Pulmonary ventilation and effect of oxygen breathing in heavy exercise.

Abstract

Summary. 1 The regulation of respiration in heavy work has been studied in young normal subjects by measuring the arterial oxygen tensions and various respiratory functions in rest and work when breathing atmospheric air and when breathing air mixtures with augmented or lowered oxygen concentrations. 2 It was found that the arterial PO2 in heavy work with pronounced hyperventilation (i. e. increased ventilation per litre oxygen uptake and decreased alveolar pCO2) was of the same magnitude (87 mmHg, range 82–94 mmHg) as in rest and light work (87 mmHg, range 79–96 mmHg). This value is lower than the reported threshold PO2 for the chemoreceptors in animals and humans. 3 Breathing of 33 per cent oxygen diminished the hyperventilation of heavy work and increased the arterial PO2 to 183 mmHg (range 161–190 mmHg). This value is well above the reported threshold PO2 for the chemoreceptors. 4 Breathing of 100 per cent oxygen further decreased the hyperventilation and increased the arterial PO2 to 663 mmHg (range 635–685 mmHg). 5 It is concluded that the hyperventilation in heavy work cannot be explained simply as the result of an arterial hypoxia. Earlier experiments with sudden changes from air breathing to oxygen breathing during work, and work experiments with about 12 per cent oxygen in the inspired air here presented, however, make the assumption probable that the chemoreceptor impulses elicited at the arterial PO2 obtaining in the air experiments sensitize the respiratory centre towards the work stimulus. Under this assumption it is possible to explain the part of the heavy exercise hyperventilation which can be eliminated by increasing the arterial PO2 up to the threshold PO2 of the chemoreceptors, as the result of a hypoxic chemoreceptor drive. Analogous with this sensitizing effect towards the work stimulus it has earlier been shown that the low oxygen stimulus also sensitizes the centre to the CO2 stimulus, whereas the combined effect of the CO2 and the work stimuli rather seems to be an additive one. 6 That part of the hyperventilation during heavy work which persists when the arterial PO2 has been increased to the threshold of the chemoreceptors is assumed to be caused by anaerobic metabolites produced in the working muscles, and its elimination by a further increase in the alveolar PO2, e. g. by changing from 33 to 100 per cent oxygen in the inspired air, is thought to be due to an effect on the metabolism of the working muscles of the increased amount of physically dissolved oxygen.