Effects of exercise training on acclimatization to hypoxia: systemic O2 transport during maximal exercise

摘要

Acclimatization to prolonged hypoxia results in the downregulation of myocardial p adrenoceptors dollar-AR) reduced maximal heart rate (Hr_(max) and cardiac output ( Q_(max)) and little or no change in maximal O2 uptake ( Vo_(2max) ). Hypoxia-induced downregulation of beta-AR is attenuated by exercise training (ET). This study tested the hypothesis that the attenuation of beta-AR downregulation by ET results in a higher Hr_(max), Q_(max) and Vo_(2max) in trained than in sedentary, acclimatized rats. After 3 weeks of treadmill training, male rats either underwent acclimatization to PI_(O2) 70 Torr for 10 days (AT), or remained in normoxia (NAT). Controls were acclimatized sedentary (AS) and non-acclimatized rats (NAS) rats. All rats exercised maximally in normoxia and in hypoxia (PIo2 70 Torr). During normoxic exercise, Vo2nm (ml/(min-kg)) was 95.8+-1.0 in AT; 87.7+- 1.7 in NAT (p<0.05); 72.5+- 1.2 in NAS (p<0.05) and 74.2+-1.4 in AS (p>0.05 AS vs. NAS). A similar distribution of Vtamax values occurred in hypoxic exercise. ET prevented the decrease in Hrmax and contributed to maintaining Qmax after acclimatization: Qmax was similar in AT and NAT, intermediate in NAS, and lowest in AS. The preservation of Qm of AT, coupled with higher arterial blood content (CaO2), resulted in AT having the highest rate of convective blood O2 delivery ( To2max = Qmax -CaCy and contributed to the elevated Vo2max values observed in this set. Our results indicate that attenuation of beta-AR downregulation by ET contributes to maintainingpreserve CW and Vo2max after acclimatization, suggesting that p-AR downregulation plays a key important role in limiting Vo2max after acclimatization.