Plasma leptin and vascular endothelial growth factor (VEGF) in normal subjects at high altitude (5050 m).

CONTEXT: High altitude (HA) is a model of severe hypoxia exposure in humans. We hypothesized that nocturnal hypoxemia or acute maximal exercise at HA might affect plasma leptin and VEGF levels. OBJECTIVES: Plasma leptin, VEGF and other metabolic variables were studied after nocturnal pulse oximetry and after maximal exercise in healthy lowlanders on the 3rd-4th day of stay in Lobuche (5050 m, HA) and after return to sea level (SL). RESULTS: Leptin was similar at SL or HA in both pre- and post-exercise conditions. Pre-exercise VEGF at HA was lower, and cortisol was higher, than at SL, suggesting that nocturnal intermittent hypoxia associated with periodic breathing at HA might affect these variables. CONCLUSIONS: Leptin levels appear unaffected at HA, whereas nocturnal hypoxic stress may affect plasma VEGF. Future HA studies should investigate the possible role of nocturnal intermittent hypoxemia on metabolism.

Exercise intolerance at high altitude (5050 m): critical power and W'.

The relationship between work rate (WR) and its tolerable duration (t(LIM)) has not been investigated at high altitude (HA). At HA (5050 m) and at sea level (SL), six subjects therefore performed symptom-limited cycle-ergometry: an incremental test (IET) and three constant-WR tests (% of IET WR(max), HA and SL respectively: WR(1) 70±8%, 74±7%; WR(2) 86±14%, 88±10%; WR(3) 105±13%, 104±9%). The power asymptote (CP) and curvature constant (W') of the hyperbolic WR-t(LIM) relationship were reduced at HA compared to SL (CP: 81±21 vs. 123±38 W; W': 7.2±2.9 vs. 13.1±4.3 kJ). HA breathing reserve (estimated maximum voluntary ventilation minus end-exercise ventilation) was also compromised (WR(1): 25±25 vs. 50±18 l min(-1); WR(2): 4±23 vs. 38±23 l min(-1); WR(3): -3±18 vs. 32±24 l min(-1)) with near-maximal dyspnea levels (Borg) (WR(1): 7.2±1.2 vs. 4.8±1.3; WR(2): 8.8±0.8 vs. 5.3±1.2; WR(3): 9.3±1.0 vs. 5.3±1.5). The CP reduction is consistent with a reduced O(2) availability; that of W' with reduced muscle-venous O(2) storage, exacerbated by ventilatory limitation and dyspnea.