Post-exercise ketosis and the hormone response to exercise

Koeslag, J. H.

doi:10.1249/00005768-198205000-00003

Cited by 52 publications

(34 citation statements)

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“…Amino acids (+0.6 mmol l -1 , Mourtzakis and Graham 2002) are mostly zwitter ions with both pK values outside the physiological pH and therefore without effect. Ketone bodies remain constant during and after 20 min of exercise (Koeslag 1982). Since there is a small Donnan effect at the capillary wall caused by the different protein concentrations in plasma and interstitial fluid (r = 0.92 for concentrations per liter solution according to Rowlands 2005), [La] if might be 9% higher than [La] plasma .…”

Section: Comparison Of Base Excess and [La] Changesmentioning

confidence: 99%

Causes of differences in exercise-induced changes of base excess and blood lactate

et al. 2006

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It has been concluded from comparisons of base excess (BE) and lactic acid (La) concentration changes in blood during exercise-induced acidosis that more H+ than La- leave the muscle and enter interstitial fluid and blood. To examine this, we performed incremental cycle tests in 13 untrained males and measured acid-base status and [La] in arterialized blood, plasma, and red cells until 21 min after exhaustion. The decrease of actual BE (-deltaABE) was 2.2 +/- 0.5 (SEM) mmol l(-1) larger than the increase of [La]blood at exhaustion, and the difference rose to 4.8 +/- 0.5 mmol l(-1) during the first minutes of recovery. The decrease of standard BE (SBE), a measure of mean BE of interstitial fluid (if) and blood, however, was smaller than the increase of [La] in the corresponding volume (delta[La](if+blood)) during exercise and only slightly larger during recovery. The discrepancy between -deltaABE and delta[La]blood mainly results from the Donnan effect hindering the rise of [La]erythrocyte to equal values like [La]plasma. The changing Donnan effect during acidosis causes that Cl- from the interstitial fluid enter plasma and erythrocytes in exchange for HCO3(-). A corresponding amount of La- remains outside the blood. SBE is not influenced by ion shifts among these compartments and therefore is a rather exact measure of acid movements across tissue cell membranes, but changes have been compared previously to delta[La]blood instead to delta[La](if+blood). When performing correct comparisons and considering Cl-/HCO3(-) exchange between erythrocytes and extracellular fluid, neither the use of deltaABE nor of deltaSBE provides evidence for differences in H+ and La- transport across the tissue cell membranes.

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Section: Comparison Of Base Excess and [La] Changesmentioning

confidence: 99%

Causes of differences in exercise-induced changes of base excess and blood lactate

et al. 2006

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“…In the absence of food restriction, non-athletes are more prone than athletes to develop post-exercise ketosis (Johnson, Walton, Krebs & Williamson, 1969a, b;Winder, Baldwin & Holloszy, 1973Rennie, Jennett & Johnson, 1974;Winder, Beattie & Holman, 1982;Koeslag, 1982). The reasons are unclear.…”

Section: Introductionmentioning

confidence: 99%

“…We confined our enquiry to the measurement of the blood 3-hydroxybutyrate and tissue glycogen concentrations because we could only obtain very small quantities of blood from each rat with certainty, and because the plasma hormone, glucose, free fatty acid, and acetoacetate concentrations have already been studied exhaustively without leading to clear conclusions (Johnson et al 1969a, b;Johnson, Rennie, Walton & Webster, 1971;Johnson & Walton, 1972;Johnson & Rennie, 1973;Winder et al 1973;Rennie, Winder & Holloszy, 1976;Holloszy, Winder, Fitts & Rennie, 1978;Koeslag, Noakes & Sloan, 1980, 1982Beattie & Winder, 1984Koeslag, Levinrad, Lochner & Sive, 1985;Adams, Irving, Koeslag, Lochner, Sandell & Wilkinson, 1987). The effects of dietary manipulation on the tissue glycogen levels and post-exercise ketosis are described elsewhere (Adams & Koeslag, 1989).…”

Section: Introductionmentioning

confidence: 99%

Carbohydrate homeostasis and post‐exercise ketosis in trained and untrained rats.

Adams

Koeslag

1988

The Journal of Physiology

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SUMMARY1. Experiments were carried out to establish what relationship there is between the concentration of ketone bodies in the blood and the concentrations of glycogen in muscle and liver of thirty-six trained and thirty-six untrained rats exercised at the same absolute load. There were, in addition. non-exercised control animals (of which thirty-six were trained and thirty-six untrained) which were studied on the same day.2. Training occurred on a level treadmill at 0 2 m/s for I h/day. 5 days a week, for 6 weeks. The untrained animals ran on the treadmill every 3rd day for 5 min to maintain familiarity with treadmill running without training them.3. At the end of the 6th week, the experimental animals ran for 1 h at 0 2 m/s on a level treadmill. Blood 3-hydroxybutyrate and tissue glycogen concentrations were measured at the beginning and immediately after exercise, and then every 30 min for 2 h.4. Physically trained rats had higher pre-and immediate post-exercise liver glycogen concentrations than untrained rats: 413 + 15 and 300+8,umol/g before exercise in trained and untrained rats respectively, and 225+8 and 166+3 /tmol/g immediately after (P < 0 05). 5. Muscle glycogen, which was also higher in trained than in untrained rats, was resynthesized at approximately the same rate in the two groups of animals (9 and 11 ,tmol/(g h), but the trained animals were able to achieve this without further depletion of liver glycogen beyond that which had occurred during exercise. In untrained animals liver glycogen concentrations continued to drop for 60 mnin beyond the end of exercise.6. The difference between the immediate post-exercise blood concentrations of 3-hydroxybutyrate of trained and untrained animals was not significant. Thereafter the level rose, within 60-90 min, to 1-31+0-04 mmol/l in the untrained animals, but to only 0-62 + 0-05 mmol/l in the trained animals (P < 0 05).7. There was a striking inverse relationship between the blood 3-hydroxybutyrate concentrations of all the animals (trained and untrained) and their simultaneous liver glycogen concentrations during the experiment (r = -0-88; P < 0-001).8. The results suggest that the phenomenon of post-exercise ketosis is associated with an inability to maintain the liver glycogen concentration after exercise.

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“…This is hypothetically a likely time for it to operate, since hyperketonaemia, increased concentrations ofnon-esterified fatty acids (reviewed by Koeslag, 1982) and rapid repletion of muscle glycogen (Garetto et al, 1984) characterize this period. The metabolite changes in the soleus, particularly in the starved rat, are consistent with inhibition of phosphofructokinase.…”

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confidence: 99%

Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

Zorzano¹,

Balon²,

Brady³

et al. 1985

Biochemical Journal

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1. Concentrations of citrate, hexose phosphates and glycogen were measured in skeletal muscle and heart under conditions in which plasma non-esterified fatty acids and ketone bodies were physiologically increased. The aim was to determine under what conditions the glucose-fatty acid cycle might be operative in skeletal muscle in vivo. 2. In keeping with the findings of others, starvation increased the concentrations of glycogen, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in heart, indicating that the cycle was operative. In contrast, it decreased glycogen and had no effect on the concentration of citrate or the fructose 6-phosphate/fructose 1,6-bisphosphate ratio in the soleus, a slow-twitch red muscle in which the glucose-fatty acid cycle has been demonstrated in vitro. 3. In fed rats, exercise of moderate intensity caused glycogen depletion in the soleus and red portion of gastrocnemius muscle, but not in heart. In starved rats the same exercise had no effect on the already diminished glycogen contents in skeletal muscle, but it decreased cardiac glycogen by 2530% . 4. After exercise, citrate and the fructose 6-phosphate/fructose 1,6-bisphosphate ratio were increased in the soleus of the starved rat. Significant changes were not observed in fed rats. 5. The data suggest that in the resting state the glucose-fatty acid cycle operates in the heart, but not in the soleus muscle, of a starved rat. In contrast, the metabolite profile in the soleus was consistent with activation of the glucose-fatty acid cycle in the starved rat during the recovery period after exercise. Whether the cycle operates during exercise itself is unclear.

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Post-exercise ketosis and the hormone response to exercise

Cited by 52 publications

References 0 publications

Causes of differences in exercise-induced changes of base excess and blood lactate

Causes of differences in exercise-induced changes of base excess and blood lactate

Carbohydrate homeostasis and post‐exercise ketosis in trained and untrained rats.

Effects of starvation and exercise on concentrations of citrate, hexose phosphates and glycogen in skeletal muscle and heart. Evidence for selective operation of the glucose-fatty acid cycle

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