The sarcoplasmic reticulum in muscle fatigue and disease: role of the sarco(endo)plasmic reticulum Ca2+-ATPase.
Skeletal muscles induced to contract repeatedly respond with a progressive loss in their ability to generate a target force or power. This condition is known simply as fatigue. Commonly, fatigue may persist for prolonged periods of time, particularly at low activation frequencies, which is called low-frequency fatigue. Failure to activate the contractile apparatus with the appropriate intracellular free calcium ([Ca2+]f) signal contributes to fatigue but the precise mechanisms involved are unknown. The sarcoplasmic reticulum (SR) is the major organelle in muscle that is responsible for the regulation of [Ca2+]f, and numerous studies have shown that SR function, both Ca2+ release and Ca2+ uptake, is impaired following fatiguing contractile activity. The major aim of this review is to provide insight into the various cellular mechanisms underlying the alterations in SR Ca2+ cycling and cytosolic [Ca2+]f that are associated both with the development of fatigue during repeated muscle contraction and with low-frequency or long-lasting fatigue. The primary focus will be on the role of the sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) in normal muscle function, fatigue, and disease.
Tupling
A Russell
AR
Department of Kinesiology, University of Waterloo, Waterloo, Ontario.
D000252:Calcium-Transporting ATPases / Q000502:physiology*; D004194:Disease; D006801:Humans; D018763:Muscle Fatigue / Q000502:physiology*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism / Q000502:physiology*; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D013997:Time Factors
D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D000252:Calcium-Transporting ATPases