Abernethy P J, Jürimäe J, Logan P A, Taylor A W, Thayer R E
Department of Human Movement Studies, University of Queensland, Brisbane, Australia.
Sports Med. 1994 Jan;17(1):22-38. doi: 10.2165/00007256-199417010-00003.
Skeletal muscle tissue is sensitive to the acute and chronic stresses associated with resistance training. These responses are influenced by the structure of resistance activity (i.e. frequency, load and recovery) as well as the training history of the individuals involved. There are histochemical and biochemical data which suggest that resistance training alters the expression of myosin heavy chains (MHCs). Specifically, chronic exposure to bodybuilding and power lifting type activity produces shifts towards the MHC I and IIb isoforms, respectively. However, it is not yet clear which training parameters trigger these differential expressions of MHC isoforms. Interestingly, many programmes undertaken by athletes appear to cause a shift towards the MHC I isoform. Increments in the cross-sectional area of muscle after resistance training can be primarily attributed to fibre hypertrophy. However, there may be an upper limit to this hypertrophy. Furthermore, significant fibre hypertrophy appears to follow the sequence of fast twitch fibre hypertrophy preceding slow twitch fibre hypertrophy. Whilst some indirect measures of fibre number in living humans suggest that there is no interindividual variation, postmortem evidence suggests that there is. There are also animal data arising from investigations using resistance training protocols which suggest that chronic exercise can increase fibre number. Furthermore, satellite cell activity has been linked to myotube formation in the human. However, other animal models (i.e. compensatory hypertrophy) do not support the notion of fibre hyperplasia. Even if hyperplasia does occur, its effect on the cross-sectional area of muscle appears to be small. Phosphagen and glycogen metabolism, whilst important during resistance activity appear not to normally limit the performance of resistance activity. Phosphagen and related enzyme adaptations are affected by the type, structure and duration of resistance training. Whilst endogenous glycogen reserves may be increased with prolonged training, typical isotonic training for less than 6 months does not seem to increase glycolytic enzyme activity. Lipid metabolism may be of some significance in bodybuilding type activity. Thus, not surprisingly, oxidative enzyme adaptations appear to be affected by the structure and perhaps the modality of resistance training. The dilution of mitochondrial volume and endogenous lipid densities appears mainly because of fibre hypertrophy.
骨骼肌组织对与抗阻训练相关的急性和慢性应激敏感。这些反应受抗阻活动的结构（即频率、负荷和恢复情况）以及相关个体的训练史影响。有组织化学和生化数据表明，抗阻训练会改变肌球蛋白重链（MHCs）的表达。具体而言，长期进行健美和力量举类型的活动分别会使表达向MHC I和IIb亚型转变。然而，尚不清楚哪些训练参数会引发MHC亚型的这些差异表达。有趣的是，运动员进行的许多训练计划似乎会使表达向MHC I亚型转变。抗阻训练后肌肉横截面积的增加主要归因于纤维肥大。然而，这种肥大可能存在上限。此外，明显的纤维肥大似乎遵循快肌纤维肥大先于慢肌纤维肥大的顺序。虽然对活体人类纤维数量的一些间接测量表明个体间没有差异，但尸检证据表明存在差异。也有使用抗阻训练方案进行调查得出的动物数据表明，长期运动可增加纤维数量。此外，卫星细胞活性与人类肌管形成有关。然而，其他动物模型（即代偿性肥大）并不支持纤维增生的观点。即使发生增生，其对肌肉横截面积的影响似乎也很小。磷酸原和糖原代谢在抗阻活动中虽很重要，但通常似乎不会限制抗阻活动的表现。磷酸原和相关酶的适应性受抗阻训练的类型、结构和持续时间影响。虽然长期训练可能会增加内源性糖原储备，但典型的等张训练少于6个月似乎不会增加糖酵解酶活性。脂质代谢在健美类型的活动中可能具有一定意义。因此，毫不奇怪，氧化酶的适应性似乎受抗阻训练的结构影响，或许还受其方式影响。线粒体体积和内源性脂质密度的稀释主要是由于纤维肥大。
