The reduction by training of CO2 output during exercise.
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5 men underwent a 10-wk endurance training programme which resulted in an 18% increase in max VO2 from a mean of 3.1 l/min. Measurements were made at 2 submaximal O2 intakes of 1.2 and 2.0 l/min to examine the physiological interdependence of mechanisms changed by training. At both levels of VO2, reductions were observed following training in cardiac frequency (fc), CO2 output (VCO2), respiratory exchange ratio (R), ventilation (VE), alveolar-arterial PO2 difference (A-aPO2) and blood lactate (La); the changes were statistically significant at the higher VO2. No change was observed in cardiac output, blood free fatty acids (FFA) and blood glycerol (gly). A small increase was found in arterial PCO2 (PaCO2) and HCO3-. Changes in fc were not significantly related to changes in other variables. The reductions in La were related to falls in VCO2 and VE, and inversely related to increases in PaCO2. Only a portion of the fall in R could be ascribed to increased usage of fat as a fuel, the main factor being a fall in lactate production. Reductions in A-aPO2 were due to decreases in PAO2 and falls in R, with no change in venous admixture. Changes in FFA and gly were small and not related to changes in other variables. Training led to an increased usage of aerobic metabolic pathways. The resultant fall in lactic acid production led to a fall in VCO2 and maintained HCO3-. These changes accounted for a marked reduction in VE following training.
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