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This investigation determined the manner in which the cardiovascular system copes with the dehydration-induced reductions in cardiac output (Q) during prolonged exercise in the heat. On two separate occasions, seven endurance-trained subjects (maximal O2 consumption 4.70 +/- 0.41 l/min) cycled in the heat (35 degrees C) for 2 h, beginning at 62 +/- 2% maximal O2 consumption. During exercise, they randomly received either 0.2 liter of fluid and became dehydrated by 4.9 +/- 0.2% of their body weight [i.e., dehydration trial (DE)] or 3.6 +/- 0.4 liter of fluid and replaced 95% of fluid losses [i.e., euhydration trial (EU)]. During the 10- to 120-min period of EU, Q, mean arterial pressure (MAP), systemic vascular resistance (SVR), cutaneous vascular resistance (CVR), and plasma catecholamines did not change while esophageal temperature stabilized at 38.0 +/- 0.1 degrees C. Conversely, after 120 min of DE, Q and MAP were reduced 18 +/- 3 and 5 +/- 2%, respectively, compared with EU (P < 0.05). This was associated with a significantly higher SVR (17 +/- 6%) and plasma norepinephrine concentration (50 +/- 19%, P < 0.05). In addition, CVR was also significantly higher (126 +/- 16 vs. 102 +/- 6% of 20-min value; P < 0.05) during DE despite a 1.2 +/- 0.1 degrees C greater esophageal temperature (P < 0.05). In conclusion, significant reductions in Q are accompanied by significant increases in SVR and plasma norepinephrine and a slight although significant decline in MAP. The cutaneous circulation participates in this systemic vasoconstriction as indicated by increases in CVR despite significant hyperthermia.

We identified the cardiovascular stress encountered by superimposing dehydration on hyperthermia during exercise in the heat and the mechanisms contributing to the dehydration-mediated stroke volume (SV) reduction. Fifteen endurance-trained cyclists [maximal O2 consumption (VO2max) = 4.5 l/min] exercised in the heat for 100-120 min and either became dehydrated by 4% body weight or remained euhydrated by drinking fluids. Measurements were made after they continued exercise at 71% VO2max for 30 min while 1) euhydrated with an esophageal temperature (T(es)) of 38.1-38.3 degrees C (control); 2) euhydrated and hyperthermic (39.3 degrees C); 3) dehydrated and hyperthermic with skin temperature (T(sk)) of 34 degrees C; 4) dehydrated with T(es) of 38.1 degrees C and T(sk) of 21 degrees C; and 5) condition 4 followed by restored blood volume. Compared with control, hyperthermia (1 degrees C T(es) increase) and dehydration (4% body weight loss) each separately lowered SV 7-8% (11 +/- 3 ml/beat; P< 0.05) and increased heart rate sufficiently to prevent significant declines in cardiac output. However, when dehydration was superimposed on hyperthermia, the reductions in SV were significantly (P < 0.05) greater (26 +/- 3 ml/beat), and cardiac output declined 13% (2.8 +/- 0.3 l/min). Furthermore, mean arterial pressure declined 5 +/- 2%, and systemic vascular resistance increased 10 +/- 3% (both P < 0.05). When hyperthermia was prevented, all of the decline in SV with dehydration was due to reduced blood volume (approximately 200 ml). These results demonstrate that the superimposition of dehydration on hyperthermia during exercise in the heat causes an inability to maintain cardiac output and blood pressure that makes the dehydrated athlete less able to cope with hyperthermia.

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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