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Vol. 84, Issue 3, 877-883, March 1998
Department of Physiology, University of the Witwatersrand, Medical School, Parktown 2193, Johannesburg, South Africa
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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We measured brain and abdominal temperatures in eight male Sprague-Dawley rats (350-450 g) exercising voluntarily to a point of fatigue in two hot environments. Rats exercised, at the same time of the day, in three different trials, in random order: rest 23°C, exercise 33°C; rest 23°C, exercise 38°C; and rest 38°C, exercise 38°C. Running time to fatigue was 29.4 ± 5.9 (SD), 22.1 ± 3.7, and 14.3 ± 2.9 min for the three trials, respectively. Abdominal temperatures, measured with intraperitoneal radiotelemeters, at fatigue in the three trials (39.9 ± 0.3, 39.9 ± 0.3, and 39.8 ± 0.3°C, respectively) were not significantly different from each other. Corresponding brain temperatures, measured with thermocouples in the hypothalamic region (40.2 ± 0.4, 40.2 ± 0.4, and 40.1 ± 0.4°C), also did not differ. Our results are consistent with the concept that there is a critical level of body temperature beyond which animals will not continue to exercise voluntarily in the heat. Also, in our study, brain temperature was higher than abdominal temperature throughout exercise; that is, selective brain cooling did not occur when body temperature was below the level limiting exercise.
hyperthermia; temperature regulation; selective brain cooling; sleep
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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HYPERTHERMIA REDUCES physical performance in many mammalian species, including rodents. Rats with body temperatures maintained above 40°C ran for only one-half the time run by those with body temperatures clamped below 38°C (6). High brain and trunk temperatures terminated running in guinea pigs (8), and heating of the rostral brain stem reduced voluntary running in hamsters (11). In some mammalian species, there appears to be a critical core temperature, below the level of heat stroke, that is transformed into a signal that limits exercise. Cheetahs stopped running when their rectal temperatures approached 40.5°C (27). Similarly, regardless of exercise duration and rate of rise in body temperature, human volunteers in the laboratory became exhausted and stopped exercising when their core temperatures approached 39.5°C (18, 22). Whether the limit to exercise resides in high brain temperature or in other body core temperatures has been investigated in only one study. Caputa and colleagues (5) altered brain temperature independently of trunk core temperature in goats and found no signs of exercise fatigue at a trunk core temperature of 43.5°C. However, when trunk core temperature was clamped at ~40°C, the animals became fatigued at brain temperatures in the range of 42-43°C, levels commonly associated with heat stroke.
Goats can maintain brain temperature below arterial blood temperature, and it is widely held that this selective brain cooling protects the brain from thermal damage during heat stress (3). If it does, and if indeed it is brain temperature that limits performance, then, under heat stress, a thermal limit will be reached more quickly in species that have weak, or no, selective brain cooling. Selective brain cooling is best developed in animals that have a carotid rete, such as the artiodactyls and felids (2, 20). In species that do not have a rete, including humans, whether and how selective brain cooling occurs remain equivocal. Selective brain cooling, however, has been observed in some species that lack a carotid rete, including horses and some rodents. McConaghy and colleagues (19) recently reported brain cooling of 0.6°C during heat exposure and 1°C during exercise in horses, the same order of magnitude of cooling as that observed in animals with a rete (2, 20). Weaker selective brain cooling was evident in exercising rats that exhibited hypothalamic temperature ~0.13°C below rectal temperature during exercise (7). Whether such weak selective brain cooling confers any role on brain temperature, in setting a thermal limit to exercise in rats, is not known. We, therefore, recorded brain and abdominal temperatures in rats exercising to fatigue under different thermal loads to investigate whether there is a critical core temperature limiting exercise and whether brain temperature plays any special role if a temperature limit to exercise is apparent.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Animals and training. Experiments were performed in eight male adult Sprague-Dawley rats weighing 350-450 g. The procedures were approved by the Animal Ethics Screening Committee of the University of the Witwatersrand (protocol no. 96/84/4). Animals were raised and housed in cages in a room with ambient temperature maintained at 22-23°C, with a 12:12-h light-dark cycle (lights on at 0600). Water and standard rat chow were provided ad libitum. The final cohort was selected from 24 4-wk-old rats that weighed 80-100 g. The animals underwent a progressive endurance-training program on a motorized treadmill in a room maintained at 23°C (relative humidity ~40%). During the first week of training, rats were induced to run by a nonpainful jet of air at the end of the belt; no electrical shock or other such painful coercion was used during the study. Rats were trained between 1400 and 1800, 5 days/wk; training commenced at a speed of 8.5 m/min for 10 min, with the treadmill belt set at a 10% slope. Each training day, speed or duration was increased so that by the end of the third week the rats were running for 40 min at 14 m/min. Fourteen rats (then 240-320 g) that ran consistently and freely on the treadmill then were selected from the initial group. These rats underwent surgery and resumed exercise training 6 days later. After 3 wk of further training, the rats were able to run for 60 min at 15 m/min on the 10% slope. The eight rats that then fully completed the experimental protocol (see Experimental procedures) constituted the final sample.
Surgery. Intra-abdominal radiotelemeters and brain thermocouple guide tubes were implanted under ketamine (0.8 ml/kg) and xylazine (0.2 ml/kg) anesthesia. The sterilized telemeters were implanted into the peritoneal cavity through a small incision in the linea alba. Polytetrafluoroethylene (Teflon) blind-ended reentrant guide tubes were implanted with their tips near the hypothalamus, according to the atlas of Paxinos and Watson (26). The position of the reentrant guide tube was verified radiographically. The brain thermocouple guide tubes were constructed from 20-gauge (0.8 mm ID, 1.1 mm OD) intravenous catheters (Jelco, Critikon, Johnson & Johnson, Bracknell, UK) that were cut to the correct length and sealed at the tip with epoxy. The brain guide tubes were secured to the skull by using dental cement and two small bone screws. Surgery lasted ~20 min.
Temperature recording. Each radiotelemeter (Mini-Mitter, Sun River, OR) was inserted with its battery (3-V lithium) coated with inert wax. Each telemeter was calibrated against a high-precision-certified glass-mercury thermometer in a water bath; the temperature of tissues subsequently surrounding each telemeter could be measured to an accuracy of 0.04°C. The frequency output from the radiotelemeters was measured with a Multimeter (Heath 2372, Mini-Mitter) and a hand-held wand receiver system (Data Sciences International). Rats were killed after completion of the study by an overdose of carbon dioxide, and the radiotelemeters were removed. There were no signs of infection, inflammation, or other tissue pathology at the telemeter sites.
Brain temperature was measured with fine (36-gauge) copper-constantan thermocouples with a 1-mm-long thermosensitive junction. Thermocouple voltages were recorded on a Hewlett-Packard 3421A data-acquisition unit (Hewlett-Packard, Santa Clara, CA), which was ice referenced by an Omega TRC III Ice Point Reference Cell (Omega Engineering, Stamford, CT). The thermocouples were calibrated in a water bath against a certified glass-mercury thermometer to a resolution of 0.025°C and to an accuracy of better than 0.05°C. Measurement of brain temperature was affected by conductive heat transfer down the reentrant guide tube and thermocouple, even though the guide tube was made of plastic rather than the more conventional steel. When ambient temperature was lower than brain temperature, as in our study, the indicated brain temperature was falsely low. We constructed a raft that acted as a model of the rat's skull. Three guide tubes were inserted into a square sheet of plastic (1.5 mm thick) and secured in position by using dental cement. The raft was floated in an insulated water bath (37-41°C) that was moved in and out of the hot room in the same way as the rat treadmill was moved subsequently. Conduction errors were determined as the difference between temperature measured in the bath, with calibrated thermocouples, at the level of the guide tube and those measured by thermocouples positioned in the guide tubes. We filled the guide tubes with castor oil, which reduced the error. Errors ranged from 0.07°C in the 38°C environment to 0.45°C in the 23°C environment; the indicated brain temperature always underestimated the actual temperature. Brain temperatures were corrected for the conduction errors in each subsequent experiment.Experimental procedures. Brain thermocouples were introduced, under light anesthesia, into brain guide tubes before each exercise trial. We elected to use light anesthesia because it reduced the distress and the handling hyperthermia otherwise associated with manipulating the rats' heads. Rats were lightly anesthetized by inhalation of enflurane (Ethrane, Abbott; 4% for induction, 2.5% for maintenance) in an oxygen-nitrous oxide mixture (1:2); anesthesia lasted 1-3 min. Comparison with the behavior of rats that had the thermocouples inserted without anesthesia showed full recovery of attention and mobility within 30 min or less. The animals rested on the treadmill in their lane (450 mm long and 100 mm wide) for a period of 60-75 min before the start of the experiment. All trials commenced at 1500, with the recording of rest temperatures for 30 min. At 1530, the treadmill was wheeled into the climatic chamber and exercise commenced. Rats were run to fatigue (see below) in three trials (trials A, B, and C), in random order. In trial A, rats rested in their treadmill lane at 23°C for 30 min and then exercised until fatigue in a hot room at 33°C. Trial B differed from trial A in that the exercise was carried out at 38°C. In trial C, the rats also exercised at 38°C but were preheated before exercise by resting in the hot room for 30 min. In all three trials, rats ran at 15 m/min (10% grade), and relative humidity was maintained at ~40%. Brain and intra-abdominal temperatures were measured at 5-min intervals and at the point of exercise fatigue. Exercise fatigue was defined as the condition in which the rat was unable to keep pace with the treadmill and lay flat on, and rode, the belt for a period of 3 min. Pilot studies showed that all rats displayed this characteristic behavior during prolonged exercise in the heat. The investigator who evaluated the degree of fatigue and switched off the treadmill motor was unaware of the body temperature prevailing at the time.
Statistics. Running time to fatigue, preexercise temperatures, and temperatures at exercise fatigue were compared among trials by using a repeated-measures analysis of variance and a Student-Newman-Keuls post hoc test where appropriate. We investigated whether there was an association between sleep or exercise and selective brain cooling by using Fisher's exact test. Values are given as means ± SD, and P < 0.05 was considered significant.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Body temperatures at exercise-induced fatigue. Figure 1 shows brain and abdominal temperatures of one animal (rat 8) as a function of time. The rat stopped exercising at approximately the same brain (~39.9°C) and abdominal temperatures (~39.8°C) in each trial. Mean brain and abdominal temperatures before exercise and at fatigue are shown in Table 1. Preexercise body temperature was determined as the mean of the last two temperatures recorded before exercise, that is, temperatures at 25 and 30 min. The preheating maneuver used in trial C resulted in preexercise brain and abdominal temperatures being significantly higher than those in trials A (P < 0.05) and B (P < 0.05) by ~0.4°C. At fatigue, neither abdominal temperatures nor brain temperatures in trials A, B, and C were significantly different from each other (Table 1). Rats remained in the hot room for 1-3 min after the cessation of exercise, and body temperatures continued to rise above fatigue levels (Fig. 1). Removal of the treadmill from the hot room may have also contributed to the additional stress hyperthermia.
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Relationships between brain and abdominal temperatures. The relationship between brain and abdominal temperatures for one rat (rat 8) during rest, exercise, and recovery from exercise is shown in Fig. 2; the responses were representative of those in all rats. Temperatures shown are those recorded at 5-min intervals and do not necessarily include temperatures measured at the point of exercise fatigue. Comparison of preexercise temperatures in each trial revealed no significant differences between brain and abdominal temperatures measured simultaneously (Table 1). However, in resting individual animals, including rat 8 (Fig. 2), we observed irregular oscillations in brain and abdominal temperatures. Brain temperature generally was slightly higher than abdominal temperature but periodically dropped below abdominal temperature, particularly, we observed, when the animal was sleeping. Rat 8, for example, slept for most of the rest period in trials A and B and also for the last 5 min before exercise in trial C. During the recovery period after exercise, all rats slept on the treadmill belt.
To analyze whether there was an association between observable behavior and selective brain cooling, we identified 5-min periods of continuous sleep or exercise and determined whether the period was associated with selective brain cooling (defined as brain temperature at least 0.1°C below abdominal temperature). Data for each rat, from all three trials (trials A, B, and C), were grouped together in a two-by-two contingency table. The average number of 5-min periods of selective brain cooling for each rat was 5.3 ± 4.5. In four rats, sleep was significantly associated with these periods of selective brain cooling (P < 0.05, Fisher's exact test).
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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Thermal limits to exercise. The main aim of our study was to determine whether rats stopped exercising in a hot environment at the same body temperature, irrespective of the actual environmental conditions. Our results indicate that there is indeed a critical level of body temperature at which exercising rats reach a point of fatigue. Abdominal temperatures at fatigue, in trials differing in ambient temperature and the rat's initial temperature, were the same (Table 1). Similarly, brain temperatures at fatigue did not differ between trials but were consistently higher than corresponding abdominal temperatures (Table 1, Fig. 3). Running time to fatigue, however, differed significantly between trials. Despite being trained to run for 60 min in a 23°C environment, rats were able to run for only one-half that time in a 33°C environment (trial A). Rats became fatigued even sooner if the ambient temperature was raised to 38°C and sooner still if their resting body temperatures were elevated before exercise (trial C). Metabolic factors related primarily to duration of exercise, for example, depletion of energy stores, therefore, were probably not responsible for the fatigue.
A common problem associated with animal studies investigating thermal limits to exercise is defining and assessing the degree of exercise fatigue. It is essential in a study such as ours that fatigue is identified by a clearly recognizable and characteristic behavior. Exercise "exhaustion," in some previous studies, was defined as the point at which the rat, when placed on its back, was unable to right itself (9, 15) or the point when the animal "collapsed" (6). Rats in those experiments were coerced to run by electrical shock, and, particularly in a hot environment, such coercion will induce them to run to a level at which heat stroke and resulting death occur (9, 14, 15). Such a procedure cannot be used to assess limits to voluntary exercise. As our end point, we used a behavioral pattern common to all rats after a period of prolonged exercise; the rat ran to the front of the treadmill belt, lay down on its belly, and "rode" to the end of the belt, at which time it stood up again and repeated the behavior. In our study, rats ran voluntarily and were only prevented from stepping off the belt by a barrier at the end of the lane. The investigator, who was unaware of the prevailing body temperature, turned off the treadmill motor after the rat had continuously displayed the characteristic fatigue behavior for 3 min. The body temperatures at which our rats became fatigued (Table 1) were not as high as those reported in other exercise studies (6, 9, 15), as might be expected in our less-coercive protocol, and were well below those evident in exercise-fatigued rats in which heat stroke fatalities occur. No rats displayed signs of heat illness (such as poor limb coordination) after exercise. Heat stroke is a complex disorder, and it is difficult to define exactly what degree and duration of hyperthermia produce injury (12, 14). Hubbard et al. (15) have reported that a rectal temperature of 40.4°C represents a threshold hyperthermia above which mortality occurs in exhausted rats, and that a final core temperature of 41.5°C will result in 50% of animals dying from heat stroke. Our results, therefore, are consistent with the hypothesis that hyperthermia precipitates feelings of fatigue at a sublethal threshold and, in so doing, establishes a safety level against heat stroke (5, 16). Rats did not stop exercising at the same absolute body temperatures but rather over a range >1°C. If a thermal limit to exercise exists, therefore, its absolute level may vary among individual animals. Our data do not allow us to conclude that a high body temperature per se is the signal causing cessation of exercise rather than another variable highly correlated with body temperature. However, studies in humans have shown that fatigue in the heat did not result from depletion of glycogen stores, reduced uptake rate of glucose or free fatty acids, reductions in muscle or skin blood flow, or accumulation of metabolites such as lactate or potassium ions (22, 23). In exercising rats and guinea pigs, blood lactate concentration is not correlated with exercise duration or body temperatures (6, 8). Our results, therefore, are consistent with the concept that a high core temperature has an effect on the central nervous system, reducing the mental drive for exercise performance (22, 23).Relationships between brain and abdominal temperatures. We investigated the relationship between brain and abdominal temperatures in rats, primarily to determine whether rats regulate brain temperature below abdominal temperature during exercise in a hot environment. If rats do not have physiologically significant selective brain cooling, then we hypothesized that high brain temperatures, rather than general body hyperthermia, might be limiting to exercise. Brain temperatures during exercise and at exercise-induced fatigue indeed were consistently higher than abdominal temperatures. In nonexercising rats, however, there were irregular oscillations in abdominal and brain temperatures, and we observed several periods of selective brain cooling (see Fig. 2, for example).
To accurately assess the degree of selective brain cooling in an animal, one ideally should measure brain temperature and central arterial blood temperature (13). It is technically difficult, however, to measure arterial temperature in such a small animal. Instead, we compared hypothalamic temperature with abdominal temperature, as others have done (1, 4, 7). It is conceivable that the telemeter may have been influenced by changes in the temperature of peripheral tissues of the rat, particularly when the rat changed posture. Also, the devices have a high thermal inertia, setting to a new temperature, after a 1°C change, in ~1 min. Hence, the telemeter may not accurately track abrupt, rapid increments (or decrements) in abdominal temperature. Another potential source of error in studies on selective brain cooling arises from the measurement of brain temperature. Brain temperature, measured by thermocouples or thermistors in reentrant guide tubes, is affected by conductive heat transfer along the thermocouple and tube. The magnitude of this conduction error is dependent on the difference between ambient temperature and brain temperature, the dimensions of the guide tube, and the material from which it is constructed. In our study, we moved the rats in and out of environments maintained at 23, 33, or 38°C, and it was essential that we corrected for the errors caused by changes in ambient temperature. Failure to correct for conduction errors may lead to artifactual evidence for selective brain cooling because the error could be as large as 0.5°C in a thermoneutral environment. An unexpected result from our study was that we occasionally recorded brain temperatures below abdominal temperatures in nonexercising rats, mostly when the rats apparently were sleeping and particularly when they were sleeping after the exercise. Selective brain cooling was more likely to occur when body temperature was low than when it was high. In some rats, and particularly in rat 8 (Fig. 2), brain temperature was depressed below abdominal temperature for some time, making it unlikely that the slow response rate of the telemeter could explain the temperature changes. A drop in brain temperature accompanies slow-wave sleep in several mammals, including cats, dogs, sheep, monkeys, and rats (1, 13, 24). Caputa and colleagues (4, 7) have argued that in rats a system of dorsal dural sinuses collects cool venous blood from the head skin and may act as an intracranial heat exchanger, cooling arterial blood perfusing the brain. They also have demonstrated an anatomic arrangement of superficial veins of the head that could function, via differential venoconstriction, to divert cool nasal blood to either the brain or the heart (4). Further studies are needed to evaluate the role of this vascular system and to investigate the possibility that a decrease in vasoconstrictor outflow, which is associated with slow-wave sleep (25), may have contributed to the selective brain cooling we observed. Despite rats possessing anatomic structures potentially capable of supporting selective brain cooling (4), we observed no cooling of the brain below abdominal temperature during exercise, including at fatigue. Instead, brain temperature was maintained at a level consistently higher than that of abdominal temperature (except in 2 of 24 experiments), even at the highest brain temperatures. The absence of brain cooling during exercise was not a consequence of our brain surgery having compromised the mechanisms because selective brain cooling did occur during rest (Fig. 2). Caputa and colleagues (4), on the other hand, reported weak selective brain cooling in warm-reared rats running at an ambient temperature of 31°C, with a threshold for selective brain cooling at 40.2°C. Only one of our rats exercised to this level of trunk core hyperthermia, so it is possible that we did not observe similar selective brain cooling simply because our rats did not reach a sufficiently high abdominal temperature. It is difficult, however, to explain how a mechanism for selective brain cooling operating only above a thermal limit to exercise could have evolved. Rats are nocturnal animals that forage and exercise at night when heat loss by convection and radiation is greatest, and it is difficult to envisage circumstances in which their body temperatures would exceed a thermal limit to exercise, in their natural habitat. In free-ranging wildebeest and springbok, selective brain cooling is inhibited during intense exercise, despite high body temperatures (17, 21). This response supports the hypothesis that, rather than protecting the brain as is usually postulated, selective brain cooling serves to reduce the drive on heat-loss mechanisms, such as sweating and panting. These thermoregulatory responses are costly in terms of water conservation, and selective brain cooling, therefore, would be advantageous to animals subject to concomitant heat stress and water deprivation. However, when the animal needs to maximize heat loss, for example, during intense exercise to escape predation, selective brain cooling can be rapidly inhibited or even abolished (in response to sympathetic outflow; Refs. 17, 21). Whether similar thermoregulatory mechanisms occur in animals without a carotid rete is not known. However, under this new interpretation, selective brain cooling in rats during exercise would appear to serve no useful thermoregulatory purpose. Rats do not lose water by sweating or panting; their major avenue of heat loss is saliva spreading (10), a method of evaporative cooling that cannot be practiced during continuous exercise. Further studies, accurately measuring brain temperature and central arterial blood temperature, are necessary to verify the existence and efficacy of selective brain cooling and its thermoregulatory role in rats. In summary, our measurements of brain and abdominal temperatures in rats exercising in the heat lend further support to the concept that a critical level of hyperthermia imposes a limit beyond which animals will not continue to exercise voluntarily. Irrespective of their initial body temperature or the environmental heat load, and therefore irrespective of duration of exercise, rats reached a point of fatigue at the same brain and the same abdominal temperatures, with brain temperatures higher than simultaneously measured abdominal temperatures. Our data also show that brain temperatures are not regulated below abdominal temperatures during exercise, at least over the range of body temperatures that do not limit exercise.| |
ACKNOWLEDGEMENTS |
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We thank the staff of the Central Animal Service for assistance with the surgical procedures and for care of the animals; Philippa Bayley, Shane Maloney, and Linda Vidulich for their help; and Claus Jessen for comments on the manuscript.
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FOOTNOTES |
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This work was funded by the Foundation for Research Development, South Africa.
Address for reprint requests: A. Fuller, Dept. of Physiology, Univ. of the Witwatersrand, Medical School, 7 York Rd., Parktown 2193, Johannesburg, South Africa (E-mail: 127andy{at}chiron.wits.ac.za).
Received 8 August 1997; accepted in final form 5 November 1997.
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Discussion
References
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H. Hasegawa, M. F. Piacentini, S. Sarre, Y. Michotte, T. Ishiwata, and R. Meeusen Influence of brain catecholamines on the development of fatigue in exercising rats in the heat J. Physiol., January 1, 2008; 586(1): 141 - 149. [Abstract] [Full Text] [PDF]
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C. Cifelli, F. Bourassa, L. Gariepy, K. Banas, M. Benkhalti, and J.-M. Renaud KATP channel deficiency in mouse flexor digitorum brevis causes fibre damage and impairs Ca2+ release and force development during fatigue in vitro J. Physiol., July 15, 2007; 582(2): 843 - 857. [Abstract] [Full Text] [PDF]
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 L. H. R. Leite, A. C. R. Lacerda, U. Marubayashi, and C. C. Coimbra Central angiotensin AT1-receptor blockade affects thermoregulation and running performance in rats Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2006; 291(3): R603 - R607. [Abstract] [Full Text] [PDF]
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H. Hasegawa, T. Ishiwata, T. Saito, T. Yazawa, Y. Aihara, and R. Meeusen Inhibition of the preoptic area and anterior hypothalamus by tetrodotoxin alters thermoregulatory functions in exercising rats J Appl Physiol, April 1, 2005; 98(4): 1458 - 1462. [Abstract] [Full Text] [PDF]
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A. G. Rodrigues, N. R. V. Lima, C. C. Coimbra, and U. Marubayashi Intracerebroventricular physostigmine facilitates heat loss mechanisms in running rats J Appl Physiol, July 1, 2004; 97(1): 333 - 338. [Abstract] [Full Text] [PDF]
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S. A. Arngrimsson, D. S. Petitt, M. G. Stueck, D. K. Jorgensen, and K. J. Cureton Cooling vest worn during active warm-up improves 5-km run performance in the heat J Appl Physiol, May 1, 2004; 96(5): 1867 - 1874. [Abstract] [Full Text] [PDF]
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A. K. Tryba and J.-M. Ramirez Response of the Respiratory Network of Mice to Hyperthermia J Neurophysiol, June 1, 2003; 89(6): 2975 - 2983. [Abstract] [Full Text] [PDF]
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 A. Fuller, P. R. Kamerman, S. K. Maloney, G. Mitchell, and D. Mitchell Variability in brain and arterial blood temperatures in free-ranging ostriches in their natural habitat J. Exp. Biol., April 1, 2003; 206(7): 1171 - 1181. [Abstract] [Full Text] [PDF]
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L. Nybo, N. H Secher, and B. Nielsen Inadequate heat release from the human brain during prolonged exercise with hyperthermia J. Physiol., December 1, 2002; 545(2): 697 - 704. [Abstract] [Full Text] [PDF]
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L. Nybo and B. Nielsen Perceived exertion is associated with an altered brain activity during exercise with progressive hyperthermia J Appl Physiol, November 1, 2001; 91(5): 2017 - 2023. [Abstract] [Full Text] [PDF]
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L. Nybo and B. Nielsen Hyperthermia and central fatigue during prolonged exercise in humans J Appl Physiol, September 1, 2001; 91(3): 1055 - 1060. [Abstract] [Full Text] [PDF]
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T. J. Walters, K. L. Ryan, L. M. Tate, and P. A. Mason Exercise in the heat is limited by a critical internal temperature J Appl Physiol, August 1, 2000; 89(2): 799 - 806. [Abstract] [Full Text] [PDF]
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J. Gonzalez-Alonso, C. Teller, S. L. Andersen, F. B. Jensen, T. Hyldig, and B. Nielsen Influence of body temperature on the development of fatigue during prolonged exercise in the heat J Appl Physiol, March 1, 1999; 86(3): 1032 - 1039. [Abstract] [Full Text] [PDF]
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), B (23°C rest,
38°C run; 
), and C (38°C
rest, 38°C run; 
). Temperatures at fatigue in each trial (A, B,
C) are indicated by dashed lines and solid symbols.
