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

Abstract

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.

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

“…This led to a marked difference in postexercise glycogen metabolism. Trained and untrained rats that had been on a normal diet partially replenished their muscle glycogen stores after exercise before replenishing their liver glycogen stores (Adams & Koeslag, 1988). In the present study the untrained animals continued this trend, but the trained animals reversed it, replenishing the liver glycogen stores apparently at the expense of the muscle glycogen stores (Figs 2 and 3).…”

“…The low-carbohydrate diet for 1 week lowered the rats' (both trained and untrained) liver glycogen concentrations by approximately 45 %, and the muscle glycogen concentrations by about 25 % of that found in laboratory rats eating normal chow under otherwise identical circumstances (Adams & Koeslag, 1988). This led to a marked difference in postexercise glycogen metabolism.…”

“…The results are compared with those of a previous study in which similar rats were not carbohydrate restricted (Adams & Koeslag, 1988 After the week of carbohydrate restriction both the trained and untrained groups were randomly subdivided into an experimental and a control group. Thus, two experimental (trained and untrained) and two control (trained and untrained) groups existed after the second subdivision.…”

Skeletal muscle PGC‐1α modulates systemic ketone body homeostasis and ameliorates diabetic hyperketonemia in mice

“…These data imply that muscle PGC‐1α is important in systemic KB homeostasis, regardless of the ketogenic stimulus. Exacerbated postexercise ketosis is associated with an untrained phenotype in both rodents and humans and can be ameliorated with exercise training (19, 20). Skeletal muscle PGC‐1α could therefore be important for the adaptation of systemic ketolytic capacity with exercise training.…”

“…Exercise can modulate the systemic response to ketosis, which is evident by the enhanced KB tolerance (29) and resistance to postexercise ketosis in trained humans (20) and rodents (19). Resistance to ketosis after exercise has been attributed to a sparing of liver glycogen content during exercise (19). However, reduction in postexercise ketosis could also be mediated by adaptations of cardiac and skeletal muscle, 2 main consumers of KBs.…”