Dietary nitrate supplementation has been purported to enhance explosive exercise performance; however, research examining the efficacy of nitrate to improve resistance exercise performance, such as weightlifting, in women is scarce. The purpose of this study was to investigate the impact of an acute nitrate dose on neuromuscular performance during barbell back squat and bench press. Eighteen resistance-trained women were assigned in a randomized, double-blinded, crossover design to consume: (1) nitrate-depleted beetroot juice (PL; negligible nitrate) and (2) nitrate-rich beetroot juice (BR; 6.7 mmol nitrate) 2.5 h prior to exercise. Participants performed explosive efforts during 1 set of 3 repetitions at 55

ABSTRACT Background and objectives Physical inactivity remains widespread despite the well-established physical and mental health benefits of regular physical activity (PA). There is an urgent need for strategies that increase both uptake and long-term adherence. The Environmental Mismatch Hypothesis proposes that natural environments may increase both engagement and performance of PA. Methodology Forty-seven healthy adults (16 females) completed a randomised, counterbalanced crossover trial. Participants undertook a 30-minute self-paced run in both a forest and an urban environment at a prescribed exertion level (rate of perceived exertion = 4/10). Performance (distance run, heart rate) and markers of intention to perform future PA (enjoyment, mood, short- and long-term intention) were assessed. Results Participants covered significantly greater distance in the forest condition (p = 0.036, Cohen’s dz = 0.2) with heart rate and RPE comparable to the urban setting. Forest-based exercise also elicited significantly greater enjoyment (p < 0.001, dz = 1.3), improved post-exercise mood (p < 0.001, dz = 0.7) and far greater intention to engage in future PA (short-term dz = 2.1; long-term dz = 2.0; both p < 0.001). Conclusions and implications Forest-based running was associated with improved performance, enjoyment, mood and motivation for future PA, relative to urban running, without an increase in physiological strain. These findings reveal that natural environments offer a promising and scalable approach to addressing physical inactivity and improving population health. Further research is required to determine the environmental drivers, the feasibility, accessibility and long-term effects across diverse and inactive populations.

Individuals of South Asian (SA) descent display a higher risk for cardiovascular disease and type 2 diabetes mellitus than their White European (WE) counterparts. Heat therapy, such as hot water immersion (HWI), can improve microvascular function and glycaemic control, although effects across racial groups are unknown. This study compared how repeated HWI influenced microvascular function, glycaemic control and markers of inflammation in males of WE and SA descent. Ten WE and SA males completed ten 60 min HWI sessions over 14 days. Before and after HWI, forearm and great toe cutaneous vascular conductance (CVC) responses to postocclusive reactive hyperaemia and local heating (LH) were measured, resting blood samples were collected, and an oral glucose tolerance test (OGTT) was conducted. Baseline great toe CVC did not differ between racial groups (P = 0.670), but forearm CVC was lower in SA (P = 0.010). For postocclusive reactive hyperaemia, forearm and great toe peak CVC and area under the curve were unchanged by HWI (P ≥ 0.300), whereas CVC during 42°C LH increased at both sites after HWI (P ≤ 0.037), as did great toe CVC during 44°C LH (P = 0.021). Glucose and insulin concentrations were elevated in SA during the OGTT (P ≤ 0.035); glucose concentration and peak insulin reduced after HWI in SA (P ≤ 0.024), but not in WE. The interleukin-6:interleukin-10 ratio was unchanged by HWI (P = 0.159), but elevated in SA (P = 0.006). Repeated HWI increased microvascular responses to LH to a similar extent between racial groups and reduced early-phase OGTT glucose concentrations in SA, although insulin sensitivity was unchanged. These findings support HWI as a health-promoting intervention.

Background and Objectives: This study examined the effects of a novel phytochemical supplement blend on markers of exercise-induced muscle damage. Methods: In a randomised, parallel group design, 24 healthy participants (14 males) consumed 300 mg of a phytochemical blend (calcium fructoborate, turmeric and pomegranate; PB) or inert placebo for 9 days (n = 12 per condition). On day 7, participants performed 150 drop jumps to induce muscle damage. Markers of neuromuscular function, muscle soreness/pain, perceived exhaustion and sleep quality, were measured pre-exercise and 24, 48, and 72 h post-exercise; systemic markers of inflammation, muscle damage, and oxidative stress were measured on these days as well post-exercise and 2.5 h post-exercise. Results: There was an interaction effect for pressure pain threshold in the vastus lateralis (p = 0.041), which was ~21% higher in PB 72 h post-exercise (p = 0.074; ds = 0.767). Perceived sleep quality was greater 72 h post-exercise in PB (p = 0.049; rrb = 0.423) and those in the PB condition reported feeling more recovered and less mentally drained post-exercise (p ≤ 0.043). There were no statistically significant between-condition differences for any markers of neuromuscular function, inflammation, oxidative stress or muscle damage (p > 0.05). Conclusion: In conclusion, a novel PB showed promise for attenuating muscle pain and perceived exhaustion, and improving sleep quality, in the days after muscle damaging exercise. The study protocol was pre-registered on the Open Science Framework Registry (registration number: qgw3a).

Nitric oxide (NO) is a critical signalling molecule in cardiovascular, metabolic, and muscular function. Endogenous NO production occurs via two primary metabolic pathways: 1) the classical nitric oxide synthases (NOS) pathway, and 2) the alternative (nitrate-nitrite-NO) pathway, in which inorganic nitrate (NO3-) is sequentially reduced to nitrite (NO2-) and other NO intermediates (e.g., S-nitrosothiol). The latter pathway relies heavily on the oral microbiota, which catalyze the two-electron partial reduction of NO3- to NO2-, which is influenced by oral physiology, microbial composition and salivary flow. While the role of exercise training in enhancing NOS-derived NO is well established, emerging evidence suggests that it may also augment NO bioavailability through the NO3--NO2--NO pathway. Furthermore, exercise training may influence the composition and functionality of oral microbiota, thereby indirectly modulating NO metabolism and oral health. However, the synergistic effects of exercise and oral microbiota on NO production remain underexplored. This review synthesises current evidence on how physical exercise may modulate both NO pathways and discusses the broader physiological implications.

Endurance performance is predicted by maximal oxygen uptake, its fractional utilisation at lactate threshold (FULT) and exercise economy. These variables are used to estimate speed or power at lactate threshold (LT) and lactate turnpoint (LTP), which serve as performance proxies. This study examined the relationships between these variables in a large cohort of runners and cyclists and quantified their relative contributions to performance prediction. 495 runners (105 females) and 393 cyclists (42 females) completed incremental exercise tests to determine maximal oxygen uptake (running [R]: 56 mL/kg/min, 3.94 L/min; cycling [C]: 52 mL/kg/min, 3.99 L/min), economy (R: 220 mL/kg/km; C: 14.7 mL/min/W), FULT (R: 78

Background: Citrulline malate (CM) supplementation has been shown to improve resistance exercise performance. However, there is limited research on the dose-response effects of CM ingestion. The aim of this study was to investigate a moderate (8 g; CM-MOD) and high (12 g; CM-HIGH) dose of CM on resistance exercise performance. Methods: Twelve resistance-trained individuals (7 females, 5 males, age = 24 ± 2 years; body mass = 70 ± 10 kg; height = 172 ± 7 cm) volunteered for this randomised, double-blind, crossover trial. Following a familiarisation trial that consisted of determining one repetition maximum, participants completed barbell bent-over rows and leg presses following acute ingestion of either 8 g CM (CM-MOD), 12 g CM (CM-HIGH), or a placebo 1 h prior to exercise. Each exercise comprised two sets of 10 repetitions (70% one-repetition maximum (RM)) and a third set to exhaustion at 70% 1 RM. Results: The linear mixed-effect model found no significant differences in the completed repetitions between exercise type but did reveal a significant main effect of CM-HIGH on repetitions completed (p = 0.032), which was not found for CM-MOD, and only increases in leg press repetitions were observed (estimated marginal means: placebo = 17; CM-MOD = 19; CM-HIGH = 20). Conclusions: In conclusion, CM-HIGH resulted in small improvements to total repetitions performed during resistance exercise performance and likely only during leg press activity, though the underlying mechanisms remain unclear and further investigation is warranted.

Sprint interval training (SIT) combined with post-exercise blood flow restriction (BFR) can augment adaptive signalling responses in skeletal muscle. However, mitochondrial adaptations to SIT with BFR are not well-understood. This study examined the effects of a 6 week SIT program with or without post-exercise BFR on skeletal muscle mitochondrial content and respiratory function, alongside physiological performance markers. Physically active males (n = 20; 25.3 ± 5.9 years; V ̇ O 2 peak ${{\dot{V}}_{{{{\mathrm{O}}}_2}{\mathrm{peak}}}}$ , 52.5 ± 4.6 mL·min-1·kg-1) completed a SIT intervention (repeated 30 s sprints interspersed with 4.5 min of rest) with (BFR; n = 12) or without (CON; n = 8) post-exercise BFR. Baseline and post-training V ̇ O 2 peak ${{\dot{V}}_{{{{\mathrm{O}}}_2}{\mathrm{peak}}}}$ and lactate thresholds were measured and muscle biopsies obtained for determination of citrate synthase (CS) activity and mitochondrial respiration [O2 flux during leak (L), ADP-stimulated oxidative phosphorylation (P) and uncoupled maximal electron transfer (E) states through mitochondrial complexes I-IV (CI-IV)]. There were time × condition interactions for CS activity (P = 0.011) and CS activity-corrected CIIE (P = 0.047) and CIVE (P = 0.010), which increased following BFR (12.1%, P = 0.040; 74.3%, P = 0.030; 64.4%, P = 0.002, respectively) but not in CON (-4.6%, P = 0.053; 9.9% P = 0.460; -7.4%, P = 0.664, respectively). There were no between-group differences in the changes in V ̇ O 2 peak ${{\dot{V}}_{{{{\mathrm{O}}}_2}{\mathrm{peak}}}}$ or any other performance markers (P ≥ 0.176). The addition of BFR to a 6 week SIT program increased mitochondrial content and uncoupled respiration in physically active males, which may have implications for improving skeletal muscle oxidative metabolism. KEY POINTS: Sprint interval training (SIT) with post-exercise BFR (SIT+BFR) augments the exercise stimulus without limiting intensity and is shown to improve maximal oxygen uptake in athletes compared to SIT alone. However, the mechanisms underpinning this response remain unclear. This study is the first to investigate the effects of SIT+BFR on citrate synthase (CS) activity and mitochondrial respiratory parameters. We demonstrate that a 6 week SIT+BFR intervention in physically active males, increased CS activity and uncoupled mitochondrial respiration compared to SIT alone. However, improvements in performance determinants in response to SIT did not differ between groups. These findings provide novel insight into the mitochondrial bioenergetic potential of BFR, when combined with SIT, and can inform recommendations for exercise training interventions.

Type 2 diabetes mellitus (T2DM) is a metabolic disease characterised by chronic hyperglycaemia, whereas obesity is a major risk factor which increases morbidity and mortality. Treatments that alter white adipose tissue to express a metabolically active brown adipose phenotype in rats may offer adjunct treatment in people with T2DM. To investigate whether inorganic nitrate supplementation from beetroot juice (BJ) alters brown adipose tissue (BAT) fat fraction and activation in humans. Thirteen older adults with T2DM (glycated haemoglobin [HbA1c]: 58 ± 13 mmol·mol-1 and body mass index: 29.1 ± 3.1 kg·m-2) completed a double-blind, randomised, balanced and placebo-controlled crossover study. Outcome measures (including BAT fat fraction; activation; plasma [nitrate] and [nitrite]) were assessed before and after 14-day of 140 mL·day-1 BJ containing inorganic nitrate (∼12.4 mmol·L1) or a placebo (∼0.1 mmol·L1). Magnetic resonance imaging (MRI) and infrared thermography (IRT) were performed to image supraclavicular BAT following a rested cooling protocol, consisting of 60-min exposure via a cold water (8.1 ± 1.2°C) perfused jacket. Respiratory parameters, including respiratory exchange ratio [RER] and mean skin temperature, were measured during the cooling protocol to confirm participants were not shivering. BJ significantly increased venous plasma [nitrate] and [nitrite] versus placebo (p < 0.001) but did not affect BAT fat fraction (p = 0.650) or activation (p = 0.152). Cooling significantly reduced mean skin temperature in BJ (-0.8 ± 0.7°C) and placebo (-0.6 ± 0.6°C) (p < 0.001) and RER remained representative of nonshivering thermogenesis throughout (0.88 ± 0.05 a.u.). 14-day of nitrate supplementation did not increase BAT fat fraction or activation in older adults with T2DM.

OBJECTIVES:Physical function-the capacity to perform tasks requiring endurance and/or strength-is a key determinant of fitness that has directly influenced Homo sapiens' survival, reproduction and health throughout our evolutionary journey. However, the last 200-300 years of global industrialization has transformed human habitats at an unprecedented rate and may now be compromising key functions that underpin our fitness (Environmental Mismatch Hypothesis). Although industrialization has delivered a range of benefits, it has simultaneously introduced novel environmental challenges (e.g., air pollution, microplastics) and reduced contact with beneficial aspects of nature (e.g., phytoncides). While negative effects of industrialization have been demonstrated for other determinants of fitness, its impact on physical function remains almost completely unexplored. MATERIALS AND METHODS:We conducted a randomized, counterbalanced crossover study to determine whether brief exposure to an industrialized environment would impair endurance performance relative to a forest environment (used as a proxy for non-industrial ancestral conditions). Twenty-five healthy adults (19 females, 6 males) completed two test sessions, each involving a 90 min environmental exposure followed by a standardized laboratory cycling test of endurance. RESULTS:Endurance performance was significantly reduced following industrial exposure (time-to-exhaustion: 13.5 ± 0.9 min) compared to forest exposure (14.6 ± 1.0 min; p = 0.007). Industrial exposure also worsened mood and led to volitional exhaustion at a lower perceived exertion, while cardiorespiratory markers recorded during the endurance test (e.g., V̇O) did not differ significantly between conditions. CONCLUSIONS:These results suggest that acute exposure to industrialized environments may reduce physical capacity, with potential consequences for evolutionary fitness.

The endocannabinoid system is a potent regulator of energy intake, but effects of cannabidiol (CBD) on appetite/eating behaviour in humans are not documented. We examined whether acute CBD ingestion affects energy intake, subjective appetite, or postprandial glucose and lipid metabolism in fifteen healthy adults (four females). A double-blind, randomized, crossover design was used. Participants ingested 298 mg CBD or placebo, with postprandial metabolic outcomes (blood-based energy substrates/hormones, and indirect calorimetry) assessed following consumption of a mixed-macronutrient breakfast 30 min later. Subjective outcomes were recorded hourly, and an ad libitum lunch provided 180 min post-CBD ingestion. Energy intake was 193 (95%CI: 80 to 306) kcal greater following CBD ingestion (CBD 979 ± 462 kcal; placebo 786 ± 280 kcal; p = 0.003; dz = 0.94 [0.32 to 1.55]). Ghrelin concentrations were 93 (37 to 148) and 107 (72 to 142) pg/mL less than placebo (p ≤ 0.01) at 120 and 180 min, respectively, following CBD. Minimum ghrelin concentration and AUC were 108 (67 to 150) pg/mL and 10.0 (16.6 to 3.3) ng/mL·180min less after CBD than placebo (p ≤ 0.01). There were no between-conditions differences in plasma glucose, triacylglycerol, non-esterified fatty acids, insulin, Glucagon-like peptide-1, energy expenditure, carbohydrate/lipid oxidation, or any subjective outcome (p > 0.05). Healthy adults ate more at lunch following CBD ingestion, providing the first evidence that CBD isolate can increase energy intake in humans. Energy intake increased despite lesser ghrelin concentrations and no differences in subjective appetite. Future research should explore mechanisms and/or utility in clinical populations.

Purpose: Inorganic nitrate (NO3-) supplementation and caffeine have been shown to have conflicting effects on various aspects of cardiovascular function. This study evaluated whether NO3- supplementation would attenuate caffeine-induced cardiovascular strain. Methods: Twenty-four (17 males; age: 24(3) years) healthy participants completed four trials in a randomized, double-blind, placebo-controlled crossover design. The trials were nitrate (NO3-)-rich (400 mg NO3-) and NO3--depleted (92 mg NO3-) beetroot powder consumed, with (BR-CAF and CAF) and without (BR and PL) 6 mg kg-1 caffeine. Brachial and central blood pressure (BP) and arterial stiffness variables were measured pre- and post-supplementation (2.5 h). Macrovascular endothelial function was assessed post-supplementation using flow mediated dilation (FMD). Results: Arterial stiffness measures of augmentation pressure (mmHg) and index (%) were higher following CAF (+3(2) mmHg and 10(9)%) than PL (+1(3) mmHg and +4(11)%) and BR (+0(3) mmHg and +1(11)%; P < 0.001-0.007), with no difference between BR-CAF (+1(3) mmHg and +3(10)%) and PL or BR (P = 0.505-0.689). Brachial BP, central BP and macrovascular endothelial function were not altered with BR or CAF compared to PL (P = 0.067-0.359). Plasma [nitrite] was higher in BR and BR-CAF than PL and CAF (P < 0.001). There were no between-group differences in plasma [cyclic guanosine monophosphate] (P = 0.370). Conclusion: Acute NO3- supplementation offset caffeine-induced increases in arterial stiffness variables. These findings improve our understanding of the cardiovascular health benefits afforded by acute NO3- consumption under cardiovascular strain.

Coenzyme Q10 (CoQ10) is an integral component of the mitochondrial electron transfer system. Most studies have administered the oxidised form of CoQ10 (ubiquinone) and observed no effects on mitochondrial respiratory function or endurance exercise performance. The reduced form of CoQ10, ubiquinol (UQH2), has greater bioavailability than ubiquinone, but the effects of UQH2 supplementation on mitochondrial respiratory function and exercise capacity are unclear. Fifty-four healthy, recreationally active males were randomised to receive either 300 mg·day− 1 UQH2 or placebo (PLA) for 6 weeks in a double-blind independent-group design. Before and after the supplementation period, skeletal muscle mitochondrial respiration variables and protein content of the mitochondrial leak proteins, adenine nucleotide translocase1 + 2 (ANT1 + 2) and uncoupling protein-3 (UCP-3), were assessed. In addition, participants completed a severe-intensity cycle test to exhaustion to assess time to the limit of tolerance (TLim) and oxygen uptake (V̇O2) kinetics. Compared to pre-supplementation and PLA, UQH2 supplementation increased plasma [CoQ10] (P < 0.05), and lowered inverse respiratory control ratio (Pre-PLA: 0.064 ± 0.034 vs. Post-PLA: 0.072 ± 0.026; Pre- UQH2: 0.073 ± 0.039 vs. Post-UQH2: 0.044 ± 0.019; P < 0.05), suggestive of improved oxidative phosphorylation coupling efficiency. There were no differences in ANT1 + 2 or UCP-3 protein content post-supplementation compared to pre-supplementation between groups (P > 0.05). End-exercise V̇O2, change in V̇O2 between 2 min and end-exercise, and TLim were not different between groups post-supplementation (P > 0.05). Six-weeks UQH2 supplementation increased plasma [CoQ10] and oxidative phosphorylation coupling efficiency, but did not alter mitochondrial leak proteins, TLim or V̇O2 kinetics during severe-intensity exercise in healthy, active males.

Heat therapy is recognised to promote cardiovascular health, and whilst most recent heat therapy investigations have focussed on continuous heat exposure, traditional sauna use often includes recovery periods. This study compared the acute effects of continuous versus intermittent whole-body heating on cardiovascular function markers in males and females. Twenty healthy participants (25 ± 3 years; 10 males, 10 females) were exposed to 2 passive heating regimens: continuous heating (CH) for 60 min and intermittent heating (IH) comprised of 3 × 20-min blocks interspersed by 15-min cooling breaks. Skin perfusion, blood pressure (BP), plasma nitrite, interleukins, body temperature, and thermal perceptual responses were assessed. Greater increases in rectal temperature (Trec) (CH: 1.2 ± 0.1 °C; IH: 0.5 ± 0.1 °C), skin perfusion, systolic blood pressure (SBP), heart rate (HR), interleukin-6 (IL-6) and plasma nitrite were found in CH compared to IH (p ≤ 0.01), but the thermal perceptual response was more unfavourable during CH (p < 0.01). Females had higher skin perfusion and plasma nitrite concentrations (p ≤ 0.04), but lower brachial and central BP than males in both conditions (p ≤ 0.01). Furthermore, females reached a higher Trec and more unfavourable thermal perception in CH (p ≤ 0.02). More pronounced cardiovascular responses were associated with higher Trec and discomfort. Females exhibited higher skin perfusion and plasma nitrite concentrations than males and reported less favourable thermal perception in CH, but not in IH.

Cardiovascular disease is more prevalent in individuals of Black-African (BA) and South-Asian (SA) descent than White-European (WE) counterparts, with vascular dysfunction identified as contributing to this disparity. Chronic heat therapy can elicit positive vascular adaptations, potentially underpinned by the repeated cardiovascular strain experienced during acute heat exposures. This study examined the cutaneous peripheral microvascular responses following acute hot (HWI) and thermoneutral (CON) water immersion between males of WE, BA, and SA descent. Thirty-one young, healthy WE (n = 10), BA (n = 10), SA (n = 11) males completed 60 minutes of HWI (39°C) and CON (36°C) with thermoregulatory, cardiovascular, and perceptual responses measured throughout. Following 60 minutes of thermoneutral rest, forearm and Great toe cutaneous vascular conductance (CVC) were recorded during cutaneous post-occlusive reactive hyperemia (PORH) and local heating (LH). Baseline CVC was similar between groups (p ≥ 0.08). During PORH, BA had lower peak forearm and Great toe CVC than WE and SA, and a reduced CVC area under the curve compared to WE (p ≤ 0.01). Furthermore, BA Great toe CVC was blunted compared to WE and SA during both 42°C (p ≤ 0.033) and 44°C (p ≤ 0.02) LH, respectively. Great toe CVC was acutely increased following HWI in responses to 44°C LH compared to CON (p ≤ 0.039), with no race × condition interaction effects. In conclusion, despite blunted microvascular responses in BA, acute HWI did not elicit distinct effects between males of WE, BA, and SA descent, although microvascular responses to LH were greater following HWI.

Postural changes elicit well-described haemodynamic effects on plasma volume, affecting blood-based hydration variables. While the time required for plasma volume stabilisation is well-established for supine rest, less is known for blood samples collected in a seated position, as is commonplace in physiology and nutrition experiments. Seventeen healthy participants (9 males; 8 females) stood stationary for 20 min in an upright position before walking on a treadmill at 4 km/h for 20 min (to simulate active travel to blood sampling locations). After walking, participants sat upright (within 7 ± 1 s), and venous blood samples were drawn from a cannula at 0, 5, 10, 20, 30 and 40 min after sitting. Time points were compared to 40 min. At 0 and 5 min, blood (0 min: -3.3

This study examined whether supplementation with collagen peptides (CP) affects appetite and post-exercise energy intake in healthy active females. In this randomised, double-blind cross-over study, fifteen healthy females (23 (sd 3) years) consumed 15 g/d of CP or a taste matched non-energy control (CON) for 7 d. On day 7, participants cycled for 45 min at ∼55 % Wmax, before consuming the final supplement. Sixty-min post supplementation an ad libitum meal was provided, and energy intake recorded. Subjective appetite sensations were measured daily for 6 d (pre- and 30 min post-supplement) and pre (0 min) to 280 min post-exercise on day 7. Blood glucose and hormone concentrations (total ghrelin, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), cholecystokinin (CCK), dipeptidyl peptidase-4 (sDPP-4), leptin, and insulin) were measured fasted at baseline (day 0), then pre-breakfast (0 min), post-exercise (100 min), post-supplement (115, 130, 145, 160 min) and post-meal (220, 280 min) on day 7. Ad libitum energy intake was ∼10 % (∼41 kcal) lower in the CP trial (P = 0·037). There was no difference in gastrointestinal symptoms or subjective appetite sensations throughout the trial (P ≥ 0·412). Total plasma GLP-1 (AUC, CON: 6369 (sd 2330); CP: 9064 (sd 3021) pmol/l; P < 0·001) and insulin (+80 % at peak) were higher after CP (P < 0·001). Plasma ghrelin and leptin were lower in CP (condition effect; P ≤ 0·032). PYY, CCK and glucose were not different between CP and placebo (P ≥ 0·100). CP supplementation following exercise increased GLP-1 and insulin concentrations and reduced ad libitum energy intake at a subsequent meal in physically active females.

The aim of this study was to determine whether inflammatory and vascular responses to passive heating differ between the early follicular phase (EFP) and the mid-luteal phase (MLP) of the menstrual cycle. Ten healthy, naturally menstruating females (26 ± 3 years of age; body mass index 21.4 ± 1.9 kg/m2) were assessed during EFP and MLP. Participants underwent 60 min whole-body passive heat exposure (71°C ± 2°C, dry heat) in both phases. Outcomes included body temperature, interleukin-6, interleukin-1 receptor antagonist and plasma nitrite concentrations, cutaneous vascular conductance, blood pressure, arterial stiffness and perceptual responses. Rectal temperature and mean skin temperature increased during heat exposure but did not differ between EFP and MLP. Likewise, heat exposure increased interleukin-6, interleukin-1 receptor antagonist and plasma nitrite concentrations, with no differences between menstrual cycle phases. However, brachial (EFP, 75 ± 4 mmHg vs MLP, 72 ± 5 mmHg; p = 0.040) and central (EFP, 75 ± 4 mmHg vs MLP, 72 ± 5 mmHg; p = 0.042) mean arterial pressures were higher in EFP than in MLP at 40 min of heat exposure. Additionally, arterial stiffness declined more in EFP (-13% ± 7%) than in MLP (-5% ± 6%; p = 0.019) from the end of heat exposure to 30 min into recovery. Perceptual responses, including thermal sensation and comfort, were similar between menstrual cycle phases, but skin wetness perception was heightened during EFP. In conclusion, the inflammatory and plasma nitrite responses to passive heating did not differ between EFP and MLP. However, some vascular function and perception parameters were affected by the menstrual cycle phase.