The acute effects of passive heat exposure on arterial stiffness, oxidative stress, and inflammation.

BACKGROUND AND OBJECTIVE: The aim of the study was to determine the acute effect of passive heat exposure (PHE) on arterial stiffness, oxidative stress (OxS) and inflammatory parameters. MATERIALS AND METHODS: Subjects were studied in thermoneutral conditions before and after PHE in a climatic chamber. Pulse wave analysis was used for assessment of central hemodynamic and arterial stiffness parameters. Venous blood samples were obtained to measure OxS and inflammatory parameters. RESULTS: Rectal temperature increased after PHE exposure compared to baseline: 37.01°C±0.19°C and 36.4°C±0.31°C, respectively (P<0.001). There was a 17% (P<0.05) decrease in large artery elasticity index (from 24.68±5.53 to 20.42±2.65mL/mmHg*10), which was predicted upon normothermic value (r=-0.878, P<0.01). However, no significant changes were found in others arterial stiffness parameters. A 30% (P<0.05) increase occurred in blood IL-6 concentration (from 0.43±0.15 to 0.56±0.23pg/mL), but OxS parameters remained significantly unchanged. CONCLUSIONS: This study describes for the first time acute PHE effects on arterial stiffness, inflammation and OxS. PHE significantly decreases large artery elasticity index and increases inflammatory IL-6 level. However, further larger investigations are needed for clarifying acute PHE effects on arterial function and biomarkers.

Effects of heat acclimation on changes in oxidative stress and inflammation caused by endurance capacity test in the heat.

BACKGROUND: The aim was to determine the effect of heat acclimation (HA) on oxidative stress (OxS) and inflammation in resting conditions and on the response pattern of these parameters to exhausting endurance exercise. METHODS: Parameters of OxS and inflammation were measured in non-heat-acclimated status (NHAS) and after a 10-day HA program (i.e., in heat-acclimated status; HAS) both at baseline and after an endurance capacity (EC) test in the heat. RESULTS: As a result of HA, EC increased from 88.62 ± 27.51 to 161.95 ± 47.80 minutes (P < 0.001). HA increased OxS level: total peroxide concentration rose from 219.38 ± 105.18 to 272.57 ± 133.39 µmol/L (P < 0.05) and oxidative stress index (OSI) from 14.97 ± 8.24 to 20.46 ± 11.13% (P < 0.05). In NHAS, the EC test increased OxS level: total peroxide concentration rose from 219.38 ± 105.18 to 278.51 ± 125.76 µmol/L (P < 0.001) and OSI from 14.97 ± 8.24 to 19.31 ± 9.37% (P < 0.01). However, in HAS, the EC test reduced OSI from 20.46 ± 11.13 to 16.83 ± 8.89% (P < 0.05). The value of log high-sensitive C-reactive protein increased from -0.32 ± 0.32 to -0.12 ± 0.34 mg/L (P < 0.05) in NHAS and from -0.31 ± 0.47 to 0.28 ± 0.46 mg/L (P < 0.001) in HAS. CONCLUSION: HA increases OxS level. However, beneficial adaptive effects of HA on acute exhaustive exercise-induced changes in OxS and inflammation parameters occur in a hot environment.

Heat acclimation increases arterial elasticity in young men.

The major physiological adaptations that occur during heat acclimation (HA) are well documented. However, no studies have provided compelling evidence about the effect of HA on arterial elastic properties. The aim of this study was to examine the changes in large artery elasticity (LAE) and small artery elasticity (SAE) concomitant with HA and to determine the potential relationships among changes in arterial elasticity, baseline aerobic fitness level, and improvement in endurance capacity (EC). During 10-day HA, the subjects (n = 21) exercised daily on a treadmill for 110 min at an intensity of 55%-60% of peak oxygen uptake in a climatic chamber preset to 42 °C and 18% relative humidity. EC was tested in the heat before and after HA. Arterial elasticity was assessed by diastolic pulse wave analysis (HDI/Pulse Wave CR-2000) at baseline and after HA. Blood samples were drawn at baseline. After HA, there was a 17% increase in LAE (from 21.19 ± 4.72 mL·mm Hg(-1) × 10 to 24.77 ± 5.91 mL·mm Hg(-1) × 10, p < 0.05) and an 18% increase in SAE (from 9.32 ± 1.76 mL·mm Hg(-1) × 100 to 10.98 ± 1.75 mL·mm Hg(-1) × 100, p < 0.01). EC increased by 86% (from 88.62 ± 27.51 min to 161.95 ± 47.80 min, p < 0.001) as a result of HA. No significant associations were revealed between changes in arterial elasticity parameters and improvement in EC or baseline aerobic fitness level. We demonstrated, for the first time, that HA has a positive impact on the parameters of arterial elasticity. Further investigations are needed to determine the mechanisms underlying these changes and the potential relationships among arterial elasticity, aerobic fitness level, and EC.