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.

Rats were trained to run on a horizontal treadmill for 2 h at 20 m/min. This activity considerably increased plasma free tryptophan (TRP) (+70%) but did not alter plasma total TRP levels and had little or no effect on plasma concentrations of the other large neutral amino acids (LNAAs) that compete with TRP for entry into the brain. Brain TRP levels increased by 80%. The only other brain LNAA to be affected by exercise was threonine, which rose moderately. The results indicate that increased plasma free TRP was specifically responsible for the increase of brain TRP after 2 h of exercise. Brain lysine was also increased whereas glycine, alanine, and gamma-aminobutyric acid were decreased. The differences between the present findings and those previously obtained following 2 h immobilization stress are discussed.

The influence of the two distinct training programmes, moderate (M) and intensive (I), on hypothalamo-pituitary-adrenal (HPA) axis was investigated, in rats. Changes in plasma concentrations of adrenocorticotropin hormone (ACTH) and corticosterone were followed in response to (i) a 60-min acute running session performed on 2nd, 4th and 6th of the seven training weeks (ii) an acute restraint stress of 40 min applied after the final training programme. After 2nd, 4th and 6th week of the two training programmes, a 60-min running resulted in an enhanced secretion of ACTH and corticosterone, compared with both the baseline values (i.e. before running) and to the sedentary (S) group. However, on 4th and 6th weeks compared with 2nd week, ACTH and corticosterone remained elevated in intensive group when they are significantly reduced in moderate group. We could suggest that a moderate training resulted in an adapted hormonal response whereas a deadapted process occurred for the intensive programme. The day after the last training session, basal ACTH, corticosterone and corticosteroid-binding globulin (CBG) capacity were not affected by training. Hypothalamic corticotropin-releasing factor tissue-content (CRF) was increased significantly in the two trained groups. When compared with the sedentary group, the body weight of the rats in the two trained groups was significantly decreased with a total adrenal mass increasing but only in intensive group. The surimposed restraint stress resulted in significant increases in plasma ACTH and corticosterone both in trained and in sedentary animals. This result suggests that the adapted HPA axis response induced by both a moderate and intensive training do not prevent against the effects of a novel stress such as restraint stress.

The expression of myosin isoforms was studied in regenerated rat soleus muscle during either normal or altered postural activity. Regeneration was induced following injury by venom from the Notechis scutatus scutatus snake. Immunohistochemical analysis showed that, in regenerating soleus muscle after 3 wk of hindlimb suspension, nearly all fibers reacted positively with the myosin heavy chain (MHC) antibody associated with fast-twitch muscle fibers (fast MHC). When 3 wk of recovery with normal weight-bearing activity followed hindlimb suspension, the regeneration soleus muscle exhibited a nearly homogeneous staining with the MHC antibody associated with the slow-twitch muscle fibers (slow MHC). These findings were in accordance with quantitative analysis of the electrophoretic separation of the native myosin isoforms. Immunohistochemical data showed that removal of weight bearing in the 21-day old regenerated soleus muscles resulted in an increase in fast MHC expression. Together, the results of the present study clearly demonstrate that the postural load is an important component in the induction of slow MHC in regenerating muscle and that the control of the expression of MHC in muscle comprising a homogeneous population of fibers deriving from satellite cells appears more homogeneous and more complete than in a nondegenerated one.

No abstract

Muscle growth, fiber size, muscle and liver glycogen, plasma hormones, and muscle glutamine concentration were evaluated in rats chronically exposed (26 days) to a simulated hypobaric altitude (HA; 6,000 m) and fed diets of varying protein concentrations (10, 20, or 40 g protein/100 g of dry matter; LP, MP, and HP, respectively). Values were compared with those measured in animals maintained under normobaric conditions and either fed ad libitum (SL groups) or pair fed equivalent quantities of food consumed by HA animals (PF groups). There was marked anorexia in response to HA exposure for all protein diets (P < 0.001). A specific effect of hypoxia on the decrease in muscle growth has been identified by comparison of the values of the muscle weight-to-body weight ratio between HA and PF groups (P < 0.05 for all dietary protein levels). Plasma insulin concentrations were lower in HA than in SL and PF rats (P < 0.05). Liver glycogen was significantly decreased by exposure to HA (P < 0.001) and high dietary protein content (P < 0.005). Hypoxia per se and decreased food intake had additive effects on soleus muscle glycogen concentrations. An increase in muscle glutamine was observed in rats fed the LP diet in comparison with the MP diet, especially in SL and PF groups (P < 0.05). These results clearly demonstrate that 1) hypobaric hypoxia per se decreases growth rate in rats and 2) increasing the dietary protein intakes in rat had no effect on the depression of muscle growth related to high altitude but had deleterious effects on glycogen deposition in liver and fast muscle.

The aim of this study was to analyze the effects of treadmill training (2 h/day, 5 days/wk, 30 m/min, 7% grade for 5 wk) on the expression of myosin heavy chain (MHC) isoforms during and after regeneration of a fast-twitch white muscle [extensor digitorum longus (EDL)]. Male Wistar rats were randomly assigned to a sedentary (n = 10) or an endurance-trained (ET; n = 10) group. EDL muscle degeneration and regeneration were induced by two subcutaneous injections of a snake toxin. Five days after induction of muscle injury, animals were trained over a 5-wk period. It was verified that approximately 40 days after venom treatment, central nuclei were present in the treated EDL muscles from sedentary and ET rats. The changes in the expression of MHCs in EDL muscles were detected by using a combination of biochemical and immunocytochemical approaches. Compared with contralateral nondegenerated muscles, relative concentrations of types I, IIa, and IIx MHC isoforms in ET rats were greater in regenerated EDL muscles (146%, P < 0.05; 76%, P < 0.01; 87%, P < 0.01, respectively). Their elevation corresponded to a decrease in the relative concentration of type IIb MHC (-36%, P < 0.01). Although type I accounted for only 3.2% of total myosin in regenerated muscles from the ET group, the cytochemical analysis showed that the proportion of positive staining with the slow MHC antibody was markedly greater in regenerated muscles than in contralateral ones. Collectively, these results demonstrate that the regenerated EDL muscle is sensitive to endurance training and suggest that the training-induced shift in MHC isoforms observed in these muscles resulted from an additive effect of regeneration and repeated exercise.

The drug test for exogenous administration of testosterone is based on the testosteronelepitestosterone ratio (TIE) in urine. Physiological and psychological stresses may alter plasma testosterone concentrations. The question is to know how much the psychological conditions of competition can modify the TIE ratio. In order to study this issue, 20 athletes practising modern pentathlon participated in a study designed to determine the effects of a pistol shooting trial on their hormonal response. Pistol shooting induces a high psychological stress without increasing energy expenditure. Venous blood samples were drawn before and after the trial according to the usual drug testing procedure. Athletes were separated into two groups: a group of young athletes ( n = 10; mean age 19 f 0.3 years) and another group of aged subjects (n = 10; mean age 45f 1.5 years). The rise in plasma testosterone concentrations reached 75 % in older subjects versus 55 % in younger ones. The plasma luteinizing hormone (LH) concentrations were not influenced by the trial. After shooting trial the elevation in cortisol concentrations was greater for oldersubjects than for younger ones (273 f 30 ng . rnl-' vs 173 f 7 ng . mt-'). The catecholamine response was identical in both groups. The urinaryT/E ratio remained unchanged after the shooting trial and always remained lowerthan the International Olympic Committee limit of 6 . These results indicate that the psychological stress associated with competition increases the production of steroid hormones (testosterone, cortisol). and that this phenornenon is more pronounced in older athletes. These hormonal changes do not influence the urinary excretion of steroid metabolites used as criterion for drug testing. On