Heat stress increases limb blood flow and cardiac output (Q̇) in humans, presumably in sole response to an augmented thermoregulatory demand of the skin circulation. Here we tested the hypothesis that local hyperthermia also increases skeletal muscle blood flow at rest and during exercise. Hemodynamics, blood and tissue oxygenation, and muscle, skin, and core temperatures were measured at rest and during exercise in 11 males across four conditions of progressive whole body heat stress and at rest during isolated leg heat stress. During whole body heat stress, leg blood flow (LBF), Q̇, and leg (LVC) and systemic vascular conductance increased gradually with elevations in muscle temperature both at rest and during exercise ( r² = 0.86–0.99; P < 0.05). Enhanced LBF and LVC were accompanied by reductions in leg arteriovenous oxygen (a-vO₂) difference and increases in deep femoral venous O₂ content and quadriceps tissue oxygenation, reflecting elevations in muscle and skin perfusion. The increase in LVC occurred despite an augmented plasma norepinephrine ( P < 0.05) and was associated with elevations in muscle temperature ( r² = 0.85; P = 0.001) and arterial plasma ATP ( r² = 0.87; P < 0.001). Isolated leg heat stress accounted for one-half of the increase in LBF with severe whole body heat stress. Our findings suggest that local hyperthermia also induces vasodilatation of the skeletal muscle microvasculature, thereby contributing to heat stress and exercise hyperemia. The increased limb muscle vasodilatation in these conditions of elevated muscle sympathetic vasoconstrictor activity is closely related to the rise in arterial plasma ATP and local tissue temperature.

The purpose of this study was to determine whether the reduction in stroke volume (SV), previously shown to occur with dehydration and increases in internal body temperatures during prolonged exercise, is caused by a reduction in left ventricular (LV) function, as indicated by LV volumes, strain, and twist (“LV mechanics”). Eight healthy men [age: 20 ± 2, maximal oxygen uptake (VO₂max): 58 ± 7 ml·kg⁻¹·min⁻¹] completed two, 1-h bouts of cycling in the heat (35°C, 50% peak power) without fluid replacement, resulting in 2% and 3.5% dehydration, respectively. Conventional and two-dimensional speckle-tracking echocardiography was used to determine LV volumes, strain, and twist at rest and during one-legged knee-extensor exercise at baseline, both levels of dehydration, and following rehydration. Progressive dehydration caused a significant reduction in end-diastolic volume (EDV) and SV at rest and during one-legged knee-extensor exercise (rest: Δ − 33 ± 14 and Δ − 21 ± 14 ml, respectively; exercise: Δ − 30 ± 10 and Δ − 22 ± 9 ml, respectively, during 3.5% dehydration). In contrast to the marked decline in EDV and SV, systolic and diastolic LV mechanics were either maintained or even enhanced with dehydration at rest and during knee-extensor exercise. We conclude that dehydration-induced reductions in SV at rest and during exercise are the result of reduced LV filling, as reflected by the decline in EDV. The concomitant maintenance of LV mechanics suggests that the decrease in LV filling, and consequently ejection, is likely caused by the reduction in blood volume and/or diminished filling time rather than impaired LV function.

Quantifying sweat gland activation provides important information when explaining differences in sweat rate between populations and physiological conditions. However, no standard technique has been proposed to measure sweat gland activation, while the reliability of sweat gland activation measurements is unknown. We examined the interrater and internal reliability of the modified-iodine paper technique, as well as compared computer-aided analysis to manual counts of sweat gland activation. Iodine-impregnated paper was pressed against the skin of 35 participants in whom sweating was elicited by exercise in the heat or infusion of methylcholine. The number of active glands was subsequently determined by computer-aided analysis. In total, 382 measurements were used to evaluate: 1) agreement between computer analysis and manual counts; 2) the interrater reliability of computer analysis between independent investigators; and 3) the internal reliability of sweat gland activation measurements between duplicate samples. The number of glands identified with computer analysis did not differ from manual counts (68 ± 29 vs. 72 ± 24 glands/cm²; P = 0.27). These measures were highly correlated ( r = 0.77) with a mean bias ± limits of agreement of −4 ± 38 glands/cm². When comparing computer analysis measures between investigators, values were highly correlated ( r = 0.95; P < 0.001) and the mean bias ± limits of agreement was 4 ± 18 glands/cm². Finally, duplicate measures of sweat gland activation were highly correlated ( r = 0.88; P < 0.001) with a mean bias ± limits of agreement of 3 ± 29 glands/cm². These results favor the use of the modified-iodine paper technique with computer-aided analysis as a standard technique to reliably evaluate the number of active sweat glands.

Cerebral autoregulation (CA) is thought to maintain relatively constant cerebral blood flow (CBF) across normal blood pressures. To determine if postural changes alter CA, we measured cerebral blood flow velocity (CBFv) in the middle cerebral arteries, mean arterial blood pressure (MABP), cardiac output (Q), and end‐tidal carbon dioxide (PETCO₂) in 18 healthy individuals (11 female and seven male; 26 ± 9 years) during repeated periods of supine and seated rest. Multiple regression was used to evaluate the influence of PETCO₂, MABP, Q, and hydrostatic pressure on CBFv. Static CA was assessed by evaluating absolute changes in steady‐state CBFv. Dynamic CA was assessed by transfer function analysis of the CBFv response to spontaneous oscillations in MABP. In the seated versus supine posture, MABP (67.2 ± 7.2 vs. 84.2 ± 12.1 mmHg; P < 0.001), CBFv (55.2 ± 9.1 vs. 63.6 ± 10.6 cm/sec; P < 0.001) and PETCO₂ (29.1 ± 2.6 vs. 30.9 ± 2.3 mmHg; P < 0.001) were reduced. Changes in CBFv were not explained by variance in PETCO₂, MABP, Q, or hydrostatic pressure. A reduction in MABP to CBFv transfer function gain while seated (P < 0.01) was explained by changes in the power spectrum of MABP, not CBFv. Our findings suggest that changes in steady‐state cerebral hemodynamics between postures do not appear to have a large functional consequence on the dynamic regulation of CBF.

A maximal aerobic capacity below the 20th percentile is associated with an increased risk of all-cause mortality (Blair 1995). Adult Adult burn surviv