Exercise have been shown to have particular insulin sensitising effects. This may relate to the training effect of skeletal muscle, whereby the oxidative capacity of the myocytes increases. The current model of insulin resistance suggests that the accumulation of intramuscular lipids may in some way interfere with the insulin signal cascade, and increased oxidative capacity in skeletal muscle may reduce this interference, thus improving insulin sensitivity. However, the nature of this relationship is not fully understood, because endurance trained athletes actually have high levels of intramuscular lipids as a result of the effects of their training, but these lipids do not seem to negatively impact the sensitivity of their myocytes. The high insulin sensitivity of myocytes in endurance trained athletes, despite high intramuscular lipid concentrations therefore creates a paradox. Further, resistance training and endurance training may have different effects on insulin resistance, with regard the mechanism by which insulin sensitivity is achieved.
Studies have compared the insulin sensitising effects of various training methods. For example, in one study1, researchers compared the insulin sensitising effects of endurance training versus resistance training in healthy normal weight female subjects over a 6 month period. Subjects were provided with standardised diet so that dietary variables that affect insulin resistance could be controlled for. Subjects then performed either jogging on a treadmill or resistance training using the main muscle groups. A control group did no exercise. The results of the study showed that the fat mass of neither the endurance, resistance or control groups changed during the study. Further, the endurance trained athletes increased their VO2 max by 29 % during their training phase, suggesting that they had derived a benefit in aerobic capacity from their training. In the resistance trained subjects both body mass and body mass indices increased, suggesting that the subjects had gained muscle (because fat mass had not changed).
The insulin sensitivity of both training groups improved. However, when the fat free mass was taken into account, the improvement remained only in the endurance trained subjects. This suggests that endurance training increases insulin sensitivity by increasing the glucose disposal per unit mass of muscle tissue, but that resistance training increases insulin sensitivity by increasing the total mass of the muscle, rather than its per unit efficiency. These results are also interesting because they support other studies that show that exercise does not cause significant changes in body fat, without concomitant improvements in diet quality. The subjects performed supervised exercise protocols and yet their total body fat did not change significantly. Other studies have shown that body fat losses are just as great in groups consuming traditional diets as they are in those consuming traditional diet and performing exercises. Therefore while exercise may have protective effects against weight gain, it is of limited efficiency at causing weight loss.
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