Extent of expiratory flow limitation influences the increase in maximal exercise ventilation in hypoxia

Abstract

Increasing ventilation ($\text{V}\text{̇}$e) during hypoxic exercise may help to defend arterial O₂ saturation (Sa_O2) and , however, many athletes experience limitations to ventilatory flow and are not able to increase $\text{V}\text{̇}$e at high workrates. Five of 19 highly trained endurance athletes screened had <5% of their tidal flow–volume loop during maximal exercise meet the boundary set by their maximal resting flow–volume loop. These five athletes were grouped as non-flow limited and compared to the five athletes who demonstrated the greatest percent of tidal volume flow limitation (56±11%) during maximal exercise (flow limited). Each athlete completed two incremental treadmill tests to exhaustion: normoxia and hypoxia (Fi_O2=0.187). Non-flow limited athletes increased $\text{V}\text{̇}$e at from normoxia to hypoxia (140.9±13.4 vs. 154.7±11.9 L/min, P<0.05), while flow limited athletes did not (159.5±9.4 vs. 162.3±6.0 L/min). The decline in Sa_O2 at from normoxia to hypoxia was not significantly different between groups. We conclude that athletes with little or no expiratory flow limitation are able to increase $\text{V}\text{̇}$e during maximal exercise in mild hypoxia, compared to athletes with significantly higher degrees of mechanical limitation. However this ‘mechanical ventilatory reserve’ does not appear to influence the ability to defend Sa_O2 or during maximal exercise in mild hypoxia.

Introduction

It has been hypothesized that a marked increase in ventilation is vital in defending arterial O₂ partial pressure (Pa_O2) and maximal oxygen uptake () during endurance exercise in hypoxia (Lawler et al., 1988, Sutton et al., 1988). Untrained individuals appear to be able to increase both minute ventilation ($\text{V}\text{̇}$e) and the ventilatory equivalent for O₂ ($\text{V}\text{̇}$e/) during maximal exercise in hypoxia compared to normoxia (Lawler et al., 1988, Gavin et al., 1998). However, the ventilatory requirement of highly trained endurance athletes during heavy exercise is reported to be substantially greater than the ventilation required by untrained individuals (Dempsey, 1986). Therefore, the endurance athlete may have little reserve to increase $\text{V}\text{̇}$e during exercise in hypoxia, and indeed many highly trained athletes reach some magnitude of mechanical limitation to ventilatory flow at (Grimby et al., 1971, Johnson et al., 1992, Norton et al., 1995).

The consequences of ventilatory flow limitations on maximal oxygen uptake and exercise performance in endurance trained athletes are only beginning to be understood. An inadequate hyperventilatory response to heavy exercise appears to contribute to the pulmonary gas exchange limitations and reduced arterial oxyhemoglobin saturation (Sa_O2) values seen in many endurance trained athletes (Dempsey et al., 1984, Harms and Stager, 1995). While a reduced alveolar P_O2 (Pa_O2) has been associated with exercise induced arterial hypoxemia at sea level and directly influences Pa_O2 (Powers et al., 1989, Harms and Stager, 1995), a widened alveolar–arterial O₂ difference has been offered as the primary factor underlying the reduced exercise Pa_O2 and Sa_O2 (Dempsey et al., 1984, Dempsey, 1986, Johnson et al., 1992). However, during exercise in hypoxia, maximizing Pa_O2 may be the only means to directly defend Pa_O2 and . Therefore, athletes who have little or no expiratory flow limitation during maximal exercise may have a distinct advantage during exercise in hypoxia over those athletes who display gross limitations to flow.

The purpose of this investigation was to determine if the extent of expiratory flow limitation influenced the response of maximal exercise ventilation to a hypoxic stimulus. Specifically, we examined the ventilatory responses to hypoxia in separate groups of endurance trained athletes displaying high and low degrees of expiratory flow limitation at . Additionally, we asked if the degree of expiratory flow limitation influenced the ability to maximize Sa_O2 and defend during exercise in acute mild hypoxia. Our working hypothesis predicted that athletes who display little or no flow limitation during maximal exercise would have a greater ability to increase $\text{V}\text{̇}$e and defend Pa_O2 (and ultimately Sa_O2) in mild hypoxia, compared to athletes displaying marked flow limitation.