Muscle glycogen concentration during recovery after prolonged severe exercise in fasting subjects

S Maehlum, L Hermansen - Scandinavian journal of clinical and …, 1978 - Taylor & Francis
S Maehlum, L Hermansen
Scandinavian journal of clinical and laboratory investigation, 1978Taylor & Francis
The influence of 12 h of fasting after prolonged severe exercise on the muscle glycogen
concentration was studied in 5 normal subjects. The subjects exercised in the post
absorptive state at 70% of max. Vo2 till exhaustion, then rested for 12 h. No food was
allowed during recovery. Blood samples and muscle biopsies were obtained before
exercise, immediately after the cessation of exercise, and after 2, 4, 6, 9 and 12 h of
recovery. Muscle glycogen content decreased from 70.4±3.0 to 21.6±3.9 mmol glucosyl …
The influence of 12 h of fasting after prolonged severe exercise on the muscle glycogen concentration was studied in 5 normal subjects. The subjects exercised in the post absorptive state at 70% of max. Vo2 till exhaustion, then rested for 12 h. No food was allowed during recovery. Blood samples and muscle biopsies were obtained before exercise, immediately after the cessation of exercise, and after 2, 4, 6, 9 and 12 h of recovery. Muscle glycogen content decreased from 70.4 ± 3.0 to 21.6 ±3.9 mmol glucosyl units/kg w.w. in response to exercise. After 4 h of recovery muscle glycogen had increased to 28.8 + 3.6 mmol glucosyl units/kg (P<0.025). During the next 8 h of recovery no further increase in glycogen concentration was observed. Mean plasma glucose concentration decreased from 5.25±0.16 to 4.37±0.18 mmol/1 during exercise (P<0.001). No change in the plasma glucose level was observed during recovery. Immunoreactive insulin (IRI) concentration decreased from 15.9±1.0 to 10.2±0.5 μU/ml (P<0.001) during exercise, and remained at this level during recovery. It is concluded that some muscle glycogen repletion may occur after prolonged, severe exercise even under fasting conditions. It is suggested that this may proceed through an increased hepatic gluconeogenesis.
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