Hydration status influences the measurement of arterial stiffness.

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-1 , respectively; P<0·05), but peripheral PWV was unaffected (861[117] versus 825[149] cm s-1 ; 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-1 ; P<0·05) and 1·0°C (-70[48] cm s-1 ; 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.

Spot Sample Urine Specific Gravity Does Not Accurately Represent Small Decreases in Plasma Volume in Resting Healthy Males.

BACKGROUND: Urine specific gravity (USG) is often used to assess hydration status, particularly around athletic competition, but it is unknown whether high USG is indicative of plasma volume (PV) reduction (i.e., hypohydration). We tested the hypothesis that if high USG is reflective of reduced PV, subsequent fluid ingestion would increase PV. PURPOSE: The purpose of this study was to examine 24-hour changes in USG and PV in individuals presenting with high and low spot USG. METHODS: Nineteen healthy males were provided food and water over 24 hours with a total water volume of 35 ml·kg-1 body mass. Absolute PV and blood volume (BV), measured using the CO-rebreathe technique, along with USG were measured before and after a 24-hour intervention period. Based on a preintervention morning spot USG, subjects were post hoc assigned to groups according to USG (≤1.020 or >1.020; low and high USG, respectively). RESULTS: Despite presenting with an elevated spot USG (1.026 ± 0.004), subsequent fluid ingestion over 24 hours did not lead to changes (∆) in PV (-75 ± 234 ml) or BV (-156 ± 370 ml) in the high USG group (p > 0.05). However, a spot USG after the 24-hour intervention in this group decreased (p = 0.018) to a level indicating improved hydration status (1.017 ± 0.007). In the low USG group, there were no changes in PV (-39 ± 274 ml), BV (-82 ± 396 ml), or USG (0.003 ± 0.007) over the 24-hour fluid intervention (all p > 0.05). CONCLUSIONS: Despite a high preintervention USG and subsequent decrease after 24-hour fluid intake, measures of PV and BV were not indicative of this seemingly improved hydration status. This suggests that a highly concentrated spot sample USG and subsequent changes are not accurately representative of PV or BV.

Effect of hypohydration on postsynaptic cutaneous vasodilation and sweating in healthy men.

Hypohydration decreases cutaneous vasodilation and sweating during heat stress, but it is unknown if these decrements are from postsynaptic (i.e., sweat gland/blood vessel) alterations. The purpose of this study was to determine if hypohydration affects postsynaptic cutaneous vasodilation and sweating responses. Twelve healthy men participated in euhydrated (EU) and hypohydrated (HY) trials, with hypohydration induced via fluid restriction and passive heat stress. Changes in cutaneous vascular conductance (CVC; %max) in response to incremental intradermal infusion of the endothelium-independent vasodilator sodium nitroprusside (SNP) and the endothelium-dependent vasodilator methacholine chloride (MCh) were assessed by laser Doppler flowmetry. Local sweat rate (LSR) was simultaneously assessed at the MCh site via ventilated capsule. At the end of the last dose, maximal CVC was elicited by delivering a maximal dose of SNP (5 × 10-2 M) for 30 min to both sites with simultaneous local heating (~44°C) at the SNP site. The concentration of drug needed to elicit 50% of the maximal response (log EC50) was compared between hydration conditions. The percent body mass loss was greater with HY vs. EU (-2.2 ± 0.7 vs. -0.1 ± 0.7%, P < 0.001). Log EC50 of endothelium-dependent CVC was lower with EU (-3.62 ± 0.22) vs. HY (-2.93 ± 0.08; P = 0.044). Hypohydration did not significantly alter endothelium-independent CVC or LSR (both P > 0.05). In conclusion, hypohydration attenuated endothelium-dependent CVC but did not affect endothelium-independent CVC or LSR responses. These data suggest that reductions in skin blood flow accompanying hypohydration can be partially attributed to altered postsynaptic function.