The aim of this study was to investigate if enhanced peripheral ammonia production during exhaustive exercise increases ammonia detoxication in brain mediated by glutamine synthesis, and subsequently influences glutamate and gamma-aminobutyric acid (GABA) levels. This neurotransmitter production is related to the metabolism of glutamine. A group of rats was trained for 6 weeks by treadmill running (TR). They were compared to a group of untrained rats (UN). At the end of training, half of TR and UN rats were submitted to one session of treadmill running until exhaustion (288+/-12 min and 62+/-5 min in TR and UN group, respectively). At exhaustion, running and control rats were sacrificed in order to collect blood and to take samples of the following brain structures: cortex, striatum and cerebellum. Treadmill running until exhaustion induced an increase in blood ammonia by 140% without significant differences between TR and UN groups. Brain ammonia increased in both groups. However, TR group exhibited values 50% higher than those observed in UN group. Brain glutamine was increased at exhaustion in all groups of running rats by 30-75% of basal value whereas the glutamate only decreased in TR rats which were able to run for a longer time. In this group, the GABA level decreased in striatum. These data confirm that enhanced brain ammonia level during exercise stimulates glutamine synthesis as a mechanism of detoxication. After several hours of running, a reduction in brain glutamate levels was observed in all brain structures in trained rats but only in the striatum in untrained animals. The reduced availability of this GABA precursor decreases GABA levels only in the striatum of TR group by 45% of the resting value. These results suggest a relation between cerebral changes in neurotransmitters and excitatory amino acids, such as glutamate and GABA, and central fatigue.

The aim of this study was to determine, in the rat, the effects of chronic exposure (7-9 weeks) to normobaric hypoxia (FIO2=0.13, equivalent to 3700 m altitude) on cardiac and skeletal muscle properties, on maximal oxygen uptake (VO2max), and endurance time to exhaustion (ETE). In addition, we evaluated the impact of endurance training (90 min of treadmill running per day, 5 days per week, for 9 weeks) on these parameters. The results were compared to normoxic rats fed ad libitum (NAL) and to normoxic pair-weight (NPW) animals in order to take into account the influence of hypoxia on growth rate. It was found that, in sedentary rats, hypoxia results in stunted growth, adrenal atrophy, a significant reduction of cross-sectional area of fast-twitch (type II) fibres, a reduced capillary-to-fibre ratio (C/F), and a reduced oxidative capacity (decreases in citrate synthase and 3-hydroxy-Acyl CoA dehydrogenase activities) of the plantaris muscle. These effects are mainly related to the anorexic effects of prolonged exposure to hypoxia. Nevertheless, hypoxic (H) rats displayed higher VO2max and ETE values when compared either to NAL or to NPW animals. Endurance training resulted, in all groups (H, NAL, NPW), in a significant change of the fibre type distribution of the plantaris which displayed an increased number of type IIA fibres and a decreased proportion of type IIB fibres. In addition, the C/F ratio and cross-sectional area of fast-twitch fibres were normalized by superimposition of training on hypoxia. Both VO2max and ETE were significantly higher in trained H rats than in NAL, but these improvements were mainly related to the reduced body weight induced by hypoxia. These data suggest that the greater aerobic capacity and tolerance for prolonged exercise induced by chronic exposure to hypoxia can be mainly accounted for by the anorexic effects of hypoxia, although other factors (e.g. increase in oxygen carrying capacity induced by hypoxia acclimatization) may play a significant role in some circumstances (e.g. in sedentary rats).

The aim of this study was to determine, in the rat, the effects of chronic exposure (7-9 weeks) to normobaric hypoxia (FIO2=0.13, equivalent to 3700 m altitude) on cardiac and skeletal muscle properties, on maximal oxygen uptake (VO2max), and endurance time to exhaustion (ETE). In addition, we evaluated the impact of endurance training (90 min of treadmill running per day, 5 days per week, for 9 weeks) on these parameters. The results were compared to normoxic rats fed ad libitum (NAL) and to normoxic pair-weight (NPW) animals in order to take into account the influence of hypoxia on growth rate. It was found that, in sedentary rats, hypoxia results in stunted growth, adrenal atrophy, a significant reduction of cross-sectional area of fast-twitch (type II) fibres, a reduced capillary-to-fibre ratio (C/F), and a reduced oxidative capacity (decreases in citrate synthase and 3-hydroxy-Acyl CoA dehydrogenase activities) of the plantaris muscle. These effects are mainly related to the anorexic effects of prolonged exposure to hypoxia. Nevertheless, hypoxic (H) rats displayed higher VO2max and ETE values when compared either to NAL or to NPW animals. Endurance training resulted, in all groups (H, NAL, NPW), in a significant change of the fibre type distribution of the plantaris which displayed an increased number of type IIA fibres and a decreased proportion of type IIB fibres. In addition, the C/F ratio and cross-sectional area of fast-twitch fibres were normalized by superimposition of training on hypoxia. Both VO2max and ETE were significantly higher in trained H rats than in NAL, but these improvements were mainly related to the reduced body weight induced by hypoxia. These data suggest that the greater aerobic capacity and tolerance for prolonged exercise induced by chronic exposure to hypoxia can be mainly accounted for by the anorexic effects of hypoxia, although other factors (e.g. increase in oxygen carrying capacity induced by hypoxia acclimatization) may play a significant role in some circumstances (e.g. in sedentary rats).

The aim of this study was to determine the impact of chronic treatment for 8 weeks with hydrocortisone acetate (5 mg kg-1 day-1) on skeletal muscles, and to evaluate whether sprint training can prevent glucocorticoid-induced muscle atrophy better than endurance training. Biochemical, histological and contractile properties were employed to determine the influence of this steroid on skeletal musculature, and the results were compared to pair-weight animals to take into account the influence of corticoids on growth rate. It was found that hydrocortisone acetate treatment results in a stunted growth, adrenal atrophy and depressed plasma corticosterone levels. Mild corticoid-induced losses of muscle mass and protein content (9%-13%) were observed in fast-twitch skeletal muscles. It appeared that the impact of corticoids is strictly directed toward type IIb fibres, which displayed a 12%-18% reduction in cross-sectional areas. No alterations occurred in plantaris contractile speed or tensions properties. Neither endurance training (30 m/min; 90 min/day; 5 days/week) nor sprint training (60 m/min; 15 min/day; 5 days/week) for 8 weeks was able to counteract the effects of corticoids. These data suggest that increased contractile activity, as induced by treadmill running, is not sufficient to counteract the muscular effects of glucocorticoids when administered at a dose of 5 mg kg-1 day-1.

The present study was designed to examine the effects of administration of a GABAergic agonist (Baclofen) on run-time to exhaustion in trained and untrained rats, and on some indicators of fatigue. Run-time to exhaustion on a treadmill set at a speed of 25 m.min-1 was significantly increased in both untrained (p < 0.01) and trained rats (p < 0.005) administered with baclofen one hour before the exercise. The animals who had run the longest time displayed the lowest concentrations of liver and muscle glycogen, and a decrease in plasma glucose concentrations (p < 0.05). The results of this investigation suggest that fatigue during prolonged exercise can be influenced by pharmacological administration of a GABAergic agonist. Indicators of fatigue such as glycemia, liver and muscular glycogen are not the limiting factors of performance and central mechanisms play a key role at exhaustion.