1. Peripheral adrenergic responses were studied in eight obese women before and after 15 days of caloric restriction (2500 kJ/day) and in eight sex- and age-matched lean controls.

2. β-Adrenergic sensitivity (defined as the dose of isoprenaline required to increase resting heart rate by 25 beats/min) was evaluated before and after the diet. Density and affinity (determined as the apparent dissociation constant) of platelet α2-adrenergic receptors, and plasma adrenaline and noradrenaline levels, were measured after overnight bed-rest and after 9 min of standardized exercise performed before and after the low caloric diet.

3. Before the diet basal antecubital venous plasma noradrenaline concentrations were lower in obese women when compared with lean women (0.94 ± 0.06 vs 1.27 ± 0.17 nmol/l, P < 0.02). Isoprenaline sensitivity did not differ between lean and obese women.

4. At rest, platelet α2-adrenoceptor density was lower in overweight than in lean women (129 ± 21 vs 168 ± 16 fmol/mg of protein, P < 0.02). Exercise significantly increased platelet α2-adrenoceptor density and decreased affinity in lean women. This decrease correlated with the rise in plasma noradrenaline.

5. In obese women exercise did not modify platelet α2-adrenoceptor density or affinity, despite a significant increase in plasma catecholamines. However, the increase in plasma noradrenaline during exercise was lower in obese women.

6. The low caloric diet produced a β-adrenergic supersensitivity.

7. We conclude that (a) obesity does not alter β-adrenergic sensitivity; (b) 15 days of caloric restriction produces a β-adrenergic supersensitive state; (c) obese women show an inability to desensitize platelet α2-adrenoceptors in response to exercise.

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