Intracellular pH and phosphate: are they limiting factors during exercise of high intensity?

Abstract

Intracellular acidosis caused by lactic acid formation and the accumulation of inorganic phosphate (Pi) by phosphocreatine (PCr) breakdown were regarded to be major factors in the process of muscle fatigue. However, recent studies on skinned and intact isolated mammalian muscle fibres at physiological temperatures have only shown minor effects of physiologically low pH values on contractility. Physiologically high concentrations of phosphate seem to reduce force and shortening velocity by a direct inhibition of acto-myosin ATPase and by a reduction in Ca-release from SR. Recent in-vivo studies using 31P MRS on human skeletal muscle seem to support these findings. During intense dynamic interval exercise, contraction velocity of the calf muscle significantly fell by about 30% within each interval while pH was increasing by about 0.3 units in average due to PCr consumption and an increase in Pi. Starting from 2nd contraction interval velocity was also initially reduced by about 20%, which corresponds with an incomplete recovery of PCr and Pi. However, also a 10% reduction in initial EMG amplitude was observed. The relative indecency of muscle fatigue from acidosis and the potential role of Pi accumulation in fatigue can also be shown in patients with myo-phosphorylase deficiency. These patients show distinct signs of fatigue after only moderate muscle load, which causes an alkalinisation and a steep PCr breakdown and Pi accumulation.