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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.

Ingestion of cold (<10°C) compared to warm (>37°C) fluid has been suggested to attenuate heat storage levels during exercise. However, modulations in sweat output may yield differences in evaporative heat loss that are greater than differences in heat transfer with the ingested fluid. The purpose of the thesis was to evaluate thermoregulatory control and human heat balance, and compare thermometrically derived values of heat storage with those derived from partitional calorimetry following water ingestion of varying temperature during exercise. We found that water ingestion of 50°C compared to 1.5°C decreases heat storage in thermoneutral environments, and further exacerbates the error of thermometric heat storage estimations. Differences in heat storage were attributed exclusively to disproportionate reductions in whole-body and local sweat output and thus evaporative heat loss potential. Ingested fluid temperature only minimally altered skin blood flow and did not influence dry heat exchange with the ambient environment.

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.

Ingestion of cold (<10°C) compared to warm (>37°C) fluid has been suggested to attenuate heat storage levels during exercise. However, modulations in sweat output may yield differences in evaporative heat loss that are greater than differences in heat transfer with the ingested fluid. The purpose of the thesis was to evaluate thermoregulatory control and human heat balance, and compare thermometrically derived values of heat storage with those derived from partitional calorimetry following water ingestion of varying temperature during exercise. We found that water ingestion of 50°C compared to 1.5°C decreases heat storage in thermoneutral environments, and further exacerbates the error of thermometric heat storage estimations. Differences in heat storage were attributed exclusively to disproportionate reductions in whole-body and local sweat output and thus evaporative heat loss potential. Ingested fluid temperature only minimally altered skin blood flow and did not influence dry heat exchange with the ambient environment.

Females exhibit lower sudomotor response than males, which has been attributed to physiological differences between sexes. It is well accepted that non-thermal factors (i.e. baroreceptors and osmoreceptors) can influence thermoeffector responses. Even though there are sex-related differences in baroreceptor modulation of thermoeffector responses, it remains unknown if differences in osmoreceptor modulation could explain the lower sudomotor response in females. Therefore, we examined if there are sex-related differences in osmoreceptor modulation of sweating and cutaneous vascular conductance (CVC). A group of nine males and nine females were passively heated while in an isosmotic and hyperosmotic state. The onset and thermosensitivity of sweating and CVC were calculated and compared between groups and conditions. We show that the delay in onset of sweating and CVC is similar between sexes. However, thermosensitivity of sweating was lower in females than males. We conclude that hyperosmolality does not modulate the decreased sudomotor activity in females.

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.

Ingestion of cold (<10°C) compared to warm (>37°C) fluid has been suggested to attenuate heat storage levels during exercise. However, modulations in sweat output may yield differences in evaporative heat loss that are greater than differences in heat transfer with the ingested fluid. The purpose of the thesis was to evaluate thermoregulatory control and human heat balance, and compare thermometrically derived values of heat storage with those derived from partitional calorimetry following water ingestion of varying temperature during exercise. We found that water ingestion of 50°C compared to 1.5°C decreases heat storage in thermoneutral environments, and further exacerbates the error of thermometric heat storage estimations. Differences in heat storage were attributed exclusively to disproportionate reductions in whole-body and local sweat output and thus evaporative heat loss potential. Ingested fluid temperature only minimally altered skin blood flow and did not influence dry heat exchange with the ambient environment.

Thesis (B.A.Hons.) from the Department of History, University of Adelaide.

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.