Obesity is a common problem in most western countries. We are investigating the metabolic basis for the inability to maintain weight loss. To date MRS measurements have been made on 5 obese and 5 non-obese subjects at their ~usual~ body weight (Wtinit). The subjects~ body weight was stabilized by adjusting the caloric intake. Following completion of studies at Wtinit the subjects diet was again adjusted to either gain 10% of their body weight or lose 10% or 20% of their body weight. Once the subjects weight stabilized at the new plateau for at least 14 days MRS measurements were repeated. MRS measurements were made at rest, during exercise, electrical stimulation and recovery. In obese and never-obese subjects no differences in the basal phosphate content and resting intracellular pH were shown. In contrast, the in vivo oxidative capacity tended to be lower in the obese subjects compared to the never-obese subjects. With progressive weight loss kPCr in the obese individuals showed a progressive increase. As a result, following weight loss the in vivo oxidative capacity of the obese subjects was higher than that of the never-obese individuals. Recently completed studies have shown that changes in the quantity of stored calories (adipose tissue) above or below that which is ~normative~ or usual for a given individual, whether lean or obese, are accompanied by changes in energy metabolism in the compartment of non-resting energy expenditure (skeletal muscle). Obese and non-obese individuals have similar responses to experimentally induced changes in caloric storage, ~defending~ adipose tissue deposits of different size by the same metabolic mechanisms. Candidate systems for effecting these changes in energy metabolism include skeletal muscle and the autonomic nervous system. In obese, never-obese and formerly-obese subjects measurements are made of systemic energy, skeletal muscle physiology, autonomic nervous system activity, and body composition.
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