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1. 1. The effect of hyperthermia on muscle release of creatine kinase (CK) was studied on an in vitro rat muscle (extensor digitorum longus) preparation. 2. 2. Release of CK from muscle was more important at 41°C than at 36°C during an in vitro test. 3. 3. After a steady-state phase, an increase in the muscle CK release appeared, before any mechanic index of muscle viability alteration. 4. 4. This final increase of CK release was observed at 36°C and at 41°C, and it could be energy dependent.

Disturbed mental status (DMS) is the most obvious sign of exertional heatstroke in humans, and is one of the main complications of severe exercise heat-stress (SHS). The cause of exertional heat-stroke has been attributed to many factors such as thermoregulatory failure or impairment of muscular function. This investigation was designed to assess muscle energy metabolism in two groups of rats running at 34°C. One group ( n = 17) stopped because of DMS (SHS rats), while the other group (n = 21) stopped because of mild or moderate exercise heat-stress (MHS rats). SHS rats ran longer and had a higher final rectal temperature ( T re ): 66.5 ± 4.2°C vs 47.3 ± 3.8°C, p p T re (0.054 ± 0.007°C min −1 vs 0.072 ± 0.008°C min −1 ) and a lower mean rate of dehydration: 0.065 ± 0.006 vs 0.084 ± 0.005% bodyweight min −1 , p p T re and that there is muscular functional impairment caused by SHS.

The present study was carried out to investigate the effect of chronic heat exposure on tyrosine hydroxylase (TH) protein content in catecholaminergic rat brain-stem areas such as the anterior (LCA) and posterior (LCP) locus coeruleus, the substantia nigra (SN), the ventral tegmental area, and the dorsomedial (DMM) and the ventrolateral medulla and in the adrenal gland (AG). Male Sprague-Dawley rats were exposed to 34 degrees C during 3, 7, or 14 days. Controls were kept at 25 degrees C for the same period. In the LCA, TH content was decreased on day 7 (-34%) and 14 (-37%) of heat exposure. In the SN, TH protein content was decreased on day 7 (-25%) and 14 (-20%) after 34 degrees C. In the DMM cell group, 14 days at 34 degrees C produced a decrease (-20%) of TH content. In all of these structures, TH content variations were correlated with body temperature variations. In the AG, TH content increased progressively to peak (+31%) after 14 days of chronic heat exposure. This increase was also associated with body temperature modification. The selective and body temperature-related response to long-term TH protein content variations following chronic heat exposure observed in the LCA, SN, DMM, and AG could represent an adaptive physiological response of these catecholaminergic cells.

An impairment of muscle energy metabolism has been suggested as a predisposing factor for, as well as a consequence of exertional heatstroke (EHS). Thirteen young men were investigated 6 months after a well-documented EHS using 31Phosphorus Magnetic Resonance Spectroscopy (31P-MRS). The relative concentrations of ATP, phosphocreatine (PCr), inorganic phosphate (Pi), phosphomonoesters (PME), and the intracellular pH (pHi) were determined at rest, during a graded standardized exercise protocol (360 active plantar flexions) and during recovery. Also the leg tissue blood flow was determined by venous occlusion plethysmography during the MRS procedure. Sixteen age-matched healthy male volunteers served as control group. In resting muscle, there were no significant differences between the groups as regards pHi, Pi/PCr, and ATP/PCr+Pi+PME ratios. During steady state exercise conditions, effective power outputs were similar for both groups at each level of exercise: 20, 35, and 50% of maximal voluntary contraction (MVC) of the calf muscle. No significant differences were shown between the two groups in Pi/PCr, pHi, or changes of leg blood flow at each level of exercise. At 50% MVC, Pi/PCr was 0.48 +/- 0.08 vs 0.47 +/- 0.05 (P = 0.96), pHi was 6.94 +/- 0.03 vs 6.99 +/- 0.02, respectively (P = 0.13). Finally, the rate of PCr resynthesis during recovery was not significantly different between the two groups: t1/2 PCr = 0.58 +/- 0.07 vs 0.50 +/- 0.05 min, respectively (P = 0.35). Therefore, no evidence of an impairment of muscle energy metabolism was shown in the EHS group during a standardized submaximal exercise using 31P-MRS performed 6 months after an EHS.

Previous studies have shown that in heat exposed rats, a decreased plasma T4 concentration was associated with a normal biologically active TSH concentration. This study was designed to clarify this apparent discrepancy in the regulation of TSH secretion. In experimental rats (34°C for 25 days) and controls (25°C), plasma total T4 was 3.2 vs. 5.7×10−8 mol/l. (P< 0.01), plasma total T3: 2.4 vs. 5.7×10−10 mol/l. (P

Changes in thyroid activity and variations in the hypthalamo-pituitary-thyroid hormone levels were examined in rats exposed to heat (34 degrees C)for3 weeks. Thyroid activity evaluated histologically (epithelium/colloid ratio, nuclear size) by radioiodine exploration (24 hrs 125 I uptake, ratio of mono- to di-125 iodotyrosines - MIT/DIT, ratio of tri- to tetra-125 iodothyronines-T3/T4, and plasma 125I-T4 and assay of plasma T4, evolves in a triphasic manner. 1.a depression phase between day 0 and day 2.5. 2. a rebound of thyroid activity between day 2.5 and day 9.3 a stabilization of thyroid parameters from day 9 to day 24. These results indicate adaptation of thyroid function to heat after 3 weeks. In phase i, plasma TSH )MeKenzie bioassay) fell to undectable levels concurrent with a 50% decrease in hypothalamic TRH (in vitro assay). Plasma TSH peaked on day 4.5, fell on day 9.5 and returned progressively to initial levels. Hypothalamic TRH returned to initial levels after 6.5 days. The rapid and simultaneous decrease in hypothalamic TRH, plasma TSH, plasma T4 and thyroid activity by the 36th hour of heat exposure (34 degrees C) suggests initiation at the hypothalamic level. In the secound phase, the rebound in thyroid activity is presumably due to the peak in circulating TSH in ralation to the marked decrease in plasma T4. The oscillations of phase 2 and the stabilization of all the thyroid parameters in phase 3 may be the reflection of an apparent discrepancy remains between a low plasma T4 and a normal or subnormal plasma TSH. A modification in the "set point" for the control of TSH secretion is discussed.

The effects of chronic exposure to high environmental temperature (34 degrees C) on T4 production rate, food-intake, growth-rate and resting metabolic rate were investigated in adult male rats. This study was designed to examine the extent of variations and possible relationships between these parameters. As compared to control rats of the same body weight kept at 25 degrees C, rats exposed to 34 degrees C for 3-4 weeks exhibited a retarded growth-rate: 2.3 vs 4.0 g/day, a reduced food-intake: 15.2 vs 23.2 g/day, a decreased T4 production-rate: 1.8 vs 2.7 micrograms/day and a decreased oxygen consumption: 4.0 vs 5.4 ml/min. Heat-exposure altered the 4 parameters to a similar extent. T4 supplementation (3 micrograms/day) which induced a decrease in plasma TSH concentration, did not restore a normal growth-rate in heat-exposed rats. The decreased food-intake of the heat-exposed rats was not associated with any significant changes in the daily pattern of variations of liver glycogen content, or in the mean daily levels of blood glucose or insulin. The ratio T3 to rT3 in plasma was not altered by chronic heat exposure. When rats which had been chronically exposed to heat (25 days at 34 degrees C) were exposed to 25 degrees C, growth-rate, food-intake and oxygen consumption rapidly increased to control values whereas the rate of T4 production remained low. It is concluded that (1) a decrease in thyroid hormone economy is not directly involved in the alterations of growth and energy expenditure in rats chronically exposed to heat, (2) heat exposure does not lead to the establishment of a fasted state resulting from a large reduction in voluntary food intake, (3) metabolic alterations induced by heat exposure are rapidly and completely reversible upon decreasing the environmental temperature.

Para conocer la distribución de velocidades de rotación de las estrellas Be, se utiliza la suposición estándar que los ejes de rotación se distribuyen uniformemente. En este trabajo usamos ángulos proyectados de polarimetría de casi 500 estrellas Be y realizamos un análisis estadístico. Además llevamos a cabo una simulación Monte Carlo cuyos resultados explican las características observadas de los ángulos, confirmando que provienen de una distribución uniforme, pero que sus ángulos proyectados poseen una estructura bimodal. Esta última característica podría cambiar las conclusiones acerca de la distribución de velocidades de rotación de estas estrellas. In order to know the distribution of rotational velocities of Be stars, a standard assumption is used, namely that the rotational axes are uniformed distributed. We use here polarimetric projected angles data from almost 500 Be stars and we make a statistical analysis. Furthermore we perform a Monte-Carlo simulation that explains the observed features of the angles, confirming that it is indeed uniform distributed, but the projected angles possess a bimodal structure. This last features may change the conclusion about the rotational velocity distribution of these stars. Fil: Curé, M.. Universidad de Valparaíso; Chile Fil: Christen, A.. Universidad de Chile; Chile Fil: Rivinius, Th.. European Southern Observatory; Chile Fil: Rial, Diego Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Investigaciones Matemáticas "luis A. Santaló"; Argentina. Universidad de Valparaíso; Chile