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Muscle temperature of mammals: cooling impairs most functional properties.

Our purpose was to study the effect of a decrease in skeletal muscle temperature on single and repeated shortening, isometric, and lengthening contractions of mammalian skeletal muscles. Fast extensor digitorum longus muscles of mice were studied in situ and in vitro at 25 and 35 degrees C. No difference in isometric force was observed, but maximum and sustained powers were reduced by 40 and 62%, respectively. With cooling, maximum power absorption, which is proportional to the external work required to lengthen the muscle, increased significantly at each velocity of lengthening from 0.5 to 4.0 optimum fiber length/s. The 10 degrees C decrease in muscle temperature produced a decrease in power that was primarily a result of the decrease in the velocity of shortening, whereas the increase in power absorption was likely due to an increase in the number of strongly bound cross bridges resulting from a decreased rate of detachment. During voluntary exercise at decreased muscle temperatures, maximum and endurance performances are inevitably impaired by the decreases in maximum and sustained power of individual motor units.

Animals↗

Biphasic fever: what triggers the second temperature rise?

The mechanism of initiation of the second body temperature (Tb) rise of the typically biphasic lipopolysaccharide (LPS) fever is not known. This study was undertaken to test the hypothesis that the second Tb rise during fever may be initiated as a direct consequence of the elevated Tb of the first febrile rise. Experiments were conducted in conscious guinea pigs implanted with intraperitoneal thermodes, intravenous catheters, and intrahypothalamic thermocouples. Intraperitoneal cooling (IPC) was performed by perfusing water (22 degrees C) through the thermode under afebrile conditions during the first (0-40 min after pyrogen injection) or second (80-120 min) phase of the biphasic LPS (2 g/kg iv) fever or during a monophasic LPS (0.5 g/kg iv) fever. Throughout IPC, the rate of heat withdrawal was maintained at 11.6 +/- 1.2 mW/g. No IPC was performed in the corresponding controls. When started immediately after LPS administration at the higher dose, IPC completely blocked the first phase of the biphasic fever. This blockade was followed by a Tb rise, which, although similar to the rise in the second phase, might alternatively be interpreted as the delayed occurrence of the first phase previously suppressed by IPC. However, we excluded the later possibility by showing the absence of an overshoot in Tb restoration after IPC applied during the second phase of biphasic fever, during monophasic fever, or under afebrile conditions. We conclude, therefore, that the second Tb rise of biphasic LPS fever is not induced by the elevated Tb of the first febrile phase. The cause of the second peak of the characteristic biphasic febrile response to intravenous LPS remains speculative.

Animals↗

Thermal dehydration-induced thirst in rats: role of body temperature.

Male Sprague-Dawley rats were used to study the possible role of hyperthermia in the thirst associated with thermal dehydration. Rats were exposed to 40 degrees C for 4 h and then allowed access to water at different times after they were transferred to 25 degrees C. Delaying the time prior to allowing the rats to drink did not significantly alter either water intake or percent rehydration even though core temperature decreased during the first 1.5 h after removal from the heat. Exposing thermally dehydrated rats to 5 degrees C for 30 min prior to allowing them access to water also failed to significantly affect water intake or percent rehydration. Thermally dehydrated rats allowed to drink while remaining in the heat did not show a significant increase in water intake during the first hour or percent rehydration over rats drinking at 25 degrees C. Nondehydrated rats did show significant increases in water intake and percent rehydration when allowed to drink in the heat. Hyperthermia does not play a role in drinking in thermally dehydrated rats but can stimulate drinking in water-replete rats.

Animals↗

Increased heat-escape/cold-seeking behavior following hypertonic saline injection in rats.

We examined the effect of hypertonic saline injection on heat-escape/cold-seeking behavior in desalivated rats. Rats were exposed to 40 degrees C heat after normal (154 mM NaCl, control) or hypertonic saline (2,500 mM NaCl) injection (1 ml/100 g body wt). The rats received a 0 degrees C air for 30 s when they entered a specific area in an experimental box. Core temperature (T(c)) surpassed 40 degrees C in both conditions when 0 degrees C air was not available. Hypertonic saline injection produced a lower baseline T(c) than control [36.9 +/- 0.2 and 37.9 +/- 0.2 degrees C (means +/- SE), P < 0.05] and a greater number of 0 degrees C air rewards during the 2-h heat with lower T(c) at the end (48 +/- 1 and 34 +/- 2, 37.6 +/- 0.1, and 37.3 +/- 0.1 degrees C in the control and hypertonic saline injection trial, respectively, P < 0.05, n = 6). However, T(c) was similar (37.7 +/- 0.2 and 37.6 +/- 0.4 degrees C in the control and hypertonic saline injection trial, n = 5) when 0 degrees C air was automatically and intermittently (35 times) given during the heat. Rats augment heat-defense mechanisms in response to osmotic stress by lowering the baseline T(c) and increasing heat-escape/cold-seeking behavior.

Animals↗

Pulse rate-rectal temperature relationships during prolonged work.

Forty-six industrial workers performed a total of 653 1-h work bouts over a wide range of work rates )142-273 W/m2) and environmental temperatures (11-35 degrees C corrected effective temperature) in the summer and winter seasons. Simultaneous measurements of heart rates and rectal temperatures were made at the end of each work period, and the relationship between heart rate and rectal temperature was computed with standard multiple linear regression techniques. The overall regression equation is: heart rate (beats/min) = 29.3 (beats/min. degrees C) x rectal temperature (degrees C) - 988.6 (beats/min). The relationship is significantly altered by work rate and job- and season-acquired acclimatization of the subjects. These data suggest that the average heart rates of industrial workers during prolonged work can be predicted from rectal temperatures with a reasonable degree of confidence if the degree of acclimatization and work rates are known. For a rectal temperature of 38.0 degrees C the expected heart rate during prolonged work ranges from 109 beats/min in acclimatized men working at low rates to 143 for unacclimatized men working at heavy rates.

Acclimatization↗