flow occlusion, we demonstrate that critical force reflects an oxygen-delivery dependent balance between motor-unit activation and peripheral fatigue development. Our findings suggest that mechanisms which determine the total force-producing capacity of exercising skeletal muscle are significantly altered during blood flow occlusion. These findings may have wide-spread implications for exercise tolerance in patient populations who experience partial vascular occlusion or altered neuromuscular reflexes.
High-levels of muscle sensory feedback restrict motor-unit activation and limit exercise tolerance. The roles of muscle fatigue development and motor-unit activation in determining the heavy-to-severe intensity threshold (critical force; CF) remain unclear. This study utilized blood flow occlusion (OCC) to determine relationships between muscle fatigue development and motor-unit activation during the determination of CF. We hypothesized that (1) OCC would exacerbate peripheral fatigue development and increase the rate of motor-unit deactivation and (2) blood flow reperfusion (REP) would result in muscle recovery and re-recruitment of motor-units despite continuous maximal effort (3) resulting in an end-exercise force not different from CF. Seven young, healthy subjects performed maximal-effort rhythmic handgrip exercise for 5-min under control conditions (CON) and during OCC and REP. Peripheral fatigue development and motor-unit activation were measured via electrical-stimulation and electromyography, respectively, during each test. OCC resulted in significantly greater peripheral fatigue development than CON (54.3±34.8%; p<0.001). Motor-unit deactivation was only observed during OCC (p<0.001). REP resulted in significant peripheral recovery (p<0.001) and the re-recruitment of motor-units (p<0.001) to levels not different from CON. While OCC resulted in a significantly greater reduction in force production compared to CON (65.7±35.6%; p<0.001), REP resulted in the restoration of maximal-effort force production (266±19N; p<0.001) to levels not different from CF (276±55N). These data suggest that CF reflects an oxygen-delivery dependent balance between motor-unit activation and peripheral fatigue development. Furthermore, this study established that mechanisms which determine the total force-producing capacity of exercising skeletal muscle are altered during OCC. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.