Effect of systemic yohimbine on the control of skin blood flow during local heating and dynamic exercise

Kenney, W. L.; Zappe, Dion H.; Tankersley, Clarke G.; Derr, Janice

doi:10.1152/ajpheart.1994.266.2.h371

Cited by 15 publications

(12 citation statements)

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“…Plateau levels of SkBF are only 50%-60% of maximum and are low relative to levels at rest under similar thermal circumstances. This reduced rate of rise is not reversed by systemic blockade of al-or az-adrenergic receptors (134,135) or by local blockade of norepinephrine release (124), which shows that the mechanism for this suppressive effect of exercise is through limiting active vasodilator outflow (rather than through exaggerated vasoconstrictor activity). Indeed, the presence of bretylium leads to a flatter plateau phase, indicating that the small further rise in SkBF mentioned above is due to a progressive withdrawal of vasoconstrictor activity (124).…”

Section: )mentioning

confidence: 94%

Cardiovascular Adjustments to Heat Stress

Johnson

Proppe

1996

Comprehensive Physiology

213

287

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Section: )mentioning

confidence: 94%

Cardiovascular Adjustments to Heat Stress

Johnson

Proppe

1996

Comprehensive Physiology

213

287

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“…This plateau phase observed during exercise occurs at much lower levels than those elicited under passive heating (50-60% peak) (7). In an effort to address the mechanism by which the suppression of skin blood flow occurs with prolonged exercise, a number of studies examined this response using systemic blockade of α 1 -(46) and α 2 -adrenoreceptors (47) or local blockade of norepinephrine release with bretylium (43). These studies showed that the attenuated rise in skin blood flow at higher levels of core temperature during prolonged exercise is primarily related to a functional limit in active vasodilator activity rather than an increase in vasoconstrictor activity.…”

Section: Thermal Factors Influencing Skin Blood Flowmentioning

confidence: 99%

Human thermoregulation: separating thermal and nonthermal effects on heat loss

Glen¹

2010

Front Biosci

106

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Human thermoregulatory control during heat stress has been studied at rest, during exercise and more recently during exercise recovery. Heat balance in the body is maintained by changes in the rate of heat loss via adjustments in skin blood flow and sweating. Independent of thermal control, the actions of nonthermal factors have important consequences in the control of heat loss responses during and following exercise. While the effect of these nonthermal factors is largely considered to be an inhibitory or excitatory stimulus which displaces the set-point about which temperature is regulated, their effects on human thermoregulatory control are far reaching. Many factors can affect the relative contribution of thermal and nonthermal influences to heat balance including exercise intensity, hemodynamic status, and the level of hyperthermia imposed. This review will characterize the physiological responses associated with heat stress and discuss the thermal and nonthermal influences on sweating and skin blood flow in humans. Further, recent calorimetric evidence for the understanding of thermal and nonthermal contributions to human heat balance will also be discussed.

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“…The mechanism behind the attenuation of the increases in CVC (i.e. attenuation phase) during exercise has recently been studied (Kenney, Tankersley, Newswanger & Puhl, 1991;Kellogg, Johnson, Kenney, P6rgola & Kosiba, 1993;Kenney, Zappe, Tankersley & Derr, 1994). The general conclusion from these investigations is that the occurrence of the CVC attenuation phase is due primarily to a withdrawal of active vasodilatation and is not the result of an increased a-adrenergic vasoconstriction superimposed upon active vasodilatation (Kenney et al 1991;Kellogg et al 1993;Kenney et al 1994).…”

mentioning

confidence: 99%

“…attenuation phase) during exercise has recently been studied (Kenney, Tankersley, Newswanger & Puhl, 1991;Kellogg, Johnson, Kenney, P6rgola & Kosiba, 1993;Kenney, Zappe, Tankersley & Derr, 1994). The general conclusion from these investigations is that the occurrence of the CVC attenuation phase is due primarily to a withdrawal of active vasodilatation and is not the result of an increased a-adrenergic vasoconstriction superimposed upon active vasodilatation (Kenney et al 1991;Kellogg et al 1993;Kenney et al 1994). While a-adrenergic vasoconstriction may or may not be involved in the general occurrence of the attenuation phase, it is not known whether changes in a-adrenergic stimulation from plasma catecholamines can affect the magnitude of CVC once the attenuation phase has been established during prolonged exercise.…”

mentioning

confidence: 99%

Plasma catecholamines and hyperglycaemia influence thermoregulation in man during prolonged exercise in the heat.

Mora-Rodríguez

González‐Alonso

Below

et al. 1996

The Journal of Physiology

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1. We manipulated plasma catecholamines (combined adrenaline and noradrenaline concentrations) to three levels during prolonged exercise to determine their effect on cutaneous and forearm vascular conductance (CVC and FVC), oesophageal temperature (T..) and cardiovascular responses.2. On three occasions, seven endurance-trained men cycled at 65% V2, max in the heat (33 1 + 0 7°C) for 120-150 min. During the control trial (150 min duration), 0 45% saline was intravenously infused (SI) starting at 30 min, at a rate that replaced a third of the fluid losses. The infusion start time and rate were identical in all three trials. During SI, plasma catecholamine levels increased progressively and were 18&2 + 2 7 pmol ml-1 at 150 min. In another trial (120 min duration), adrenaline was infused (AI) at 0 1 jug kg-1 min-' and plasma catecholamine levels were elevated 6 pmol ml-' above SI during the 60-120 min period. In a third trial (150 min duration), an 18% glucose solution was infused (GI) at a rate that maintained plasma glucose levels above 11 mm and plasma catecholamine levels were 5 0-5 5 pmol ml-' lower (P < 0'05) than SI from 120-150 min.3. Heat production and sweat rate were not different during the three trials and neither was the decline in stroke volume, cardiac output and mean arterial pressure.4. Soon after beginning AI, CVC decreased 15%, TRes increased by 04 + 0.1°C and heart rate increased by 6 + 1 beats min-; these significant (P < 0 05) differences from SI were maintained throughout the bout. As a result of GI, FVC was 15% higher than SI and TRe and heart rate were attenuated by 0 3 + 0.1°C and 7 + 1 beats min-' at 150 min compared with SI (P < 0'05).5. In conclusion, large increases in plasma catecholamine levels cause hyperthermia during exercise by vasoconstricting the skin. The mechanisms by which hyperglycaemia (i.e. 11 mM) attenuates hyperthermia are less clear and may be due to others factors besides attenuation of the plasma catecholamine response to exercise.The cutaneous circulation in humans is one of the major routes for heat dissipation during exercise in the heat and is affected by many factors including local temperature, circulating autacoids and hormones, and nervous system reflexes (Rowell, 1986). The cutaneous vasculature lacks fl-adrenergic receptors but is richly supplied with a-receptors that cause vasoconstriction when stimulated. a-Adrenergic vasoconstriction can be induced either by noradrenaline released from sympathetic vasoconstrictor nerve endings in the skin or by plasma catecholamines (Rowell, 1986).It is not well understood how vasodilatation occurs in the non-acral cutaneous vasculature. Substantial vasodilatation, beyond that which occurs with just the withdrawal of sympathetic vasoconstrictor tone when core temperature increases, is termed active vasodilatation. Active vasodilatation is considered to be an active process because it requires an intact sympathetic innervation to the skin (Edholm, Fox & Macpherson, 1957), but the specific neurotransmitter and underlyi...

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Effect of systemic yohimbine on the control of skin blood flow during local heating and dynamic exercise

Cited by 15 publications

References 0 publications

Cardiovascular Adjustments to Heat Stress

Cardiovascular Adjustments to Heat Stress

Human thermoregulation: separating thermal and nonthermal effects on heat loss

Plasma catecholamines and hyperglycaemia influence thermoregulation in man during prolonged exercise in the heat.

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