A Single Dose of Ibuprofen Impacts IL-10 Response to 164-km Road Cycling in the Heat.

Purpose: The purpose was to determine the effect of a single-dose prophylactic ibuprofen use before a 164-km road cycling event in high ambient temperature on the circulating cytokine and leukocyte responses. Methods: Twenty-three men (53 ± 8 y, 172.0 ± 22.0 cm, 85.1 ± 12.8 kg, 19.6 ± 4.4% body fat) completed a 164-km self-paced recreational road cycling event in a hot, humid, sunny environment (WBGT = 29.0 ± 2.9°C) after consuming 600 mg of ibuprofen (n = 13) or a placebo (n = 10). Blood samples were obtained one to two hours before (PRE) and immediately after (POST) the event, and analyzed for concentrations of circulating cytokines interleukins (IL)-1ß, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, GM-CSF, IFN-γ, and TNF-α and leukocytes (total leukocytes, granulocytes, monocytes, and lymphocytes). Results: Event completion time was 400.2 ± 74.8 min. Concentrations of all cytokines (except IL-1ß, IL-2, IL-5, IL-12, GM-CSF, and IFN-γ) and of all leukocyte subsets increased from PRE to POST. Ibuprofen ingestion attenuated the increase in IL-10 (86% increase with Ibuprofen; 270% increase with placebo). Conclusions: Consuming 600 mg of Ibuprofen prior to a 164-km road cycling event in a hot-humid environment attenuates exercise-induced increases in the concentration of the anti-inflammatory cytokine IL-10, but does not alter the effect of the exercise event on concentrations of other circulating cytokines or leukocyte subset concentrations.

Reliability of 24-h void frequency as an index of hydration status when euhydrated and hypohydrated.

BACKGROUND/OBJECTIVES: Void frequency (VF) is significantly correlated to hydration status, but it is unknown whether VF is reliable when an individual is repeatedly euhydrated (EU) or hypohydrated (HY). The purpose of this study was to test the reliability of VF when individuals were EU or HY on multiple occasions. SUBJECTS/METHODS: Fourteen males (age 22±2 years, mass 79.1±12.8 kg) completed three EU trials achieved with 24-h ad libitum fluid intake, and 14 males (age 22±2 years, mass 78.6±10.4 kg) completed three HY trials achieved with 24-h fluid restriction. Twenty-four hour urine was collected and analyzed for specific gravity (USG) and VF. Subjects voided at a 'normal urgency' (rated a '2' on a 0-4 perceptual scale) throughout each 24-h period. RESULTS: Twenty-four hour USG was greater and VF was lower when HY (1.026±0.003 and 5±2, respectively) versus EU (1.014±0.003 and 7±2; both P<0.05). Intra-class correlations for VF between the three trials at each hydration status were deemed acceptable (0.863 and 0.849 for EU and HY, respectively). Within-subject coefficients of variation for VF were 15±9 and 21±14% for the EU and HY trials. CONCLUSIONS: VF is a reliable index of 24-h hydration status when healthy young males are EU or HY and voiding at a consistent 'urgency'.

Effect of passive heat stress on arterial stiffness in smokers versus non-smokers.

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.

24-h Void number as an indicator of hydration status.

BACKGROUND/OBJECTIVES: Few user-friendly hydration assessment techniques exist for the general population to use on a daily basis. The present study evaluated void number over 24 h as a potential hydration assessment tool. SUBJECTS/METHODS: Male and female subjects collected urine for 24 h while adequately hydrated (n=44; 22 ± 4 years, 168 ± 16 cm, 73 ± 15 kg) or fluid restricted (n=43; 22 ± 3 years, 175 ± 10 cm, 81 ± 24 kg). As a control, participants were asked to void when feeling the 'first urge to void' on a commonly used urge scale and noted the volume of each void. For each sample, 24-h urine volume, osmolality (U(OSM)), specific gravity (U(SG)) and color were measured in the laboratory. RESULTS: As designed, the level of urge upon voiding was consistent throughout the study (2 ± 0; 'first urge to void'). Samples were classified by U(SG) as either euhydrated (U(SG)<1.020) or hypohydrated (U(SG) ⩾ 1.020). Grouping by U(OSM) did not change results. Euhydrated versus hypohydrated individuals had greater 24-h urine volume (1933 ± 864 versus 967 ± 306 ml, respectively) and lower urine color (2 ± 1 versus 5 ± 1), U(SG) (1.012 ± 0.004 versus 1.025 ± 0.004) and UOSM (457 ± 180 versus 874 ± 175 mOsm/kg H2O; all P<0.001). Euhydrated individuals voided more than hypohydrated individuals over the 24-h period (5 ± 2 versus 3 ± 1 voids; P<0.001). Additionally, void number inversely correlated with hydration status as identified by U(SG) (r=-0.50; P<0.05) and U(OSM) (r=-0.56; P<0.05). CONCLUSIONS: 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.

Heat stress does not augment ventilatory responses to presyncopal limited lower body negative pressure.

Simulated haemorrhage, e.g. lower body negative pressure (LBNP), reduces central blood volume and mean arterial pressure, while ventilation increases. Passive whole-body heat stress likewise increases ventilation. The objective of this project was to test the hypothesis that ventilatory responses to reductions in central blood volume and arterial pressure during simulated haemorrhage are enhanced when individuals are heat stressed rather than normothermic. Eight healthy men (34 ± 9 years old, 176 ± 6 cm tall and 80.2 ± 4.2 kg body weight) underwent a simulated haemorrhagic challenge via LBNP until presyncope on two separate occasions, namely normothermic control and whole-body heat-stress trials. Baseline ventilation and core and mean skin temperatures were not different between trials (all P > 0.05). Prior to LBNP, heat stress increased core (from 36.8 ± 0.2 to 38.2 ± 0.2°C, P < 0.05) and mean skin temperatures (from 33.9 ± 0.5 to 38.1 ± 0.6°C, P < 0.05), as well as minute ventilation (from 8.01 ± 2.63 to 13.68 ± 6.68 l min(-1), P < 0.01). At presyncope, mean arterial pressure and middle cerebral artery blood velocity decreased in both trials (P < 0.05). At presyncope, ventilation increased to 23.22 ± 6.78 (P < 0.01) and 25.88 ± 10.16 l min(-1) (P < 0.01) in the normothermic and hyperthermic trials, respectively; however, neither the increase in ventilation from the pre-LBNP period nor the absolute ventilation was different between normothermic and hyperthermic trials (P > 0.05). These data suggest that the increase in ventilation during simulated haemorrhage induced via LBNP is not altered in heat-stressed humans.

Effects of dehydration and fluid ingestion on cognition.

The effects of exercise-induced dehydration and fluid ingestion on men's cognitive performance were assessed. Eleven young men attended separate sessions in which each individual cycled in a controlled environment at 60 % of V.O (2max) for periods of 15, 60, or 120 min without fluid replacement or 120 min with fluid replacement. Immediately following the assigned submaximal exercise period, the participant completed a graded exercise test to voluntary exhaustion. An executive processing test and a short-term memory test were performed prior to and immediately following exercise. Choice-response times during the executive processing test decreased following exercise, regardless of the level of dehydration. Choice-response errors increased following exercise, but only on trials requiring set shifting. Short-term memory performance improved following exercise, regardless of the level of dehydration. Changes in cognitive performance following exercise are hypothesized to be related to metabolic arousal following strenuous physical activity.