In order to test the hypothesis that dietary restriction may have a negative influence on physiological and psychological adaptation to a judo competition, we examined the effects of weight loss induced by restricting energy and fluid intake on the physiology, psychology, and physical performance of judo athletes. Twenty male judoka were randomly assigned to one of two groups (Group A: called diet, n = 10; height 174.8 +/- 1.9 cm, body weight 75.9 +/- 3.1 kg; they were asked to lose approximately 5 % of their body weight through self-determined means during the week before the competition; Group B: called control, n = 10; height 176.4 +/- 1.1 cm, body weight 73.3 +/- 6.3 kg maintained their body weight during the week before the competition). A battery of tests was performed during a baseline period (T1), on the morning of a simulated competition (T2) and 10 min after the end of the competition (T3). The test battery included assessment for body composition, performance tests, evaluation of mood, determination of metabolic and hormonal responses. Dietary data were collected using a 7-day diet record. The nutrient analysis indicated that all the athletes followed a low carbohydrate diet whatever the period of the investigation. For the Group A, the food restriction (- 4 MJ per day) resulted in significant decreases of the body weight and altered the mood by increasing Fatigue, Tension and decreasing Vigour. Dietary restriction had also a significant influence on metabolic and endocrine parameters and was associated with poor performance. After the competition, significant decreases of the levels in testosterone, T/C ratio, alkali reserve, and free fatty acid were observed in both groups, whereas the plasma concentrations in insulin, ammonia, urea, and uric acid were increased. In conclusion, our results suggest that the combination of energy restriction and intense exercise training, which causes weight reduction before a competition, adversely affects the physiology and psychology of judo athletes and impairs physical performance before the competition. Our data are the first to demonstrate that a competition including five 5-min bouts induced the same changes of physiological and psychological variables and performance whatever the dietary intake (dietary restriction or not) during the seven days before the competition.

Neuroprotective functions of erythropoietin (Epo) are thought to involve a heteroreceptor composed of both Epo receptor (Epo-R) and common beta chain (betac). Here, we measured the response of hippocampal Epo system components (Epo, Epo-R and betac) during neurodegenerative processes following pilocarpine-induced status epilepticus (SE), and examined whether recombinant human Epo (rHuEpo) could support neuronal survival. We evidence that Epo is induced in astroglia following SE, in particular within areas displaying delayed neuronal death. In addition, we demonstrate for the first time that rHuEpo reduces considerably hippocampal neurodegeneration following SE. rHuEpo may thus supplement astroglial induction of Epo to promote enhanced hippocampal neuronal survival following SE. We also show that Epo-R is expressed by neurons and astrocytes mainly, while betac is barely detectable in basal conditions and induced in reactive microglia exclusively following SE. Altogether, our results suggest that Epo/rHuEpo exerts neuroprotection, through Epo-R signaling and independently of betac, and, therefore, may be anti-epileptogenic.

Exposure to intermittent hypoxia (IH), such as occurs in sleep-disordered breathing, is associated with increased apoptosis in vulnerable brain regions as well as with spatial reference memory deficits in adult and developing rats. The latter are more susceptible to IH, suggesting that early exposure to IH may have long-term consequences. Rats were exposed to 14 d of room air (RA) or IH starting at postnatal d 10. Working memory was then assessed in the water maze at 4 mo of age using a delayed matching to place task in which the rats were required to locate a submerged platform hidden in a novel location on the first trial (T1 or acquisition trial), and then remember that position after a delay (T2 or test trial). Mean escape latencies and swim distances were derived and the savings (T1-T2) were used as a measure of working memory. Male but not female rats exposed to IH showed working memory deficits at both a 10-and 120-min delay (for both latency and pathlength). Additionally, Sholl analysis of Golgi-stained neurons revealed decreased dendritic branching in the frontal cortex, but not the hippocampus, of male rats exposed to IH. Norepinephrine concentrations, dopamine turnover, and tyrosine hydroxylase activity were increased similarly in males and females. However, increased dopamine concentrations were present only in the frontal cortex of female rats. In conclusion, exposure to IH during a critical developmental period is associated with long-term alterations in frontal cortical dopaminergic pathways that may underlie gender differences in neurobehavioral deficits. OSA is a highly prevalent condition that affects 2-3% of all children (1-3). It is characterized by the repetitive development of either complete or partial upper airway occlusion that leads to periodic hypoxemia and hypercapnia and to recurring arousals. In recent years, it has become apparent that OSA imposes substantial neurobehavioral morbidity (4 -6), particularly of functions pertaining to the PFC (7), and that such alterations in attention, executive, and intellectual function may not be completely reversible (8). The recent development of a rodent model, whereby IH is applied during sleep, has allowed for improved delineation of some of the potential mechanisms underlying the morbid consequences of OSA (8 -17). Furthermore, a unique period of neuronal susceptibility emerged, such that developing rats exposed to IH displayed reduced apoptosis during the immediate postnatal period but markedly enhanced neuronal cell loss between 10 and 25 d of age, compared with adult animals (18). Furthermore, exposure to IH during this period was associated with marked reductions in the ability to acquire a spatial task in the water maze and with locomotor hyperactivity in males but not in females (9). The potential irreversibility of the IH-induced effects was further suggested by Decker and colleagues (19), who reported altered dopaminergic transmission in rats exposed perinatally

SUMMARY1. The peripheral, arterial chemoreceptors in the carotid body are active and responsive in the fetus. At birth, when oxygenation increases, the chemoreceptors are silenced. Over the next few days the sensitivity is reset toward the adult level and the chemoreceptors influence breathing during normal conditions. In order to investigate the underlying mechanisms of this resetting we examined the strength of the chemoreflex in newborn rats and correlated this to the contents of dopamine and noradrenaline in the carotid bodies of the newborn pups and near-term fetuses. Furthermore, turnover rates of dopamine and noradrenaline were determined in newborn rats up to 1 week of age by analysis of catecholamine decreases after inhibition of synthesis with a-methyl-p-tyrosine.2. Chemoreceptor influence was assessed by the method of 'physiological chemodenervation' with hyperoxia of 15-20 s duration in unanaesthetized rat pups. Relative changes in ventilation elicited by hyperoxia were determined by body plethysmography. We found no change in ventilation on the day of birth either in vaginally born rats or in near-term pups delivered by Caesarean section. After 1 day there was a significant decrease in ventilation of -19-4 + 2'3 % (mean + S.E.M.) and at 7 days of age the decrease was -28-8 + 2-2 %, suggesting an increasing influence from the peripheral chemoreceptors.3. The contents of dopamine and noradrenaline were measured by highperformance liquid chromatography. Dopamine increased from 3.7 + 04 pmol (pair of carotid bodies)-' in the fetus to a peak of 15-9 + 2-6, 6-12 h after birth followed by a decline to 7-1 + 0-7 at 7 days of age. Noradrenaline levels increased from 1-3 + 0 3 in the fetus to 9'6 + 1 1 pmol (pair of carotid bodies)-' after 4 days. The turnover rate of dopamine decreased from 4-4 pmol (pair of carotid bodies)-' h-1 0-6 h after birth to 1-0 at 6-12 h of age. The turnover rate of noradrenaline also decreased over the first hours following delivery.4. Since dopamine is an inhibitory neuromodulator in this system, we suggest that the increase in sensitivity seen after the first day of life is, at least in part, due to a decrease in the release of dopamine and thus a removal of an inhibitory mechanism.MS 7746

Erythropoietin receptor (EpoR) binding mediates neuroprotection by endogenous Epo or by exogenous recombinant human (rh)Epo.The level of EpoR gene expression may determine tissue responsiveness to Epo. Thus, harnessing the neuroprotective power of Epo requires an understanding of the Epo-EpoR system and its regulation. We tested the hypothesis that neuronal expression of EpoR is required to achieve optimal neuroprotection by Epo. The ventral limbic region (VLR) in the rat brain was used because we determined that its neurons express minimal EpoR under basal conditions, and they are highly sensitive to excitotoxic damage, such as occurs with pilocarpine-induced status epilepticus (Pilo-SE). We report that (i) EpoR expression is significantly elevated in nearly all VLR neurons when rats are subjected to 3 moderate hypoxic exposures, with each separated by a 4-day interval; (ii) synergistic induction of EpoR expression is achieved in the dorsal hippocampus and neocortex by the combination of hypoxia and exposure to an enriched environment, with minimal increased expression by either treatment alone; and (iii) rhEpo administered after Pilo-SE cannot rescue neurons in the VLR, unless neuronal induction of EpoR is elicited by hypoxia before Pilo-SE. This study thus demonstrates using environmental manipulations in normal rodents, the strict requirement for induction of EpoR expression in brain neurons to achieve optimal neuroprotection. Our results indicate that regulation of EpoR gene expression may facilitate the neuroprotective potential of rhEpo.hypoxia ͉ environmental enrichment ͉ epilepsy ͉ limbic system ͉ enviromimetic

We examined changes in the haematological, metabolic, immunological, hormonal, and psychological fields using selected variables in 20 professional soccer players. over the course of a competitive season. The team performance was assessed by computing the winning percentage. A symptom checklist was used to assess the severity of upper respiratory tract infections. A high-intensity training programme induced a significant increase in cortisol and uric acid concentrations. Despite lower glutamine concentrations than the normal range throughout the study, infection occurred only in two of the soccer players. Moreover, the levels of immunological factors IgA, IgG, and IgM, and the haematological parameters were unaltered. Subsequent decreased performance coincided with changes in specific mood states of the team. Our results show some alterations on the metabolic, hormonal, and psychological variables over the five fields studied, suggesting that combined psychological and physiological changes during training are of primary interest to monitor the training stress in relation to performance in team sport.

To determine whether prenatal hypoxia increases the risk of developing cardiovascular disorders as an adult and, if so, the identity of the cell mechanisms involved in such dysfunction, we evaluated the sympathoadrenal system and central areas related to cardiovascular events during development and the cardiovascular parameters in adults. Pregnant rats were exposed to hypoxia (10% oxygen) from embryonic day (E) 5 to E20 and the offspring studied at 1, 3, 9 and 12 weeks of age for neurochemistry and at 12 weeks of age for cardiovascular analysis. In the 1-, 3- and 9-week-old offspring, the levels and utilization of catecholamines were reduced in sympathetic ganglia, in target organs, in adrenals and in the rostral part of the A2 cell group in the nucleus tractus solitarius, but were increased in the locus coeruleus. In the 12-week-old adult offspring, the lowered autonomic nervous activity was restricted to cardiac-related structures, i.e. the stellate ganglion, heart and adrenals. In adult rats, prenatal hypoxia did not affect the cardiac parameters under resting conditions but increased blood pressure and the variability of blood pressure and heart rate under stress conditions. The altered metabolic activity of the sympathoadrenal system and related central areas during development and at adulthood for most structures might be part of the potential mechanisms contributing to cardiovascular disorders in adults.

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