Burgomaster Kirsten A, Heigenhauser George J F, Gibala Martin J
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada L8S 4K1.
J Appl Physiol (1985). 2006 Jun;100(6):2041-7. doi: 10.1152/japplphysiol.01220.2005. Epub 2006 Feb 9.
Our laboratory recently showed that six sessions of sprint interval training (SIT) over 2 wk increased muscle oxidative potential and cycle endurance capacity (Burgomaster KA, Hughes SC, Heigenhauser GJF, Bradwell SN, and Gibala MJ. J Appl Physiol 98: 1895-1900, 2005). The present study tested the hypothesis that short-term SIT would reduce skeletal muscle glycogenolysis and lactate accumulation during exercise and increase the capacity for pyruvate oxidation via pyruvate dehydrogenase (PDH). Eight men [peak oxygen uptake (VO2 peak)=3.8+/-0.2 l/min] performed six sessions of SIT (4-7x30-s "all-out" cycling with 4 min of recovery) over 2 wk. Before and after SIT, biopsies (vastus lateralis) were obtained at rest and after each stage of a two-stage cycling test that consisted of 10 min at approximately 60% followed by 10 min at approximately 90% of VO2 peak. Subjects also performed a 250-kJ time trial (TT) before and after SIT to assess changes in cycling performance. SIT increased muscle glycogen content by approximately 50% (main effect, P=0.04) and the maximal activity of citrate synthase (posttraining: 7.8+/-0.4 vs. pretraining: 7.0+/-0.4 mol.kg protein -1.h-1; P=0.04), but the maximal activity of 3-hydroxyacyl-CoA dehydrogenase was unchanged (posttraining: 5.1+/-0.7 vs. pretraining: 4.9+/-0.6 mol.kg protein -1.h-1; P=0.76). The active form of PDH was higher after training (main effect, P=0.04), and net muscle glycogenolysis (posttraining: 100+/-16 vs. pretraining: 139+/-11 mmol/kg dry wt; P=0.03) and lactate accumulation (posttraining: 55+/-2 vs. pretraining: 63+/-1 mmol/kg dry wt; P=0.03) during exercise were reduced. TT performance improved by 9.6% after training (posttraining: 15.5+/-0.5 vs. pretraining: 17.2+/-1.0 min; P=0.006), and a control group (n=8, VO2 peak=3.9+/-0.2 l/min) showed no change in performance when tested 2 wk apart without SIT (posttraining: 18.8+/-1.2 vs. pretraining: 18.9+/-1.2 min; P=0.74). We conclude that short-term SIT improved cycling TT performance and resulted in a closer matching of glycogenolytic flux and pyruvate oxidation during submaximal exercise.
我们实验室最近的研究表明，在两周内进行6次冲刺间歇训练（SIT）可提高肌肉氧化能力和骑行耐力（Burgomaster KA, Hughes SC, Heigenhauser GJF, Bradwell SN, and Gibala MJ. J Appl Physiol 98: 1895 - 1900, 2005）。本研究检验了以下假设：短期SIT可减少运动期间骨骼肌糖原分解和乳酸积累，并增加通过丙酮酸脱氢酶（PDH）进行丙酮酸氧化的能力。8名男性[峰值摄氧量（VO2峰值）=3.8±0.2升/分钟]在两周内进行了6次SIT（4 - 7次30秒的“全力”骑行，每次骑行后恢复4分钟）。在SIT前后，在静息状态下以及在两阶段骑行测试的每个阶段后（该测试包括在约60%VO2峰值下骑行10分钟，随后在约90%VO2峰值下骑行10分钟），获取股外侧肌活检样本。受试者在SIT前后还进行了一次250千焦的计时赛（TT），以评估骑行表现的变化。SIT使肌肉糖原含量增加了约50%（主效应，P = 0.04），柠檬酸合酶的最大活性增加（训练后：7.8±0.4对训练前：7.0±0.4摩尔·千克蛋白质-1·小时-1；P = 0.04），但3 - 羟酰基辅酶A脱氢酶的最大活性没有变化（训练后：5.1±0.7对训练前：4.9±0.6摩尔·千克蛋白质-1·小时-1；P = 0.76）。训练后PDH的活性形式更高（主效应，P = 0.04），并且运动期间净肌肉糖原分解（训练后：100±16对训练前：139±11毫摩尔/千克干重；P = 0.03）和乳酸积累（训练后：55±2对训练前：63±1毫摩尔/千克干重；P = 0.03）减少。训练后TT表现提高了9.6%（训练后：15.5±0.5对训练前：17.2±1.0分钟；P = 0.006），而一个对照组（n = 8，VO2峰值=3.9±0.2升/分钟）在未进行SIT的情况下，相隔两周进行测试时，表现没有变化（训练后：18.8±1.2对训练前：18.9±1.2分钟；P = 0.74）。我们得出结论，短期SIT改善了骑行TT表现，并使次最大运动期间糖原分解通量和丙酮酸氧化更紧密匹配。
