Key pointsr Despite an attenuated fluctuation in ovarian hormone concentrations in well-trained women, one in two of such women believe their menstrual cycle negatively impacts training and performance.r Forthcoming large international events will expose female athletes to hot environments, and studies evaluating aerobic exercise performance in such environments across the menstrual cycle are sparse, with mixed findings.r We have identified that autonomic heat loss responses at rest and during fixed-intensity exercise in well-trained women are not affected by menstrual cycle phase, but differ between dry and humid heat.r Furthermore, exercise performance is not different across the menstrual cycle, yet is lower in humid heat, in conjunction with reduced evaporative cooling.r Menstrual cycle phase does not appear to affect exercise performance in the heat in well-trained women, but humidity impairs performance, probably due to reduced evaporative power. AbstractWe studied thermoregulatory responses of ten well-trained [VO 2max , 57 (7) ml min −1 kg −1 ] eumenorrheic women exercising in dry and humid heat, across their menstrual cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), to assess autonomic regulation, then self-paced intensity (30 min work trial), to assess behavioural regulation. Trials were in early-follicular (EF) and mid-luteal (ML) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT, 27°C). During rest and fixed-intensity exercise, rectal temperature was ß0.2°C higher in ML than EF (P < 0.01) independent of environment (P = 0.66). Mean skin temperature did not differ between menstrual phases (P ࣙ 0.13) but was higher in DRY than HUM (P < 0.01). Local sweat rate and/or forearm blood flow differed as a function of menstrual phase and environment (interaction: P ࣘ 0.01). Exercise performance did not differ between phases [EF: 257 (37), ML: 255 (43) kJ, P = 0.62], but was 7 (9)% higher in DRY than HUM [263 (39), 248 (40) kJ; P < 0.01] in conjunction with equivalent autonomic regulation and thermal strain but higher evaporative cooling [16 (6) W m 2 ; P < 0.01]. In well-trained women exercising in the heat: (1) menstrual phase did not affect performance, (2) humidity impaired performance due to reduced evaporative cooling despite matched WBGT and (3) behavioural responses nullified thermodynamic and autonomic differences associated with menstrual phase and dry vs. humid heat. Abbreviations BP, blood pressure; BSA, body surface area; C, rate of heat transfer from convection; C res , rate of respiratory conductive heat transfer; E, rate of evaporative heat loss; EF, early follicular; E max , maximal evaporative capacity of the environment; E req , required evaporative cooling for heat balance; E res , rate of respiratory evaporative heat transfer; FBF, forearm blood flow; FVR, forearm vascular resistance; h c , convective heat transfer coefficient; HR, heart rate; HSI, heat strain index; IAAF, International Association of At...

Key points One in two female athletes chronically take a combined, monophasic oral contraceptive pill (OCP). Previous thermoregulatory investigations proposed that an endogenous rhythm of the menstrual cycle still occurs with OCP usage. Forthcoming large international sporting events will expose female athletes to hot environments differing in their thermal profile, yet few data exist on how trained women will respond from both a thermoregulatory and performance stand‐point. In the present study, we have demonstrated that a small endogenous rhythm of the menstrual cycle still affects Tcore and also that chronic OCP use attenuates the sweating response, whereas behavioural thermoregulation is maintained. Furthermore, humid heat affects both performance and thermoregulatory responses to a greater extent than OCP usage and the menstrual cycle does. Abstract We studied thermoregulatory responses of ten well‐trained (V̇O2 max , 57 ± 7 mL min−1 kg−1) women taking a combined, monophasic oral contraceptive pill (OCP) (≥12 months) during exercise in dry and humid heat, across their active OCP cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), aiming to assess autonomic regulation, and then a self‐paced intensity (30‐min work trial) to assess behavioural regulation. Trials were conducted in quasi‐follicular (qF) and quasi‐luteal (qL) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT) (27°C). During rest and exercise at 125 W, rectal temperature was 0.15°C higher in qL than qF (P = 0.05) independent of environment (P = 0.17). The onset threshold and thermosensitivity of local sweat rate and forearm blood flow relative to mean body temperature was unaffected by the OCP cycle (both P > 0.30). Exercise performance did not differ between quasi‐phases (qF: 268 ± 31 kJ, qL: 263 ± 26 kJ, P = 0.31) but was 5 ± 7% higher during DRY than during HUM (273 ± 29 kJ, 258 ± 28 kJ; P = 0.03). Compared to matched eumenorrhoeic athletes, chronic OCP use impaired the sweating onset threshold and thermosensitivity (both P < 0.01). In well‐trained, OCP‐using women exercising in the heat: (i) a performance‐thermoregulatory trade‐off occurred that required behavioural adjustment; (ii) humidity impaired performance as a result of reduced evaporative power despite matched WBGT; and (iii) the sudomotor but not behavioural thermoregulatory responses were impaired compared to matched eumenorrhoeic athletes.

The current study investigated whether ambient heat augments the inflammatory and post-exercise hepcidin response in women, and if menstrual phase and/or self-pacing modulate these physiological effects. Eight trained females (age: 37±7 y; VO2max: 46±7 mL∙kg-1∙min-1; peak power output: 4.5±0.8 W∙kg-1) underwent 20 min of fixed-intensity cycling (100 and 125 W) followed by a 30-min work trial (≈75% VO2max) in a moderate (MOD: 20±1 °C, 53±8% relative humidity) and warm-humid (WARM: 32±0 °C, 75±3% relative humidity) environment in both their early follicular (days 5±2) and mid-luteal (days 21±3) phases. Mean power output was 5±4 W higher in MOD than in WARM (p=0.02) such that the difference in core temperature rise was limited between environments (-0.29±0.18 °C in MOD, p<0.01). IL-6 and hepcidin both increased post-exercise (198% and 38%, respectively), however, neither were affected by ambient temperature or menstrual phase (all p>0.15). Multiple regression analysis demonstrated that the IL-6 response to exercise was explained by leukocyte and platelet count (r2=0.72, p<0.01) and the hepcidin response to exercise was explained by serum iron and ferritin (r2=0.62, p<0.01). During exercise participants almost matched their fluid loss (0.48±0.18 kg·h-1) with water intake (0.35±0.15 L·h-1) such that changes in body mass (-0.3±0.3%) and serum osmolality (0.5±2.0 mOsm·kg-1) were minimal or negligible, indicating a behavioral fluid-regulatory response. These results indicate that trained, iron sufficient women suffer no detriment to their iron regulation in response to exercise with acute ambient heat stress or between menstrual phases on account of a performance-physiological trade-off.

We hypothesized that the performance of prior heavy exercise would speed pulmonary oxygen uptake (VO2) kinetics (i.e. described by a time constant, τVO2) and reduce the amplitude of muscle deoxygenation (deoxy[heme]) kinetics in the supine (S) but not upright (U) body positions. 17 healthy men completed heavy intensity constant work rate exercise tests in S and U consisting of two bouts of 6 min cycling separated by 6 min cycling at 20 W. Pulmonary VO2 was measured breath-by-breath; total- and deoxy[heme] were determined via time-resolved-NIRS at three muscle sites. Priming exercise reduced τVO2 in S (bout 1: 36 ± 10 vs. bout 2: 28 ± 10 s, P < 0.05) but not U (bout 1: 27 ± 8 vs. bout 2: 25 ± 7 s, P > 0.05). The deoxy[heme] amplitude was increased following priming in S (bout 1: 25-28 vs. bout 2: 30-35 μM, P < 0.05) but not U (bout 1: 13-18 vs. bout 2: 17-25 μM, P > 0.05), whereas baseline total[heme] was enhanced in S (bout 1: 110-179 vs. bout 2: 128-185 μM, P < 0.05) and U (bout 1: 123-186 vs. bout 2: 137-197 μM, P < 0.05). Priming exercise increased total[heme] in both S and U, likely indicating enhanced diffusive O2 delivery. However, the observation that following priming the amplitude of the deoxy[heme] response was increased in S suggests that the reduction in τVO2 subsequent to priming was related to a combination of both enhanced intracellular O2 utilization and increased O2 delivery.

Oxygen uptake (VO2) kinetics are slowed in the supine (S) position due to impaired muscle O2 delivery (QO2), however, these conclusions are predicated on single-site measurements in superficial muscle using continuous-wave near-infrared spectroscopy (NIRS). This study aimed to determine the impact of body position (i.e. upright U vs. S) on deep and superficial muscle deoxygenation (deoxy[heme]) using time-resolved (TR-) NIRS, and how these relate to slowed pulmonary VO2 kinetics. 17 healthy men completed constant power tests during 1) S heavy intensity exercise; and 2) U exercise at the same absolute work rate, with a subset of 10 completing additional tests at the same relative work rate as S. Pulmonary VO2 was measured breath-by-breath and, deoxy- and total[heme] were resolved via TR-NIRS in the superficial and deep vastus lateralis and superficial rectus femoris. The fundamental phase VO2 time constant was increased during S compared to U (S: 36±10 vs. U: 27±8 s, P<0.001). The deoxy[heme] amplitude (S: 25-28 vs. U: 13-18 µM, P<0.05) and total[heme] amplitude (S: 17-20 vs. U: 9-16µM, P<0.05) were greater in S compared to U and were consistent for the same absolute (above data) and relative work rates (n=10, all P<0.05). The greater deoxy- and total[heme] amplitudes in S vs. U supports that reduced perfusive QO2 in S, even within deep muscle, necessitated a greater reliance on fractional O2 extraction and diffusive QO2. The slower VO2 kinetics in S vs. U demonstrates that, ultimately, these adaptations were insufficient to prevent impairments in whole-body oxidative metabolism.