Weight reduction by exercises & changes in the muscle structure & function
The following article is straight from my forth coming book:
Preserving the muscle is worth while loosing weight. According to many reports dieting can help loose weight but exercise regimen added to diet regimen leads to preservation of muscle mass while loosing weight. For example Janssen I et al reported that independent of sex, the combination of diet and exercise results in a preservation of skeletal muscle mass, a preferential reduction of abdominal subcutaneous adipose tissue, and improved functional capacity by comparison to diet alone. And more importantly in response to diet or diet and exercise-induced weight loss, reductions in total adiposity, subcutaneous and visceral adipose tissue distribution are not different in obese men and women. Let us discuss some recent evidences of importance of muscle & it’s changes in weight loss.
Weight reduction & muscle fiber ultrastructural change: In obesity, skeletal muscle insulin resistance may be associated with smaller mitochondria. Toledo FG et al (2006) reported a combined intervention of weight loss and physical activity in previously sedentary obese adults is associated with enlargement of mitochondria and an increase in the mitochondrial content in skeletal muscle. These findings indicate that in obesity with insulin resistance, ultrastructural mitochondrial plasticity is substantially retained and, importantly, that changes in the morphology of mitochondria are associated with improvements in insulin resistance.
Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome: Aerobic conditioned muscle shows increased oxidative metabolism or glucose relative to untrained muscle at a given absolute exercise intensity. The STRRIDE study (studies of a targeted risk reduction intervention through defined exercise) is an aerobic exercise intervention in men and women with features of metabolic syndrome. Hittel DS et al (2005) reported serial measurement of fasting plasma lactate from 62 subjects from the same exercise group demonstrated a significant decrease of circulating lactate with training. They also reported evidence for sex-specific (only in women) molecular remodeling of muscle’s component of mitochondrial respiratory complex (III). These biochemical adaptations complement existing molecular models for improved glucose tolerance with exercise intervention in prediabetic individuals.
Effects of weight loss and physical activity on muscle lipid content and droplet size: He J et al (2004) reported intramyocellular lipid does not decrease in response to weight loss and physical activity in obese, previously sedentary individuals, yet the lipid within muscle is dispersed into smaller droplets. This change in the size of lipid droplets, likely coupled with a concomitant increase in oxidative enzyme capacity, is correlated to improved insulin sensitivity.
Skeletal muscle dictates the fibrinolytic state after exercise training in overweight men with characteristics of metabolic syndrome: While there is indisputable evidence supporting the beneficial role of aerobic exercise in reducing cardiovascular risk factors, there are few dose-response studies of this relationship. Increasingly, it is thought that the cardiovascular benefits of exercise are significantly influenced by adaptations within skeletal muscle and its vasculature. However, little is known about the molecular mechanisms underlying these adaptations. Hittel DS et al (2003) reported in a STRRIDE study that the rigors of exercise directly induce fibrinolytic genes and protein cascades, both within muscle, and in the systemic circulation. This finding is particularly significant given that the metabolic syndrome is an independent risk factor for peripheral vascular disease and thrombotic events within the heart and brain. We conclude that aerobic exercise training induces both local and systemic changes in fibrinolysis and vascular homeostasis that are probably protective against cardiovascular disease.
Weight reduction & muscle fiber ultrastructural change: In obesity, skeletal muscle insulin resistance may be associated with smaller mitochondria. Toledo FG et al (2006) reported a combined intervention of weight loss and physical activity in previously sedentary obese adults is associated with enlargement of mitochondria and an increase in the mitochondrial content in skeletal muscle. These findings indicate that in obesity with insulin resistance, ultrastructural mitochondrial plasticity is substantially retained and, importantly, that changes in the morphology of mitochondria are associated with improvements in insulin resistance.
Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome: Aerobic conditioned muscle shows increased oxidative metabolism or glucose relative to untrained muscle at a given absolute exercise intensity. The STRRIDE study (studies of a targeted risk reduction intervention through defined exercise) is an aerobic exercise intervention in men and women with features of metabolic syndrome. Hittel DS et al (2005) reported serial measurement of fasting plasma lactate from 62 subjects from the same exercise group demonstrated a significant decrease of circulating lactate with training. They also reported evidence for sex-specific (only in women) molecular remodeling of muscle’s component of mitochondrial respiratory complex (III). These biochemical adaptations complement existing molecular models for improved glucose tolerance with exercise intervention in prediabetic individuals.
Effects of weight loss and physical activity on muscle lipid content and droplet size: He J et al (2004) reported intramyocellular lipid does not decrease in response to weight loss and physical activity in obese, previously sedentary individuals, yet the lipid within muscle is dispersed into smaller droplets. This change in the size of lipid droplets, likely coupled with a concomitant increase in oxidative enzyme capacity, is correlated to improved insulin sensitivity.
Skeletal muscle dictates the fibrinolytic state after exercise training in overweight men with characteristics of metabolic syndrome: While there is indisputable evidence supporting the beneficial role of aerobic exercise in reducing cardiovascular risk factors, there are few dose-response studies of this relationship. Increasingly, it is thought that the cardiovascular benefits of exercise are significantly influenced by adaptations within skeletal muscle and its vasculature. However, little is known about the molecular mechanisms underlying these adaptations. Hittel DS et al (2003) reported in a STRRIDE study that the rigors of exercise directly induce fibrinolytic genes and protein cascades, both within muscle, and in the systemic circulation. This finding is particularly significant given that the metabolic syndrome is an independent risk factor for peripheral vascular disease and thrombotic events within the heart and brain. We conclude that aerobic exercise training induces both local and systemic changes in fibrinolysis and vascular homeostasis that are probably protective against cardiovascular disease.
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