Fatigue during high-intensity endurance exercise: the interaction between metabolic factors and thermal stress.

The purpose of this study was to examine the effects of hot (37° C) and cool (10° C) environments on cycling time to exhaustion (TTE), pH, lactate, and core temperature (Tc). Eleven endurance-trained subjects completed 4 TTE trials: Hot 80% VO2max (H80), Cool 80% (C80), Hot 100% (H100), and Cool 100% VO2max (C100). Esophageal temperature and blood was sampled before, every 5 minutes, at exhaustion, and 3 minutes after exercise and analyzed for lactate, pH, and HCO3-.

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage.

End-tidal carbon dioxide tension (Pet(CO(2))) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on Pet(CO(2)) being an accurate surrogate for arterial carbon dioxide tension (Pa(CO(2))), the latter being the physiologically relevant variable. This study tested the hypothesis that Pet(CO(2)) provides an accurate assessment of Pa(CO(2)) during the aforementioned conditions.

Exercise-associated hyponatremia: the influence of pre-exercise carbohydrate status combined with high volume fluid intake on sodium concentrations and fluid balance.

To evaluate the effect of hydration and carbohydrate (CHO) status on plasma sodium, fluid balance, and regulatory factors (IL-6 & ADH) during and after exercise; 10 males completed the following conditions: low CHO, euhydrated (fluid intake = sweat loss) (LCEH); low CHO, dehydrated (no fluid) (LCDH); high CHO, euhydrated (HCEH); and high CHO, dehydrated (HCDH). Each trial consisted of 90-min cycling at 60% VO(2) max in a 35°C environment followed by 3-h rehydration (RH). During RH, subjects received either 150% of sweat loss (LCDH & HCDH) or an additional 50% of sweat loss (LCEH and HCEH).

Methodological assessment of skin and limb blood flows in the human forearm during thermal and baroreceptor provocations.

Skin blood flow responses in the human forearm, assessed by three commonly used technologies-single-point laser-Doppler flowmetry, integrated laser-Doppler flowmetry, and laser-Doppler imaging-were compared in eight subjects during normothermic baseline, acute skin-surface cooling, and whole body heat stress (Δ internal temperature=1.0±0.2 degrees C; P<0.

Nitric oxide synthase inhibition attenuates cutaneous vasodilation during postmenopausal hot flash episodes.

Objective: The purpose of this study was to test the hypothesis that local inhibition of nitric oxide and prostaglandin synthesis attenuates cutaneous vasodilator responses during postmenopausal hot flash episodes.

Methods: Four microdialysis membranes were inserted into the forearm skin (dorsal surface) of eight postmenopausal women (mean +/- SD age, 51 +/- 7 y). Ringer solution (control), 10 mM ketorolac (Keto) to inhibit prostaglandin synthesis, 10 mM N-l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase, and a combination of 10 mM Keto + 10 mM l-NAME were each infused at the separate sites.

Influence of commonly employed resistance exercise protocols on circulating IL-6 and indices of insulin sensitivity.

The purpose of this project was to examine the influence of resistance exercise (RE) intensities, resulting in different total volume loads on circulating interleukin-6 (IL-6), insulin and glucose response (IGR) to a carbohydrate feeding (CHO), and whether RE-induced IL-6 was associated with postexercise IGR. Fourteen men (21.7 +/- 1.

Effect of whole body heat stress on peripheral vasoconstriction during leg dependency.

The venoarteriolar response (VAR) increases vascular resistance upon increases in venous transmural pressure in cutaneous, subcutaneous, and muscle vascular beds. During orthostasis, it has been proposed that up to 45% of the increase in systemic vascular tone is due to VAR-related local mechanism(s). The objective of this project was to test the hypothesis that heat stress attenuates VAR-mediated cutaneous and whole leg vasoconstriction.

Effects of heat stress on dynamic cerebral autoregulation during large fluctuations in arterial blood pressure.

Impaired cerebral autoregulation during marked reductions in arterial blood pressure may contribute to heat stress-induced orthostatic intolerance. This study tested the hypothesis that passive heat stress attenuates dynamic cerebral autoregulation during pronounced swings in arterial blood pressure. Mean arterial blood pressure (MAP) and middle cerebral artery blood velocity were continuously recorded for approximately 6 min during normothermia and heat stress (core body temperature = 36.

The effects of reduced end-tidal carbon dioxide tension on cerebral blood flow during heat stress.

Passive heat stress reduces arterial carbon dioxide partial pressure (P(aCO2)) as reflected by 3 to 5 Torr reductions in end-tidal carbon dioxide tension (P(ETCO2)). Heat stress also reduces cerebrovascular conductance (CBVC) by up to 30%. While is a strong regulator of CBVC, it is unlikely that the relatively small change in during heating is solely responsible for the reductions in CBVC.