Ventilatory capacities at sea level and high altitude.

Because air is less dense at high altitude (HA), airway resistance is reduced and maximum inspiratory and expiratory flows are greater than at sea level (SL). Despite the reduction in airway resistance, ventilatory muscle endurance may be decreased by hypobaric hypoxia and, thus, may be a factor in limiting exercise at HA. To explore the effects of HA on ventilatory capacities and their relation to ventilatory demands of exercise, we measured 15-s maximum voluntary ventilation (MVV), 15-min maximum sustainable ventilation (MSV), and maximum airway pressures (Plmax and PEmax) in 18 healthy young men at SL and HA (Pikes Peak, 4300 m, or hypobaric chamber, PB approximately 460 mmHg). In eight of these subjects ventilatory capacities were compared with exercise ventilations. We also measured the effects of 36% O2 on the MSV in 12 of the subjects exposed to simulated altitude. Similar results were obtained at either simulated or actual HA. We found that MVV increased (p < 0.001) by 20% and the MSV (p < 0.001) by 15% at HA. Administration of 36% O2 at HA increased MSV further by 5% with no effect on MVV. No effect of HA on maximum inspiratory and expiratory pressures was found. We confirmed previous findings of modest increases in forced 1-s expired volume (FEV1) and slight decreases in forced vital capacity (FVC) at HA. At both SL and HA, the MSV exceeded the ventilatory demands of submaximal cycle exercise that could be sustained for about 30 min. During progressive cycle exercise to exhaustion, however, peak VE was not different from MVV, either at SL or HA. We conclude that the small, but significant, increase in MSV with 36% O2 administration at HA suggests that hypoxia decreases ventilatory endurance for flow loads as determined by the MSV. Thus, the possibility that ventilatory limits have a role in cessation of exercise at high altitude cannot be ruled out.