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Acute incremental exercise, sprint exercise, as well as chronic intermittent hypoxia each decrease muscle Na+K+ATPase activity

R.J. Aughey1, J.A. Hawley2, C.J. Gore3, A.G. Hahn3, D.T. Martin3, S.A. Clark2, N.E. Townsend3, T. Kinsman3, M.J. Ashenden3, K.E. Fallon3, G.J. Slater3, A.P. Garnham4, C.M. Chow5 and M.J. McKenna1, 1Centre for Rehabilitation, Exercise and Sports Science, Victoria University of Technology, Melbourne, 2RMIT University, Melbourne, 3Australian Institute of Sport, Canberra, 4Deakin University, Melbourne, and 5University of Sydney, NSW 2006, Australia.

The Na+K+ATPase enzyme is vital in maintaining skeletal muscle excitability. Athletes commonly use hypoxic exposure to improve athletic performance, favouring the live high, train low approach (LHTL). Paradoxically, muscle Na+K+ATPase content is reduced by chronic hypoxia (Fraser et al., 2002), which would be expected to reduce muscle performance. Muscle maximal Na+K+ATPase activity is also decreased with fatiguing single-leg kicking exercise (Fraser et al., 2002), although the effects of acute intense cycle exercise are unknown. We therefore investigated the effects of acute incremental and sprint exercise and of LHTL on muscle Na+K+ATPase activity and exercise performance.

Two studies were performed, where control subjects slept and trained in Canberra (altitude ∼600m), whilst the LHTL groups slept in a hypoxic room (study 1, 3000m for 23-nights; study 2, 2650 m for 20-n), and trained at 600m. In study 1, 13 endurance athletes were assigned to either a control (CON, n=6) or LHTL group (n=7). In study 2, 21 endurance athletes were assigned to a control (CON2, n=7), 20 consecutive night LHTL (LHTLc, n=7), or an intermittent 20 night LHTL (LHTLi, 4 x [5-n LHTL then 2-n CON]) group. The lower simulated altitude and intermittent exposure in study 2 were used to reflect common athletic practice. A vastus lateralis muscle biopsy was taken at rest and immediately after incremental exercise prior to (Pre) & after (Post) 23-n of LHTL (study 1); and at rest and immediately after ∼1-min sprint exercise prior to (Pre) and after (Post) 20-n LHTL (study 2.) The timecourse of adaptation was investigated in study 2 via an additional rest and post sprint exercise muscle biopsy taken after 5-n of LHTL. Muscle was analysed for maximal in vitro Na+K+ATPase (K+ stimulated, 3-O-MFPase) activity. Arterialised venous plasma [K+] was analysed during and following incremental (study 1) and sprint exercise (study 2).

Muscle 3-O-MFPase activity was depressed to a similar extent after both incremental (-12.4±0.8%, study 1, exercise effect, P<0.05) and sprint exercise (-12.3±0.5%, study 2, exercise effect, P<0.05). In study 1, the change in resting 3-O-MFPase activity (Pre Post) was greater in LHTL (-2.9±1.1%, P<0.05) than CON (0.4±0.5%, NS). In study 2, resting muscle 3-O-MFPase was also reduced from Pre to Day 5 in both LHTLc and LHTLi groups (-2.1±0.4% and -2.3±0.2% respectively, P<0.05), but was unchanged in CON (0.3±0.9%, NS). Resting 3-O-MFPase activity (Day 5 Post) was unchanged in LHTLc and CON (-0.8±0.7% and 0.5±0.6 respectively, NS), but was reversed and increased in LHTLi (3.5±1.2%). The Pre - Post change in resting 3-O-MFPase activity was lowered in LHTLc (-2.9±0.7%, P<0.05), remained unchanged in CON (0.8±1.0%), but tended to increase in LHTLi (1.1 ± 1.2%). Plasma [K+] rose with exercise and then declined post-exercise (P<0.05) in each study, but was unchanged by LHTL, LHTLc and LHTLi (data not shown).

In conclusion, markedly different exercise regimes each acutely depressed skeletal muscle maximal Na+K+ATPase activity, with no residual effect evident after 5d recovery. This effect was reproducible, suggesting an obligatory response to heavy exercise. LHTL at 3000m for 23-n, and at 2650m for 20-n each induced only a small reduction in resting Na+K+ATPase activity, which was reversed with inclusion of normoxic nightly exposure. In contrast to continuous hypoxic exposure, LHTL caused only a small depression in Na+K+ATPase activity. This was insufficient to adversely affect muscle performance or plasma K+ regulation, but may be energetically advantageous and might explain why exercise performance is not impaired with LHTL.

Fraser, S.F., Li, J.L., Carey, M.F., Wang, X.N., Sangkabutra, T., Sostaric, S., Selig, S.E., Kjeldsen, K. & McKenna, M.J. (2002) Journal of Applied Physiology, 93, 1650-1659.

Green, H., Roy, B., Grant, S., Burnett, M., Tupling, R., Otto, C., Pipe, A. & McKenzie, D. (2000) Journal of Applied Physiology, 88, 634-640.

This work was partially funded by an Australian Research Council SPIRT grant (C00002552).