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Female Wistar strain rats were swim trained six hours/day, five days/week, for eight weeks. Animals were sacrificed after 2, 4, 6, or 8 weeks of training, or after 8 weeks of training followed by 7, 14, or 21 days of detraining. The red vastus and soleus muscles were removed and assayed for succinate dehydrogenase (SDH) levels.. Sedentary rats were sacrificed during the detraining time period to provide control values of SDH activity in the two muscles. The SDH values of the red vastus muscle were significantly higher than those obtained from the controls after eight weeks of training, but higher in the soleus by six weeks of training. These elevated levels of SDH were maintained for at least seven days after training ceased in both muscles. By the 14th day of detraining, SDH levels of both muscles had dropped drastically, but were still significantly higher than control values. After 21 days of detraining the SDH levels of the two muscles were only slightly lower than those obtained after 14 days of detraining.The results indicate that:1) there is no loss in the training-induced increased oxidative capacity of the muscle following seven days of inactivity, and 2) there was a significant loss in this training effect by 14 days, though a total loss was not observed even after 21 days of detraining. These results should be of interest to people who train at a moderate intensity and must miss a series of training sessions due to injury or illness.

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Previous reports of the effects of tetrodotoxin (TTX)-induced muscular disuse have demonstrated alterations in muscle force, speed, and fatiguability that might suggest changes in the quality of contractile proteins. These studies were extended to the effects of TTX-induced disuse on the Ca$ sp{2+}$-activation characteristics of myofibrillar ATPase of the rat gastrocnemius. Atrophic responses after TTX treatment were as previously reported with a significant decrease in left gastrocnemius weight (g) compared to the control-pump (C) group (1.25 $ pm$ 0.04 for C vs 0.72 $ pm$ 0.04 for TTX, X $ pm$ SEM, p $ leq$ 0.01). Myofibrillar protein yield (mg$ cdot$g$ sp{-1}$ wet weight) was also depressed (92.8 $ pm$ 4.6 for C vs 70.3 $ pm$ 3.7 for TTX; p $ leq$ 0.01). Maximum ATPase of myofibrils (nmol Pi$ cdot$mg$ sp{-1} cdot$min$ sp{-1}$) was decreased (424 $ pm$ 46 for C vs 199 $ pm$ 27 for TTX, p $ leq$ 0.01). Furthermore, the Hill n which reflects the cooperative aspects of Ca$ sp{2+}$-activation of the myofibrillar ATPase was significantly depressed (1.58 $ pm$ 0.07 for C vs 1.29 $ pm$ 0.09 for TTX; p $ leq$ 0.05) after TTX treatment. The results of the present study suggest that muscle perturbations that result from TTX-induced disuse are at least partially related to changes in the myofibrillar fraction.

Typescript. / Thesis (Ph. D.)--University of Hawaii, 1970. / Bibliography: leaves [74]-79. / viii, 79 l illus., charts, tables