Relationship Between Metabolic By-Products and Nervous System Failure/Fatigue
Fatigue has generally been defined as an acute impairment of exercise/sport performance that includes both an increase in the perceived effort necessary to exert a desired force or power output, and the inability to produce the desired force or power output. The majority of research to date looking at fatigue has focused upon substrate utilization, however, what is relatively unknown is the contribution the nervous system has upon fatigue. Therefore, the purpose of this dissertation was to investigate potential mechanisms that relate to neural fatigue. An additional purpose was to determine if there were any relationships between metabolic by-products and EMG characteristics following exercise. The first investigation sought to determine changes in EMG M-wave amplitude of the gastrocnemius following the calf raise exercise. There were no significant changes in M-wave EMG amplitude following exercise. The second investigation compared changes in muscle contractile properties and EMG characteristics of the VL, RF, and VM following a high-intensity exercise. There was a significant decrease in MDF of the VL only. Additionally, there was a decrease in peak force and rate of force development. The last investigation utilized the same exercise protocol as the second investigation, but added the supplementation of aspartate and sodium bicarbonate. Both supplements were effective in reducing ammonia concentrations following exercise. Additionally, supplementation with sodium bicarbonate resulted in an increase in rate of force development following exercise. As for EMG characteristics, there was a significant decrease in MDF for the RF, but not the VL. There were no significant changes in PF or EMG amplitude. Currently, no relationship between the metabolic and nervous systems during times of fatigue can be determined at this point.
Fatigue, Metabolism, Nervous System, Ammonia, Rate of Force Development, Peak Force, Electromyography
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