SKELETAL-MUSCLE FATIGUE IN NORMAL SUBJECTS AND HEART-FAILURE PATIENTS- IS THERE A COMMON MECHANISM

Skeletal muscle fatigue develops gradually during all forms of exercis e, and develops more rapidly in heart failure patients. The fatigue me chanism is still not known, but is most likely localized to the muscle cells themselves. During high intensity exercise the perturbations of the Na+ and K+ balance in the exercising muscle favour depolarization , smaller action potentials and inexcitability. The Na+,K+ pump become s strongly activated and limits, but does not prevent the rise in extr acellular Na+,K+ pump concentration and intracellular Na+ concentratio n. However, by virtue of its electrogenic property the pump may contri bute in maintaining excitability and contractility by keeping the cell s more polarized than the ion gradients predict. With prolonged exerci se perturbations of Na+ and K+ are smaller and fatigue may be associat ed with altered cellular handling of Ca2+ and Mg2+. Release of Ca2+ fr om the sarcoplasmic reticulum (SR) is reduced in the absence of change s of the cellular content of Ca2+ and Mg2+. in heart failure several c linical reports indicate severe electrolyte perturbations in skeletal muscle. However, in well controlled studies small or insignificant cha nges are found. We conclude that with high intensity exercise perturba tions of Na+ and K+ in muscle cells may contribute to fatigue, whereas with endurance type of exercise and in heart failure patients the ske letal muscle fatigue is more likely to reside in the intracellular con trol of Ca2+ release and reuptake.