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Endurance & Strength Exercise Prevents Insulin Resistance in general Populations
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"EXERCISE MODULATION OF SKELETAL MUSCLE INSULIN SENSITIVITY AND LIPID METABOLISM"
This text was excerpted from:
"Skeletal muscle lipid deposition and insulin resistance: effect of dietary fatty acids and exercise"
American Journal of Clinical Nutrition, Vol. 85, No. 3, 662-677, March 2007
Michael P Corcoran, Stefania Lamon-Fava and Roger A Fielding
1 From the Lipid Metabolism Laboratory (MPC and SL-F) and the Nutrition, Exercise Physiology, and Sarcopenia Laboratory (RAF), Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA
The authors concluded:
"...Overall, it seems clear that a long-term exercise program, composed of both endurance and strength training, along with reductions in saturated fat intake, will prevent the occurrence of insulin resistance in the general population and improve insulin sensitivity in the obese population...."
Endurance exercise improves skeletal muscle insulin sensitivity, and the mechanism of action is fairly well described. Notable points in skeletal muscle insulin signal modulation via this type of exercise include increases in GLUT4 protein concentrations and increased activities of both glycogen synthase and hexokinase, the enzyme that phosphorylates glucose (203, 204). As previously mentioned, endurance athletes are quite insulin-sensitive yet have high IMTG concentrations (17). Some studies have shown that placing sedentary adults on an endurance exercise program improves insulin sensitivity while increasing IMTG concentrations (16, 205). The effect of exercise is, of course, whole-body mediated, but in these studies, the improved insulin sensitivity in the presence of increased IMTG concentrations is most likely the result of more efficient lipid turnover in that the muscle is becoming more adept at lipid uptake, transport, utilization, and oxidation. Indeed, Menshikova et al (206) showed improvements in mitochondrial biogenesis and electron transport chain activity in older persons after 12 wk of endurance training. Bruce et al (14) obtained similar results in obese persons, although their IMTG concentrations remained relatively unchanged. Therefore, the capacity for lipid oxidation is increased, yet given the IMTG increase noted in some of these studies, greater FFA delivery and uptake must also be occurring (207, 208). The increase in lipid uptake most likely represents, again, an adaptation by the muscle to the increased metabolic demands that arise from strenuous physical exertion. This, coupled with increased FFA delivery to the exercising muscles, an expected physiologic response, would help to explain increased IMTG concentrations. The improvements in insulin sensitivity despite the increase in IMTG are likely related to reductions in deleterious lipid metabolites from a greater lipid flux. In the study by Bruce et al (14), obese subjects were exposed to endurance training, which yielded reductions in both intramyocellular DAG and ceramide content. Reductions in lipid metabolite concentrations may partly explain the improvements in GLUT4 translocation and activities of hexokinase and glycogen synthase. There is also some evidence suggesting that endurance training reduces susceptibility of skeletal muscle to lipid peroxidation (209). This may lead to further improvements in mitochondrial function. Lastly, the antiinflammatory effects of exercise are well known [reviewed by Petersen and Pedersen (210)], and studies have shown that exercise reduces TNF-a concentrations, which may in part explain the increases in GLUT4 expression.
In addition to endurance exercise, resistance training should also be regarded as an essential component in an individual's daily lifestyle. From a physiologic point of view, it is well recognized that endurance exercise increases capillary density, improves blood flow to the muscles and skeletal muscle mitochondrial biogenesis, and enhances translational stability of key proteins involved in insulin signal transduction (203). However, endurance exercise does not substantially affect skeletal muscle hypertrophy and strength compared with resistance training. Because resistance training increases skeletal muscle mass (211), it can augment whole-body glucose disposal capacity (212-214). Furthermore, studies have shown that even a single resistance exercise training session can improve insulin sensitivity for up to 24 h after cessation of exercise (214-216) and that these benefits are possibly attributed in part to reductions in IMTG stores (217). At first, this may seem contradictory to studies that have shown increases in IMTG from endurance exercise, which imply a discrepancy dependent on exercise type. However, it is important to distinguish between a single training session and multiple training sessions. Many studies examining a single endurance bout have also shown reductions in IMTG concentrations (218-220). It is widely agreed that to really achieve any substantial long-lasting benefit from physical exercise, the activity must be consistently repeated throughout one's life. A single training session of either endurance or resistance exercise will undoubtedly lead to reduced IMTG concentrations, because these lipids have been shown to be a major fuel source in both exercise types, depending on the intensity of the exercise; though, admittedly, this is still rather controversial [reviewed by van Loon (221)]. The enhanced lipid turnover seen with endurance exercise (14, 222) is a consequential adaptation to the metabolic demands of the body. Unfortunately, studies on the metabolic demands of resistance training are few. This is likely due to the methodologic difficulties associated with the non-steady state conditions of this type of exercise. Regardless, studies that use exercise, be it endurance or resistance training, have consistently shown improvements in skeletal muscle insulin sensitivity, and any so called "paradox" with regard to IMTG concentrations is explained when examining lipid turnover.
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