Heat production during exercise in pregnancy: discerning the contribution of total body weight.

Studies have reported enhanced thermoregulatory function as pregnancy progresses; however, it is unclear if differences in thermoregulation are attributed to weight gain or other physiological changes. This study aimed to determine if total body weight will influence thermoregulation (heat production (Hprod)), heart rate, and perceptual measurements in response to weight-bearing exercise during early to late pregnancy. A cross-sectional design of healthy pregnant women at different pregnancy time points (early, T1; middle, T2; late, T3) performed a 7-stage weight-bearing incremental exercise protocol. Measurements of Hprod, HR, and RPE were examined. Two experimental groups were studied: (1) weight matched and (2) non-weight matched, in T1, T2, and T3. During exercise, equivalent Hprod at T1 (326 ± 88 kJ), T2 (330 ± 43 kJ), and T3 (352 ± 52 kJ) (p = 0.504); HR (p = 0.830); and RPE (p = 0.195) were observed in the WM group at each time point. In the NWM group, Hprod (from stages 1-6 of the exercise) increased across pregnancy time points, T1 (291 ± 76 kJ) to T2 (347 ± 41 kJ) and T3 (385 ± 47 kJ) (p < 0.001). HR increased from T1 to T3 in the warm-up to stage 6 (p = 0.009). RPE did not change as pregnancy time point progressed (p = 0.309). Total body weight, irrespective of pregnancy time point, modulates Hprod and HR during exercise. Therefore, accounting for total body weight is crucial when comparing thermoregulatory function during exercise across pregnancy.

Does prepregnancy weight change have an effect on subsequent pregnancy health outcomes? A systematic review and meta-analysis.

International guidelines recommend women with an overweight or obese body mass index (BMI) aim to reduce their body weight prior to conception to minimize the risk of adverse perinatal outcomes. Recent systematic reviews have demonstrated that interpregnancy weight gain increases women's risk of developing adverse pregnancy outcomes in their subsequent pregnancy. Interpregnancy weight change studies exclude nulliparous women. This systematic review and meta-analysis was conducted following MOOSE guidelines and summarizes the evidence of the impact of preconception and interpregnancy weight change on perinatal outcomes for women regardless of parity. Sixty one studies met the inclusion criteria for this review and reported 34 different outcomes. We identified a significantly increased risk of gestational diabetes (OR 1.88, 95% CI 1.66, 2.14, I2  = 87.8%), hypertensive disorders (OR 1.46 95% CI 1.12, 1.91, I2  = 94.9%), preeclampsia (OR 1.92 95% CI 1.55, 2.37, I2  = 93.6%), and large-for-gestational-age (OR 1.36, 95% CI 1.25, 1.49, I2  = 92.2%) with preconception and interpregnancy weight gain. Interpregnancy weight loss only was significantly associated with increased risk for small-for-gestational-age (OR 1.29 95% CI 1.11, 1.50, I2  = 89.9%) and preterm birth (OR 1.06 95% CI 1.00, 1.13, I2  = 22.4%). Our findings illustrate the need for effective preconception and interpregnancy weight management support to improve pregnancy outcomes in subsequent pregnancies.

Heat loss responses at rest and during exercise in pregnancy: A scoping review.

BACKGROUND: The teratogenic risk associated with maternal hyperthermia (i.e., core temperature ≥39.0 °C) has been a crucial motive in understanding thermoregulatory responses in pregnancy. To date, a substantial number of studies have focused on core temperature responses in a wide range of exercise intensities, duration, and ambient temperatures. Fortunately, none have reported core temperatures exceeding 39.0 °C. Nonetheless, there are limited studies that have provided substantial insight into both dry and evaporative heat loss mechanisms involved in facilitating the maintenance of core temperature (≥39.0 °C) during heat stress in pregnant women. The purpose of this scoping review was to summarize the available literature that has assessed heat loss responses in studies of human pregnancy. METHODS: A search strategy was developed combining the terms pregnancy, thermoregulation, and adaptation. A systematic search was performed in the following databases: PubMed, Embase, Scopus, and ProQuest. Studies eligible for inclusion included pregnant women between the ages of 18-40 years old, and at least one measurement of the following: sweating, blood flow, skin temperature, and behavioural responses. Retrieved data were categorized as evaporative (sweating), dry or behavioural heat loss responses and summarized narratively. RESULTS: Thirty-three studies were included in this review (twenty-nine measured physiological responses and four measured behavioural responses). Studies suggest that during exercise, evaporative (sweating) and dry (skin blood flow and temperature) heat loss responses increase from early to late pregnancy in addition to greater cardiac output, blood volume and reduced vascular resistance. Behavioural practices related to heat loss responses are also influenced by cultural/religious expectations, personal preferences and sociodemographics. CONCLUSION: The findings from this review suggest that pregnancy modifies evaporative (sweating), dry and behavioural heat loss. However, future studies have an opportunity to compare heat loss measurements accounting for gestational weight gain and thermal sensation/comfort scale to associate physiological responses with perceptual responses across pregnancy.

Physical activity and gestational weight gain predict physiological and perceptual responses to exercise during pregnancy.

BACKGROUND: Exercise is known to improve the health of the pregnant woman and her child. Studies that have evaluated physiological parameters during prenatal exercise have conflicting results. Better understanding of these physiological responses can modify exercise prescriptions, safety, and monitoring strategies. We examined the association between age, prepregnancy body mass index (BMI), gestational weight gain (GWG), and physical activity (PA) levels, factors that may influence a change in physiological (HR, VO2 responses) and perceptual (RPE) responses to acute exercise throughout pregnancy. METHODS: Twenty-two healthy pregnant women (31.4 ± 3.7 years) performed a Submaximal incremental Walking Exercise Test (SWET). Early- (13-18 weeks), mid- (24-28 weeks), and late-pregnancy (34-37 weeks) were compared. VO2 (L/min; ml/kg/min), HR (bpm), and RPE were collected at the end of each test stage. PA was determined by accelerometry. We associated PA levels, GWG, prepregnancy BMI, and age with HR, RPE, and VO2 responses. RESULTS: HR, RPE, and absolute VO2 were higher in late-pregnancy compared to earlier time points (p < .05; η2 = 0.299-0.525). Regression models were built for HR (all time points), RPE (early- and late-pregnancy), and VO2 (L/min; late-pregnancy). HR (late-pregnancy) was predicted by time in vigorous PA, GWG, age, and prepregnancy BMI (r2 = 0.645; SEE = 5.84). RPE (late-pregnancy) was predicted by sedentary time, GWG, prepregnancy BMI, and age (r2 = 0.662; SEE = 1.21). CONCLUSION: Physiological/perceptual responses were higher in late-pregnancy compared to other time points and associated with combined PA, GWG, prepregnancy BMI, and age. These findings can be used to modify exercise prescriptions and designs for future PA interventions in pregnant women.

Energy Intake Requirements in Pregnancy.

Energy intake requirements in pregnancy match the demands of resting metabolism, physical activity, and tissue growth. Energy balance in pregnancy is, therefore, defined as energy intake equal to energy expenditure plus energy storage. A detailed understanding of these components and their changes throughout gestation can inform energy intake recommendations for minimizing the risk of poor pregnancy outcomes. Energy expenditure is the sum of resting and physical activity-related expenditure. Resting metabolic rate increases during pregnancy as a result of increased body mass, pregnancy-associated physiological changes, i.e., cardiac output, and the growing fetus. Physical activity is extremely variable between women and may change over the course of pregnancy. The requirement for energy storage depends on maternal pregravid body size. For optimal pregnancy outcomes, women with low body weight require more fat mass accumulation than women with obesity, who do not require to accumulate fat mass at all. Given the high energy density of fat mass, these differences affect energy intake requirements for a healthy pregnancy greatly. In contrast, the energy stored in fetal and placental tissues is comparable between all women and have small impact on energy requirements. Different prediction equations have been developed to quantify energy intake requirements and we provide a brief review of the strengths and weaknesses and discuss their application for healthy management of weight gain in pregnant women.

Interactive effects of age and hydration state on human thermoregulatory function during exercise in hot-dry conditions.

AIM: Ageing and hypohydration independently attenuate heat dissipation during exercise; however, the interactive effects of these factors remain unclear. We assessed the hypothesis that ageing suppresses hypohydration-induced reductions in whole-body heat loss during exercise in the heat. METHODS: On two occasions, eight young (mean [SD]: 24 [4] years) and eight middle-aged (59 [5] years) men performed 30-minute bouts of light (heat production of 175 W m-2 ) and moderate (275 W m-2 ) cycling (separated by 15-minute rest) in the heat (40°C, 15% relative humidity) when euhydrated and hypohydrated (~4% reduction in body mass). Heat production and whole-body net heat exchange (evaporative heat loss + dry heat gain) were measured via indirect and direct calorimetry (respectively) and heat storage was calculated via their temporal summation. RESULTS: Net heat exchange was reduced, while heat storage was elevated, in the middle-aged men during moderate exercise when euhydrated (both P ≤ 0.01). In the young, evaporative heat loss was attenuated in the hypohydrated vs euhydrated condition during light (199 ± 6 vs 211 ± 10 W m-2 ; P ≤ 0.01) and moderate (287 ± 15 vs 307 ± 13 W m-2 ; P ≤ 0.01) exercise, but was similar in the middle-aged men, averaging 223 ± 6 and 299 ± 15 W m-2 , respectively, across conditions (both P ≥ 0.32). Heat storage was thereby exacerbated by hypohydration in the young (both P < 0.01) but not the middle-aged (both P ≥ 0.32) during both exercise bouts and, as a result, was similar between groups when hypohydrated (both P ≥ 0.50). CONCLUSION: Hypohydration attenuates heat loss via sweating in young but not middle-aged men, indicating that ageing impairs one's ability to mitigate further sweat-induced fluid loss during hypohydration.

Menstrual cycle phase does not modulate whole body heat loss during exercise in hot, dry conditions.

Menstrual cycle phase has long been thought to modulate thermoregulatory function. However, information pertaining to the effects of menstrual phase on time-dependent changes in whole body dry and evaporative heat exchange during exercise-induced heat stress and the specific heat load at which menstrual phase modulates whole body heat loss remained unavailable. We therefore used direct calorimetry to continuously assess whole body dry and evaporative exchange in 12 habitually active, non-endurance-trained, eumenorrheic women [21 ± 3 (SD) yr] within the early-follicular, late-follicular, and midluteal menstrual phases during three 30-min bouts of cycling at increasing fixed exercise intensities of 40% (Low), 55% (Moderate), and 70% (High) peak oxygen uptake, each followed by a 15-min recovery, in hot, dry conditions (40°C, 15% relative humidity). This model elicited equivalent rates of metabolic heat production among menstrual phases ( P = 0.80) of ~250 (Low), ~340 (Moderate), and ~430 W (High). However, dry and evaporative heat exchange and the resulting changes in net heat loss (dry ± evaporative heat exchange) were similar among phases (all P > 0.05), with net heat loss averaging 216 ± 43 (Low), 287 ± 63 (Moderate), and 331 ± 75 W (High) across phases. Accordingly, cumulative body heat storage (summation of heat production and loss) across all exercise bouts was similar among phases ( P = 0.55), averaging 464 ± 122 kJ. For some time, menstrual cycle phase has been thought to modulate heat dissipation; however, we show that menstrual cycle phase does not influence the contribution of whole body dry and evaporative heat exchange or the resulting changes in net heat loss or body heat storage, irrespective of the heat load. NEW & NOTEWORTHY Menstrual phase has long been thought to modulate thermoregulatory function in eumenorrheic women during exercise-induced heat stress. Contrary to that perception, we show that when assessed in young, non-endurance-trained women within the early-follicular, late-follicular, and midluteal phases during three incremental exercise-induced heat loads in hot, dry conditions, menstrual phase does not modify whole body dry and evaporative heat exchange or the resulting changes in body heat storage, regardless of the heat load employed.

Hyperthermia and cardiovascular strain during an extreme heat exposure in young versus older adults.

We examined whether older individuals experience greater levels of hyperthermia and cardiovascular strain during an extreme heat exposure compared to young adults. During a 3-hour extreme heat exposure (44°C, 30% relative humidity), we compared body heat storage, core temperature (rectal, visceral) and cardiovascular (heart rate, cardiac output, mean arterial pressure, limb blood flow) responses of young adults (n = 30, 19-28 years) against those of older adults (n = 30, 55-73 years). Direct calorimetry measured whole-body evaporative and dry heat exchange. Body heat storage was calculated as the temporal summation of heat production (indirect calorimetry) and whole-body heat loss (direct calorimetry) over the exposure period. While both groups gained a similar amount of heat in the first hour, the older adults showed an attenuated increase in evaporative heat loss (p < 0.033) in the first 30-min. Thereafter, the older adults were unable to compensate for a greater rate of heat gain (11 ± 1 ; p < 0.05) with a corresponding increase in evaporative heat loss. Older adults stored more heat (358 ± 173 kJ) relative to their younger (202 ± 92 kJ; p < 0.001) counterparts at the end of the exposure leading to greater elevations in rectal (p = 0.043) and visceral (p = 0.05) temperatures, albeit not clinically significant (rise < 0.5°C). Older adults experienced a reduction in calf blood flow (p < 0.01) with heat stress, yet no differences in cardiac output, blood pressure or heart rate. We conclude, in healthy habitually active individuals, despite no clinically observable cardiovascular or temperature changes, older adults experience greater heat gain and decreased limb perfusion in response to 3-hour heat exposure.

Type 1 diabetes modulates cyclooxygenase- and nitric oxide-dependent mechanisms governing sweating but not cutaneous vasodilation during exercise in the heat.

Both cyclooxygenase (COX) and nitric oxide synthase (NOS) contribute to sweating, whereas NOS alone contributes to cutaneous vasodilation during exercise in the heat. Here, we evaluated if Type 1 diabetes mellitus (T1DM) modulates these responses. Adults with (n = 11, 25 ± 5 yr) and without (n = 12, 24 ± 4 yr) T1DM performed two bouts of 30-min cycling at a fixed rate of heat production of 400 W in the heat (35°C); each followed by a 20- and 40-min recovery period, respectively. Sweat rate and cutaneous vascular conductance (CVC) were measured at four intradermal microdialysis sites treated with either 1) lactated Ringer (vehicle control site), 2) 10 mM ketorolac (nonselective COX inhibitor), 3) 10 mM NG-nitro-l-arginine methyl ester (nonselective NOS inhibitor), or 4) a combination of both inhibitors. In nondiabetic adults, separate and combined inhibition of COX and NOS reduced exercise sweat rate (P ≤ 0.05), and the magnitude of reductions were similar across sites. In individuals with T1DM, inhibition of COX resulted in an increase in sweat rate of 0.10 ± 0.09 and 0.09 ± 0.08 mg ·: min-1 ·: cm-2 for the first and second exercise bouts, respectively, relative to vehicle control site (P ≤ 0.05), whereas NOS inhibition had no effect on sweating. In both groups, NOS inhibition reduced CVC during exercise (P ≤ 0.05), although the magnitude of reduction did not differ between the nondiabetic and T1DM groups (exercise 1: -28 ± 10 vs. -23 ± 8% max, P = 0.51; exercise 2: -31 ± 12 vs. -24 ± 10% max, P = 0.38). We show that in individuals with T1DM performing moderate intensity exercise in the heat, NOS-dependent sweating but not cutaneous vasodilation is attenuated, whereas COX inhibition increases sweating.

Heart rate variability during high heat stress: a comparison between young and older adults with and without Type 2 diabetes.

We examined whether older individuals with and without Type 2 diabetes (T2D) experience differences in heart rate variability (HRV) during a 3-h exposure to high heat stress compared with young adults. Young (Young; n = 22; 23 ± 3 yr) and older individuals with (T2D; n = 11; 59 ± 9 yr) and without (Older; n = 25; 63 ± 5 yr) T2D were exposed to heat stress (44°C, 30% relative humidity) for 3 h. Fifty-five HRV measures were assessed for 15 min at baseline and at minutes 82.5-97.5 (Mid) and minutes 165-180 (End) during heat stress. When compared with Young, a similar number of HRV indices were significantly different (P < 0.05) in Older (Baseline: 35; Mid: 29; End: 32) and T2D (Baseline: 31; Mid: 30; End: 27). In contrast, the number of HRV indices significantly different (P < 0.05) between Older and T2D were far fewer (Baseline: 13, Mid: 1, End: 3). Within-group analyses demonstrated a greater change in the Young group's HRV during heat stress compared with Older and T2D; the number of significantly different (P < 0.05) HRV indices between baseline and End were 42, 29, and 20, for Young, Older, and T2D, respectively. Analysis of specific HRV domains suggest that the Young group experienced greater sympathetic activity during heat stress compared with Older and T2D. In conclusion, when compared with young, older individuals with and without T2D demonstrate low HRV at baseline and less change in HRV (including an attenuated sympathetic response) during 3 h high heat stress, potentially contributing to impaired thermoregulatory function.

The effect of plasma osmolality and baroreceptor loading status on postexercise heat loss responses.

We examined the separate and combined effects of plasma osmolality and baroreceptor loading status on postexercise heat loss responses. Nine young males completed a 45-min treadmill exercise protocol at 58 ± 2% V̇o2 peak, followed by a 60-min recovery. On separate days, participants received 0.9% NaCl (ISO), 3.0% NaCl (HYP), or no infusion (natural recovery) throughout exercise. In two additional sessions (no infusion), lower-body negative (LBNP) or positive (LBPP) pressure was applied throughout the final 45 min of recovery. Local sweat rate (LSR; ventilated capsule: chest, forearm, upper back, forehead) and skin blood flow (SkBF; laser-Doppler flowmetry: forearm, upper back) were continuously measured. During HYP, upper back LSR was attenuated from end-exercise to 10 min of recovery by ∼0.35 ± 0.10 mg·min(-1)·cm(-2) and during the last 20 min of recovery by ∼0.13 ± 0.03 mg·min(-1)·cm(-2), while chest LSR was lower by 0.18 ± 0.06 mg·min(-1)·cm(-2) at 50 min of recovery compared with natural recovery (all P < 0.05). Forearm and forehead LSRs were not affected by plasma hyperosmolality during HYP (all P > 0.28), which suggests regional differences in the osmotic modulation of postexercise LSR. Furthermore, LBPP application attenuated LSR by ∼0.07-0.28 mg·min(-1)·cm(-2) during the last 30 min of recovery at all sites except the forehead compared with natural recovery (all P < 0.05). Relative to natural recovery, forearm and upper back SkBF were elevated during LBPP, ISO, and HYP by ∼6-10% by the end of recovery (all P < 0.05). We conclude that 1) hyperosmolality attenuates postexercise sweating heterogeneously among skin regions, and 2) baroreceptor loading modulates postexercise SkBF independently of changes in plasma osmolality without regional differences.

A comparison of thermoregulatory responses to exercise between mass-matched groups with large differences in body fat.

We sought to determine 1) the influence of adiposity on thermoregulatory responses independently of the confounding biophysical factors of body mass and metabolic heat production (Hprod); and 2) whether differences in adiposity should be accounted for by prescribing an exercise intensity eliciting a fixed Hprod per kilogram of lean body mass (LBM). Nine low (LO-BF) and nine high (HI-BF) body fat males matched in pairs for total body mass (TBM; LO-BF: 88.7 ± 8.4 kg, HI-BF: 90.1 ± 7.9 kg; P = 0.72), but with distinctly different percentage body fat (%BF; LO-BF: 10.8 ± 3.6%; HI-BF: 32.0 ± 5.6%; P < 0.001), cycled for 60 min at 28.1 ± 0.2 °C, 26 ± 8% relative humidity (RH), at a target Hprod of 1) 550 W (FHP trial) and 2) 7.5 W/kg LBM (LBM trial). Changes in rectal temperature (ΔTre) and local sweat rate (LSR) were measured continuously while whole body sweat loss (WBSL) and net heat loss (Hloss) were estimated over 60 min. In the FHP trial, ΔTre (LO-BF: 0.66 ± 0.21 °C, HI-BF: 0.87 ± 0.18 °C; P = 0.02) was greater in HI-BF, whereas mean LSR (LO-BF 0.52 ± 0.19, HI-BF 0.43 ± 0.15 mg·cm(-2)·min(-1); P = 0.19), WBSL (LO-BF 586 ± 82 ml, HI-BF 559 ± 75 ml; P = 0.47) and Hloss (LO-BF 1,867 ± 208 kJ, HI-BF 1,826 ± 224 kJ; P = 0.69) were all similar. In the LBM trial, ΔTre (LO-BF 0.82 ± 0.18 °C, HI-BF 0.54 ± 0.19 °C; P < 0.001), mean LSR (LO-BF 0.59 ± 0.20, HI-BF 0.38 ± 0.12 mg·cm(-2)·min(-1); P = 0.04), WBSL (LO-BF 580 ± 106 ml, HI-BF 381 ± 68 ml; P < 0.001), and Hloss (LO-BF 1,884 ± 277 kJ, HI-BF 1,341 ± 184 kJ; P < 0.001) were all greater at end-exercise in LO-BF. In conclusion, high %BF individuals demonstrate a greater ΔTre independently of differences in mass and Hprod, possibly due to a lower mean specific heat capacity or impaired sudomotor control. However, thermoregulatory responses of groups with different adiposity levels should not be compared using a fixed Hprod in watts per kilogram lean body mass.

Muscle metaboreceptors modulate postexercise sweating, but not cutaneous blood flow, independent of baroreceptor loading status.

We examined whether sustained changes in baroreceptor loading status during prolonged postexercise recovery can alter the metaboreceptors' influence on heat loss. Thirteen young males performed a 1-min isometric handgrip exercise (IHG) at 60% maximal voluntary contraction followed by 2 min of forearm ischemia (to activate metaboreceptors) before and 15, 30, 45, and 60 min after a 15-min intense treadmill running exercise (>90% maximal heart rate) in the heat (35°C). This was repeated on three separate days with continuous lower body positive (LBPP, +40 mmHg), negative (LBNP, -20 mmHg), or no pressure (Control) from 13- to 65-min postexercise. Sweat rate (ventilated capsule; forearm, chest, upper back) and cutaneous vascular conductance (CVC; forearm, upper back) were measured. Relative to pre-IHG levels, sweating at all sites increased during IHG and remained elevated during ischemia at baseline and similarly at 30, 45, and 60 min postexercise (site average sweat rate increase during ischemia: Control, 0.13 ± 0.02; LBPP, 0.12 ± 0.02; LBNP, 0.15 ± 0.02 mg·min(-1)·cm(-2); all P < 0.01), but not at 15 min (all P > 0.10). LBPP and LBNP did not modulate the pattern of sweating to IHG and ischemia (all P > 0.05). At 15-min postexercise, forearm CVC was reduced from pre-IHG levels during both IHG and ischemia under LBNP only (ischemia: 3.9 ± 0.8% CVCmax; P < 0.02). Therefore, we show metaboreceptors increase postexercise sweating in the middle to late stages of recovery (30-60 min), independent of baroreceptor loading status and similarly between skin sites. In contrast, metaboreflex modulation of forearm but not upper back CVC occurs only in the early stages of recovery (15 min) and is dependent upon baroreceptor unloading.

Running economy, not aerobic fitness, independently alters thermoregulatory responses during treadmill running.

We sought to determine the independent influence of running economy (RE) and aerobic fitness [maximum oxygen consumption (V̇O 2max)] on thermoregulatory responses during treadmill running by conducting two studies. In study 1, seven high (HI-FIT: 61 ± 5 ml O2 · kg(-1) · min(-1)) and seven low (LO-FIT: 45 ± 4 ml O2 · kg(-1) · min(-1)) V̇O 2max males matched for physical characteristics and RE (HI-FIT: 200 ± 21; LO-FIT: 200 ± 18 ml O2 · kg(-1) · km(-1)) ran for 60 min at 1) 60%V̇O 2max and 2) a fixed metabolic heat production (Hprod) of 640 W. In study 2, seven high (HI-ECO: 189 ± 15.3 ml O2 · kg(-1) · km(-1)) and seven low (LO-ECO: 222 ± 10 ml O2 · kg(-1) · km(-1)) RE males matched for physical characteristics and V̇O 2max (HI-ECO: 60 ± 3; LO-ECO: 61 ± 7 ml O2 · kg(-1) · min(-1)) ran for 60 min at a fixed 1) speed of 10.5 km/h and 2) Hprod of 640 W. Environmental conditions were 25.4 ± 0.8°C, 37 ± 12% RH. In study 1, at Hprod of 640 W, similar changes in esophageal temperature (ΔTes; HI-FIT: 0.63 ± 0.20; LO-FIT: 0.63 ± 0.22°C; P = 0.986) and whole body sweat losses (WBSL; HI-FIT: 498 ± 66; LO-FIT: 497 ± 149 g; P = 0.984) occurred despite different relative intensities (HI-FIT: 55 ± 6; LO-FIT: 39 ± 2% V̇O 2max; P < 0.001). At 60% V̇O 2max, ΔTes (P = 0.029) and WBSL (P = 0.003) were greater in HI-FIT (1.14 ± 0.32°C; 858 ± 130 g) compared with LO-FIT (0.73 ± 0.34°C; 609 ± 123 g), as was Hprod (HI-FIT: 12.6 ± 0.9; LO-FIT: 9.4 ± 1.0 W/kg; P < 0.001) and the evaporative heat balance requirement (Ereq; HI-FIT: 691 ± 74; LO-FIT: 523 ± 65 W; P < 0.001). Similar sweating onset ΔTes and thermosensitivities occurred between V̇O 2max groups. In study 2, at 10.5 km/h, ΔTes (1.16 ± 0.31 vs. 0.78 ± 0.28°C; P = 0.017) and WBSL (835 ± 73 vs. 667 ± 139 g; P = 0.015) were greater in LO-ECO, as was Hprod (13.5 ± 0.6 vs. 11.3 ± 0.8 W/kg; P < 0.001) and Ereq (741 ± 89 vs. 532 ± 130 W; P = 0.007). At Hprod of 640 W, ΔTes (P = 0.910) and WBSL (P = 0.710) were similar between HI-ECO (0.55 ± 0.31°C; 501 ± 88 g) and LO-ECO (0.57 ± 0.16°C; 483 ± 88 g), but running speed was different (HI-ECO: 8.2 ± 0.6; LO-ECO: 7.2 ± 0.4 km/h; P = 0.025). In conclusion, thermoregulatory responses during treadmill running are not altered by V̇O 2max, but by RE because of differences in Hprod and Ereq.