ABSTRACT
Theperformanceofskeletalmusclesislimitedbythedevelopmentoffatigue(i.e., adeclineinperformancewithtimeofactivity,manifestedasreducedforce, diminishedcontractilespeed,andslowerrelaxation).Thecombinationofreduced forceandlowershorteningvelocityresultsinreducedmechanicalpoweroutput, whichisofgreatfunctionalimportanceduringmosttypesofphysicalactivity. Fatigueiscausedmainlybyintramuscularfactors:thus,neitherthecentralnervous system(CNS),themotornerve,northeneuromuscularjunctionsetasignificant limitformuscleperformance(forreviewseeBigland-RitchieandWoods,1984). Inthischapterwewilldealwithmetabolicalterationswithinthemusclefibresthat maybeimportantforthereducedperformanceinfatigue.Wewilldealmainlywith effectsonisometricforceproduction,becausethisiswheremostexperimentaldata isavailableandthecausalrelationsprobablybestunderstood;towardtheendwe willverybrieflydiscussknownmetabolicinfluencesonshorteningspeedand relaxationrate.Wewillprimarilyconsiderfatigueproducedbybriefmaximal contractions,repeatedatshortintervals,leadingtoseverefatiguewithinafew minutes.Thistypeofintermittentmaximalactivityisknowntocauselargechemical changesand,therefore,isagoodmodelforstudiesoftheroleofmetabolicfactors inthedevelopmentoffatigue.Metabolicfactorsmayalsobeinvolvedinfatigue
Recent studies have shown that force decline in fatigue is due to both direct impairment of cross-bridge function and to changes in intracellular activation. Three principal fatigue mechanisms can now be identified (Westerblad and Allen, 1991): (1) reduction of the maximum tension (i.e., the tension at saturating Ca2+ levels), (2) reduced myofibrillar Ca 2+ sensitivity, and (3) reduced Ca2+ levels during tetanic contractions. Some metabolic factor(s) may be implicated in all these three mechanisms, or they may be related to different metabolic alterations-such putative relations will be discussed in detail later in the chapter.
