Gas exchange kinetics during constant-load exercise were measured to investigate the possibility that excess CO2 output during exercise might not be dependent on hyperventilation. Five healthy males performed twelve minutes of cycle exercise, including two minutes of 0 W pedaling, at 20, 40, 50, 60, 70, and 80% of their maximal work rate (WRmax) determined on the basis of preliminary ramp exercise of 30 W/min. Minute ventilation, O2 uptake, and CO2 output were measured breath-by-breath. Excess CO2 output and CO2 stores were calculated, assuming that the respiratory quotient (RQ) in tissue is constant during constant-load exercise and that the respiratory exchange ratio at the mouth level is equal to the RQ during the steady-state phase. Excess CO2 output was observed at levels of WR greater than 40% WRmax after initial CO2 storage, where VCO2/VE decreased gradually as though in parallel with the kinetics of CO2 storage. VO2/VE, however, appeared to be constant after the initial peak. These data suggest that VE is closely correlated with VO2 rather than VCO2 during constant-load exercise, indicating that excess CO2 output to compensate lactate production is independent of hyperventilation.
A study was conducted for further investigation of the mechanism of notch formation of heart rate (HR) in sudden strenuous exercise (SSE), and rapid increase in stroke volume (SV) right after SSE which were the questions arised in the prior experiment. Six healthy male students volunteered for the study. A bicycle ergometer was prepared for SSE. The intensity and duration of SSE were 100%VO2max and 1 min, respectively. Warming-up consisting of 80%VO2max for 5 min, preceeded SSE. The interval between SSE and warming-up varied from 5 to 30 min. A control experiment was also conducted without warming-up. The main results obtained were as follows : 1) Diastolic time (DT) temporarily elongated when a notch of HR was formed at the early stage of SSE. Warming-up prevented this formation. No notch was observed throughout total electromechanical systolic time (QS2), left ventricular ejection time (LVET) or preejection time (PEP) . 2) DT was prolonged immediately after SSE, while LVET, PEPi (PEP index, Weissler's equation) were shortened. PEP/LVET did not change in the initial stage of the recovery period, while electrical systolic time (QT) and QS2 shortend and QT/QS2 increased temporarily. These results suggest the following conclusions : 1) Notch formation observed in heart rate is due to the temporary extension of DT at the early stage of SSE. 2) Decrease in afterload may be the main cause for the rapid increase in stroke volume after SSE, though other factors such as increase in preload, myocardial contractility and sympathetic tone should also be considered.