Point:counterpoint Comments

To the Editor: Lamb and Stephenson (3) argue, based on reductionist approaches in isolated and skinned muscle fibers at rest, that lactate and proton accumulation during periods of contraction may augment force production by relieving inhibition of excitation-contraction coupling processes at the sarcolemma, SR and contractile apparatus. The reductionist approaches give insight to mechanisms that may be involved in the regulation of cellular processes, but the results are initially valid only for the experimental conditions used. Even with consideration of temperature effects (1), there are in vivo and in situ metabolic, biochemical and molecular evidence that lactate and proton accumulation within contracting muscle, directly and indirectly, contribute to fatigue and that this is effected by a number of factors including downregulation of pH-sensitive enzyme systems (2, 5). Although there may be simultaneous beneficial effects of increased lactate or protons on some E-C coupling processes at the sarcolemma, these are over-ridden by other, simultaneous, inhibitory effects on the contractile machinery (1) and energy production (5) that occur as a result of lactate and proton accumulation. The suggestion that fast glycotic fibers benefit from lactate accumulation on the basis of the high Km for MCT4 (3) is illogical. Fast glycolytic fibers, during high intensity exercise, are tolerant of large excursions of metabolite and electrolyte concentrations, some of which are relatively slowly restored (4). However, retention of produced lactate by fast glycolytic fibers provides a preferred energy source for resynthesizing glycogen after cessation of contraction. Why get rid of a most important, readily usable postcontraction energy source?