REDUCTION BY TRAINING OF CO2 OUTPUT DURING EXERCISE

Abstract

A 10 wk endurance training program of 5 men resulted in an 18% increase in maximum .ovrhdot.VO2 [O2 consumption at work] from a mean of 3.1 1/min. Measurements were made at 2 submaximal O2 intakes of 1.2 and 2.0 1/min to examine the physiological interdependence of mechanisms changed by training. At both levels of .ovrhdot.VO2, reductions occurred following training in cardiac frequency (fc), CO2 output (.ovrhdot.VCO2), respiratory exchange ratio (R), ventilation (.ovrhdot.VE), alveolar-arterial PO2 [partial pressure of O2] difference (A-aPO2) and blood lactate (La); the changes were statistically significant at the higher .ovrhdot.VO2. No change was observed in cardiac output, blood free fatty acids (FFA) and blood glycerol (gly). Arterial PCO2 [partial pressure of CO2] (PaCO2) and .**GRAPHIC**. increased slightly. Changes in fc were not significantly related to changes in other variables. The reductions in La were related to falls in .ovrhdot.VCO2 and .ovrhdot.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 increased aerobic metabolism. The resultant fall in lactic acid production led to a fall in .ovrhdot.VCO2 and maintained .**GRAPHIC**. These changes accounted for a marked reduction in .ovrhdot.VE following training.