MECHANISMS OF CONTROL OF SKIN BLOOD-FLOW DURING PROLONGED EXERCISE IN HUMANS

Exercise in a warm environment raises internal temperature and leads to a rapid increase in skin blood flow (SkBF). As exercise continues, and internal temperature approaches 38-degrees-C, the rate of rise of SkBF is markedly attenuated despite further significant increases in internal temperature. To find whether this attenuation is mediated by increased cutaneous active vasoconstrictor activity or by a reduced rate of rise of active vasodilator activity, each of 12 male subjects had 0.64 cm2 forearm skin sites iontophoretically treated with bretylium tosylate for selective local blockade of noradrenergic vasoconstrictor nerves. SkBF was monitored there and at adjacent untreated control sites by laser-Doppler blood flowmetry (LDF). Whole body skin temperature (T(sk)) was controlled by water-perfused suits, and esophageal temperature (T(es)) was monitored as an index of internal temperature. Mean arterial pressure (MAP) was monitored and cutaneous vascular conductance was calculated as LDF/MAP. Sweat rate was also monitored by dew point hygrometry in 11 subjects. T(sk) was raised to 38-degrees-C, after which subjects began 20-30 min of exercise on a bicycle ergometer. The rate of the initial rapid increase in SkBF with increasing T(es) was not altered by bretylium treatment (P > 0.05 between sites). The attenuation of the rate of rise during the latter phase of exercise was not abolished by bretylium treatment (P > 0.05 between sites); instead, there was a trend for the attenuation to be enhanced at those sites. We conclude that the attenuated rate of rise of SkBF is due to limitation of active vasodilator activity and not due to increased vasoconstrictor tone. Active vasoconstrictor activity appears to be progressively withdrawn during the later phases of prolonged exercise.