Introduction
As homeotherms, humans have the ability to control thermoregulatory mechanisms: physiological processes that are critical to maintaining core temperature within a very narrow limit. Although peripheral temperature fluctuates regularly & often largely in response to ambient temperature, core temperature must be maintained within a tight window in order for the human body to function properly. Throughout the course of circadian rhythm, the body’s core temperature can fluctuate by up to 0.5C. Only through exercise, illness, & external heat stress will the body stray outside its normal core temperature range of 36.1C-37.8C (Weller, 2005). Mechanisms that maintain normothermic core body conditions consist of processes that either dissipate (to counteract hyperthermia) or generate (to counteract hypothermia) heat in response to internal or external thermal stimuli (Charkoudian, 2003). The consequences of having a core temperature outside of this narrow range without compensation via thermoregulatory mechanisms can result in heat-related illness, injury, or death. Thermoregulatory control of the human body is found within the brain in the preoptic anterior hypothalamus (POAH). This portion of the central nervous system acts much like a thermostat in that it receives afferent input from central & peripheral thermoreceptors, integrates the afferent signal, & generates an efferent signal in response to the information (Boulant, 2000). The POAH produces & coordinates several physiological & behavioural responses to heat imbalance. However, the process by which heat is mechanically dissipated remains enigmatic. While the complete mechanism is still unclear, current understanding suggests a classic feedback loop where temperature deviates from a steady-state, & as a result physiological mechanisms return the temperature to its set-point. The current body of knowledge recognises the POAH 's role in receiving, integrating, & weighing central & peripheral afferent signals. …show more content…
Efferent sympathetic signals originating from the POAH travel by way of the ipsilateral brainstem through the tegmentum of the pons & the medullary raphe nuclei, which terminate on the preganglionic neurons in the intermediolateral column of the spinal cord (Smith & Johnson, 2016). The efferent signal departs from the ventral horn & passes into the sympathetic trunk via the white ramus communicans (Smith & Johnson, 2016). Efferent signals terminate & act post-synaptically on several effectors, which includes endothelial cells found within cutaneous blood vessels & subcutaneous glands. Sympathetic adrenergic nerves release norepinephrine & other neurotransmitters, which interact with …show more content…
Subjects were placed in heated water & wrapped in thermal blankets with the purpose of elucidating the connection between an increase in skin & core temperatures & an increase in sympathetic neural activity. This study also sought to determine if localised cooling of the hand triggered a local or systemic response. This study sought out to test several hypotheses; It was hypothesized that healthy humans subjected to heat stress will experience increased cholinergic & adrenergic activity, inducing vasodilation in peripheral cutaneous blood vessels & activation of subcutaneous eccrine glands. The activation of eccrine glands is expected to trigger the secretion of sweat which will result in a decrease in skin resistance. In response to heat stress, it is hypothesized that the body will maintain core body temperature, regardless of peripheral temperature fluctuations. To preserve core body temperature, it is expected that cardiac output (heart rate & stroke volume) will increase to maintain arterial blood pressure in response to decreased total peripheral resistance. Respiratory rate is expected to increase, while tidal volume is expected to remain constant; this combination should result in an increase in minute ventilation. It is hypothesized that volunteers subjected to the localised cooling protocol will not undergo systemic
As homeotherms, humans have the ability to control thermoregulatory mechanisms: physiological processes that are critical to maintaining core temperature within a very narrow limit. Although peripheral temperature fluctuates regularly & often largely in response to ambient temperature, core temperature must be maintained within a tight window in order for the human body to function properly. Throughout the course of circadian rhythm, the body’s core temperature can fluctuate by up to 0.5C. Only through exercise, illness, & external heat stress will the body stray outside its normal core temperature range of 36.1C-37.8C (Weller, 2005). Mechanisms that maintain normothermic core body conditions consist of processes that either dissipate (to counteract hyperthermia) or generate (to counteract hypothermia) heat in response to internal or external thermal stimuli (Charkoudian, 2003). The consequences of having a core temperature outside of this narrow range without compensation via thermoregulatory mechanisms can result in heat-related illness, injury, or death. Thermoregulatory control of the human body is found within the brain in the preoptic anterior hypothalamus (POAH). This portion of the central nervous system acts much like a thermostat in that it receives afferent input from central & peripheral thermoreceptors, integrates the afferent signal, & generates an efferent signal in response to the information (Boulant, 2000). The POAH produces & coordinates several physiological & behavioural responses to heat imbalance. However, the process by which heat is mechanically dissipated remains enigmatic. While the complete mechanism is still unclear, current understanding suggests a classic feedback loop where temperature deviates from a steady-state, & as a result physiological mechanisms return the temperature to its set-point. The current body of knowledge recognises the POAH 's role in receiving, integrating, & weighing central & peripheral afferent signals. …show more content…
Efferent sympathetic signals originating from the POAH travel by way of the ipsilateral brainstem through the tegmentum of the pons & the medullary raphe nuclei, which terminate on the preganglionic neurons in the intermediolateral column of the spinal cord (Smith & Johnson, 2016). The efferent signal departs from the ventral horn & passes into the sympathetic trunk via the white ramus communicans (Smith & Johnson, 2016). Efferent signals terminate & act post-synaptically on several effectors, which includes endothelial cells found within cutaneous blood vessels & subcutaneous glands. Sympathetic adrenergic nerves release norepinephrine & other neurotransmitters, which interact with …show more content…
Subjects were placed in heated water & wrapped in thermal blankets with the purpose of elucidating the connection between an increase in skin & core temperatures & an increase in sympathetic neural activity. This study also sought to determine if localised cooling of the hand triggered a local or systemic response. This study sought out to test several hypotheses; It was hypothesized that healthy humans subjected to heat stress will experience increased cholinergic & adrenergic activity, inducing vasodilation in peripheral cutaneous blood vessels & activation of subcutaneous eccrine glands. The activation of eccrine glands is expected to trigger the secretion of sweat which will result in a decrease in skin resistance. In response to heat stress, it is hypothesized that the body will maintain core body temperature, regardless of peripheral temperature fluctuations. To preserve core body temperature, it is expected that cardiac output (heart rate & stroke volume) will increase to maintain arterial blood pressure in response to decreased total peripheral resistance. Respiratory rate is expected to increase, while tidal volume is expected to remain constant; this combination should result in an increase in minute ventilation. It is hypothesized that volunteers subjected to the localised cooling protocol will not undergo systemic