6.6. Compensatory effects of stretch and exercise

Immobilization and glucocorticoid treatment cause muscle atrophy and loss of muscle proteins. Muscle stretch during immobilization is known to prevent muscle wasting and even induce muscle growth (Goldspink 1977, Savolainen et al. 1988). In the present study, muscle stretch partly prevented muscle atrophy during immobilization in rat plantarflexors: SOL and GM. In these muscles the overall loss of muscle weight was more rapid than in the dorsiflexors: EDL and TA. Stretch also partly prevented most of the changes in mRNA level, prolyl 4-hydroxylase activity and type IV collagen concentration, and totally prevented the increase in proMMP-2 and MMP-2 quantity in plantarflexors. Endurance running completely prevented the loss of muscle weight during dexamethasone treatment in rat SOL, and partially in EDL. This is in accordance with earlier studies on endurance running during glucocorticoid treatment (Hickson & Davis 1981, Seene & Viru 1982, Falduto et al. 1992). Endurance running might be an effective stimulus especially for the slow SOL, whereas interval-type uphill running seems to lack all effects on any of the muscles. Endurance running also partly prevented the increase in type IV collagen concentration in one muscle, while uphill running had no preventive effects on collagen turnover. At first, exercise combined with dexamethasone treatment seemed to be too strenuous for the animals, since their body weights decreased even more than with sole steroid treatment. This negative effect of exercise disappeared when treatments continued for ten days. The prevention of the anti-anabolic changes in skeletal muscle during glucocorticoid treatment is clinically very relevant, since glucocorticoid treatments are commonly used in various conditions, e.g. in the therapy of fibrotic conditions of the liver (Tanner & Powell 1979), lung (Turner-Warwick et al. 1980) and skin (Griffiths 1966), and e.g. organ transplant therapy (Hickson & Marone 1993). For the functional capacity of these patients, it is important to prevent as much as possible the negative changes in muscle tissue.

The utilization of stretch during immobilization in rats seems to have more preventive effects than light exercise during dexamethasone treatment. The exercise might have been too mild to prevent the changes in ECM during the first ten days, although prevention of muscle atrophy was observed. Longer-lasting exercise might have had more effect on the progressive muscle loss. Even though the exercise protocols were light, they probably correlate well to the exercise that can be used as daily exercise in human patients. With more strenuous exercise the effects might have been more pronounced, although their value would have been purely theoretical. However, exercise itself was able to cause increased mRNA level of type IV collagen in SOL, which is in accordance with earlier findings showing that endurance training increases total collagen biosynthesis (Takala et al. 1983), and that even a single bout of strenuous exercise can cause an increase in the mRNA levels of collagens I, III and IV in rat skeletal muscles (Koskinen et al. 2001).

The problem with immobilizing muscles in lengthened positions is the shortening of the antagonist muscles. At least in rat legs, it seems to be most advantageous to use full plantarflexion, since musculoskeletal anatomy causes dorsiflexors to be shortened much less in plantarflexion than plantarflexors in dorsiflexion (Witzmann et al. 1982). Dorsiflexors seem to be able to tolerate the slight shortening, whereas plantarflexors may even benefit from the stretch. This is definitely practical when the ankle is immobilized, and the same idea could be utilized in the immobilization of other joints as well.