The purpose of this study was to evaluate the effects on physical performance of three levels of energy intake during a 5-day period of prolonged physical exercise and relative sleep deprivation. A group of 27 male soldiers were randomly assigned to three groups receiving either 1800 kcal.24 h-1 (7560 kJ, LC), 3200 kcal.24 h-1 (13440 kJ, MC) or 4200 kcal.24 h-1 (17,640 kJ, HC). They took part in a 5-day combat course (CC) of heavy and continuous physical activities, with less than 4 h sleep per day. Performance capacity was tested just before and at the end of CC. Maximal oxygen uptake (VO2max) was determined during an exhausting incremental exercise test on a cycle ergometer. Anaerobic performance was measured from the time during which exercise could be maintained at supra maximal loads on a cycle ergometer. After CC, the subjects receiving LC exhibited a 14% decrease in power output at exhaustion in the incremental exercise test [from 325 (SEM 8) to 278 (SEM 9) W, P < 0.001] and a significant decrease in VO2max of 8% [from 3.74 (SEM 0.06) to 3.45 (SEM 0.05) 1.min-1, P < 0.05]. The remaining two experimental groups demonstrated the same mechanical and metabolic performances on days 1 and 5. Anaerobic performance was not influenced by energy intake and the field course. Blood samples were obtained at rest on days 1 and 5. At the end of CC, the data demonstrated a significant decrease in blood glucose concentrated ion (P < 0.01) for LC diet only.(ABSTRACT TRUNCATED AT 250 WORDS)

The glucose disappearance rate measured after IV glucose injection (1g/kg body wt) remained unchanged between 12 and 21 day of gestation in the rat. In contrast, insulin secretion in response to IV glucose was markedly increased on day 19 and 21 of pregnancy, suggesting resistance to endogenous insulin. Glucose kinetics (glucose production, utilization and clearance) in response to various doses of IV insulin have been studied in anaesthetised post-absorbtive 19 day pregnant and virgin rats using 6-(3)H glucose. With the supramaximal dose of insulin (4 U/kg body wt) no differences in glucose kinetics were found between pregnant and virgin rats. In contrast, with the two lower doses of insulin (0.15 and 0.05 U/kg body wt) glucose production was inhibited by 36 plus or minus 3% and 13 plus or minus 2% (Mean plus or minus SEM) respectively in virgin rats, but was not decreased in pregnant rats. When the effect of insulin on glucose clearance was expressed as % of the maximal effect obtained with 4 U/kg body weight, the rise in glucose clearance in response to the two lower doses of insulin (0.15 and 0.05 U/kg body wt) was lower in pregnant (57.5 plus or minus 6 and 27. 4 plus or minus 4%) than in virgin rats (73.3 plus or minus 6 and 42.2 plus or minus 7%). These results suggest that a decreased sensitivity to insulin appears in late pregnancy in the rat and could involve both liver and skeletal muscle.

The development of fatty acid metabolism was studied in isolated hepatocytes from newborn rats. Ketone-body production from oleate is increased 6-fold between 0 and 16 h after birth. This increase is related to an enhanced beta-oxidation rather than to a channeling of acetyl-CoA from the tricarboxylic acid cycle to ketone-body synthesis. The increase in oleate oxidation is not related to a decreased esterification rate, as the latter is already low at birth and does not decrease further. At birth, lipogenic rate is 2-3-fold lower than in fed adult rats and it decreases to undetectable values in 16 h-old rats. A 90% inhibition of lipogenesis in hepatocytes of newborn rats (0 h) by glucagon and 5-(tetradecyloxy)-2-furoic acid does not lead to an increased oxidation of non-esterified fatty acids. This suggests that the inverse relationship between lipogenesis and ketogenesis in the starved newborn rat is not responsible for the switch-on of fatty acid oxidation at birth. Moreover, ketogenesis from octanoate, a medium-chain fatty acid the oxidation of which is independent of carnitine acyltransferase, follows the same developmental pattern at birth as that from oleate.

We studied the effects of prolonged physical activities on resting heart rate variability (HRV) during a training session attended by 23 cadets of the French military academy. This course lasts 1 month and is concluded by a 5-day field exercise simulation with physical and psychological stress. Data collection took place before (B) and immediately at the end (E) of the course. It included HRV recordings during a stand test (5 minutes lying down and 5 minutes standing), with a Polar R-R monitor, followed by blood sampling to assay plasma testosterone. The results (B and E) showed that the testosterone level fell by approximately 28.6 +/- 7%, indicating a high level of fatigue. During the stand test, the total power (TP) of the HRV spectrum increased in a supine position. The TP of B was 5,515.7 ms2 (SE, 718.4) and of E was 13018.9 ms2 (SE, 2,539.2; p < 0.001). High-frequency (HF) normalized values increased and low-frequency (LF) normalized values fell, regardless of position (HF normalized values and LF normalized values: supine, p < 0.01, p < 0.05; standing, p < 0.05, p < 0.01, respectively). LF:HF ratio fell 66.2 (SE, 12.9%; p < 0.01) in a lying position. During the time-domain analysis of HRV, differences between adjacent normal R-R intervals more than 50 milliseconds, expressed as a percentage, and differences between the coupling intervals of adjacent normal RR intervals increased in the lying position (p < 0.001). These results as a whole suggest that parasympathetic nervous system activity increases with fatigue.

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