Final answer:
Exercise-induced fatigue involves both central and peripheral mechanisms. The CNS adjusts muscle contraction speed, while peripheral factors include ATP depletion and lactic acid buildup. Muscle fatigue is therefore a multifaceted phenomenon that cannot be attributed solely to peripheral or central factors.
Step-by-step explanation:
In examining the mechanisms for exercise-induced fatigue, the vast majority of the evidence points to both the central nervous system and peripheral factors. Fatigue, or muscle failure, is a complex process influenced by a variety of physiological changes. The central nervous system (CNS) plays a critical role in regulating muscle contraction speed and responding to local muscle conditions. Peripheral fatigue, which includes factors such as ATP depletion, lactic acid buildup, ion imbalances, and muscle damage, is also significant in contributing to the overall experience of muscle fatigue.
ATP is essential for muscle contractions and during intense exercise, ATP reserves are reduced leading to declined muscle function. Sustained high-intensity exercise can lead to a buildup of lactic acid, which affects intracellular pH and enzyme activity. This is more apparent in fast-twitch muscle fibers which rely more on anaerobic metabolism, subsequently leading to faster fatigue compared to slow-twitch fibers that primarily use aerobic metabolism and fatigue more slowly.
Ultimately, muscle fatigue is a multifaceted phenomenon that includes both CNS and peripheral factors like the condition of the alpha motor neuron in the spinal cord, lactic acid levels, ATP availability, oxygen delivery, and psychological factors. Hence, while peripheral mechanisms such as energy depletion and metabolite accumulation are substantial, the CNS's contribution to fatigue, including motor neuron excitability and mental state, is also recognized as a contributing factor to exercise-induced muscle fatigue.