Chronic intermittent hypoxia and incremental cycling exercise independently depress muscle in vitro maximal Na+-K+-ATPase activity in well-trained athletes

Athletes commonly attempt to enhance performance by training in normoxia but sleeping in hypoxia [live high and train low (LHTL)]. However, chronic hypoxia reduces muscle Na⁺-K⁺-ATPase content, whereas fatiguing contractions reduce Na⁺-K⁺-ATPase activity, which each may impair performance. We examined whether LHTL and intense exercise would decrease muscle Na⁺-K⁺-ATPase activity and whether these effects would be additive and sufficient to impair performance or plasma K⁺ regulation. Thirteen subjects were randomly assigned to two fitness-matched groups, LHTL (n = 6) or control (Con, n = 7). LHTL slept at simulated moderate altitude (3,000 m, inspired O₂ fraction = 15.48%) for 23 nights and lived and trained by day under normoxic conditions in Canberra (altitude ~600 m). Con lived, trained, and slept in normoxia. A standardized incremental exercise test was conducted before and after LHTL. A vastus lateralis muscle biopsy was taken at rest and after exercise, before and after LHTL or Con, and analyzed for maximal Na⁺-K⁺-ATPase activity [K⁺-stimulated 3-O-methylfluorescein phosphatase (3-O-MFPase)] and Na⁺-K⁺-ATPase content ([³H]ouabain binding sites). 3-O-MFPase activity was decreased by –2.9 ± 2.6% in LHTL (P < 0.05) and was depressed immediately after exercise (P < 0.05) similarly in Con and LHTL (–13.0 ± 3.2 and –11.8 ± 1.5%, respectively). Plasma K⁺ concentration during exercise was unchanged by LHTL; [3H]ouabain binding was unchanged with LHTL or exercise. Peak oxygen consumption was reduced in LHTL (P < 0.05) but not in Con, whereas exercise work was unchanged in either group. Thus LHTL had a minor effect on, and incremental exercise reduced, Na⁺-K⁺-ATPase activity. However, the small LHTL-induced depression of 3-O-MFPase activity was insufficient to adversely affect either K⁺ regulation or total work performed.

Modeling intermittent cycling performance in hypoxia using the critical power concept

PURPOSE: This study investigated the efficacy of an intermittent critical power model, termed the "work-balance" (W'BAL) model, during high-intensity exercise in hypoxia. METHODS: Eleven trained, male cyclists (mean ± SD; age 27 ± 6.6 yr, V[Combining Dot Above]O2peak 4.79 ± 0.56 L.min) completed a maximal ramp test and a 3 min "all-out" test to determine critical power (CP) and work performed above CP (W'). On another day an intermittent exercise test to task failure was performed. All procedures were performed in normoxia (NORM) and hypoxia (HYPO; FiO2 ≈ 0.155) in a single-blind, randomized and counter-balanced experimental design. The W'BAL model was used to calculate the minimum W' (W'BALmin) achieved during the intermittent test. W'BALmin in HYPO was also calculated using CP + W' derived in NORM (N+H). RESULTS: In HYPO there was an 18% decrease in V[Combining Dot Above]O2peak (4.79 ± 0.56 vs 3.93 ± 0.47 L.min ; P<0.001) and a 9% decrease in CP (347 ± 45 vs 316 ± 46 W; P<0.001). No significant change for W' occurred (13.4 ± 3.9 vs 13.7 ± 4.9 kJ; P=0.69; NORM vs HYPO). The change in V[Combining Dot Above]O2peak was significantly correlated with the change in CP (r = 0.72; P=0.01). There was no difference between NORM and HYPO for W'BALmin (1.1 ± 0.9 kJ vs 1.2 ± 0.6 kJ). The N+H analysis grossly overestimated W'BALmin (7.8 ± 3.4 kJ) compared with HYPO (P<0.001). CONCLUSION: The W'BAL model produced similar results in hypoxia and normoxia, but only when model parameters were determined under the same environmental conditions as the performance task. Application of the W'BAL model at altitude requires a modification of the model, or that CP and W' are measured at altitude.