The effects of alanine, glucose and starch ingestion on the ketosis produced by exercise and by starvation.

Abstract

SUMMARY1. Several investigators have found that the development of post-exercise ketosis is not counteracted by glucose ingestion. Post-exercise ketosis might therefore have more in common with diabetic ketoacidosis than with starvational ketosis.2. The effects of ingesting 100 g ofglucose, alanine or starch were therefore studied in subjects rendered hyperketonaemic by prolonged running on a low carbohydrate diet, or by 65 h of starvation. These substances were also ingested by normal post-prandial subjects.3. The runners developed post-exercise ketosis (1I81 +S.D. 0-81 mmol/l), which was counteracted by alanine and glucose, but only minimally by starch.4. Fasting caused a variable ketosis (2-19 +S.D. 1-63 mmol/l), also counteracted by glucose and less by starch, but alanine caused vomiting.5. Glucose and alanine lowered the blood ketone body levels of the post-prandial subjects.6. The rising ketone body levels in starvation and after exercise were accompanied by simultaneous increases in the plasma insulin/glucagon ratios; in both, glucose ingestion increased the ratio further, while alanine decreased it.7. It is concluded that there is no essential difference between established post-exercise and starvational ketosis, and that the blood fuel-hormone changes do not correlate with the changes in blood ketone body concentration.

The effects of post‐exercise glucose and alanine ingestion on plasma carnitine and ketosis in humans.

“…1 B). These findings would support the conclusions of other authors who have suggested that alanine decreases plasma ketone body levels post-exercise (Koeslag et al 1982) or after somatostatin infusion (Nosadini, Alberti, Johnson, Del Prato, Marescotti & Dune, 1981) by increasing oxaloacetate availability for citrate synthase-catalysed condensation with acetyl CoA.…”

“…While the fundamental processes that regulate the metabolism of acetyl CoA within the mitochondrion have not been elucidated, catalytic amounts of oxaloacetate are thought to be of primary importance for the oxidation of this molecule (Lehninger, 1946). Alanine is thought to inhibit ketosis during fasting and following exercise by entering the tricarboxlic acid cycle as oxaloacetate to increase the oxidation of acetyl CoA (Zammit, 1981; Koeslag, Noakes & Sloan, 1982). Carnitine buffers variations of acetyl CoA by forming acetyl carnitine (Pearson & Tubbs, 1967).…”

Glycogen Metabolism and Post‐exercise Ketosis in Carbohydrate‐restricted Trained and Untrained Rats

“…The hormones which might influence the development of post-exercise ketosis have been shown to act paradoxically during the recovery from exercise (Koeslag, Noakes & Sloan, 1982;Koeslag, Levinrad, Lochner & Sive, 1985;Adams, Irving, Koeslag, Lochner, Sandell & Wilkinson, 1987), and to change with the diet in the same way that post-exercise ketosis changes with the previous day's carbohydrate intake (Koeslag et al 1980). The present findings therefore support the hypothesis that the availability of mobilizable carbohydrate after exercise is an important (but probably not the sole) determinant of the development of post-exercise ketosis.…”

Beta‐adrenergic blockade restores glucose's antiketogenic activity after exercise in carbohydrate‐depleted athletes.

“…These procedures have previously been shown to induce the development of a marked post-exercise ketosis which reaches a plateau at about 2 h after the cessation of exercise (Koeslag, Noakes & Sloan, 1980;Koeslag, 1982;Koeslag et al 1982;Koeslag et al 1985).…”

“…Established post-exercise ketosis is readily abolished by the ingestion of glucose 2 h after exercise (Koeslag, Noakes & Sloan, 1982). Glucose ingestion immediately after exercise, on the other hand, has only a minimal, and very short-lived influence on the development of post-exercise ketosis (Koeslag, Levinrad, Lochner & Sive, 1985).…”