Determinants and control of breathing during muscular exercise.

Abstract

IntroductionExercise hyperpnoea is considered to be one of the major remaining challenges to understanding the control of human systemic function. The topic is currently in an exciting phase, both with respect to novel perspectives on its control and the application of novel techniques to investigate previously proposed mechanisms. However, despite this, the integrative aspects of the control that so closely regulates arterial PCO 2 (PaCO 2 ) and pH (pHa) during moderate exercise, and which constrains the fall in pHa at higher work rates, seem no less elusive.We attempt in this review to provide a current perspective on the mechanisms proposed to contribute to the exercise hyperpnoea in humans (typically under laboratory conditions) using, as a frame of reference, the diVerent regulatory demands of the diVerent temporal and intensity domains.

Effect of inspiratory threshold loading on ventilatory kinetics during constant-load exercise

“…This transition has been characterized as having three phases (6,24): phase 1 is the rapid increase in oxygen uptake (V O 2 ), carbon dioxide output (V CO 2 ), and ventilation (V E) in the first 15-20 s of exercise; phase 2 is the exponential increase; and phase 3 is the final steady-state response. Phase 1 reflects the sudden increase in cardiac output (25), and the phase 2 response is known to be influenced by the carotid bodies (26,28). Thus studying phase 2 allows for the exploration of the ventilatory adaptation to exercise load, especially the time constants (), which represent the time to reach 63% of the steady-state response of the ventilatory parameters.…”

Ventilatory response to exercise does not evidence electroencephalographical respiratory‐related activation of the cortical premotor circuitry in healthy humans

“…A constant work rate exercise results in an immediate increase in ventilation that rises exponentially until an isocapnic steady state is reached (Whipp & Ward 1998). Early on, exercise increases the production of carbon dioxide (CO 2 ): in response, ventilation augments to regulate the arterial partial pressure of CO 2 .…”

“…When exercise intensifies and the lactate threshold is crossed, metabolic acidosis sets in, requiring additional ventilatory compensation. A constant work rate exercise results in an immediate increase in ventilation that rises exponentially until an isocapnic steady state is reached (Whipp & Ward 1998). Recent experiments have identified a subset of neurons within the mesencephalic locomotor region that sends direct inputs to neurons in the respiratory generator (Gariepy et al 2012) and thus seems intimately involved in the coupling between respiration and locomotion (Gariepy et al 2012).…”

Exercise performance and quality of life is more impaired in Eisenmenger syndrome than in complex cyanotic congenital heart disease with pulmonary stenosis

“…In healthy people there is an increase of P ET CO 2 under exercise till the respiratory compensation point and then a progressive decline till exhaustion. [28] In patients with major cardiac shunts or large ventilation/perfusion mismatch there are low P ET CO 2 values at rest that further decline from the beginning of the exercise test on. [29] This could be shown in our total patient group of cyanotic patients.…”