The initial skin blood flow response to rapid local heating is an axon reflex, which may be mediated by calcitonin gene‐related peptide and substance P released from C‐fibres. We investigated the role of nitric oxide (NO) and noradrenaline on the temperature threshold for the axon reflex during gradual local heating. 36 subjects participated in two studies. Using microdialysis, we examined the following interventions: NO synthase inhibition (10 mmN^G‐nitro‐l‐arginine methyl ester, l‐NAME); low‐dose NO infusion (1.0 μm sodium nitroprusside, SNP); adrenergic blockade (10 mm bretylium tosylate); and low‐dose (0.1 μm) noradrenaline infusion. Laser‐Doppler flowmetry was used to measure red blood cell flux. Skin was heated at a rate of 0.1°C min⁻¹ from 33°C to 40°C. Compared to control skin sites, the axon reflex response was shifted to a higher temperature in 4 subjects in the l‐NAME sites (control, 37.0 ± 0.3°C, n= 16; l‐NAME, 39.8 ± 0.1°C, n= 4; P < 0.001) and absent in 12 subjects. The response was also absent in l‐NAME plus low‐dose SNP sites and not altered by low‐dose SNP infusion alone. Adrenergic blockade, with and without low‐dose noradrenaline infusion, also abolished the axon reflex response in all subjects. Low‐dose noradrenaline infusion alone shifted the axon reflex to a significantly lower temperature threshold compared to control sites (control, 38.2 ± 0.5°C; noradrenaline, 37.7 ± 0.4°C, P < 0.05, n= 5). These results suggest that endogenous NO and noradrenaline contribute to the temperature threshold of the axon reflex response during gradual local heating of the skin.

The purpose of this study was to investigate the oxygen cost of running barefoot vs. running shod on the treadmill as well as overground. 10 healthy recreational runners, 5 male and 5 female, whose mean age was 23.8±3.39 volunteered to participate in the study. Subjects participated in 4 experimental conditions: 1) barefoot on treadmill, 2) shod on treadmill, 3) barefoot overground, and 4) shod overground. For each condition, subjects ran for 6 min at 70% vVO₂max pace while VO₂, heart rate (HR), and rating of perceived exertion (RPE) were assessed. A 2 × 2 (shoe condition x surface) repeated measures ANOVA revealed that running with shoes showed significantly higher VO₂ values on both the treadmill and the overground track (p<0.05). HR and RPE were significantly higher in the shod condition as well (p<0.02 and p<0.01, respectively). For the overground and treadmill conditions, recorded VO₂ while running shod was 5.7% and 2.0% higher than running barefoot. It was concluded that at 70% of vVO₂max pace, barefoot running is more economical than running shod, both overground and on a treadmill.

Women have decreased orthostatic tolerance compared with men, and anecdotal evidence suggests women are more susceptible to orthostatic intolerance in warm environments. Because estrogen and progesterone affect numerous physiological variables that may alter orthostatic tolerance, the purpose of our study was to compare orthostatic tolerance across the menstrual cycle phases in women during combined orthostatic and heat stress and to compare these data with those of men. Eight normally menstruating women and eight males (22 ± 4.0 and 23 ± 3.5 yr, respectively) completed the protocol. Women were studied during their early follicular (EF), ovulatory (OV), and midluteal (ML) phases. Men were studied twice within 2–4 wk. Heart rate, cardiac output, blood pressure, core temperature (T_c), and cutaneous vascular conductance (CVC) were measured during three head-up tilt tests, consisting of two tilts in the thermoneutral condition and one tilt after a 0.5°C rise in T_c. There was no difference in orthostatic tolerance across the menstrual cycle phases, despite higher CVC in the ML phase after heating (EF, 42.3 ± 4.8; OV, 40.1 ± 3.7; ML, 57.5 ± 4.5; P < 0.05). Orthostatic tolerance in the heat was greater in men than women ( P < 0.05). These data suggest that although many physiological variables associated with blood pressure regulation fluctuate during the menstrual cycle, orthostatic tolerance in the heat remains unchanged. Additionally, our data support a clear sex difference in orthostatic tolerance and extend upon previous data to show that the sex difference in the heat is not attributable to fluctuating hormone profiles during the menstrual cycle.

Oral contraceptive pills (OCPs) are a popular contraception method. Currently, lower-dose ethinyl estradiol formulations are most commonly prescribed, although they have been linked to increased arterial vascular risk. The aim of this study was to investigate endothelial function in healthy young women using lower-dose ethinyl estradiol OCPs. We examined flow-mediated, endothelium-dependent and nitroglycerin-mediated, endothelium-independent vasodilation of the brachial artery, comparing two doses of ethinyl estradiol/levonorgestrel OCPs in 15 healthy young women on two study days: once during the active phase and once during the placebo phase of an OCP cycle. Group low dose (LD) ( n = 7) active pills contained 150 μg levonorgestrel/30 μg ethinyl estradiol versus Group very low dose (VLD) ( n = 8) with 100 μg levonorgestrel/20 μg ethinyl estradiol. Endothelium-dependent vasodilation was lower during the active phase in Group VLD (5.33 ± 1.77% vs. 7.23 ± 2.60%; P = 0.024). This phase difference was not observed in Group LD (8.00 ± 0.970% vs. 7.61 ± 1.07%; P = 0.647). Endothelium-independent vasodilation did not differ between phases in either group. Finally, we measured endothelium-dependent vasodilation in two additional women who received 10 μg of unopposed ethinyl estradiol. Endothelium-dependent vasodilation was increased by unopposed ethinyl estradiol compared with the placebo phase (10.88 ± 2.34% vs. 6.97 ± 1.83%). These results suggest that levonorgestrel may antagonize the activity of ethinyl estradiol. Thus both the progestin type and estradiol dose need to be considered when assessing arterial vascular risk of OCP use in women.