Date of Award

1989

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

First Advisor

Steve Dodd

Abstract

Three studies were performed to determine the relationship between blood lactate, CO$\sb2$ flow to the lung, and ventilation during exercise. First, the method of determining the lactate threshold by use of log-log and semilog transformations developed by Beaver and his colleagues was modified to provide an objective method of determining the threshold which resulted in a significantly better fit (p $<$.05) of the log-log model to the data. Second, to test the theory that the increase in CO$\sb2$ flow to the lung due to bicarbonate buffering of H+ from lactic acid causes the rise in ventilation out of proportion to VO$\sb2$ at the ventilatory threshold, the lactate thresholds of these subjects were used to predict their ventilatory thresholds. The lactate threshold determined by the modified log-log model/method was a poor predictor with an insignificant relationship between the lactate and ventilatory thresholds (p $>$.05). In the third study, six subjects were tested during 4 sessions to determine the relationship between ventilation and CO$\sb2$ flow to the lung during exercise and also during rest and exercise while CO$\sb2$ was being inhaled. This relationship was expressed by the regression of minute ventilation (V$\sb{\rm E}$) vs. the minute rate of CO$\sb2$ expired (V$\sb{\rm T}$CO$\sb2$). Results showed no significant differences (p $>$.05) between the slopes of the V$\sb{\rm E}$-V$\sb{\rm T}$CO$\sb2$ regression during rest and exercise with CO$\sb2$ inhalation, but the intercepts were significantly different (p $<$.05). The slope of the V$\sb{\rm E}$-V$\sb{\rm T}$CO$\sb2$ regression during incremental exercise was significantly greater than during rest with CO$\sb2$ inhalation, with the intercepts not significantly different, showing that the regression at rest with CO$\sb2$ inhalation could not be extended to explain the ventilatory response to exercise. However, the ventilatory response to incremental exercise could be explained by dividing the response into two components: (1) that component dependent upon CO$\sb2$ flow to the lung, and (2) a component independent of CO$\sb2$ flow to the lung and quantified by the difference in intercepts between the ventilatory response to V$\sb{\rm T}$CO$\sb2$ at rest and during exercise with CO$\sb2$ inhalation. In conclusion, these studies do not support the theory that CO$\sb2$ flow is the primary stimulus of exercise hyperpnea.

Pages

101

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