ACUTE AND CHRONIC RESPONSE OF SKELETAL-MUSCLE TO RESISTANCE EXERCISE

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 recove ry) 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). Specific ally, chronic exposure to bodybuilding and power lifting type activity produces shifts towards the MHC I and IIb isoforms, respectively. How ever, it is not yet clear which training parameters trigger these diff erential expressions of MHC isoforms. Interestingly, many programmes u ndertaken by athletes appear to cause a shift towards the MHC I isofor m. Increments in the cross-sectional area of muscle after resistance t raining can be primarily attributed to fibre hypertrophy. However, the re 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 indi rect measures of fibre number in living humans suggest that there is n o interindividual variation, postmortem evidence suggests that there i s. There are also animal data arising from investigations using resist ance training protocols which suggest that chronic exercise can increa se 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 hyperplas ia. 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 l imit the performance of resistance activity. Phosphagen and related en zyme adaptations are affected by the type, structure and duration of r esistance training. Whilst endogenous glycogen reserves may be increas ed with prolonged training, typical isotonic training for less than 6 months does not seem to increase glycolytic enzyme activity. Lipid met abolism may be of some significance in body building type activity. Th us, not surprisingly, oxidative enzyme adaptations appear to be affect ed by the structure and perhaps the modality of resistance training. T he dilution of mitochondrial volume and endogenous lipid densities app ears mainly because of fibre hypertrophy.