41 research outputs found

    An exploratory study of short-term camping in Antarctica: Hormonal and mood states changes

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    Long-term Antarctic expedition’s studies indicated harmful or positive behavioral and psychophysiological adaptive changes that arise from adversities in isolated, confined, and extreme environments. Whereas most of the published studies focused on overwintering situations, most Brazilian Antarctic Program summer expeditions consist of short-term stays. We evaluated the influence of a permanence in Antarctic short-term (13-day) summer camp on the hormonal responses and mood states in eight volunteers. Data collection was carried out at the beginning (initial measure, days 3 to 5) and the end (final measurement, days 10 to 12) of the camping. Morning and evening samples of saliva were obtained to measure the testosterone and cortisol concentrations. Morning blood drops were used to determine thyroid-stimulating hormone (TSH) and thyroxine (T4) concentration. The volunteers also answered a mood states questionnaire. During the short-term camp, T4 (3.92 ± 0.75 vs 2.21 ± 0.71 μg.dL-1) and T4/TSH (3.16 ± 0.97 vs 1.79 ± 0.74 AU) reduced, without concomitant changes in TSH (1.28 ± 0.17 vs 1.30 ± 0.09 μU.mL-1), and salivary cortisol increased (2,392 ± 1,153 vs 4,440 ± 1,941 pg.mL-1) resulting in greater cortisol amplitude (calculated from the difference between morning and evening measurement, 1,400 ± 1,442 vs 3,230 ± 2,046). In men, testosterone increased as well (26.2 ± 12.5 vs 67.8 ± 45.8, all differences with P<0.05). There was a moderate effect in mood states evidenced by increased anger and fatigue, and reduced vigor. At the end of the camp, the change in cortisol correlated with anger, and the final cortisol values with anger and tension. We concluded that staying in a short-term summer camp in Antarctica induced endocrine and mood state changes, indicators of stress reaction

    O exercício físiico induz ajustes termorregulatorios ecardiovasculares que sao mediados pela neurotransmissãocolinérgica dos nucleos ventromediais hipotalâmicos

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    Exportado OPUSMade available in DSpace on 2019-08-14T09:00:01Z (GMT). No. of bitstreams: 1 disserta__o___samuel_wanner.pdf: 2603407 bytes, checksum: a6681f20381639459f1fefdcf57f571a (MD5) Previous issue date: 28O objetivo do presente estudo foi avaliar a participação dos receptores colinérgicos muscarínicos dos núcleos ventromediais hipotalâmicos (VMH) na dissipação de calor, nos ajustes cardiovasculares e na fadiga durante o exercício em esteira rolante (24 m.min-1, 5% inclinação). Os ratos foram submetidos a duas condições experimentais separadas por um intervalo de pelo menos dois dias. A temperatura da pele da cauda, a temperatura interna e a pressão arterial foram medidas após a injeção de 200 nL de solução de metilatropina 2,5 x 10-2 M (Atr) ou NaCl 0,15 M (Sal) nos VMH. A injeção de Atr nos VMH amplificou os aumentos da temperatura interna induzidos pelo exercício e causou um atraso do aumento da temperatura da cauda. O maior ac´umulo de calor necessário para desencadear os mecanismos de dissipação de calor observado nos ratos injetados com Atr nos VMH pode ter sido responsável pela redução de 37% no desempenho dos animais (21, 0 ± 2, 9 min Atr vs. 33, 5 ± 3, 4 min Sal; n = 8; p < 0,001). O bloqueio colin´ergico dos VMH tamb´em antecipou os ajustes da pressão arterial (valor máximo da pressão arterial média: 132, 6 ± 3, 9 mmHg aos 3 min Atr vs. 125, 2 ± 4, 1 mmHg aos 9 min Sal; n = 7), os quais foram relacionados ao percentual do tempo total de exercício. Nós concluímos que os receptores colinérgicos muscarínicos nos VMH modulam a atividade simpática e a dissipação de calor durante o exercício físco. Além disso, os ajustes induzidos pela neurotransmissão colin´ergica intra-ventromedial podem determinar o tempo de exercício até a fadiga.The aim of this study was to evaluate the participation of cholinergic muscarinic receptors in the ventromedial hypothalamic nuclei (VMH) on heat balance, cardiovascular adjustments and central fatigue during treadmill exercise (24 m.min-1, 5% inclination). Rats were submittedto two experimental situations separated by an interval of at least two days. Tail skin temperature, core body temperature (Tb) and arterial pressure were measured after the injection of 200 L of 2,5 x 10-2 M methylatropine (Atr) or 0.15 M NaCl solution (Sal) into the VMH. Atr injection into the VMH amplified the exercise-induced increase in Tb andresulted in a delay in the rise of skin temperature. The increased heat storage needed to trigger the heat loss mechanisms observed in VMH Atr-treated rats may be responsible for the 37% decrease in the performance of these animals (21.0 ± 2.9 min Atr vs. 33.5 ± 3.4 minSal; n = 8; p 0.001). Cholinergic blockade of VMH has also acelerated the blood pressure adjustments (mean arterial pressure maximal value: 132.6 ± 3.9 mmHg at 3 min Atr vs. 125.2±4.1 mmHg at 9 min Sal; n = 7), which were related to the percentage of total exercise time. We conclude that cholinergic muscarinic receptors in the VMH modulate sympatheticactivation and facilitate heat loss during exercise. Furthermore, these adjustments induced by intra-ventromedial cholinergic neurotransmission determine exercise time until fatigue

    O exercício físico induz ajustes termorregulatórios e cardiovasculares que são mediados pela neurotransmissão colinérgica dos núcleos ventromediais hipotalâmicos

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    Exportado OPUSMade available in DSpace on 2019-08-11T04:27:03Z (GMT). No. of bitstreams: 1 mestrado_final.pdf: 2603407 bytes, checksum: a6681f20381639459f1fefdcf57f571a (MD5) Previous issue date: 28O objetivo do presente estudo foi avaliar a participação dos receptores colinergicos muscarínicos dos núcleos ventromediais hipotalâmicos (VMH) na dissipação de calor, nos ajustes cardiovasculares e na fadiga durante o exercício em esteira rolante (24 m.min 1, 5% inclinação). Os ratos foram submetidos a duas condições experimentais separadas por um intervalo de pelo menos dois dias. A temperatura da pele da cauda, a temperatura interna e a pressão arterial foram medidas após a injeção de 200 _L de solução de metilatropina 2,5 x 10 2 M (Atr) ou NaCl 0,15 M (Sal) nos VMH. A injeção de Atr nos VMH amplificou os aumentos da temperatura interna induzidos pelo exercício e causou um atraso do aumento da temperatura da cauda. O maior acúmulo de calor necessário para desencadear os mecanismos de dissipação de calor observado nos ratos injetados com Atr nos VMH pode ter sido responsável pela redução de 37% no desempenho dos animais (21, 0 ± 2, 9 min Atr vs. 33, 5 ± 3, 4 min Sal; n = 8; p _ 0,001). O bloqueio colinérgico dos VMH também antecipou os ajustes da pressão arterial (valor máximo da pressão arterial média: 132, 6 ± 3, 9 mmHg aos 3 min Atr vs. 125, 2 ± 4, 1 mmHg aos 9 min Sal; n = 7), os quais foram relacionados ao percentual do tempo total de exercício. Nós concluímos que os receptores colinérgicos muscarínicos nos VMH modulam a atividade simpática e a dissipação de calor durante o exercício físico. Além disso, os ajustes induzidos pela neurotransmissão colinérgica intra-ventromedial podem determinar o tempo de exercício at´e a fadiga.The aim of this study was to evaluate the participation of cholinergic muscarinic receptors in the ventromedial hypothalamic nuclei (VMH) on heat balance, cardiovascular adjustments and central fatigue during treadmill exercise (24 m.min1, 5% inclination). Rats were submitted to two experimental situations separated by an interval of at least two days. Tail skin temperature, core body temperature (Tb) and arterial pressure were measured after the injection of 200 _L of 2,5 x 102 M ethylatropine (Atr) or 0.15 M NaCl solution (Sal) into the VMH. Atr injection into the VMH amplified the exercise-induced increase in Tb and resulted in a delay in the rise of skin temperature. The increased heat storage needed to trigger the heat loss mechanisms observed in VMH Atr-treated rats may be esponsible for the 37% decrease in the performance of these animals (21.0 ± 2.9 min Atr vs. 33.5 ± 3.4 min Sal; n = 8; p _ 0.001). Cholinergic blockade of VMH has also acelerated the blood pressure adjustments (mean arterial pressure maximal value: 132.6 ± 3.9 mmHg at 3 min Atr vs. 125.2±4.1 mmHg at 9 min Sal; n = 7), which were related to the percentage of total exercise time. We conclude that cholinergic muscarinic receptors in the VMH modulate sympathetic activation and facilitate heat loss during exercise. Furthermore, these adjustments induced by intra-ventromedial cholinergic eurotransmission determine exercise time until fatigue

    Hypothalamic temperature of rats subjected to treadmill running in a cold environment.

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    Different strategies for cooling the body prior to or during physical exercise have been shown to improve prolonged performance. Because of ethical and methodological issues, no studies conducted in humans have evaluated the changes in brain temperature promoted by cooling strategies. Therefore, our first aim sought to measure the hypothalamic temperature (Thyp) of rats subjected to treadmill running in a cold environment. Moreover, evidence suggests that Thyp and abdominal temperature (Tabd) are regulated by different physiological mechanisms. Thus, this study also investigated the dynamics of exercise-induced changes in Thyp and Tabd at two ambient temperatures: 25°C (temperate environment) and 12°C (cold). Adult male Wistar rats were used in these experiments. The rats were implanted with a guide cannula in the hypothalamus and a temperature sensor in the abdominal cavity. After recovery from this surgery, the rats were familiarized with running on a treadmill and were then subjected to the two experimental trials: constant-speed running (20 m/min) at 12°C and 25°C. Both Thyp and Tabd increased during exercise at 25°C. In contrast, Thyp and Tabd remained unchanged during fatiguing exercise at 12°C. The temperature differential (i.e., Thyp - Tabd) increased during the initial min of running at 25°C and thereafter decreased toward pre-exercise values. Interestingly, external cooling prevented this early increase in the temperature differential from the 2nd to the 8th min of running. In addition, the time until volitional fatigue was higher during the constant exercise at 12°C compared with 25°C. Together, our results indicate that Thyp and Tabd are regulated by different mechanisms in running rats and that external cooling affected the relationship between both temperature indexes observed during exercise without environmental thermal stress. Our data also suggest that attenuated hypothalamic hyperthermia may contribute to improved performance in cold environments

    Comparative effects of two heat acclimation protocols consisting of high-intensity interval training in the heat on aerobic performance and thermoregulatory responses in exercising rats.

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    Acclimation resulting from low- to moderate-intensity physical exertion in the heat induces several thermoregulatory adaptations, including slower exercise-induced increases in core body temperature. However, few studies have investigated the thermoregulatory adaptations induced by high-intensity interval training (HIIT) protocols. Thus, the present study aimed to compare the adaptations in rats' thermoregulatory parameters and aerobic performance observed after two different heat acclimation regimens consisting of HIIT protocols performed in a hot environment. Twenty-three adult male Wistar rats were initially subjected to an incremental-speed exercise at 32°C until they were fatigued and then randomly assigned to one of the following three heat acclimation strategies: passive heat exposure without any exercise (untrained controls-UN; n = 7), HIIT performed at the maximal aerobic speed (HIIT100%; n = 8) and HIIT performed at a high but submaximal speed (HIIT85%; n = 8). Following the two weeks of interventions, the rats were again subjected to a fatiguing incremental exercise at 32°C, while their colonic temperature (TCOL) was recorded. The workload performed by the rats and their thermoregulatory efficiency were calculated. After the intervention period, rats subjected to both HIIT protocols attained greater workloads (HIIT100%: 313.7 ± 21.9 J vs. HIIT85%: 318.1 ± 32.6 J vs. UN: 250.8 ± 32.4 J; p < 0.01) and presented a lower ratio between the change in TCOL and the distance travelled (HIIT100%: 4.95 ± 0.42°C/km vs. HIIT85%: 4.33 ± 0.59°C/km vs. UN: 6.14 ± 1.03°C/km; p < 0.001) when compared to UN rats. The latter finding indicates better thermoregulatory efficiency in trained animals. No differences were observed between rats subjected to the two HIIT regimens. In conclusion, the two HIIT protocols induce greater thermoregulatory adaptations and performance improvements than passive heat exposure. These adaptations do not differ between the two training protocols investigated in the present study

    Total exercise time for the animals that were implanted with a guide cannula in the VMH or in the peri-VMH area.

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    <p>Constant-speed running (20 m/min and 5% inclination) was performed at ambient temperatures of 25°C and 12°C (panel A). #<i>P</i><0.05 compared with the experimental trials at 25°C. The curves presented in the panel B show the maximum exercise duration tolerated by the rats subjected to the constant exercise sessions (panel B). The data are expressed as the number of rats that continued to run at specific time points at each ambient temperature.</p

    Coronal sections taken from the Paxinos and Watson atlas (2007) showing the location of the thermistor tips (panels A–D).

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    <p>The numbers above the schematic representation of each hypothalamic section indicate the distance (in mm) between the section plane and the bregma. Legends: 3V, 3rd ventricle; DMD, dorsomedial hypothalamic nucleus, dorsal part; f, fornix; MeAD, medial amygdaloid nucleus, anterodorsal part; mt, mammillothalamic tract; PeF, perifornical nucleus; PeFLH, perifornical part of lateral hypothalamus; PH, posterior hypothalamus; sox, supraoptic decussation; STM, bed nucleus of the stria terminalis, medial division; VMH, ventromedial hypothalamus nucleus. Photomicrographs of coronal sections (50 µm, cresyl violet staining) showing the location of the thermistor tips in two rats: one rat had a thermistor inserted into the frontal cortex, and the another animal had a thermistor inserted into the <i>caudate putamen nucleus</i> (panels E and F).</p
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