Norton K I, Squires B, Norton L H, Craig N P, McGrath P, Olds T S
Human Bioenergetics Laboratory, School of Sport and Leisure Studies, University of New South Wales, Australia.
Eur J Appl Physiol Occup Physiol. 1995;70(2):115-25. doi: 10.1007/BF00361538.
This study investigated the influence of an exercise stimulus on pulmonary ventilation (VE) during severe levels of exercise in a group of ten athletes. The altered ventilation was assessed in relation to its effect on blood gas status, in particular to the incidence and severity of exercise induced hypoxaemia. Direct measurements of arterial blood were made at rest and during the last 15 s of two intense periods of cycling; once at an intensity found to elicit maximal oxygen uptake (VO2max; MAX) and once at an intensity established to require 115% of VO2max (SMAX). Oxygen uptake (VO2) and ventilatory markers were continually recorded during the exercise and respiratory flow-volume loops were measured at rest and during the final 30 s of each minute for both exercise intensities. When compared to MAX exercise, the subjects had higher ventilation and partial pressure of arterial oxygen (PaO2) during the SMAX intensity. Regression analysis for both conditions indicated the levels of PaO2 and oxygen saturation of arterial blood (SaO2) were positively correlated with relative levels of ventilation during exercise. It was apparent that mechanical constraints to ventilate further were not present during the MAX test since the subjects were able to elevate VE during SMAX and attenuate the level of hypoxaemia. This was also confirmed by analysis of the flow volume recordings. These data support the conclusions firstly, that overwhelming mechanical constraints on VE were not present during the MAX exercise, secondly, the subjects exhibiting the most severe hypoxaemia had no consistent relationship with any measure of expiratory flow limitation, and thirdly, ventilatory patterns during intense exercise are strong predictors of blood gas status.
