SUMMARY1. The development of post-exercise ketosis is not abolished by the ingestion of glucose immediately after exercise, despite inducing high insulin/glucagon ratios in the peripheral (and therefore by implication in the portal) blood.2. To investigate the possibility of autonomic control of the liver influencing its sensitivity to the major counter-regulatory hormones, we administered 50 g glucose, either on its own, or together with 0 5 mg prazosine, 40 mg propranolol, or 15 mg propantheline, to forty-seven 48 h carbohydrate-starved athletes who had just run 25 km.3. The blood 3-hydroxybutyrate concentration rose from 0 30 + 0 05 (mean + S.E. of mean) to 0-52 + 0-08 mmol/l with exercise, and then to 1-32 + 0-40 mmol/l at 6 h after exercise in subjects who had ingested only glucose after exercise.4. The effects of prazosine and propantheline on the blood ketone body concentration at 2 h after exercise was not statistically significant. Propranolol, on the other hand, significantly lowered the blood 3-hydroxybutyrate concentration (compared with controls) to 0 09+0 03 mmol/l at 3 h (P < 0-01), and 0-35 +0-08 mmol/l at 6 h (P < 0X01) after exercise.5. The plasma insulin, glucagon, glucose and free fatty acid concentrations were unaffected by propranolol, indicating that the antiketogenesis was the result of a direct effect on ketone body metabolism.6. Since /1-adrenergic blockade has not previously been shown to have antiketogenic activity, except in somatostatin-induced hyperketonaemia, it is concluded that its effectiveness in post-exercise ketosis can probably be ascribed to a functional hepatic insulin and glucagon deficiency.