Abstract
Many stressors cause an increase in ventilation in humans. This is predominantly reported as an increase in minute ventilation (V̇E). But, the same V̇E can be achieved by a wide variety of changes in the depth (tidal volume, V(T) ) and number of breaths (respiratory frequency, ƒ(R) ). This review investigates the impact of stressors including: cold, heat, hypoxia, pain and panic on the contributions of ƒ(R) and V(T) to V̇E to see if they differ with different stressors. Where possible we also consider the potential mechanisms that underpin the responses identified, and propose mechanisms by which differences in ƒ(R) and V(T) are mediated. Our aim being to consider if there is an overall differential control of ƒ(R) and V(T) that applies in a wide range of conditions. We consider moderating factors, including exercise, sex, intensity and duration of stimuli. For the stressors reviewed, as the stress becomes extreme V̇E generally becomes increased more by ƒ(R) than V(T) . We also present some tentative evidence that the pattern of ƒ(R) and V(T) could provide some useful diagnostic information for a variety of clinical conditions. In The Physiological Society's year of 'Making Sense of Stress', this review has wide-ranging implications that are not limited to one discipline, but are integrative and relevant for physiology, psychophysiology, neuroscience and pathophysiology.