Metabolic homeostasis during exercise

Leptin therapy has corrected obesity in a child with congenital leptin deficiency. In obese individuals, the presence of circulating high levels of leptin has been attributed to resistance or some other defect in the leptin receptors. This apparent paradox of high leptin levels associated with obesity is analogous to insulin resistance seen in type 2 diabetes mellitus. In general, in the vast majority of obese patients, the molecular defects remain unknown. Diet and exercise are the mainstays in the management of obesity. 

At rest, skeletal muscle utilizes the catabolism of fatty acids and branched-chain amino acids to maintain cellular 

---

A potential drawback of such a hierarchical system is that it is nonrobust to perturbations. Changes in ventilatory load, for example, would disrupt the ventilatory command from the feedforward signal. This is at variance with the experimental observation of a load compensation response of the controller which protects ventilation against perturbations of the mechanical plant at rest and during exercise [Poon et al, 1987a, b Poon, 1989a, b]. Furthermore, if the prime objective of the controller were indeed to meet the metabolic demand (i.e., to maintain chemical homeostasis), then the hierarchical control system seems to perform quite poorly it is well known that arterial chemical homeostasis is readily disrupted environmental changes. 

Brass, E.P, Hoppel, C.L., and Hiatt, W.R., Effects of intravenous L-carnitine on carnitine homeostasis and fuel metabolism during exercise in humans. Clin. Pharmacol. Then, 55, 681-692, 1994. 

The chemoreflex model provides a satisfactory explanation for the chemical regulation of ventilation as well as respiratory instability. However, it fails to explain a fundamental aspect of ventilatory control experienced by everyone in everyday life the increase in ventilation during muscular exercise. Typically, Ve increases in direct proportion to the metabolic demand (VCO2, VO2) such that the outputs of the chemical plant. Equation 11.1 and Equation 11.2, are well regulated at constant levels from rest to exercise. As a result, homeostasis of arterial blood chemistry is closely maintained over a wide range of work rates. The dilemma is if increases in metaboHc rate are not accompanied by corresponding increases in chemical feedback, then what causes exercise hyperpnea ... 

---