The impact of exercise on insulin action in Type 2 Diabetes Mellitus: Relationship to Prevention and Control (Part 1)

Colberg, S.R. 2006. Insulin. 1(3): 85-98.

Complex interaction between insulin and insulin action, counterregulatory hormone release, blood glucose regulation and physical activity.

INSULIN AND OTHER HORMONAL RESPONSES TO ACUTE EXERCISE

Immediate response once a person exercise in order to maintain blood glucose level. Through hepatic gluconeogenesis and glycogenolysis, blood glucose level will be maitaned at the normal level as carbohydrates are the main source of energy during exrcise.

Catecholamines and glucagon are th emost immediate ciounterregualtory hormones released during exercise which signal the liver to release more glucose.

Epinephrine raises heart rate and signal the exercising muscle to break down stored glycogen and triglyserides and at the same time supresses insulin release from Beta-cells. The release of glucagon from from pancreatic alpha cell is inversely related to portal levels circulating insulin during exercise.

Norepinephrine, cortisol and growth hormone help to redistribute blood to the exercising muscle - providing alternate fuels.

Both decrements in insulin and increments in glucagon play important roles in the prevention of hypoglycemia during exercise by stimulating increments of hepatic glucose production.

In people with DM, insufficient decrease in protal vein insulin levels can impair teh production of adequate blood glucose and potentially causing hypuglycemia.

Prolonged/endurance exercise may cause hypoglycemia due to the extreme demands of glucose whereby intense exercise heavy weight lifting or sprinting) may result in hyperglycemia due to high release of epinephrine and norepinephrine.

Patients treated with insulin injection normally experience the absence of the physiologic exercise-induced decrease in insulin level. The blood glucose level among this group of patients may fall considerably faster even with the compensatory mechanism work to increase glucose production.

Antecedent moderate intensity exercise has been shown to blunt autonomic, neuroendocrine and metabolic counterregulatory responses to subsequent exercise or to hypoglycemia even in people without DM. At rest, average human body uses a fuel mix of ~ 60% fat and 40% CHO, however during exercise, CHO becoem the main source during exercise and it is crucial during intense workouts. Plasma FFA can also be used but contribute the most duirng mild- to moderate-intensity workouts.

TRAINING, INSULIN ACTION AND PHYSICAL ACTIVITY

Most obese individual with Type 2 DM experience a decrease in their blood glucose levels during mild- to moderate intensity exercise. The magnitude is related to the duration and intensity as well as pre-exercise glycemic control and theindividual's training state.

The ability of more intense or prolonged exercise to acutely enhance insulin sensitivity results in more effective postexercise glycemic control in people with insulin resisiatbnce or Type 2 DM. Exercise training can result in a more lasting effect on action of insulin.

Insulin sensitvity can be acutely improved by regular exercise without loosing weight and also without showing a true muscle adaption. More prolonged physical training can enhance both the responsiveness of muscles to insulin as well basal blood glucose uptake.

In healthy young men, 6 weeks of moderate intensity work out cycling performed for 1 hour, 5 days a week was capable to increase not only insulin sensitivity but also their glucose effectiveness for at least a week after the last session of exercise.

Insulin sensitivity affected by individual age and training status.

In elderly, research shown improvement in both aerobic power and insulin action after high-intensity aerobic training and this result is much higher as compared to those in younger age group who followed teh same training.

Older women shown improvement in insulin sensitivity from the acute effect of last training session rather than the chronic training adaptation. Elderly subjects were not impaired by age but rather by physical inactivity. Acute effect of recent exercise are more prominent, however, regular participation in physical activity is required for a prolong improvements in glucose homeostasis and insulin action.

High intensity training clearly improves insulin sensitivity but the same effect could be obtained. Exercise duration may play mire important role than training intensity to improve insluin action in overweight people. After 14 weeks of moderate exercise training, postmenapausal women shown a decrease in body weight and total body fat. The strongest predictor of improved insulin action in women with T2DM was enhanced fasting rate of fat oxidation, and both exercise and both exercise and weight loss increased postabsorptive fat oxidation as well. Dieting alone could reduce subcutaneous fat but not vesceral fat without exercise being added in the regimen plan.

Resistance training can acutely raise blood glucose levels due to its high intensity and exaggearted counterregulartory hormonal response, resistance training in general appears to be beneficial to glycemic control and insulin sensitivity particularly in individuals with T2DM.