Ventilatory Responses to Exercise

Regulation of ventilation is complex and under the influence of several mechanisms. The primary mechanism during exercise is a neural input that likely originates from the same area of the motor cortex in the brain that is telling the skeletal muscles to exercise. This would explain the rapid increase and decrease of minute ventilation (VE) with the onset and cessation, respectively, of exercise. However, a "fine tuning" of exercise VE is accomplished primarily by the peripheral chemoreceptors, most likely by the CO2 chemoreceptors. The following graph illustrates the different control mechanisms during and after a sub-lactate threshold exercise.

The data below is taken from a single subject who performed an incremental treadmill test. In the figure below, the linear relationship of energy expenditure (VO2) and exercise intensity (running velocity) is demonstrated.

In the next figure, minute ventilation (VE) is plotted against the relative exercise intensity (% of VO2max) and demonstrates a curvilinear or alinear relationship. Thus, at low to moderate intensities, there is a linear relationship between minute ventilation and exercise intensity but, after a certain exercise intensity, minute ventilation increases at a more rapid rate than before.

In the next figure, VCO2 is plotted against exercise intensity and also displays a curvilinear response.

A question arises as to the explanation of the VE and VCO2 responses at higher exercise intensities. Note that the inflection point on both graphs occurs at a similar percent of VO2max. To answer this question, look at the following graph which shows the relationship of blood lactate accumulation at increasing exercise intensities.

Note the occurrence of the lactate threshold–point at which blood lactate begins accumulating more rapidly–then compare the percent of VO2max at which it occurs with the occurrences of the inflection points on the above VE and VCO2 graphs. As blood lactate concentration increases (i.e. after the lactate threshold), so does the accumulation of H+. The H+ stimulates the peripheral pH chemoreceptors located in the aortic arch and explains the rapid rise in VE at intensities higher than the lactate threshold. In order to counteract the decreasing blood pH, buffers in the blood remove some of the H+. The primary buffer is the bicarbonate ion (HCO3-) and, when the H+ and HCO3- reach the lungs, they are rapidly converted into CO2 and H2O and expired. This explains the VCO2 inflection point which occurs at a similar time to the lactate threshold.