MECHANISMS OF CONTROL OF SKIN BLOOD-FLOW DURING PROLONGED EXERCISE INHUMANS

Exercise in a warm environment raises internal temperature and leads t o a rapid increase in skin blood flow (SkBF). As exercise continues, a nd internal temperature approaches 38-degrees-C, the rate of rise of S kBF is markedly attenuated despite further significant increases in in ternal temperature. To find whether this attenuation is mediated by in creased 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 t osylate for selective local blockade of noradrenergic vasoconstrictor nerves. SkBF was monitored there and at adjacent untreated control sit es by laser-Doppler blood flowmetry (LDF). Whole body skin temperature (T(sk)) was controlled by water-perfused suits, and esophageal temper ature (T(es)) was monitored as an index of internal temperature. Mean arterial pressure (MAP) was monitored and cutaneous vascular conductan ce was calculated as LDF/MAP. Sweat rate was also monitored by dew poi nt 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 atten uation of the rate of rise during the latter phase of exercise was not abolished by bretylium treatment (P > 0.05 between sites); instead, t here 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 limitatio n of active vasodilator activity and not due to increased vasoconstric tor tone. Active vasoconstrictor activity appears to be progressively withdrawn during the later phases of prolonged exercise.