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1Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas, Dallas, Texas; 2Penn State Heart and Vascular Institute, Penn State College of Medicine, Hershey, Pennsylvania; and 3Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas
Submitted 25 January 2007 ; accepted in final form 17 July 2007
Skin surface cooling improves orthostatic tolerance through a yet to be identified mechanism. One possibility is that skin surface cooling increases the gain of baroreflex control of efferent responses contributing to the maintenance of blood pressure. To test this hypothesis, muscle sympathetic nerve activity (MSNA), arterial blood pressure, and heart rate were recorded in nine healthy subjects during both normothermic and skin surface cooling conditions, while baroreflex control of MSNA and heart rate were assessed during rapid pharmacologically induced changes in arterial blood pressure. Skin surface cooling decreased mean skin temperature (34.9 ± 0.2 to 29.8 ± 0.6°C; P < 0.001) and increased mean arterial blood pressure (85 ± 2 to 93 ± 3 mmHg; P < 0.001) without changing MSNA (P = 0.47) or heart rate (P = 0.21). The slope of the relationship between MSNA and diastolic blood pressure during skin surface cooling (–3.54 ± 0.29 units·beat–1·mmHg–1) was not significantly different from normothermic conditions (–2.94 ± 0.21 units·beat–1·mmHg–1; P = 0.19). The slope depicting baroreflex control of heart rate was also not altered by skin surface cooling. However, skin surface cooling shifted the "operating point" of both baroreflex curves to high arterial blood pressures (i.e., rightward shift). Resetting baroreflex curves to higher pressure might contribute to the elevations in orthostatic tolerance associated with skin surface cooling.
autonomic nervous system; baroreflex gain; thermoregulation; blood pressure regulation; baroreceptors
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