Glycogen Storage and Use Term Paper

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Glycogen Storage and Use

Exercise and diabetes: Beneficial effects

Diabetes is increasing in the United States and throughout the world due to the ever-growing adoption of an unhealthy lifestyle, including poor diet and lack of physical activity. Obesity is a characteristic often present in individuals with diabetes, and in order for the occurrences of diabetes to be reduced and the effects of diabetes to be minimized, efforts must be put in place to encourage weight loss and the maintenance of a healthy weight. It is expected that obesity and diabetes will reach epidemic proportions unless prompt action is taken to counteract these conditions (Albu & Raja-Khan, 2003).

Lifestyle factors have been identified that are associated with glycemic control and body mass in individuals with diabetes. Grylls et al. (2003) found that reducing dietary saturated fat and excess body weight may be useful for improving glycemic control in older adults with diabetes. Moreover, a change in diet and increased physical activity are beneficial because they assist in weight control, and therefore, improve glycemic control.

Albu & Raja-Khan (2003) note that the provision of intensive glycemic control in patients with diabetes reduced microvascular complications and improved mortality. However, weight reduction and glycemic control are often difficult to achieve in diabetic patients suffering from obesity because increasing insulin resistance and progressive beta-cell dysfunction necessitate the administration of increasingly higher doses of insulin, which furthermore leads to weight gain. Moreover, exercise is an essential factor in the successful management of diabetes in obese patients.

Insulin insensitivity is a common problem among diabetic patients. Along with a decrease in weight, exercise has also been found to improve insulin sensitivity. Cuff et al. (2003) investigated whether a combined resistance and aerobic training program would improve insulin sensitivity compared with aerobic training alone in women with type 2 diabetes, who were also post-menopausal. The results indicated that glucose infusion rates increased significantly in the group that participated in combined resistance and aerobic training. This group also demonstrated a significantly greater increase in muscle density compared to the group that took part in aerobic exercise only. The researchers concluded from these findings that adding resistance training to aerobic training enhanced glucose disposal, and hence improved insulin sensitivity, in postmenopausal women with type 2 diabetes.

Physical activity has been shown to have beneficial effects on insulin sensitivity in normal as well as insulin resistant populations, such as diabetics. Borghouts & Keizer (2000) explain how up to two hours after exercise, glucose uptake is elevated partly due mechanisms independent of insulin, which probably involve a contraction-induced increase in the amount of GLUT4 associated with the T-tubules and the plasma membrane. A single episode of exercise can increase insulin sensitivity for at least 16 hours after the exercise in both healthy and insulin insensitive individuals. Acute exercise also enhances GLUT4 translocation stimulated by insulin. Contributing to this effect, are increases in muscle GLUT4 protein content, and the depletion of muscle glycogen stores that occurs with exercise may play a role in this process. The authors explain how, through multiple adaptations in the transport and metabolism of glucose, physical training maximizes the effect that exercise has on insulin sensitivity. Moreover, physical training plays an extremely important role in the treatment and prevention of insulin sensitivity in relation to diabetes.

Another study conducted by Casteneda et al. (2002) investigated whether and to what extent high-intensity progressive resistance training (PRT) had on glycemic control in patients with type 2 diabetes. The results indicated that sixteen weeks of PRT resulted in reduced levels of plasma glycosylated hemoglobin and increased muscle glycogen stores. This level of physical activity also reduced the dosage of prescribed diabetes medication in 72% of the patients involved. Control subjects, on the other hand, showed no change in glycosylated hemoglobin, a reduction in muscle glycogen stores, and a 42% increase in medications for diabetes. Based on these results, the researchers concluded that PRT along with standard care is an effective and feasible means of improving glycemic control among patients with type 2 diabetes.

The improvements that physical activity causes in insulin sensitivity among obese diabetic patients may also be associated with enhanced fat oxidation. Goodpaster et al. (2003) explain insulin resistance in skeletal muscle entails dysregulation of both fatty acid and glucose metabolism. These researchers therefore sought to examine whether a combined intervention of weight loss and physical activity influences fasting rates of insulin-stimulated glucose disposal and fat oxidation. The results of the study indicated that the strongest predictor of improved sensitivity to insulin was enhanced fasting rates of fat oxidation. Moreover, exercise in combination with weight loss enhances post-absorptive fat oxidation. According to the researchers, this process is an important component to the improvement in insulin sensitivity among obese diabetic patients.

Exercise has been found to not only have effects on insulin sensitivity, but also on insulin release. Along with insulin release, physical activity has also been found to play a role in glucoregulation (Marliss & Vranic, 2002). Marliss & Vranic (2002) explain how, unlike exercise at lesser intensities, in intense exercise, glucose is the exclusive fuel used by muscles. This glucose must be moved from liver and muscle glycogen in both the fasted and fed states. Therefore, regulation of glucose production (GP) and glucose utilization (GU) during intense exercise has to be different from exercise that is less intense. Lower intensity exercise often results in declined plasma glucose. During low intensity exercise, insulin secretion is inhibited by the activation of beta-cell alpha-adrenergic receptors. Intense exercise, on the contrary, results in GP rising seven to eightfold and GU rising three to fourfold. Therefore, increases in glycemia result and decreases in insulin occur minimally or not at all. The researchers conclude that the clinical challenge posed by this phenomenon is to reproduce the normal recovery period hyperinsulinemia in patients with diabetes, who often report exercise-induced hyperglycemia.

The process of glucose uptake into muscle and its subsequent storage as glycogen is essential for energy homeostasis in skeletal muscle is stimulated by insulin, and is therefore impaired in diabetes (Yeaman et al., 2001). Yeaman et al. (2001) explain how although glycogen synthesis is an insulin-regulated pathway, it is also regulated in a manner independent of insulin. The authors provide the example of how glycogen synthesis in muscle is stimulated significantly after intense exercise, with much of this stimulation being independent of insulin. Furthermore, glucose and glycogen content of the muscle are important to the stimulation of glycogen synthesis, and therefore may be important to the understanding of the impaired glycogen synthesis process seen in diabetic patients.

During exercise, an enzyme that is activated is called the AMP-activated protein kinase (AMPK) (Musi & Goodyear, 2003; Grahame Hardie, 2003). This enzyme is also activated pharmacologically through metformin, an antidiabetic agent. Musi & Goodyear (2003) maintain that AMPK plays a crucial role in the stimulation of muscle glucose uptake, and this is evident through studies that have demonstrated that the activation of AMPK through exercise is associated with increases in glucose uptake through an insulin-independent mechanism. These effects have also been demonstrated with the pharmacological agent based on AMPK. The researchers conclude that the effects that exercise, and therefore AMPK, has on muscle glucose uptake makes this enzyme a key component to the treatment of diabetes.

However, Hojlund et al. (2003) furthermore examined how the reduced function of AMPK might play a role in insulin resistance seen in diabetes. These researchers concluded based on their findings that changes in AMPK activity and expression are not likely to be affect lipid oxidation and glycogen synthesis in obese diabetic patients.

Overall, evidence is overwhelmingly in support of the benefits that exercise has for patients with diabetes. Physical activity may allow patients to improve insulin sensitivity, feel healthier, and may possibly even allow medication dosages to be reduced. As with…

Sources Used in Documents:


Albu, J. & Raja-Khan, N. (2003). The management of the obese diabetic patient. Primary Care, 30(2), 465-91.

Borghouts, L. & Keizer, H. (2000). Exercise and insulin sensitivity: A review. International Journal of Sports Medicine, 21(1), 1-12.

Casteneda, C., Layne, J., Munoz-Orians, L., Gordon, P., Walsmith, J., Foldvari, M., Roubenoff, R., Tucker, K., Nelson, M. (2002). A randomized controlled trial of resistance exercise training to improve glycemic control in older adults with type 2 diabetes. Diabetes Care, 25(12), 2335-41.

Cradock, S. (1997). The role of exercise in diabetes management. Community Nurse, 3(3), 23-4.

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