Non-thermal influences on the control of skin blood flow have minimal effects on heat transfer during exercise

During exercise, circulatory reflexes ensure that the cardiac output is sufficiently elevated to meet the oxygen delivery requirements of the contracting skeletal muscles and the heat delivery requirements of the body to the skin. The latter requirements are met by increasing skin blood flow. These increases are largely driven by elevations in the body temperatures, although non-thermal effects on the control of skin blood flow occur in certain conditions. These effects are largely the consequence of high and/or low baroreflex stimulation. Even in the face of such non-thermal effects, which occur during exercise in the heat, the body's requirements for heat transfer from core to skin are largely met by the increased skin blood flow. Thus, non-thermal effects on the control of skin blood flow are relatively unimportant in the body's overall regulatory response to exercise.     

The role of non-thermal factors in the control of skin blood flow during exercise

Arguments in favor of the importance of non-thermal factors in the control of skin circulation are presented. Such factors include exercise, posture, water and electrolyte balance, state of training, and acclimatization. The first three factors probably elicit their effects via high- and low-pressure baroreceptors, while the mechanisms involved for the remainder are unknown.     

Neural control of muscle blood flow during exercise.

Activation of skeletal muscle fibers by somatic nerves results in vasodilation and functional hyperemia. Sympathetic nerve activity is integral to vasoconstriction and the maintenance of arterial blood pressure. Thus the interaction between somatic and sympathetic neuroeffector pathways underlies blood flow control to skeletal muscle during exercise. Muscle blood flow increases in proportion to the intensity of activity despite concomitant increases in sympathetic neural discharge to the active muscles, indicating a reduced responsiveness to sympathetic activation. However, increased sympathetic nerve activity can restrict blood flow to active muscles to maintain arterial blood pressure. In this brief review, we highlight recent advances in our understanding of the neural control of the circulation in exercising muscle by focusing on two main topics: 1) the role of motor unit recruitment and muscle fiber activation in generating vasodilator signals and 2) the nature of interaction between sympathetic vasoconstriction and functional vasodilation that occurs throughout the resistance network. Understanding how these control systems interact to govern muscle blood flow during exercise leads to a clear set of specific aims for future research.     

Fluid ingestion during exercise increases skin blood flow independent of increases in blood volume.

The purpose of this experiment was to determine whether fluid ingestion attenuates the hyperthermia and cardiovascular drift that occurs during exercise dehydration due to increases in blood volume. In addition, forearm blood flow, which is indicative of skin blood flow, was measured to determine whether the attenuation of hyperthermia and cardiovascular drift during exercise with fluid ingestion is due to higher skin blood flow. On three different occasions, seven trained cyclists [mean age, body weight, and maximum oxygen uptake: 23 +/- 3 yr, 73.9 +/- 10.5 kg, and 4.75 +/- 0.34 (SD) l/min, respectively] cycled at a power output equal to 62-67% maximum oxygen uptake for 2 h in a warm environment (33 degrees C, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or a volume of a carbohydrate-electrolyte fluid replacement solution (FR) sufficient to replace 80 +/- 2% of sweat loss or were intravenously infused with 5.3 ml/kg of a blood volume expander (BVX; 6% dextran in saline). The infusion of 398 +/- 23 ml of BVX maintained blood volume at levels similar to that when 2,404 +/- 103 ml of fluid were ingested during FR and greater than that when no fluid was ingested during the 2nd h of exercise (P less than 0.05). However, BVX and NF resulted in similar esophageal and rectal temperatures, forearm blood flow, and elevations in serum osmolality and sodium concentration during 2 h of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Laser-Doppler and plethysmographic skin blood flow during exercise and during acute heat stress in the sauna

Forearm skin blood flow was measured in six male subjects by laser-Doppler flowmetry (LDF) and venous occlusion plethysmography (VOP) during constant-load (125-200 W) upright bicycle exercise in a warm environment (X + SD, ta 34.6 +/- 0.2 degrees C) and during a 15 min sauna bath (ta 69.0 +/- 2.8 degrees C). During the sauna test the LDF values correlated well with the VOP measurements in the initial phase of active cutaneous vasodilation, after which the LDF values almost leveled off in spite of a steady increase in VOP measurements. During the exercise the mean VOP and LDF values rose in parallel with each other to steady state levels. The relationship between the results of the two methods proved to be nonlinear. It was concluded that different parameters were measured by VOP and LDF. The latter measured mainly the integrated velocity of blood flow in the outermost cutaneous tissue, and this velocity seemed to be partly dependent on the level of the arterial inflow (VOP), but also on the prevailing pressure-flow and pressure-volume relations in the cutaneous vascular bed.     

Effect of continuous negative-pressure breathing on skin blood flow during exercise in a hot environment

To assessthe impact of continuous negative-pressure breathing (CNPB) on theregulation of skin blood flow, we measured forearm blood flow (FBF) byvenous-occlusion plethysmography and laser-Doppler flow (LDF) at theanterior chest during exercise in a hot environment (ambienttemperature = 30°C, relative humidity = ~30%). Seven malesubjects exercised in the upright position at an intensity of 60% peakoxygen consumption rate for 40 min with and without CNPB after 20 minof exercise. The esophageal temperature(T_es) in both conditionsincreased to 38.1°C by the end of exercise, without any significantdifferences between the two trials. Mean arterial pressure (MAP)increased by ~15 mmHg by 8 min of exercise, without any significantdifference between the two trials before CNPB. However, CNPB reducedMAP by ~10 mmHg after 24 min of exercise (P < 0.05). The increasein FBF and LDF in the control condition leveled off after 18 min ofexercise above a T_es of37.7°C, whereas in the CNPB trial the increase continued, with arise in T_es despite the decreasein MAP. These results suggest that CNPB enhances vasodilation of skinabove a T_es of ~38°C bystretching intrathoracic baroreceptors such as cardiopulmonarybaroreceptors.

     

Nonthermoregulatory control of human skin blood flow

Although it is well accepted that skin blood flow (SkBF) in humans is controlled by thermoregulatory reflexes, the conclusion that the cutaneous circulation is also controlled by reflexes of nonthermoregulatory origin is not universally held. This review considers the extent to which the cutaneous circulation participates in baroreceptor-mediated reflexes and in the reflexes associated with exercise. Exercise is explored in some detail, because it elicits both thermoregulatory and nonthermoregulatory reflexes. The overall conclusion reached is that thermoregulatory control of SkBF is subject to modification by or competition from several other sources. The fundamental pattern for control of SkBF is described by the threshold and slope of the SkBF-internal temperature relationship. Reflex effects of skin temperature act to shift the threshold of this relationship such that lower levels of skin temperature are associated with higher threshold internal temperatures at which cutaneous vasodilation begins. Similarly, baroreceptor reflexes, reflexes associated with exercise, and effects of some cardiovascular disease also operate against this background. Although modification of the SkBF-internal temperature slope is occasionally seen, the most consistent effect of these nonthermoregulatory factors is to elevate the threshold internal temperature for cutaneous vasodilation. The consequence of this modification of thermoregulatory control of SkBF is that temperature regulation will often suffer when increases in SkBF are delayed or limited. Blood flow to other regions, possibly including active skeletal muscle, may also be compromised when thermoregulatory demands for SkBF are high.     

Control of coronary blood flow during exercise

Under normal physiological conditions, coronary blood flow is closely matched with the rate of myocardial oxygen consumption. This matching of flow and metabolism is physiologically important due to the limited oxygen extraction reserve of the heart. Thus, when myocardial oxygen consumption is increased, as during exercise, coronary vasodilation and increased oxygen delivery are critical to preventing myocardial underperfusion and ischemia. Exercise coronary vasodilation is thought to be mediated primarily by the production of local metabolic vasodilators released from cardiomyocytes secondary to an increase in myocardial oxygen consumption. However, despite various investigations into this mechanism, the mediator(s) of metabolic coronary vasodilation remain unknown. As will be seen in this review, the adenosine, K(+)(ATP) channel and nitric oxide hypotheses have been found to be inadequate, either alone or in combination as multiple redundant compensatory mechanisms. Prostaglandins and potassium are also not important in steady-state coronary flow regulation. Other factors such as ATP and endothelium-derived hyperpolarizing factors have been proposed as potential local metabolic factors, but have not been examined during exercise coronary vasodilation. In contrast, norepinephrine released from sympathetic nerve endings mediates a feed-forward betaadrenoceptor coronary vasodilation that accounts for approximately 25% of coronary vasodilation observed during exercise. There is also a feed-forward alpha-adrenoceptor-mediated vasoconstriction that helps maintain blood flow to the vulnerable subendocardium when heart rate, myocardial contractility, and oxygen consumption are elevated during exercise. Control of coronary blood flow during pathophysiological conditions such as hypertension, diabetes mellitus, and heart failure is also addressed.     

Cerebral blood flow during static exercise in humans

Cerebral blood flow (CBF) was determined in humans at rest and during four consecutive unilateral static contractions of the knee extensors. Each contraction was maintained for 3 min 15 s with the subjects in a semisupine position. The contractions corresponded to 8, 16, 24, and 32% of the maximal voluntary contraction (MVC) and utilized alternate legs. CBF (measured by the 133Xe clearance technique) was expressed by a noncompartmental flow index (ISI). Heart rate and mean arterial pressure increased from resting values of 73 (55-80) beats/min and 88 (74-104) mmHg to 106 (86-138) beats/min and 124 (102-146) mmHg, respectively (P less than 0.0005), during the contraction at 32% MVC. Arterial PCO2 and central venous pressure did not change. Corrected to the average resting PCO2, CBF during control was 55 (35-73) ml.100 g-1.min-1 and remained constant during contractions. Cerebral vascular resistance increased from 1.5 (1.0-2.2) to 2.4 (1.4-3.0) mmHg. 100 g.min.ml-1 (P less than 0.025) at 32% of MVC. There was no difference in CBF between the two hemispheres at rest or during exercise. In contrast to dynamic leg exercise, static leg exercise is not associated with an increase in global CBF when measured by the 133Xe clearance technique.     

Effect of mild essential hypertension on control of forearm blood flow during exercise in the heat

Six essential hypertensive (resting mean arterial pressure, MAP greater than 110 mmHg) and eight normotensive (resting MAP less than 95 mmHg) men, aged 30-58 yr, were tested during 1 h of dynamic leg exercise in the heat. Environmental conditions were fixed at 38 degrees C dry-bulb temperature and 28 degrees C wet-bulb temperature; exercise intensity was preset to approximate 40% of each subject's maximal aerobic capacity (actual range 38-43%). Forearm blood flow (FBF) was measured by impedance plethysmography. The intergroup difference in arterial pressure was maintained but not increased or decreased during exercise in the heat. FBF increased in both groups, but the increase was significantly less for the hypertensive subjects. FBF showed a significant linear correlation (different from 0) with core temperature in seven of eight control subjects but in none of the hypertensive subjects. The magnitude of FBF increase was inversely proportional to resting MAP (r = -0.89). It was concluded that essential hypertensive subjects respond to exercise in the heat with a diminished FBF response related to an alteration in control relative to central (core temperature) influences. This may be due to an imbalance between thermal and nonthermal (baroreflex) mechanisms controlling cutaneous blood flow.     

Sweating and skin blood flow during exercise: effects of age and maximal oxygen uptake

Individuals greater than or equal to 60 yr of age are more susceptible to hyperthermia than younger people. However, the mechanisms involved remain unclear. To gain further insight, we examined the heat loss responses of 7 young (24-30 yr) and 13 older (58-74 yr) men during 20 min of cycle exercise [67.5% maximal O2 uptake (VO2max)] in a warm environment (30 degrees C, 55% relative humidity). Forearm blood flow (FBF) and chest sweat rate (SR) were plotted as a function of the weighted average of mean skin and esophageal temperatures [Tes(w)] during exercise. The sensitivity and threshold for each response were defined as the slope and Tes(w) at the onset of the response, respectively. When the young sedentary men were compared with a subgroup (n = 7) of the older physically active men with similar VO2max, the SR and FBF responses of the two groups did not differ significantly. However, when the young men were compared with a subgroup of older sedentary men with a similar maximal O2 pulse, the SR and FBF sensitivities were significantly reduced by 62 and 40%, respectively. These findings suggest that during a short exercise bout either 1) there is no primary effect of aging on heat loss responses but, rather, changes are associated with the age-related decrease in VO2max or 2) the decline in heat loss responses due to aging may be masked by repeated exercise training.