POST-EXERCISE KETOSIS

doi:10.1016/S0140-6736(69)90931-3

The Lancet

Volume 294, Issue 7635, 27 December 1969, Pages 1383-1385

https://doi.org/10.1016/S0140-6736(69)90931-3 Get rights and content

Abstract

The effects of ingestion of glucose after strenuous exercise on the concentrations of blood glucose, glycerol, and ketone-bodies, and plasma-free-fatty-acids (F.F.A.) have been studied in a group of twelve subjects. The results have been compared with those of oral glucose-tolerance tests at rest in eight of the same subjects and after administration of glucose to three subjects undergoing a prolonged fast (72 hours). The findings support the following hypothesis regarding the nature of post-exercise ketosis. In severe exercise the need for respiratory fuels is increased, and adipose-tissue triglyceride is mobilised as an alternative fuel to glucose, as indicated by the rise of blood-glycerol and plasma-F.F.A. The increased concentration of F.F.A. and the depletion of hepatic glycogen cause an increased rate of ketone-body formation by the liver because in this situation ketone-body production is approximately proportional to the concentration of F.F.A. in the blood-plasma. During the exercise the extra ketone bodies formed also serve as a fuel of respiration and therefore do not accumulate. After cessation of exercise the raised concentration of F.F.A. results in a continued high rate of ketone-body formation which shows itself as post-exercise ketosis. The rise in the concentrations of F.F.A. with exercise modifies the glucose-tolerance curve, which shows a higher peak and a delayed fall, presumably because F.F.A. competes with glucose as a fuel of respiration and thus inhibits glucose utilisation.

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Citation Excerpt :
Ketone body oxidation becomes a significant contributor to overall energy mammalian metabolism within extrahepatic tissues in myriad physiological states, including fasting, starvation, the neonatal period, post-exercise, pregnancy, and adherence to low-carbohydrate diets. Circulating total ketone body concentrations in healthy adult humans normally exhibit circadian oscillations between approximately 100 and 250 μM, rise to ∼1 mM after prolonged exercise or 24 hr of fasting, and can accumulate to as high as 20 mM in pathological states like diabetic ketoacidosis (Cahill, 2006; Johnson et al., 1969b; Koeslag et al., 1980; Robinson and Williamson, 1980; Wildenhoff et al., 1974). The human liver produces up to 300 g of ketone bodies per day (Balasse and Féry, 1989), which contribute between 5% and 20% of total energy expenditure in fed, fasted, and starved states (Balasse et al., 1978; Cox et al., 2016).
Ketone body metabolism is a central node in physiological homeostasis. In this review, we discuss how ketones serve discrete fine-tuning metabolic roles that optimize organ and organism performance in varying nutrient states and protect from inflammation and injury in multiple organ systems. Traditionally viewed as metabolic substrates enlisted only in carbohydrate restriction, observations underscore the importance of ketone bodies as vital metabolic and signaling mediators when carbohydrates are abundant. Complementing a repertoire of known therapeutic options for diseases of the nervous system, prospective roles for ketone bodies in cancer have arisen, as have intriguing protective roles in heart and liver, opening therapeutic options in obesity-related and cardiovascular disease. Controversies in ketone metabolism and signaling are discussed to reconcile classical dogma with contemporary observations.
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This can be expected to promote depletion of hepatic glycogen stores while simultaneously promoting adipocyte lipolysis and hence providing the liver with more substrate for ketogenesis. Although blood ketone levels don’t notably rise during exercise – owing to rapid muscle oxidation of ketone bodies – a post-exercise rise in blood ketones has often been reported (“post-exercise ketosis”) [173,174]. Continuing carbohydrate avoidance following exercise, coupled with administration of the supplements described above, might represent a practical strategy for enabling significant ketosis to be achieved in the context of less than 24 h of carb restriction – for example, with the “mini-fast with exercise” strategy for achieving and maintaining leanness [175,176].
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This chapter covers the biochemistry and clinical chemistry of long-chain fatty acids, triacylglycerols, phospholipids, cholesterol, and ketones. The two most important functions of lipids are energy storage and membrane structure. Triacylglycerols are by far the most important lipids with regard to energy storage, and phospholipids and cholesterol are the most important lipid membrane constituents. Lipids serve other functions, including being precursors for steroids and bile acids (cholesterol), thermal insulation (triacylglycerols), and electrical insulation. Virtually all lipids are insoluble in water, which greatly complicates their handling in the body. Because of their insolubility, lipids must rely on proteins for transport for any significant distance in the body. This chapter begins with a discussion on long-chain fatty acids, and then discusses the structure, properties, and synthesis of triacylglycerol, and assays triacylglycerol. Structure and properties of phospholipids are also discussed. The chapter also elaborates properties of cholesterol and lipoproteins. The chapter concludes with a discussion on biochemistry of ketones including their synthesis and catabolism.
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ORIGINAL ARTICLESPOST-EXERCISE KETOSIS

Abstract

Lancet

Life Sci.

Lancet

Proc. R. Soc. B

Q. J. exp. Physiol.

Klin. Wschr.

J. Lab. clin. Med.

Ann. N.Y. Acad. Sci.

J. clin. Invest.

Diabetologia

ORIGINAL ARTICLES
POST-EXERCISE KETOSIS