BARORECEPTOR MODULATION OF CUTANEOUS VASODILATOR AND SUDOMOTOR RESPONSES TO THERMAL-STRESS IN HUMANS

1. The influence of baroreceptor unloading on cutaneous vasodilatation was investigated in ten human subjects during dynamic supine cycle er gometer exercise at 28 degrees C. Increases in forearm skin blood flow (venous occlusion plethysmography) and arterial blood pressure (non-i nvasive) were measured and used to calculate forearm vascular conducta nce while local chest sweating rate was measured by dem-point hygromet ry. Subjects performed two similar exercise protocols with and without baroreceptor unloading induced by application of -40 mmHg lower body negative pressure (LBNP). The LBNP condition was reversed (i.e. either removed or applied) after 15 min while exercise continued for an addi tional 20 min. 2. During exercise without LBNP, the body core temperat ure threshold for vasodilatation (measured as oesophageal temperature, T-c) averaged 37.06 +/- 0.12 degrees C (+/- S.E.M) and increased to 3 7.30 +/- 0.09 degrees C (P < 0.05) during exercise with LBNP. The rate of rise of forearm vascular conductance (FVC) per unit increase in T- c (an expression of thermal sensitivity) and peak FVC at 15 min was si gnificantly attenuated during baroreceptor unloading. These effects we re rapidly reversed when LBNP was turned off. 3. Baroreceptor unloadin g during the first 15 min of exercise attenuated the local chest sweat ing rate, which was also reversed when LBNP was removed. 4. The time c ourse and quickness in which baroreceptor unloading modulated thermore gulatory control of skin blood flow and local chest sweat rate suggest s that the interaction between these two homeostatic mechanisms is pri marily neurally mediated. The ability of baroreceptor activity to modu late both control of skin blood flow and sweating suggests a common si te of interaction, more proximal than the effector organs, and involvi ng the active vasodilator system.