SUMMARY1. The breathing pattern, that is the relation between tidal volume (VT) and the inspiratory (T1) and expiratory (TE) durations, has been studied for individual breaths (forty in each steady state).2. Five healthy subjects were studied in steady-state exercise on a bicycle ergometer breathing air; three of them were also studied in hypercapnia, at rest and during exercise, and two of them also during exercise on a treadmill.3. Tidal volume and respiratory frequency both increased with work load. The increase in frequency was largely due to a progressive decrease in TE; T, also decreased. 5. A simple model of the respiratory cycle which fits both the observed mean and breath-by-breath patterns and which involves no new assumptions is presented.
The ventilatory response to hypoxia (PAO2 55 and 45 Torr) at each of four levels of PACO2 was studied in five healthy subjects before and after a rise in rectal temperature of 1.4 degrees C had been induced by means of a heated flying suit. At a given level of chemical drive both ventilation and mean inspiratory flow increased after heating, frequency relatively more than tidal volume. In isoventilation comparisons mean inspiratory flow was identical in normo- and hyperthermia, whereas the durations of inspiration (TI) and expiration (TE) were proportionately shortened. It is suggested that a rise in temperature shortens TI by affecting a central "clock" and that TE changes are secondary to changes in end-inspiratory volume. The euoxic CO2 response in hyperthermia was suggestive of multiplication between CO2 and temperature. Hypoxic sensitivity was significantly increased, indicating a temperature effect on the arterial chemoreceptors. The breathing pattern was in either temperature condition identical in euoxia and in hypoxia.
Petersen, E. S. and H. Vejby‐Christensen. Effect of body temperature on steady state ventilation and metabolism in exercise. Acta physiol. scand. 1073. 89. 342–351.
Four healthy subjects were studied at rest and during steady slate of work at normal room and body temperature, and at elevated body temperature (38.5o C) in a climatic chamber. Ventilation, oxygen uptake, carbon dioxide elimination, heart rate, and blood lactate and pyruvate concentrations were measured. At equal work loads ventilation was not different, although respiratory rate was consistently higher and tidal volume lower at elevated temperature. Oxygen uptake was lower, and the ventilatory equivalent therefore higher in hyperthermia than in normothermia. Blood lactate concentration was higher both at rest and at all work loads indicating an increased anaerobic energy yield in hyperthermia. The study indicates the existence of a temperature threshold near 38o C, above which a relative hyperventilation is seen. The observed hyperventilation is hardly caused by changes in the [H+]‐stimulus, and it is suggested that hyperthermia per se or through interaction with other stimuli might constitute the additional ventilatory drive.
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