Pulmonary Gas Exchange Dynamics and the Tolerance to Muscular Exercise: Effects of Fitness and Training.
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Departments of Physiology and Anesthesiology. School of Medicine. UCLA. U. S. A. Oxygen uptake (VO<SUB>2</SUB>) kinetics are generally agreed to be first-order for moderate work rates with a time constant (γVO<SUB>2</SUB>) that is thought to reflect the kinetics of intramuscular creatine phosphate depletion. However, when there is a concomitant lactic acidosis, VO<SUB>2</SUB> is appreciably longer, reflecting an additional, delayed and slowed component that leads to γVO<SUB>2</SUB>s greater than the aerobic equivalent of that work rate and which therefore invalidates current techniques for VO<SUB>2</SUB> deficit estimation. This "excess" VO<SUB>2</SUB> is no more than ∼250-300 ml/min at work rates for which [lactate] and [H<SUP>+</SUP>]a can be stabilized. At higher work rates which demand sustained and progressive increases in [lactate] and [H<SUP>+</SUP>] a, however, VO<SUB>2</SUB> also continues to increase progressively, yielding excess VO<SUB>2</SUB>S > 1 l/min at exhaustion. The trajectory of excess VO<SUB>2</SUB> therefore is to the maximum VO<SUB>2</SUB> : the resulting exercise limitation becomes progressively more pronounced the higher the work rate, which accounts for the hyperbolic character of the power-duration curve. Factors which speed VO<SUB>2</SUB> kinetics in this domain reduce the excess VO<SUB>2</SUB> mechanism and lead to improved exercise performance. We have demonstrated that, in addition to appropriately-designed training regimens, induction of a metabolic acidosis prior to exercise speeds VO<SUB>2</SUB> kinetics at high work rates, reducing the increase in both [lactate] and [H<SUP>+</SUP>] a and reducing the CO<SUB>2</SUB> Ioad to ventilation during the transient phase of the work. The optimum procedure for inducing these improved pulmonary gas-exchange kinetics, however, remains to be determined
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