Short- and long-term modulation of the exercise ventilatory response

Abstract

The importance of adaptive control strategies (modulation and plasticity) in the control of breathing during exercise has become recognized only in recent years. In this review, we discuss new evidence for modulation of the exercise ventilatory response in humans, specifically, short- and long-term modulation. Short-term modulation is proposed to be an important regulatory mechanism that helps maintain blood gas homeostasis during exercise.

Figure 1

Short-term modulation of the exercise ventilatory response in younger men. Top Panel: slope of the exercise ventilatory response ($\Delta \stackrel{.}{\mathrm{V}}\mathrm{E}∕\Delta \stackrel{.}{\mathrm{V}}{\mathrm{CO}}_2$) from rest to each work rate. Bottom Panel: change in end-tidal PCO₂ (PET_CO2) from rest to each work rate. DS, dead space.

Figure 2

Typical flow-volume loops in younger men. Left Panel: at rest and each work rate with no added dead space, indicating main effect of exercise on lung volumes; Right Panel: without (Control) and with each added dead space volume during exercise at 50 W, indicating main effect of dead space on lung volumes. Max loop, maximal flow-volume loop at rest; EILV, end-inspiratory lung volume; EELV, end-expiratory lung volume. Adapted from Wood etal. 2009.

Figure 3

Short-term modulation of the exercise ventilatory response in older men. Slope of the exercise ventilatory response ($\Delta \stackrel{.}{\mathrm{V}}\mathrm{E}∕\Delta \stackrel{.}{\mathrm{V}}{\mathrm{CO}}_2$) from rest to each work rate.

Figure 4

Proposed neural mechanism of STM. Exercise increases ventilation via activation of premotor neurons in the brain stem, driving spinal respiratory motor neurons to activate respiratory muscle contraction. The addition of external dead space activates brain stem raphe serotonergic neurons that project to the ventral spinal cord, increasing serotonin release in the vicinity of respiratory motor neurons. This amplifies the descending respiratory drive resulting in greater ventilation at a given exercise intensity (see text for full details). 5-HT, serotonin.

Figure 5

Hypothetical mechanisms modulating the exercise ventilatory response when dead space is increased (STM) with the central command for locomotion and feedback. Model assumes that the primary feedforward stimulus for ventilation [1] does not necessarily need to be altered for ventilation to be augmented during STM. However, during STM respiratory muscle drive is increased via increased excitability of spinal motor neurons [2] to synaptic inputs from descending feedforward stimulus for ventilation.