Journal
CURRENT OPINION IN PHYSIOLOGY
Volume 10, Issue -, Pages 118-127Publisher
ELSEVIER
DOI: 10.1016/j.cophys.2019.05.004
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Funding
- American Heart Association postdoctoral fellowship [19POST34380411]
- National Institute of Aging [AG048262]
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Energetic demand from high-intensity exercise can easily exceed ATP synthesis rates of mitochondria leading to a reliance on anaerobic metabolism. The reliance on anaerobic metabolism results in the accumulation of intracellular metabolites, namely inorganic phosphate (P-i) and hydrogen (H+), that are closely associated with exercise-induced reductions in power. Cellular and molecular studies have revealed several steps where these metabolites impair contractile function demonstrating a causal role in fatigue. Elevated Pi or H+ directly inhibits force and power of the cross-bridge and decreases myofibrillar Ca2+ sensitivity, whereas P-i also inhibits Ca2+ release from the sarcoplasmic reticulum (SR). When both metabolites are elevated, they act synergistically to cause marked reductions in power, indicating that fatigue during high-intensity exercise has a bioenergetic basis.
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