It is well documented that aerobic exercise training provides an individual with a pronounced thermoregulatory and circulatory advantage during exercise in the heat. The ability to prevent excessive hyperthermia during conditions of high thermal and circulatory strain is dependent on a complex interaction between reflexes that regulate heat dissipating mechanisms and non-thermoregulatory (circulatory) reflexes. The long-term objectives of this project are to describe the physiological mechanisms involved in the interaction between control systems which regulated arterial blood pressure and those which regulate body temperature. We are particularly interested in baroreflex control of cutaneous vasoconstrictor activity and how it is influenced by thermal status and/or physical fitness. Our specific aims of over the next five years are: l) to characterize spatial heterogeneities in baroreflex mediated cutaneous vasoconstriction 2) to demonstrate attenuated baroreceptor mediated increases in sympathetic vasoconstrictor activity in hyperthermic humans. 3) to identify the mechanism by which thermoregulatory responses to thermal stress are attenuated by baroreceptor unloading. 4) to examine the role of oropharyngeal reflexes in reversing the inhibitory influence of dehydration on heat loss mechanisms in thermally stressed humans. To accomplish these goals we will create topographical perfusion maps of relatively large areas of the skin microvasculature with the aid of a computer-guided stereotaxic laser Doppler velocimetry system, monitor sympathetic vasoconstrictor nerve activity directly via microneurographic techniques, and modify local sympathetic adrenergic responses in the skin with selective adrenergic blocking agents. We will relate the circulatory and thermoregulatory responses (i.e. changes in sympathetic nerve activity, skin blood flow, or sweating) to their primary physiological stimuli (i.e. changes in central venous or carotid artery pressure or body core temperature). We expect to demonstrate that baroreflex control of circulatory function is altered by the thermal status of the individual and is dependent, in part, on their level of aerobic fitness. In addition, we expect to demonstrate that the interaction between baroreceptor and thermoregulatory control of skin blood flow occurs at a site more proximal than the cutaneous arterioles. Thermal status will be manipulated using passive heating and/or exercise while baroreceptor mediated increases in sympathetic nerve activity will be accomplished by application of lower body negative pressure and/or carotid neck pressure. These studies should improve our understanding of the control of arterial blood pressure during conditions of thermal stress and provide new knowledge about the mechanisms that humans employ to resist syncope in conditions of high circulation and thermal stress.