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Long-term metabolic and skeletal muscle adaptations to short-sprint training: implications for sprint training and tapering.

机译:长期代谢和骨骼肌对短跑训练的适应性:对短跑训练和渐缩的影响。

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The adaptations of muscle to sprint training can be separated into metabolic and morphological changes. Enzyme adaptations represent a major metabolic adaptation to sprint training, with the enzymes of all three energy systems showing signs of adaptation to training and some evidence of a return to baseline levels with detraining. Myokinase and creatine phosphokinase have shown small increases as a result of short-sprint training in some studies and elite sprinters appear better able to rapidly breakdown phosphocreatine (PCr) than the sub-elite. No changes in these enzyme levels have been reported as a result of detraining. Similarly, glycolytic enzyme activity (notably lactate dehydrogenase, phosphofructokinase and glycogen phosphorylase) has been shown to increase after training consisting of either long (>10-second) or short (<10-second) sprints. Evidence suggests that these enzymes return to pre-training levels after somewhere between 7 weeks and 6 months of detraining. Mitochondrial enzyme activity also increases after sprint training, particularly when long sprints or short recovery between short sprints are used as the training stimulus. Morphological adaptations to sprint training include changes in muscle fibre type, sarcoplasmic reticulum, and fibre cross-sectional area. An appropriate sprint training programme could be expected to induce a shift toward type IIa muscle, increase muscle cross-sectional area and increase the sarcoplasmic reticulum volume to aid release of Ca(2+). Training volume and/or frequency of sprint training in excess of what is optimal for an individual, however, will induce a shift toward slower muscle contractile characteristics. In contrast, detraining appears to shift the contractile characteristics towards type IIb, although muscle atrophy is also likely to occur. Muscle conduction velocity appears to be a potential non-invasive method of monitoring contractile changes in response to sprint training and detraining. In summary, adaptation to sprint training is clearly dependent on the duration of sprinting, recovery between repetitions, total volume and frequency of training bouts. These variables have profound effects on the metabolic, structural and performance adaptations from a sprint-training programme and these changes take a considerable period of time to return to baseline after a period of detraining. However, the complexity of the interaction between the aforementioned variables and training adaptation combined with individual differences is clearly disruptive to the transfer of knowledge and advice from laboratory to coach to athlete.
机译:肌肉对冲刺训练的适应性可以分为代谢和形态变化。酶适应是短跑训练的主要新陈代谢适应,所有三个能量系统的酶都显示出适应训练的迹象,并且有一些证据表明训练后恢复到基线水平。在一些研究中,由于短跑训练的结果,肌激酶和肌酸磷酸激酶的增加很小,精英短跑运动员似乎比次精英更能迅速分解磷酸肌酸(PCr)。由于失调,这些酶水平没有变化的报道。类似地,在经过长冲刺(> 10秒)或短冲刺(<10秒)训练后,糖酵解酶的活性(尤其是乳酸脱氢酶,磷酸果糖激酶和糖原磷酸化酶)已显示出增加。有证据表明,这些酶经过7周至6个月的减量训练后恢复到训练前的水平。短跑训练后,线粒体酶的活性也增加,特别是当长冲刺或短冲刺之间的短暂恢复用作训练刺激时。冲刺训练的形态适应包括肌肉纤维类型,肌浆网和纤维横截面积的变化。适当的冲刺训练计划可能会导致向IIa型肌肉转移,增加肌肉截面积和增加肌浆网体积以帮助释放Ca(2+)。然而,冲刺训练的训练量和/或频率超过对个人最佳的训练次数和/或频率,将导致向较慢的肌肉收缩特性的转变。相反,尽管肌肉萎缩也很可能发生,但训练似乎会使收缩特性向IIb型转移。肌肉传导速度似乎是一种潜在的非侵入性方法,用于监测对冲刺训练和训练的收缩变化。总之,对冲刺训练的适应显然取决于冲刺的持续时间,重复之间的恢复,总训练次数和次数。这些变量对冲刺训练程序的代谢,结构和性能适应具有深远影响,经过一段时间的训练后,这些变化需要相当长的时间才能恢复到基线。但是,上述变量与训练适应之间相互作用的复杂性以及个体差异显然会破坏从实验室到教练再到运动员的知识和建议的传递。

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