Ross A, Leveritt M
School of Human Movement Studies, University of Queensland, St Lucia, Queensland, Australia.
Sports Med. 2001;31(15):1063-82. doi: 10.2165/00007256-200131150-00003.
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.
肌肉对短跑训练的适应性可分为代谢变化和形态变化。酶的适应性是对短跑训练的主要代谢适应，所有三种能量系统的酶都显示出对训练的适应性迹象，并且有一些证据表明在停止训练后会恢复到基线水平。在一些研究中，短跑训练后肌激酶和肌酸磷酸激酶略有增加，精英短跑运动员似乎比次精英运动员更能快速分解磷酸肌酸（PCr）。停止训练后，这些酶的水平未见变化。同样，无论是长距离（>10秒）还是短距离（<10秒）短跑训练后，糖酵解酶活性（特别是乳酸脱氢酶、磷酸果糖激酶和糖原磷酸化酶）都有所增加。有证据表明，在停止训练7周至6个月后，这些酶会恢复到训练前的水平。短跑训练后线粒体酶活性也会增加，尤其是当长距离短跑或短距离短跑间的短恢复时间用作训练刺激时。对短跑训练的形态学适应包括肌纤维类型、肌浆网和纤维横截面积的变化。一个合适的短跑训练计划有望促使向IIa型肌肉转变，增加肌肉横截面积并增加肌浆网体积以帮助钙离子（Ca2+）释放。然而，超过个体最佳量的短跑训练量和/或频率会导致向较慢的肌肉收缩特性转变。相比之下，停止训练似乎会使收缩特性向IIb型转变，尽管也可能发生肌肉萎缩。肌肉传导速度似乎是监测对短跑训练和停止训练反应的收缩变化一种潜在的非侵入性方法。总之，对短跑训练的适应显然取决于短跑的持续时间、重复间的恢复、训练总量和频率。这些变量对短跑训练计划的代谢、结构和性能适应有深远影响，并且在一段时间的停止训练后，这些变化需要相当长的时间才能恢复到基线水平。然而，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不利于知识和建议从实验室向教练再向运动员的传递。
