Previous studies suggest that fast-twitch skeletal muscle overloaded by surgical removal of synergists contains a greater percent of slow-twitch fibers than normal muscle. Therefore we examined subcellular systems known to represent biochemical properties of slow-twitch skeletal muscle by measuring myosin ATPase, Ca2+ regulation of myofibril ATPase, Ca2+ uptake of sarcoplasmic reticulum (SR), and marker enzymes of glycogenolysis in normal soleus (NS) and in normal (NP) and surgically overloaded (OP) plantaris muscles of adult female rats. The OP muscles were 65% larger than NP muscles (P less than 0.001). Specific activity of myosin and myofibril ATPase was approximately 25% lower in OP compared with NP muscle (P less than 0.05). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of myosin revealed the presence of more slow and less fast myosin light-chain components in OP muscles. Although SR of NP muscle took up more Ca2+ than OP muscle during the initial for both groups. Marker regulatory enzymes of glycogenolysis collectively were reduced by 40% in OP compared with NP muscle (P less than 0.001). Collectively the data are consistent with the concept that some muscle fiber types were converted from "fast" to "slow" in the OP muscle.

We determined the effects of surgically induced functional overload (O) on rodent fast-twitch plantaris (P) and slow-twitch soleus (S) skeletal muscle substrate oxidative capacity. Compared with normal control muscles of weight-matched rats, bilateral overload produced 68 and 23% increases in the wet weight of OP and OS muscles, respectively (p less than 0.05). Total protein concentrations of the O muscles remained unchanged relative to controls. The enzymatic capacity to oxidize pyruvate, palmitate, and alpha-glycerophosphate was unchanged in OP muscles relative to controls. Certain ketone oxidative enzyme markers were increased in the whole as well as in the inner "red" and outer "white" regions of OP muscle. Citrate synthase activity (a marker for tricarboxylic acid cycle oxidative capacity) was decreased in the whole and in the red region but unchanged in the white region of OP muscles. In contrast, the above measurements were significantly decreased in the OS muscles compared with controls (p less than 0.05). These findings suggest that there is both an expansion and a change in composition of the mitochondrial pool of enlarged P muscle. The effects on OS muscle, however, suggest the possibility that the oxidative capacity is not altered parallel with the enlargement, although fibre-typing (fast-twitch to slow-twitch) changes and altered mitochondrial composition could also contribute in part to the change.

This study was designed to test the hypothesis that rats trained with marked reductions in exercise heart rate respond with adaptations indicative of increased intrinsic myocardial performance. Therefore, we measured changes in maximum work capacity (VO2max), biochemical-functional indexes of cardiac contractile capacity, and skeletal muscle oxidative capacity in normal-trained (NT) rats and in rats trained while receiving the selective cardiac beta 1-blocking drug atenolol (AT). Training consisted of treadmill running at approximately 80% VO2max (untrained) for 1-h duration, 6 days/wk, for a total of 8 wk. Exercise heart rate of the AT group was markedly reduced and averaged 140 beats/min below the NT group for any given session. Compared with sedentary controls, VO2max was increased by 11%, and red vastus lateralis muscle citrate synthase activity was increased by 28% in both AT and NT groups (P less than 0.05). There were no differences between trained and nontrained groups with regard to Ca2+-regulated myofibril adenosinetriphosphatase. In situ derived left ventricular pressure and the maximum rate of left ventricular pressure development were not augmented relative to sedentary control values when the trained hearts were either stimulated inotropically or maximally afterloaded . These findings suggest that maximum exercise capacity can be enhanced in rodents conditioned with and without limited elevation in exercise heart rate; however, this reduction of exercise heart rate acceleration does not provide a stimulus to enhance the intrinsic functional capacity of the rodent heart.

Monosodium Glutamate (MSG) is used as flavour enhancer, with potential beneficial effects due to its nutritional value. Given the decline in kidney functions during aging, we investigated the impact of MSG voluntary intake on the kidney of male mice, aged 6 or 18 months. For 2 months, they freely consumed water (control group), sodium chloride (0.3% NaCl) or MSG (1% MSG) in addition to standard diet. Young animals consuming sodium chloride presented signs of proteinuria, hyperfiltration, enhanced expression and excretion of Aquaporin 2 and initial degenerative reactions suggestive of fibrosis, while MSG-consuming mice were similar to controls. In old mice, aging-related effects including proteinuria and increased renal corpuscle volume were observed in all groups. At an advanced age, MSG caused no adverse effects on the kidney compared to controls, despite the presence of a sodium moiety, similar to sodium chloride. These data show that prolonged MSG intake in mice has less impact on kidney compared to sodium chloride, that already in young animals induced some effects on kidney, possibly related to hypertension.

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