Limiting Factors of Maximal Oxygen Uptake at Altitude

摘要

Tnhe authors of this interesting article (Calbet andnLundby, 2009) conclude in the abstract that ‘‘hypoxianreduces Vo2max because it limits O2 diffusion in the lung.’’ Innmy opinion they ascribe too little importance to convectionalnpulmonary transport and too much to the diffusion pressurengradient from the lungs to the mitochondria. A main effect ofnaltitude is the reduction of molecule number in each liter ofninspired air. For simplification, consider an ascent to 5500 mnthat reduces barometric pressure to one-half. To transport annequal amount of oxygen into the alveoli as at sea level, thenventilation at BTPS conditions has to be doubled, corresponding to unchanged Ve at STPD. This is clearly impossiblenat high performance levels, such as Vo2max. Even if possible,nthe oxygen pressure in inspired air remains halved, whilenPio2 u0001 Pao2 must be equal to that at sea level for unchangednoxygen uptake. Only an increased ventilation at STPD cannincrease the mass transport of this gas, increasing again Pao2nto partly reestablish the pulmonary diffusion pressure. This isnpossible only at very moderate altitudes during hard exercise.nThe next step, oxygen diffusion from the alveoli into blood,ndepends on the difference between Pao2 and mean capillarynPo2ntimes diffusion capacity. Since the lower limit of venousnPo2 at exhausting exercise (*10 mmHg; Sutton et al., 1988)ncan hardly be reduced, only an increase in diffusion capacity,neither by increasing lung capillary or erythrocyte area, improves oxygen transport. All additional acclimatization effects in the rest of the body are mitigating deleteriousnconsequences of lung failure, but cannot compensate fornthem. Blunting of peak Q is not ‘‘contributing to the limitationnof Vo2max,’’ (Calbet and Lundby, 2009) if all oxygen diffusedninto the blood can be transported.