Forced calorie restriction is seen as a solution to obesity and weight gain. However, studies attest to the failure of forced calorie regimens to cause effective long term fat loss. Obesity is a metabolic disorder caused by poor diet and improper nutrient intakes, and is characterised by insulin resistance and non-alcoholic fatty liver. The idea that obesity is caused by a positive energy balance is therefore problematic because it implies that energy restriction is a solution to weight gain. The main problem with application of a forced calorie restrictive regimens to an overweight person is the fact that the hypothalamus perceives the overweight or obese state akin to that of starvation. Although fat mass is plentiful, the inability of the individual to tap into those reserves, because of the presence of both leptin and insulin resistance, causes there to be a lack of available energy. In response the hypothalamus down regulates energy expenditure, and uses skeletal muscle as a source of fuel.
The catabolism of skeletal muscle during forced calorie restrictive diets is reflected in a fall in resting metabolic rate during the course of the diet. The subject believes they are achieving their goals because body weight is falling, but in reality much of the initial weight lost in such energy restrictive diets, is skeletal muscle. Low energy diets are known to cause detrimental changes to skeletal muscle and result in fatigue and an inability of muscle to correctly undergo the cyclical contraction-relaxation required for proper force generation. A number of studies have investigated the effects of energy restriction on skeletal muscle, and the metabolic changes that result. For example, in one study1, researchers analysed the metabolic and structural changes to skeletal muscle during a low energy diet in morbidly obese subjects. A baseline diet of 2500 kcal per day was administered while muscle biopsies were repeatedly taken from the gastrocnemius muscle. The subjects then consumed a hypocaloric diet of 400 kcal for 2 weeks.
The results showed that the low energy intake resulted in a significant decrease in the muscle enzymes phosphofructokinase and succinate dehydrogenase as well as decreases in glutamine, glycine and alanine. These changes may reflect a catabolic state in the skeletal muscle tissue, with low glutamine levels particularly associated with the catabolic state. In addition, type II fibre atrophy was observed in the subjects on the low energy diet. The atrophy of muscle tissue is not unexpected from those who have reviewed the literature because reductions in circulating and active thyroid hormones and skeletal muscle loss are known side effects of low calorie diets. Another finding of this study was an increase in the intracellular calcium content of the muscle. This is problematic because it may signify a reduction in plasma calcium caused by inadequate dietary calcium. High intracellular and low extracellular calcium caused by inadequate dietary calcium is termed the calcium paradox, and may signify insulin resistance and a diseased state.
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