Format

Send to

Choose Destination
Curr Opin Physiol. 2019 Aug;10:118-127. doi: 10.1016/j.cophys.2019.05.004. Epub 2019 May 10.

Bioenergetic basis of skeletal muscle fatigue.

Author information

1
Department of Biological Sciences, Marquette University, Milwaukee, WI.
2
Department of Physical Therapy, Marquette University, Milwaukee, WI.

Abstract

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 (Pi) 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 Pi 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.

KEYWORDS:

31P-MRS; Ca2+ handling; acidosis; cross-bridge mechanics; diprotonated phosphate; inorganic phosphate; metabolism; muscle fatigue

PMID:
31342000
PMCID:
PMC6656370
[Available on 2020-08-01]
DOI:
10.1016/j.cophys.2019.05.004

Supplemental Content

Loading ...
Support Center