No description available.

Exercise and/or heat-induced dehydration is associated with decreases in plasma volume (hypovolemia) and increases in plasma osmolality (hyperosmolality), which are thought to stimulate peripheral baroreceptors and central osmoreceptors respectively. Independently, plasma hyperosmolality and baroreceptor unloading have been shown to attenuate sweating and cutaneous vasodilation during heat stress, and therefore, negatively impact body temperature regulation. However, to date little is known regarding the combined influence of plasma hyperosmolality and baroreceptor unloading on thermoefferent activity. Therefore, we evaluated the separate and combined effects of baroreceptor unloading (via lower body negative pressure, LBNP) and plasma hyperosmolality (via infusion of 3% NaCl saline) on heat loss responses of sweating and cutaneous vascular conductance (CVC) during progressive whole-body heating. We show that the combined nonthermal influences of plasma hyperosmolality and baroreceptor unloading additively delay the onset threshold for CVC, relative to their independent effects. In contrast, baroreceptor unloading has no influence on the sweating response regardless of osmotic state. These divergent roles of plasma hyperosmolality and the baroreflex on heat loss responses might serve to enhance blood pressure and body core temperature regulation during dehydration and heat stress.

Exercise and/or heat-induced dehydration is associated with decreases in plasma volume (hypovolemia) and increases in plasma osmolality (hyperosmolality), which are thought to stimulate peripheral baroreceptors and central osmoreceptors respectively. Independently, plasma hyperosmolality and baroreceptor unloading have been shown to attenuate sweating and cutaneous vasodilation during heat stress, and therefore, negatively impact body temperature regulation. However, to date little is known regarding the combined influence of plasma hyperosmolality and baroreceptor unloading on thermoefferent activity. Therefore, we evaluated the separate and combined effects of baroreceptor unloading (via lower body negative pressure, LBNP) and plasma hyperosmolality (via infusion of 3% NaCl saline) on heat loss responses of sweating and cutaneous vascular conductance (CVC) during progressive whole-body heating. We show that the combined nonthermal influences of plasma hyperosmolality and baroreceptor unloading additively delay the onset threshold for CVC, relative to their independent effects. In contrast, baroreceptor unloading has no influence on the sweating response regardless of osmotic state. These divergent roles of plasma hyperosmolality and the baroreflex on heat loss responses might serve to enhance blood pressure and body core temperature regulation during dehydration and heat stress.

Exercise and/or heat-induced dehydration is associated with decreases in plasma volume (hypovolemia) and increases in plasma osmolality (hyperosmolality), which are thought to stimulate peripheral baroreceptors and central osmoreceptors respectively. Independently, plasma hyperosmolality and baroreceptor unloading have been shown to attenuate sweating and cutaneous vasodilation during heat stress, and therefore, negatively impact body temperature regulation. However, to date little is known regarding the combined influence of plasma hyperosmolality and baroreceptor unloading on thermoefferent activity. Therefore, we evaluated the separate and combined effects of baroreceptor unloading (via lower body negative pressure, LBNP) and plasma hyperosmolality (via infusion of 3% NaCl saline) on heat loss responses of sweating and cutaneous vascular conductance (CVC) during progressive whole-body heating. We show that the combined nonthermal influences of plasma hyperosmolality and baroreceptor unloading additively delay the onset threshold for CVC, relative to their independent effects. In contrast, baroreceptor unloading has no influence on the sweating response regardless of osmotic state. These divergent roles of plasma hyperosmolality and the baroreflex on heat loss responses might serve to enhance blood pressure and body core temperature regulation during dehydration and heat stress.

Exercise and/or heat-induced dehydration is associated with decreases in plasma volume (hypovolemia) and increases in plasma osmolality (hyperosmolality), which are thought to stimulate peripheral baroreceptors and central osmoreceptors respectively. Independently, plasma hyperosmolality and baroreceptor unloading have been shown to attenuate sweating and cutaneous vasodilation during heat stress, and therefore, negatively impact body temperature regulation. However, to date little is known regarding the combined influence of plasma hyperosmolality and baroreceptor unloading on thermoefferent activity. Therefore, we evaluated the separate and combined effects of baroreceptor unloading (via lower body negative pressure, LBNP) and plasma hyperosmolality (via infusion of 3% NaCl saline) on heat loss responses of sweating and cutaneous vascular conductance (CVC) during progressive whole-body heating. We show that the combined nonthermal influences of plasma hyperosmolality and baroreceptor unloading additively delay the onset threshold for CVC, relative to their independent effects. In contrast, baroreceptor unloading has no influence on the sweating response regardless of osmotic state. These divergent roles of plasma hyperosmolality and the baroreflex on heat loss responses might serve to enhance blood pressure and body core temperature regulation during dehydration and heat stress.

This study sought to determine the independent influence of hypoxia on thermoregulatory responses to exercise in compensable and uncompensable hot conditions. Eight participants completed three experimental trials of cycling in either normoxia (21% O2) or hypoxia (13% O2) in order to manipulate relative exercise intensity (%VO2peak), since VO2peak was reduced by ~30% in hypoxia. When trials were matched for %VO2peak, changes in core temperature and local sweat rates (LSR) were significantly lower in the hypoxic trial as a result of a lower rate of metabolic heat production (Hprod) in order to maintain a similar %VO2peak compared to normoxia. However, when Hprod was fixed between normoxic and hypoxic trials the systematic differences in core temperature and LSR were eliminated. Conversely, at a fixed Hprod skin blood flow (SkBF) was greater in hypoxia compared to normoxia by ~40%. Despite improvements in SkBF, the potential for maximum heat loss was unaffected during an incremental humidity ramp protocol, resulting in no difference between normoxia and hypoxia in the critical ambient vapour pressures at which core temperature inflected upwards. These data further demonstrate, using a within-subjects design, that metabolic heat production, irrespective of large differences in %VO2peak, determines thermoregulatory responses during exercise. Furthermore, this study suggests that the influence of large differences in skin blood flow on heat dissipation may be lesser than previously thought.

The current thesis examined whether sex-differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrates that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W•°C-1, p=0.05) during exercise performed at a fixed rate of metabolic heat production. The second study shows that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W•m-2 (496 ± 139 vs. 483 ± 185 W•m-2•°C-1, p=0.91) and 300 W•m-2 (283 ± 70 vs. 211 ± 66 W•m-2•°C-1, p=0.17), only becoming greater in males at a requirement for heat loss of 350 W•m-2 (197 ± 61 vs. 82 ± 27 W•m-2•°C-1, p=0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg•min-1•cm-2, p=0.02) and methylcholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg•min-1•cm-2, p=0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.

The current thesis examined whether sex-differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrates that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W•°C-1, p=0.05) during exercise performed at a fixed rate of metabolic heat production. The second study shows that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W•m-2 (496 ± 139 vs. 483 ± 185 W•m-2•°C-1, p=0.91) and 300 W•m-2 (283 ± 70 vs. 211 ± 66 W•m-2•°C-1, p=0.17), only becoming greater in males at a requirement for heat loss of 350 W•m-2 (197 ± 61 vs. 82 ± 27 W•m-2•°C-1, p=0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg•min-1•cm-2, p=0.02) and methylcholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg•min-1•cm-2, p=0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.

The current thesis examined whether sex-differences in local and whole-body heat loss are evident after accounting for confounding differences in physical characteristics and rate of metabolic heat production. Three experimental studies were performed: the first examined whole-body heat loss in males and females matched for body mass and surface area during exercise at a fixed rate of metabolic heat production; the second examined local and whole-body heat loss responses between sexes during exercise at increasing requirements for heat loss; the third examined sex-differences in local sweating and cutaneous vasodilation to given doses of pharmacological agonists, as well as during passive heating. The first study demonstrates that females exhibit a lower whole-body sudomotor thermosensitivity (553 ± 77 vs. 795 ± 85 W•°C-1, p=0.05) during exercise performed at a fixed rate of metabolic heat production. The second study shows that whole-body sudomotor thermosensitivity is similar between sexes at a requirement for heat loss of 250 W•m-2 (496 ± 139 vs. 483 ± 185 W•m-2•°C-1, p=0.91) and 300 W•m-2 (283 ± 70 vs. 211 ± 66 W•m-2•°C-1, p=0.17), only becoming greater in males at a requirement for heat loss of 350 W•m-2 (197 ± 61 vs. 82 ± 27 W•m-2•°C-1, p=0.007). In the third study, a lower sweat rate to the highest concentration of acetylcholine (0.27 ± 0.08 vs. 0.48 ± 0.13 mg•min-1•cm-2, p=0.02) and methylcholine (0.41 ± 0.09 vs. 0.57 ± 0.11 mg•min-1•cm-2, p=0.04) employed was evidenced in females, with no differences in cholinergic sensitivity. Taken together, the results of the current thesis show that sex itself can modulate sudomotor activity, specifically the thermosensitivity of the response, during both exercise and passive heat stress. Furthermore, the results of the third study point towards a peripheral modulation of the sweat gland as a mechanism responsible for the lower sudomotor thermosensitivity in females.

O sinal de fluxo cutâneo obtido via fluxometria Laser Doppler (SFLD) tem flutuações de baixas frequências que estão relacionadas a mecanismos de controle do fluxo microvascular. Análises espectrais, via transformada de Fourier e transformada de wavelet, têm sido usadas para correlacionar as flutuações de SFLD com os seguintes mecanismos de controle de fluxo: metabólico, metabólico NO-dependente, neurogênico e miogênico, nos respectivos intervalos de frequência 0,005-0,0095 Hz, 0,0095-0,02 Hz, 0,02-0,05 Hz e 0,05-0,15 Hz. A potência do sinal, em cada intervalo de frequência, geralmente é usada como uma medida da atividade do mecanismo de controle microvascular relacionado. Uma vez que os métodos usados de análise são espectrais, as características das flutuações do SFLD, em cada intervalo de frequência, no domínio do tempo são desconhecidas. Como consequência, há ausência de critérios objetivos para medir adequadamente, em cada intervalo de frequência, os parâmetros hemodinâmicos relacionados. O objetivo deste trabalho foi caracterizar e quantificar flutuações temporais, espaciais e espaço-temporais do SFLD em cada faixa de frequência, usando um método no domínio do tempo. Os fluxos basais (320C) e termicamente estimulados à (420C) das regiões volares de antebraços de 20 voluntários saudáveis foram coletados em duas regiões próximas e analisados. As análises dos dados obtidos indicam que janelas temporais pequenas (1 minuto) são aceitáveis para a quantificação do fluxo médio, e que janelas temporais maiores são necessários para quantificar as flutuações de fluxo. A análise espaço-temporal revelou uma forte correlação entre sinais (em todas as bandas, exceto na banda B5) das duas regiões investigadas, durante longos intervalos de tempo, quando as duas regiões estudadas foram termicamente estimuladas, e menor variabilidade intragrupo quando comparada à obtida para os valores médios das flutuações, sugerindo que o intervalo de tempo de correlação é um parâmetro promissor para estudar mecanismos de controle do fluxo microvascular. / The laser Doppler flow signal from the skin (LDFS) has low-frequency fluctuations which are related to microvascular mechanisms of flow control. The Fourier and the wavelet spectral analysis has been used to correlate fluctuations in the LDFS with the metabolic, metabolic NO-dependent, neurogenic and myogenic mechanisms of control in the frequency intervals 0.005-0.0095 Hz, 0.0095-0.02 Hz, 0.02-0.05 Hz and 0.05-0.15 Hz, respectively. The signal power, in each frequency interval, is generally used as a measure of the activity of the related mechanism of microvascular control. Since spectral analysis methods have been used, the time-domain characteristics of the fluctuations in the LDFS in each frequency interval are unknown. As a consequence, there is a lack of objective criteria to properly measure, in each frequency interval, the related hemodynamic parameters. The aim of this work was characterizing and quantifying temporal, spatial and spatial-temporal fluctuations in the LDFS in each frequency band, using a time-domain method. Baseline (320C) and thermally stimulated (420C) LDFS of volar forearms from 20 healthy volunteers were collected from two close regions and analyzed. The data obtained indicate that short-time windows (1 minute) are acceptable for quantifying the mean flow, and that larger time-windows are needed for quantifying the flow fluctuations. The spatialtemporal analysis revealed strong correlations between signals (all bands, except B5) from the two investigated regions, during large time intervals when thermally stimulated, and lower intragroup variability than the ones obtained for the mean values of fluctuations, suggesting that the time interval of correlation is a promising parameter for studying mechanisms of microvascular flow control.