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Journal Article
Research Support, Non-U.S. Gov't
Sprint interval training in hypoxia stimulates glycolytic enzyme activity.
Medicine and Science in Sports and Exercise 2013 November
PURPOSE: 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.
METHODS: 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 (MAX nor and TT nor) and hypoxia (MAX hyp and TT hyp). A needle biopsy was taken from musculus vastus lateralis at rest 5-6 d after the last exercise session.
RESULTS: 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 MAX nor (+7%) and MAX hyp (+9%) were slightly increased (P < 0.05), whereas values were constant in NOR. V·O 2max in MAX nor and TT performance in TT nor and TT hyp 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.
CONCLUSION: SIT in hypoxia up-regulated muscle phosphofructokinase activity and the anaerobic threshold more than SIT in normoxia but did not enhance endurance exercise performance.
METHODS: 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 (MAX nor and TT nor) and hypoxia (MAX hyp and TT hyp). A needle biopsy was taken from musculus vastus lateralis at rest 5-6 d after the last exercise session.
RESULTS: 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 MAX nor (+7%) and MAX hyp (+9%) were slightly increased (P < 0.05), whereas values were constant in NOR. V·O 2max in MAX nor and TT performance in TT nor and TT hyp 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.
CONCLUSION: 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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