Sprint Interval Training in Hypoxia Stimulates Glycolytic Enzyme Activity

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In this study, we compared the effect of sprint interval training (SIT) in normoxia versus hypoxia on muscle glycolytic and oxidative capacity, monocarboxylate transporter content, and endurance exercise performance.


Healthy male volunteers (18–30 yr) performed 6 wk of SIT on a cycling ergometer (30-s sprints vs 4.5-min rest intervals; 3 d·wk−1) in either normobaric hypoxia (HYP, FiO2 = 14.4%, n = 10) or normoxia (NOR, FiO2 = 20.9%, n = 9). The control group did not train (CON, n = 10). Training load was increased from four sprints per session in week 1 to nine sprints in week 6. Before and after SIT, subjects performed a maximal incremental exercise test plus a 10-min simulated time trial on a cycle ergometer in both normoxia (MAXnor and TTnor) and hypoxia (MAXhyp and TThyp). A needle biopsy was taken from musculus vastus lateralis at rest 5–6 d after the last exercise session.


SIT increased muscle phosphofructokinase activity more in HYP (+59%, P < 0.05) than that in NOR (+17%), whereas citrate synthase activity was similar between groups. Compared with the pretest, power outputs corresponding to 4 mmol blood lactate in HYP during MAXnor (+7%) and MAXhyp (+9%) were slightly increased (P < 0.05), whereas values were constant in NOR. V˙O2max in MAXnor and TT performance in TTnor and TThyp were increased by ∼6%–8% (P < 0.05) in either group. The training elevated monocarboxylate transporter 1 protein content by ∼70% (P < 0.05). In CON, all measurements were constant throughout the study.


SIT in hypoxia up-regulated muscle phosphofructokinase activity and the anaerobic threshold more than SIT in normoxia but did not enhance endurance exercise performance.

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