No abstract

The purpose of this study was to determine the effect of altered metabolic acid-base status on the changes in ventilation in the transition from heavy exercise above anaerobic threshold to rest. Seven subjects ingested, in a randomized and blind manner, either NaHCO3 or CaCO3 (placebo) at a dose of 300 mg.kg-1 body mass and ran on a treadmill for five minutes (90% VO2max and above anaerobic threshold) on ten different occasions. Changes in minute ventilation in the exercise transitions were studied by starting and stopping the treadmill abruptly with a remote switch. The fast increase in ventilation at the start of exercise was not accompanied by a corresponding fast drop in ventilation at the end of exercise (P less than or equal to 0.001) and the effects of chemicals on these changes were not significantly different (P greater than 0.05). A single-component exponential model, without a time delay, was used to determine the time constants of off-transitional decay in ventilation for the two chemicals in each subject. Parametric and non-parametric statistical tests revealed that the time constants were not as significantly different as the venous pH measurements which were significantly higher with NaHCO3 (P less than or equal to 0.001). The results indicate that the absence of fast change in ventilation at the end of heavy exercise is not due to lactic acidosis and the consequent slow ventilatory changes in the off-transition of heavy exercise are at least partly mediated by non-humoral factors such as a central neural reverberatory mechanism.

The purpose of this study was to determine the role of lactic acidosis in the ventilatory response to heavy exercise above anaerobic threshold. Seven subjects ingested either NaHCO₃ or CaCO₃ at a dose of 300 mg/kg body weight and ran on a motor-driven treadmill at a work load corresponding to 90% of V_O2max and above anaerobic threshold for a period of 5 min while minute ventilation and Pet_Co were recorded breath by breath. A total of 10 runs, 5 with CaCO₃ and 5 with NaHCO₃ in a randomized and blind order, were done in each subject. Statistical analyses of the effects of the chemicals on minute ventilation during the 15 s between min 4.75 and 5 of exercise showed that the differences in ventilation did not reach statistical significance (p > 0.05) in 5 of the 7 subjects. Venous pH measurements at the end of exercise revealed a significant increase with NaHCO₃ (p « 0.05). It is concluded that lactic acidosis is not an essential determinant of ventilatory response to heavy exercise above anaerobic threshold in the majority of the subjects.

Transitions from rest to exercise and vice versa are reported to be associated with instantaneous changes in minute ventilation and the changes in the off-transitions are thought to be the reverses of those in the on-transitions. Such changes have been observed mainly in mild-moderate exercise and their extrapolation to heavy exercise above anaerobic threshold is unwarranted. Hence, the purpose of this study was to determine the changes in ventilation in the transition from heavy exercise above anaerobic threshold to rest. Five healthy volunteers ran on a motor-driven treadmill at a constant work-load corresponding to 80% VO2max and above anaerobic threshold. Changes in minute ventilation and end-tidal PCO2 in the on- and off-transitions were determined breath by breath by starting and stopping the treadmill abruptly. The results indicate that, contrary to what is reported for mild-moderate exercise, an instantaneous drop in ventilation is absent in the off-transition of heavy exercise above anaerobic threshold. The gradual decline in minute ventilation may be due to a sustained respiratory drive from a central neural reverberatory mechanism, blood-borne respiratory stimuli and/or a peripheral neurogenic drive originating in the so-called metaboloreceptors.

The purpose of this study was to examine the effects of duration and the concomitant ventilatory drift of heavy exercise on the changes in ventilation following the cessation of exercise. Seven male subjects ran on a motor-driven treadmill at a constant work-rate of 90% of VO2max for either 5 min or 7 min on 60 occasions. The exercise was terminated abruptly by stopping the treadmill with a remote switch while recording inspired minute ventilation (VI) breath by breath. The fast drop in VI at the end of exercise is significantly less than the corresponding increase at the onset of exercise (P less than 0.05) and this difference is greater with longer duration of exercise. The time constants of the slow ventilatory decline are significantly increased following 7 min of exercise (P less than 0.05). They are also positively related to the drift in VI that occurs with the continuation of heavy exercise beyond 3 min. This relationship is however not statistically significant (P greater than 0.05). These results indicate that the rate of ventilatory decline is slower after the end of a longer duration of exercise and this is caused by mechanism/s that also contribute/s to the ventilatory drift of heavy exercise. As, of the many different possibilities, only the respiratory after-discharge (central neural reverberatory) mechanism is likely to be more activated with a longer duration of exercise and on the basis of our previous observations (Jeyaranjan et al. 1988, 1989), the results suggest that the mechanism of after-discharge is an important mediator of ventilatory response during as well as after the cessation of heavy exercise.