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Thesis (Ph. D.)--Ohio State University, 2005. / Title from second page of PDF file. Document formatted into pages; contains xix, 347 p.; also includes graphics. Includes bibliographical references (p. 183-192). Available online via OhioLINK's ETD Center

1. This series of studies was undertaken to examine the adrenergic regulation of carbohydrate metabolism during exercise. Recreationally active males were tested during moderate to intense exercise on a stationary cycle ergometer. Venous and arterial plasma obtained from indwelling catheters was analysed for hormonal and metabolite responses, and hepatic glucose production and glucose uptake were measured using the tracer-dilution method with stable isotopes. Muscle samples were obtained by the needle biopsy technique to examine muscle glycogen utilisation and the flux of related muscle metabolites using enzymatic, fluorometric and radioisotopic techniques. 2. During moderate exercise adrenaline infusion induced a marked hyperglycemia and this was due to reduced glucose uptake rather than enhanced hepatic glucose production. The reduction in glucose uptake was most likely mediated by a decrease in glucose phosphorylation, as indicated by the accumulation of glucose 6-phosphate with adrenaline infusion. 3. The hyperglycemic response to intense exercise was prevented by the administration of α- and β-adrenergic antagonists. Adrenergic blockade was without effect on hepatic glucose production whereas glucose uptake was enhanced when compared with control subjects. These data support the notion that adrenergic mechanisms are more important in restraining glucose uptake than enhancing hepatic glucose production during intense exercise. Other glucoregulatory factors are responsible for the increase in glucose production during intense exercise. 4. Elevated plasma adrenaline levels during moderate exercise in untrained men increases skeletal muscle glycogen breakdown and PDH activation which results

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The tail-cast suspension system was used as a ground-based model of weightlessness to study the effects of reduced weight-bearing (unloading) and attendant atrophy on carbohydrate metabolism in the rat soleus muscle. Changes in glycogen metabolism during unloading were biphasic. The initial phase, which took place during the first 24 hours, was characterized by increased glycogen concentrations, the result of decreased glycogenolysis. This glycogen accumulation in turn decreased the glycogen synthase activity ratio. These alterations were maintained thereafter. A similar glycogen increase was seen in the soleus unloaded by hypogravity. A rapid decline in glucose uptake also occurred during this initial phase of unloading, both in the absence and presence of insulin. During the second phase of this unloading response, beyond 24 hours, there was an increase in the sensitivity of the soleus to insulin for glucose uptake that coincided with the onset of muscle atrophy. However, this increased insulin sensitivity was not seen for glycogen synthesis, indicating differential regulation of these two processes by insulin. The enhanced insulin sensitivity likely resulted from an increase in the binding capacity for the hormone, resulting from no increased turnover of the insulin receptor during unloading. Additionally, the onset of increased insulin sensitivity coincided with a return to normal of basal glucose uptake, despite the continued unloading. When the 3-day unloaded soleus was reloaded, carbohydrate metabolism returned to normal after a triphasic response. Within two hours, the glycogen concentration decreased below control levels, due to increased glycogenolysis. During the second phase of reloading, from two to 24 hours, glycogen accumulated dramatically due to an enhanced capacity of the muscle for glycogenesis. Insulin sensitivity returned to normal by 24 hours of reloading. In the final phase, beyond 24 hours, glycogen decreased to control values. An uncoupling of the inverse relationship between glycogen and the activity ratio of glycogen synthase was seen beyond four hours of reloading. These effects of unloading and reloading were not due to systemic factors, as the extensor digitorum longus was unaffected. It is apparent that the unloaded soleus is a potent model with which to study the individual factors that regulate carbohydrate metabolism in skeletal muscle.

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