The purpose of this investigation was to evaluate the effects of 24-h carbohydrate-poor diet on metabolic and hormonal responses induced by prolonged exercise in both follicular (FP) and luteal (LP) phases of the menstrual cycle. At mid-FP and at mid-LP, seven eumenorrheic young women [means +/- SE; chronological age, 21.1 +/- 0.6 yr; O2 uptake (VO2) peak, 43.7 +/- 2.0 ml X kg-1 X min-1; body fat, 19.2 +/- 2.0%] were subjected to a 90-min bicycle exercise period at an intensity representing 63% of their measured VO2 peak. Venous blood samples obtained before and during exercise were analyzed for levels of substrates (glucose, lactate, free fatty acids, glycerol) and hormones (luteinizing hormone, progesterone, estradiol, insulin, glucagon, cortisol, catecholamines). Contrary to FP, a significant (P less than 0.01) decrease in blood glucose concentration was observed after 70 and 90 min of exercise during LP. Significant phase differences were also observed for blood lactate (highest in FP), cortisol (highest in LP), and progesterone (highest in LP). Although not significantly different, tendencies for menstrual phase dissociations were noticed for some of the other measured variables. Hence, a menstrual phase dissociation in circulating glucose level, unmasked by a prolonged exercise performed after a 24-h carbohydrate-poor diet, suggests to the authors a specific metabolic involvement for gonadotrophic and/or gonadal hormones.

Eight male subjects (24 +/- 1 years old) performed graded ergocycle exercises in normoxic (N) and acute hypoxic (H) conditions (14.5% O2). VO2max decreased from 55.5 +/- 1.3 to 45.8 +/- 1.4 ml . kg-1 . min-1 in H condition. Plasma glucose and free fatty acid concentrations remained unchanged throughout exercise in both conditions. Increase in blood lactate concentration was associated with relative workload in both conditions. At VO2max lactate concentrations were similar in the two conditions, plasma insulin, glucagon, and LH concentrations did not significantly change in either. Plasma delta 4-androstenedione and testosterone increased in a similar manner in both conditions. Finally plasma norepinephrine concentration reached at VO2max was significantly lower in hypoxia. These results suggest that acute moderate hypoxia does not affect metabolic and hormonal responses to short exercise performed at similar relative workloads, i.e. when the reduction of VO2max due to hypoxia is taken into consideration. The lower catecholamine response to maximal exercise under acute hypoxia might suggest that the sympathetic response could be related to relative as well as absolute workloads.

In order to describe fluid-electrolyte shift and endocrine response to exercise under moderate acute hypoxia, 8 healthy male subjects (24 +/- 3 years old) were evaluated at 40, 60, 80 and 100% VO2 max in normoxic (N) and hypoxic (H) conditions (14.5% O2). VO2 max decreased from 55.5 +/- 1.3 to 45.8 +/- 1.4 ml/kg X min in H condition. Plasma volume reductions with increasing relative workloads were similar in N (9.4%) and H (9.9%) conditions. The rise in plasma osmolality was in part related to blood lactate accumulation which occurred in both conditions. However, variations in plasma solute content and osmolality suggested that exercise under hypoxia results in a greater electrolyte loss from vascular space and in a greater K+ loss from working skeletal muscles. Increase in catecholamine concentrations were similar in normoxic and hypoxic conditions except for lower maximal norepinephrine concentration under hypoxia. Finally, although plasma renin activity increased with workload in both conditions, plasma aldosterone did not significantly change. This dissociation between renin and aldosterone suggest that aldosterone release during exercise might depend upon other factors. However, changes in plasma potassium concentration do not appear as an important stimulus for aldosterone secretion during exercise.

Extant literature dealing with metabolic and hormonal adaptations to exercise following carbohydrate (CHO) reduced diets is not sufficiently precise to allow researchers to partial out the effects of reduced blood glucose levels from other general effects produced by low CHO diets. In order to shed light on this issue, a study was conducted to examine the effects of a 24-h CHO-poor diet on substrate and endocrine responses during prolonged (75 min; 60% Vo2max) glucose-infused leg exercise. Eight subjects exercised on a cycle ergometer in the two following conditions: 1) after a normal diet (CHON), and 2) after a 24-h low CHO diet (CHOL). In both conditions, glucose was constantly infused intravenously (2.2 mg . kg-1 . min-1) from the 10th to the 75th min of exercise in relatively small amounts (10.4 +/- 0.8 g). No significant differences in blood glucose concentrations were found between the two conditions at rest and during exercise although a significant increase (p less than 0.01) in glucose level was observed in both conditions after 40 min of exercise. The CHOL as compared to the CHON condition, was associated with significantly (p less than 0.05) lower resting concentrations of insulin, muscle glycogen (8.7 vs 10.6 g . kg-1), and triacylglycerol, and greater concentrations of beta-hydroxybutyrate (0.5 vs 0.2 mmol . L-1), and free fatty acids. During exercise, the CHOL condition as compared to the CHON condition, was associated with significantly (p less than 0.05) lower insulin and R values, as well as greater free fatty acid (from min 20 to 60) and epinephrine (min 60 to 75) concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

The purpose of the present investigation was to evaluate the effects of a small infusion of pyruvate into the hepatic portal vein on the pancreatic hormone response during exercise (30-min treadmill run; 26 m/min, 0% grade) in adrenodemedullated rats. Resting and exercising rats were infused with either pyruvate (5% solution; 0.016 ml/min) into the portal vein, pyruvate into the jugular vein, or saline into the portal vein. Peripheral and portal blood glucose concentrations were decreased (P < 0.01) similarly in all groups after the exercise period. Peripheral insulin, glucagon, and norepinephrine levels, either at rest or after exercise, were not significantly affected by the infusions. The response of portal pancreatic hormone concentrations to exercise was, however, reduced by the pyruvate infused into the portal and jugular veins for insulin and into the portal vein only for glucagon. The normal increase in peripheral glucagon-insulin molar ratio during exercise was shut down by the infusion of pyruvate into the portal vein but not by the infusion of pyruvate into the jugular vein or by the infusion of saline. These results indicate that a small blood infusion of pyruvate, even in the presence of a decreasing blood glucose level, can attenuate substantially the pancreatic hormone response during exercise in adrenodemedullated rats.