ECSS Paris 2023: CP-PN04
INTRODUCTION: Exercise performed in hot environments is associated with exacerbated physiological strain and reduced endurance performance1,2. However, most studies assess neuromuscular function following exercise to task failure, where longer exercise duration in the thermoneutral environment may confound the isolated effects of heat stress. This study aimed to evaluate the effects of cycling exercise performed in the heat, within the heavy-intensity domain, on endurance performance and knee-extensor neuromuscular function using both task-failure and isotime experimental designs. METHODS: Thirteen physically active participants (11 males, 2 females; V̇O₂max: 43 ± 5 mL·kg⁻¹·min⁻¹) completed a step–ramp–step test under thermoneutral (20 ± 2 °C; 55 ± 7% relative humidity) and hot (38 ± 2 °C; 43 ± 9%) conditions. Participants subsequently performed constant work-rate cycling at Δ80% between the gas-exchange threshold and the maximal metabolic steady state, determined separately for each condition, until task failure. An additional isotime trial was conducted under thermoneutral conditions, with exercise duration matched to the time to task failure (TTF) observed in the heat condition. Maximal voluntary contraction (MVC), voluntary activation (VA), and evoked knee-extensor forces (single twitch, Qtw; low- and high-frequency doublets, Db100 and Db10; Db10/Db100 ratio) were assessed pre-exercise and up to 3 h post-exercise to quantify performance fatigability. RESULTS: TTF was significantly reduced in the heat (31±14 min) compared with thermoneutral conditions (60±24 min; p<0.001). Skin temperature was higher in the heat(36.8±0.6 °C;), compared to thermoneutral (34.5±1.0 °C; p<0.001) environment, whereas post-exercise core temperature was slightly but significantly greater following thermoneutral exercise (38.1±0.5 °C) compared with heat (37.7±0.5 °C; p=0.017). Following task failure, no condition × time interactions were observed for MVC (p=0.422), VA (p=0.277), Qtw (p=0.079), Db10 (p=0.182), Db100 (p=0.021, not confirmed by Bonferroni post hoc), or Db10/Db100 ratio (p=0.082). Significant main effects of time relative to baseline were observed for MVC (up to 3 h post-exercise), Db10, and Db100 (all p<0.001), with no evidence of central fatigue. For the isotime comparisons, only main effects of time were observed for MVC, Qtw, Db10, and Db10/Db100 ratio (all p<0.001). CONCLUSION: Cycling exercise performed in a hot environment markedly reduces endurance performance but does not exacerbate neuromuscular impairments compared with thermoneutral conditions when exercise duration is controlled. The observed global and peripheral fatigue responses appear primarily attributable to exercise time rather than heat stress per se. 1. HARGREAVES (2008); 2. TATTERSON et al. (2003)
Read CV Alessandro ZagattoECSS Paris 2023: CP-PN04
INTRODUCTION: The behavioural responses available to humans are far more effective than physiological mechanisms for dealing with thermal discomfort and imbalance, typically evoked by perception of the thermal environment. Whilst perception of the environment is a holistic amalgamation of human senses, there is some evidence that humans prioritise visual information over other senses. Unfortunately, the current evidence exploring the relationship between visual manipulations and thermal perception is limited to ambient environments (1). Therefore, we tested the experimental hypothesis that (in)congruent visual manipulations would alter behavioural, physiological, and perceptual responses during exercise in the heat. METHODS: Twelve participants (6 female) (mean ± SD, age: 23.2 ± 3.5 years; height 76.0 ± 8.4 cm; mass 72.4 ± 10.3 kg; VO2max 36.3 ± 7.0 mL·kg·min-1) were exposed to three different visual environments [Control (No Virtual Reality (No VR)), an arid environment (Hot VR), and a snow environment (Cold VR)] whilst in a hot climatic chamber (35 °C, 50 % r.h.) in a randomised controlled cross over design. Participants completed a fixed-RPE protocol (6/10 CR-10 scale) on a cycle ergometer until power output dropped below 70% of their starting power. Behavioural (starting Watts, exercise duration), physiological (rectal temperature), and perceptual (thermal sensation, thermal comfort, and skin wettedness) measures were recorded throughout. RESULTS: The visual manipulations had no effect on exercise duration (control: 19.9±6.4, Hot VR: 19.4±6.8, Cold VR 18.4±7.3 mins; p = .468, ω2 = .03) or starting power (control: 131±21, Hot VR: 125±37, Cold VR 140±37 W; p = .077, ω2 = .03). Similarly, the visual manipulation did not alter any perceptual (p values = .116 to .808, ω2 = .00 to .02) or physiological (p values = .397 to .770, ω2 = .00 to .01) variables. CONCLUSION: The novel findings from this experiment suggest that visual manipulation using VR did not alter behavioural thermoregulation, perceptual, or thermophysiological variables during a fixed-RPE cycling protocol in a hot environment. Therefore, the hypothesis is rejected. Further research is needed to explore the utility of VR, and visual manipulations in the selection, preparation and protection of athletes and workers performing in extreme environments. 1. Mayes, H. S., Navarro, M., Satchell, L. P., Tipton, M. J., Ando, S., & Costello, J. T. (2023). The effects of manipulating the visual environment on thermal perception: A structured narrative review. Journal of Thermal Biology, 112, 103488.
Read CV Joseph CostelloECSS Paris 2023: CP-PN04
INTRODUCTION: Heat stress increases cardiovascular mortality, likely through ischemic pathways. Although myocardial blood flow rises during passive heating, the pressure–time determinants of coronary perfusion and their interaction with ventricular loading remain incompletely defined due to measurement limitations. The hypothesis that disease phenotypes operate with a reduced coronary perfusion reserve margin that is further compressed during thermal stress was assessed using computational models of heat stress. METHODS: A validated CircAdapt model was calibrated to represent an older adult phenotype and extended to heart failure with preserved ejection fraction (HFpEF) and pulmonary hypertension (PH). Acute heat stress was imposed using literature-aligned perturbations in systemic vascular resistance, chronotropy, and inotropy across progressive increases equivalent to 0.5, 1.0, and 1.5 °C elevations in core temperature observed during passive heating in older adults (1). Primary outcomes included coronary perfusion pressure (CPP), a diastolic pressure–time index (DPTI), and left ventricular end-diastolic pressure (LVEDP). RESULTS: At baseline, diseased phenotypes exhibited lower CPP (HFpEF 44.2 mmHg; PH 42.6 mmHg) compared with the older phenotype (53.4 mmHg), alongside higher LVEDP. Baseline DPTI was likewise reduced in HFpEF and PH relative to older. Progressive heat stress produced modest reductions in CPP across all phenotypes (1.5 °C: HFpEF 41.5 mmHg; PH 41.0 mmHg; older 50.6 mmHg), preserving between-group separation at each thermal level. DPTI declined proportionally with increasing thermal load in all groups, remaining consistently lower in disease. LVEDP increased across phenotypes, maintaining higher absolute filling pressures in HFpEF and PH (13.7 and 13.6 mmHg at 1.5 °C) compared with older (10.7 mmHg). Across thermal increments, disease phenotypes operated with a persistently narrower perfusion–demand margin rather than an accelerated deterioration slope. CONCLUSION: Although heat imposes similar relative perfusion compression across phenotypes, diseased hearts operate closer to subendocardial supply–demand imbalance throughout. This reduced reserve margin provides a mechanistic framework linking thermal stress to ischemic vulnerability. Further computational studies are warranted to explore the determinants of cardiac perfusion during passive heating and to examine subfactors that may predispose certain individuals to thermal intolerance. Reference 1. Gagnon D, Romero SA, Ngo H, Poh PY, Cramer MN, Jay O. Healthy aging does not compromise the augmentation of cardiac function during heat stress. Journal of Applied Physiology. 2016;121(4):885–893. doi:10.1152/japplphysiol.00337.2016.
Read CV Edward AshworthECSS Paris 2023: CP-PN04