Effect of streptozotocin-induced diabetes on glycogen resynthesis in fasted rats post-high-intensity exercise

Abstract

It has recently been shown that food intake is not essential for the resynthesis of the stores of muscle glycogen in fasted animals recovering from high-intensity exercise. Because the effect of diabetes on this process has never been examined before, we undertook to explore this issue. To this end, groups of rats were treated with streptozotocin (60 mg/kg body mass ip) to induce mild diabetes. After 11 days, each animal was fasted for 24 h before swimming with a lead weight equivalent to 9% body mass attached to the tail. After exercise, the rate and the extent of glycogen repletion in muscles were not affected by diabetes, irrespective of muscle fiber composition. Consistent with these findings, the effect of exercise on the phosphorylation state of glycogen synthase in muscles was only minimally affected by diabetes. In contrast to its effects on nondiabetic animals, exercise in fasted diabetic rats was accompanied by a marked fall in hepatic glycogen levels, which, surprisingly, increased to preexercise levels during recovery despite the absence of food intake.

Anti-diabetic effects of Campomanesia xanthocarpa (Berg) leaf decoction

“…In addition, glucagon levels are high in this condition, stimulating glycogenolysis and gluconeogenesis, and resulting in reduced liver glycogen (Jhiang, Zhang, 2003). Thus, the reduced glycogen levels in diabetic patients can be explained by reduced glycogen synthesis, and also by an increase in glycogenolysis and gluconeogenesis (Ferreira et al, 2001;Grover et al, 2002;Savage et al, 2007). On the other hand, hepatic glycogen of the diabetic rats treated with C. xanthocarpa decoct was similar to the untreated control group, suggesting that this treatment was able to restore or preserve liver glycogen.…”

Continuous and Intermittent Exercise Training and Glucose Metabolism in Neonatal Alloxan Administered Rats

“…Both the basal and insulin-stimulated activity of the glycogen synthase enzyme is impaired in the skeletal muscle of T2DM, which may have an important role in the development of glucose intolerance and insulin resistance [38][39][40][41]. The liver glycogen content of adult rats with diabetes is increased compared with control rats, and high intensity training reduces these stores [42]. Therefore, in the present study, glycogen concentrations in the gastrocnemius muscle, liver and heart were measured to verify the infl uence of training on the storage of this substrate in alloxan animals.…”

Lactate availability is not the major factor limiting muscle glycogen repletion during recovery from an intense sprint in previously active fasted rats

“…The rats were kept at approximately 20°C on a 12·h:12·h L:D photoperiod and had unlimited access to water and a standard laboratory chow diet (Glen Forrest Stockfeeders, Glen Forrest, Western Australia 6071: 55% digestible carbohydrate, 19% protein, 5% lipid and 21% nondigestible residue by mass). Before experiments, the rats were fasted for 24·h to deplete most of their stores of liver glycogen (Ferreira et al, 2001) and to prevent food present in the gut from providing carbon precursors for the replenishment of muscle glycogen post-exercise. On the day of each experiment, the animals were exercised and killed by cardiac excision between 9.00 and 12.00·h.…”

“…In contrast, the partial conversion of lactate into muscle glycogen in other species, such as humans and rats, has been proposed to explain, in part, why their muscle glycogen stores are only partially replenished after a sprint (Hermansen and Vaage, 1977;Astrand et al, 1986;Hatta et al, 1988;Bangsbo et al, 1992;Choi et al, 1994;Nikolovski et al, 1996;Peters et al, 1996;Bangsbo et al, 1997;Ferreira et al, 2001). If, as predicted above, the amount of accumulated lactate is the primary factor limiting the extent of muscle glycogen repletion post-intense exercise, one would predict that under conditions where a large proportion of muscle glycogen is oxidised by sustained moderate intensity exercise prior to a sprint, only the glycogen converted to lactate (and to a lesser extent to the glycolytic intermediates) during that sprint would be expected to be replenished, thus leading to the partial replenishment of muscle glycogen.…”