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An abstract of the article "Limb uptake of total and platelet derived circulating microvesicles in normothermic and heat stressed, healthy humans" by M. Rakobowchuk, E. N.Wilhelm, S. J. Trangmar and J. González-Alonso is presented.

Introduction: The haemodynamic responses of skeletal muscle to localised changes in tissue temperature are still poorly understood, despite the widespread therapeutic use of heating and cooling. We aimed to systematically identify these responses both at rest and during one-legged exercise over a wide range of physiologically relevant temperatures. Methods: Leg tissue temperatures in 7 males (age 22±1 years) were altered at rest over 1hr through the use of frozen gel packs (cooling) or a water perfused suit (heating). Core, skin and deep muscle (Tm) temperatures were measured throughout. Haemodynamic alterations in 3 major arteries of the leg (common, superficial, and profunda femoral arteries: CFA, SFA, and PFA) were assessed using duplex Doppler ultrasound, with the contralateral leg providing control measures. Systemic haemodynamic responses were measured non-invasively using infrared plethysmography. Following each intervention, CFA flow was measured during incremental single-legged knee extensor exercise in the experimental or control leg (10±1, 16±1, 23±2, and 30±2W). All values are means ± SEM, with Tm and flows analysed using RM-ANOVA and conductance using linear regression. Results: At rest, 1 hr of localised cooling (Tm 34.9±0.3°C to 29.5±0.6°C; p<0.05) led to small but significant decreases in blood flow to all three vessels (40-60ml.min-1 or 15-25%; p<0.05), with heating (Tm 34.5±0.5°C to 36.8±0.1°C; p<0.05) leading to significant increases (100-360ml.min-1 or 63-99%; p<0.05). Blood flow through the PFA (the major supply artery of the thigh skeletal muscle and therefore representative of muscle blood flow) showed significant alterations following both interventions (25% decrease and 63% increase respectively; p<0.05). PFA vascular conductance showed a strong linear relationship with muscle temperature during both interventions (R²=0.95 and 0.96; p<0.01), with the sensitivity of the response increasing considerably at ~35 °C (i.e. normal resting muscle temperature; 0.11 ±0.03 to 0.70±0.07ml.min-1.mmHg-1.°C-1). Systemic and control leg values remained unchanged. During exercise, prior cooling of the leg had no effect on CFA flows. In contrast, exercise following heating resulted in significantly higher CFA flows throughout the duration of the protocol (~500ml.min-1; p<0.05). Conclusions: These findings suggest that local temperature exerts significant effects on skeletal muscle haemodynamics both at rest and during exercise over a wide range of temperatures, but with significantly increased sensitivity observed at temperatures ≥ 35°C. The maintenance of an increased blood flow throughout exercise following heating suggests an independent role for temperature in the hyperaemic exercise response, potentially mediated through the rapid increases in local muscle and blood temperature experienced when undertaking dynamic muscular contractions. [ABSTRACT FROM AUTHOR]

Background: Dehydration accrued during prolonged exercise in the heat induces significant cardiovascular strain on the human body characterised by reductions in cardiac output, active muscle and skin blood flow, arterial blood pressure, vascular conductance and an overall impaired exercise capacity (1). However, it is presently unknown whether progressive dehydration during exercise in the heat reduces blood flow to the brain, thereby impairing aerobic metabolism. A hyperthermic-hyperventilation induced lowering of the PaCO2 may reduce blood flow to the brain, assuming that reductions in middle cerebral artery velocity (MCA Vmean) reflect reductions in cerebral blood flow (CBF) (2,3,4,5). This study tested the hypothesis that progressive dehydration reduces CBF during prolonged exercise in the heat, in part through mechanisms associated with PaCO2, but without impairing brain VO2. Methods: We assessed blood flow in the internal carotid artery (CBF) using Doppler ultrasonography and middle cerebral artery velocity (MCA Vmean) in ten cyclists (VO2PEAK: 59 ± 2 ml/kg/min), who performed two hours of prolonged cycling exercise in a warm environment (182 ± 6 W; 35°C), without fluids to induce moderate dehydration (DEH; 3.1 ± 0.3 % body mass loss). Subjects returned one week laterto repeat the protocol, but with regular fluid ingestion to maintain hydration status (Control). Blood samples were obtained from the brachial artery and left internal jugular vein (DEH only) to measure a-vO2 differences and for the calculation of brain VO2. All data are mean ± SEM and were compared with ANOVA and Pearson correlation (SPSS). Results: During dehydration CBF and MCA Vmean increased by 13 ± 3% from rest to 30 min (p<0.05). Thereafter CBF declined to resting values with flow at 120 min significantly lower than at 30, 60 and 90 min (p<0.001). During control, CBF and MCA Vmean increased from rest to 30 min and were subsequently maintained throughout exercise (Increase > 25%, p<0.05). Reductions in CBF and MCA Vmean during DEH were accompanied with significant increases (p<0.05) in a-vO2 diff resulting in an unchanged brain VO2. PaCO2 declined in accordance with flow and velocity (p<0.05) with changes in flow correlated to changes in PaCO2 (R² = 0.75, p<0.001), supporting a role for PaCO2 in cerebral vasoconstriction. Discussion: The present findings show that progressive dehydration during prolonged exercise results in a marked reduction in CBF, whereas in control CBF did not decline. Compensatory increases in cerebral oxygen extraction allow for the maintenance of brain VO2 throughout exhaustive exercise. These findings suggest that a reduction in brain VO2 is an unlikely mechanism underpinning exercise capacity during prolonged, exhaustive exercise with dehydration. [ABSTRACT FROM AUTHOR]

Human limb muscle and skin perfusion alters with changes in tissue temperature evoked by heating or cooling and these processes may involve temperature sensitive regulatory mechanisms. We have previously shown that passive heating and exercise increase limb tissue blood flow in humans in association with the increases in muscle temperature and plasma adenosine 5'-triphosphate concentration [ATP] (1,2). Reduced haemoglobin O2 saturation is thought to be the main stimulus for erythrocyte ATP release in the muscle microcirculation (3,4). Recent evidence, however, suggests that temperature is another potent stimulus. Here we tested the hypothesis that the release of the vasodilator mediator ATP from human erythrocytes is sensitive to physiological reductions and increases in blood temperature independently of oxygenation induced ATP release in the human forearm circulation. To accomplish this aim, we measured forearm blood flow (FBF; Doppler ultrasound), deep venous blood temperature (Tb), retrograde venous plasma [ATP], blood gas parameters and calculated forearm vascular conductance (FVC) in the experimental and the control contralateral forearm in 7 males (19 ± 2 years) during 1 hour of passive heating using a water perfused cuff and 1 hour of passive cooling using ice with 1 hour of rest in between. All data are mean ± SEM and were compared with ANOVA and Pearson correlation (SPSS). With heating T increased from 34.0 ± 0.5 to 36.8 ± 0.1°C (p<0.05) while with cooling Tb decreased from 34.4 ± 0.4 to 29.1 ± 0.7°C (p<0.05). Plasma [ATP] doubled with heating from 0.21 ± 0.03 to 0.43 ± 0.05 µmol.l-1 (p<0.05) but did not change with cooling remaining at 0.23 ± 0.03-1 µmol.l-1 similar to values in the control forearm. FBF progressively and significantly increased with heating from 124 ± 11 to 418 ± 10 ml.min-1 (p<0.05) and decreased with cooling from 121 ± 11 to 90 ± 14 ml.min-1 (p<0.05). Similar significant responses were observed with FVC, indicating that flow changes with heating and cooling were due to vasodilatation and vasoconstriction, respectively. In contrast, control forearm values for Tb, [ATP], FBF and FVC were unchanged throughout the study. During heating and cooling, FBF and FVC were exponentially correlated to Tb (R² = 0.86 and 0.87, respectively; p<0.01) and [ATP] (both R² = 0.85; p<0.01). Contrary to the reported involvement of the O2 saturation pathway, plasma [ATP] remained unchanged during cooling despite decreasing O2 saturation from 62 ± 4 to 35 ± 4% (p<0.05) but increased with heating when O2 saturation was elevated from 59 ± 6 to 82 ± 4% (p<0.05). These findings suggest that ATP from erythrocytes may be an important mechanism regulating human limb muscle and skin perfusion in conditions that alter blood and tissue temperature. Furthermore, it seems that temperature works through a distinct pathway to that sensitive to blood oxygenation. [ABSTRACT FROM AUTHOR]