Respiratory drive and breathing pattern during exercise in man.

Changes in respiratory drive, as assessed by mouth occlusion pressure (P0.1), and in breathing pattern were studied in 19 healthy subjects who exercised on a cycle ergometer with work loads ranging from loadless pedalling up to the highest load that could be sustained for 4 min. In the P0.1 studies, experiments were carried out both at normal atmospheric pressure and during hyperbaric conditions in which the density (D) of the respired gas was increased. Analyses of observed changes in P0.1 and in the interrelations of minute ventilation (V), tidal volume (VT), inspiratory (TI), expiratory (TE) and total breath (Ttot) durations, and lung volumes yielded the following results and conclusions: Analyses of inspiratory and expiratory volume threshold curves in terms of the relations between end-inspiratory volume and TI on one hand, and end-expiratory volume and TE on the other, suggest that the termination of inspiration during cycle exercise is dependent on volume-related afferent feedback from the lungs and/or chest wall, not only in the high but also in the low volume range, and expiratory muscle activity occurs already at low exercise intensities, combined with active control of expiratory flow, end-expiratory volume and TE as exercise hyperpnea intensifies. TI/Ttot increased with V and work intensity through a number of mechanisms which accelerate the increase in mean expiratory flow compared with that in mean inspiratory flow (VT/TI), the change in timing presumably reducing the oxygen cost of respiration at any given exercise-induced ventilatory demand. With increments in work load, P0.1 increased at higher rates than V and VT/TI, both in the normo- and hyperbaric conditions. Respiratory impedance, P0.1/(VT/TI), increased with both D and VT/TI. The relationship of P0.1, D and VT/TI approximated the equation P0.1 = K X D0.5(VT/TI)b, where K varies among subjects due to differences in i.a. vital capacity, and b has a value close to 1.5. The observed changes in P0.1 suggest that the respiratory drive was reflexly enhanced in response to loading as airway resistance increased with D and/or VT/TI, whereby any depression of V or VT/TI attributable to the increased respiratory impedance was counteracted.