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, ventila tory muscle endurance may be decreased by hypobaric hypoxia and, thus, may be a factor in limiting exercise at HA. To explore the effects oi HA on ventilatory capacities and their relation to ventilatory demand s of exercise, we measured 15-s maximum voluntary ventilation (MVV), 1 5-min maximum sustainable ventilation (MSV), and maximum airway pressu res (PImax and PEmax) in 18 healthy young men at SL and HA (Pikes Peak , 4300 m, or hypobaric chamber, PB similar to 460 mmHg). In eight of t hese subjects ventilatory capacities were compared with exercise venti lations. We also measured the effects of 36% O-2 on the MSV in 12 of t he subjects exposed to simulated altitude. Similar results were obtain ed at either simulated or actual HA. We found that MW increased (p < 0 .001) by 20% and the MSV (p < 0.001) by 15% at HA. Administration of 3 6% O-2 at HA increased MSV further by 5% with no effect on MVV. No eff ect of HA on maximum inspiratory and expiratory pressures was found. W e confirmed previous findings of modest increases in forced 1-s expire d volume (FEV1) and slight decreases in forced vital capacity (FVC) at HA. At both SL and HA, the MSV exceeded the ventilatory demands or su bmaximal cycle exercise that could be sustained for about 30 min. Duri ng progressive cycle exercise to exhaustion, however, peak (V) over do t E was not different from MW, either at SL or HA. We conclude that th e small, but significant, increase in MSV with 36% O-2 administration at HA suggests that hypoxia decreases ventilatory endurance for flow l oads 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.