We examined the effect of high local forearm skin temperature (Tloc) on reflex cutaneous vasodilator responses to elevated whole-body skin (Tsk) and internal temperatures. One forearm was locally warmed to 42 degrees C while the other was left at ambient conditions to determine if a high Tloc could attenuate or abolish reflex vasodilation. Forearm blood flow (FBF) was monitored in both arms, increases being indicative of increases in skin blood flow (SkBF). In one protocol, Tsk was raised to 39-40 degrees C 30 min after Tloc in one arm had been raised to 42 degrees C. In a second protocol, Tsk and Tloc were elevated simultaneously. In protocol 1, the locally warmed arm showed little or no change in blood flow in response to increasing Tsk and esophageal temperature (average rise = 0.76 +/- 1.18 ml X 100 ml-1 X min-1), whereas FBF in the normothermic arm rose by an average of 8.84 +/- 3.85 ml X 100 ml-1 X min-1. In protocol 2, FBF in the normothermic arm converged with that in the warmed arm in three of four cases but did not surpass it. We conclude that local warming to 42 degrees C for 35-55 min prevents reflex forearm cutaneous vasodilator responses to whole-body heat stress. The data strongly suggest that this attenuation is via reduction or abolition of basal tone in the cutaneous arteriolar smooth muscle and that at a Tloc of 42 degrees C a maximum forearm SkBF has been achieved. Implicit in this conclusion is that local warming has been applied for a duration sufficient to achieve a plateau in FBF.

We compared laser-Doppler velocimetry with plethysmographically determined changes in skin blood flow (SkBF) in five studies on four men. Increments in SkBF were induced by raising whole-body skin temperature to 39 degrees C for 50-70 min. We found laser-Doppler blood flow (LDF) to correlate well with total forearm blood flow (FBF) within each study (r = 0.94-0.98), but the relationship varied among studies. Thus the slopes for the LDF vs. FBF relationship varied from 40 to 122 mV X ml-1 X 100 ml X min. The value for LDF at zero FBF, extrapolated from the regression relationships, ranged from 246 to 599 mV above the value for LDF set with the probe on a stationary object. The value for LDF when blood flow to the arm was mechanically occluded ranged from 110 to 230 mV. In a second series, we measured the LDF values from six sites on forearms of each of four normothermic men. There was marked regional variation, with 1.8- to 5.7-fold ranges in LDF within a given subject. Values for LDF during occlusion of the forearm were more consistent within and between subjects. Thus LDF appears to provide a good indicator of the response pattern of SkBF from the region of illuminated skin. However, variability in the relationship to total SkBF (probably arising from variation in the number of perfused capillaries in the small volume of tissue) and uncertainties in the value of LDF at zero SkBF make quantitative use difficult.

Cutaneous vascular responses to dynamic exercise have been well characterized, but it is not known whether that response pattern applies to isometric handgrip exercise. We examined cutaneous vascular responses to isometric handgrip and dynamic leg exercise in five supine men. Skin blood flow was measured by laser-Doppler velocimetry and expressed as laser-Doppler flow (LDF). Arterial blood pressure was measured noninvasively once each minute. Cutaneous vascular conductance (CVC) was calculated as LDF/mean arterial pressure. LDF and CVC responses were measured at the forearm and chest during two 3-min periods of isometric handgrip at 30% of maximum voluntary contraction and expressed as percent changes from the preexercise levels. The skin was normothermic (32 degrees C) for the first period of handgrip and was locally warmed to 39 degrees C for the second handgrip. Finally, responses were observed during 5 min of dynamic two-leg bicycle exercise (150-175 W) at a local skin temperature of 39 degrees C. Arm LDF increased 24.5 +/- 18.9% during isometric handgrip in normothermia and 64.8 +/- 14.1% during isometric handgrip at 39 degrees C (P less than 0.05). Arm CVC did not significantly change at 32 degrees C but significantly increased 18.1 +/- 6.5% during isometric handgrip at 39 degrees C (P less than 0.05). Arm LDF decreased 12.2 +/- 7.9% during dynamic exercise at 39 degrees C, whereas arm CVC fell by 35.3 +/- 4.6% (in each case P less than 0.05). Chest LDF and CVC showed similar responses.(ABSTRACT TRUNCATED AT 250 WORDS)

Measurement of minimal vascular resistance has proved useful in quantifying structural changes in regional circulations. Accurate measurement of minimal vascular resistance requires full relaxation of all resistance vessels within the region under examination. The usual procedure in humans involves the measurement of maximal forearm blood-flow following 6-10 min of forearm ischaemia. We conducted this study to find whether forearm skin was fully vasodilated by this procedure. Peak forearm blood-flow was measured by plethysmography in six healthy subjects following 10 min of ischaemia while the arm was at a neutral temperature (33 degrees C) and while the arm was locally warmed to 42 degrees C. Peak reactive hyperaemia blood-flow was significantly elevated by local heating (P less than 0.001) to 79.6 ml 100 ml-1 min-1 from a value of 50.2 ml 100 ml-1 min-1 during normothermia. Peak reactive hyperaemia blood-flow in the contralateral unheated forearm showed no significant change between the two periods of ischaemia (P greater than 0.05). These findings were confirmed in four subjects by laser Doppler velocimetry, which gives a linear index of skin blood-flow. In normothermic conditions, this index rose to 0.89 V following 10 min of ischaemia and to 1.26 V with local warming to 42 degrees C (P less than 0.001). Ischaemia plus local warming did not cause a further significant rise in this index of skin blood-flow (1.35 V, P greater than 0.05). These data suggest that 10 min of ischaemia during normothermia is insufficient to relax fully cutaneous resistance vessels and that maximal forearm blood-flow is underestimated by this procedure.

The roles of the mode of contraction (i.e., dynamic or static) and the active muscle mass as determinants of the cardiovascular responses to exercise were studied. Six healthy men performed static handgrip (SHG), dynamic handgrip (DHG), static two-knee extension (SKE), and dynamic two-knee extension (DKE) to local muscular fatigue in approximately 6 min. Increases in mean arterial pressure were similar for each mode of contraction, 29 +/- 5 and 30 +/- 3 mmHg in SHG and DHG and 56 +/- 2 and 48 +/- 2 mmHg in SKE and DKE (P greater than 0.05) but larger for KE than HG (P less than 0.001). Cardiac output increased more for dynamic than for static exercise and for each mode more for KE than HG (P less than 0.001). Systemic resistance was lower for dynamic than static exercise and fell from resting levels by approximately 1/3 during DKE. The magnitude of the pressor response was related to the active muscle mass but independent of the contraction mode. However, the mode of contraction affected the circulatory changes contributing to the pressor response. Equalization of the pressor responses was achieved by proportionately larger increases in cardiac output during dynamic exercise.