Ventilatory Changes During Exercise

Mild to moderate dynamic exercise results in changes in the ventilatory response to compensate for the corresponding increase in the metabolic rate. This response has always been considered to be stereotypical and unmalleable, but recent studies have suggested otherwise. This paper begins by explaining current thinking about ventilatory changes during mild exercise. The inspired ventilation increase in response to mild exercise is thought to be brought about by the activation of multiple neural pathways, and by mechanical and chemical receptors in the periphery. Descending inputs from supramedullary locations in the central nervous system may combine with these effects to bring about a ventilatory increase. The level of pulmonary ventilation is determined by the interactions of these various pathways.

Reversible short-term alterations in synaptic strength or cellular properties in these neural circuits can modify the ventilatory response and alter respiratory behavior accordingly. Structural and/or functional system changes may become more permanent in the long term adjustment. The article then reviews evidence for changes in neural function which might be responsible for these modulations.

In going from rest to mild exercise, ventilation increase exponentially until a steady-state is reached, usually within three to five minutes, and further adjustments are made as the strength or duration of the exercise changes. It has been accepted for some time that the init

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pnia was shown to be preserved in goats through a small external dead space. To maintain this dead space during exercise, they suggest that a modulatory process involving activation of serotonin receptors may be necessary. This was supported by a study in which the use of methysergide, a serotonin receptor antagonist, attenuated the ventilatory response during exercise, increased dead space, and induced a loss of carbon dioxide partial pressure regulation from rest to exercise. However, systemic methysergide had no effect on ventilatory control during exercise alone. This suggests that serotonin receptor-dependent modulatory mechanisms are only activated to elicit an appropriate exercise ventilatory response if other respiratory stimuli are also involved. Further studies with serotonin-receptor antagonists given intrathecally into the cerebrospinal fluid suggested that short term modulation of the ventilatory response to exercise with increased dead space requires spinal seratonergic receptors. The raphe neurons in the brainstem when stimulated electrically elicit augmentation of phrenic nerve activity, and raphe neurons have been shown to be activated by exercise in rats. These neurons are also stimulated in cats by walkin

Category: Medical - V