When obese and non-obese females exercised at a fixed metabolic heat production and euhydration was maintained, there were no differences in body temperature between groups.

In conclusion, over 24 h, individuals with a higher void number were euhydrated (that is, had less concentrated hydration biomarkers) than those with a lower void number. Based on these data, void number might be utilized as a simple and feasible hydration assessment for the general public, as it utilizes no equipment or technical expertise.

In non-smokers, passive heat stress increases shear stress and vasodilation, decreasing arterial stiffness. Smokers, who reportedly have arterial dysfunction, may have similar improvements in arterial stiffness with passive heat stress. Therefore, we examined the effects of an acute bout of whole-body passive heat stress on arterial stiffness in smokers vs. non-smokers. Thirteen smokers (8.8 ± 5.5 [median = 6] cigarettes per day for > 4 years) and 13 non-smokers matched for age, mass, height, and exercise habits (27 ± 8 years; 78.8 ± 15.4 kg; 177.6 ± 6.7 cm) were passively heated to 1.5 °C core temperature (T C) increase. At baseline and each 0.5 °C T C increase, peripheral (pPWV) and central pulse wave velocity (cPWV) were measured via Doppler ultrasound. No differences existed between smokers and non-smokers for any variables (all p > .05), except cPWV slightly increased from baseline (526.7 ± 81.7 cm · s(-1)) to 1.5 °C ΔT C (579.7 ± 69.8 cm · s(-1); p < 0.005), suggesting heat stress acutely increased central arterial stiffness. pPWV did not change with heating (grand mean: baseline = 691.9 ± 92.9 cm · s(-1); 1.5 °C ΔT C = 691.9 ± 79.5 cm · s(-1); p > 0.05). Changes in cPWV and pPWV during heating correlated (p < 0.05) with baseline PWV in smokers (cPWV: r = -0.59; pPWV: r = -0.62) and non-smokers (cPWV: r = -0.45; pPWV: r = -0.77). Independent of smoking status, baseline stiffness appears to mediate the magnitude of heating-induced changes in arterial stiffness.

VF is a reliable index of 24-h hydration status when healthy young males are EU or HY and voiding at a consistent 'urgency'.

Consensus guidelines have attempted to standardize the measurement and interpretation of pulse wave velocity (PWV); however, guidelines have not addressed whether hydration status affects PWV. Moreover, multiple studies have utilized heat stress to reduce arterial stiffness which may lead to dehydration. This study utilized two experiments to investigate the effects of dehydration on PWV at rest and during passive heat stress. In experiment 1, subjects (n = 19) completed two trials, one in which they arrived euhydrated and one dehydrated (1·2[1·0]% body mass loss). In experiment 2, subjects (n = 11) began two trials euhydrated and in one trial did not receive water during heat stress, thus becoming dehydrated (1·6[0·6]% body mass loss); the other trial subjects remained euhydrated. Using Doppler ultrasound, carotid-to-femoral (central) and carotid-to-radial (peripheral) PWVs were measured. PWV was obtained at a normothermic baseline, and at a 0·5°C and 1°C elevation in rectal temperature (via passive heating). In experiment 1, baseline central PWV was significantly higher when euhydrated compared to dehydrated (628[95] versus 572[91] cm s , respectively; P<0·05), but peripheral PWV was unaffected (861[117] versus 825[149] cm s ; P>0·05). However, starting euhydrated and becoming dehydrated during heating in experiment 2 did not affect PWV measures (P>0·05), and independent of hydration status peripheral PWV was reduced when rectal temperature was elevated 0·5°C (-74[45] cm s ; P<0·05) and 1·0°C (-70[48] cm s ; P<0·05). Overall, these data suggest that hydration status affects measurements of central PWV in normothermic, resting conditions. Therefore, future guidelines should suggest that investigators ensure adequate hydration status prior to measures of PWV.