This study evaluated exercise modality [i.e. self-paced (SP) or fixed-intensity (FI) exercise] as a modulator of body temperature regulation under uncompensable heat stress. Eight well-trained male cyclists completed (work-matched) FI and SP cycling exercise bouts in a hot (40.6 ± 0.2°C) and dry (relative humidity 23 ± 3%) environment estimated to elicit 70% of [Formula: see text]O(2)max. Exercise intensity (i.e. power output) decreased over time in SP, which resulted in longer exercise duration (FI 20.3 ± 3.4 min, SP 23.2 ± 4.1 min). According to the heat strain index, the modification of exercise intensity in SP improved the compensability of the thermal environment which, relative to FI, was likely a result of the reductions in metabolic heat production (i.e. [Formula: see text]O(2)). Consequently, the rate of rise in core body temperature was higher in FI (0.108 ± 0.020°C/min) than in SP (0.082 ± 0.016°C/min). Interestingly, cardiac output, stroke volume, and heart rate during exercise were independent of exercise modality. However, core body temperature (FI 39.4 ± 0.3°C, SP 39.1 ± 0.4°C), blood lactate (FI 2.9 ± 0.8 mmol/L, SP 2.3 ± 0.7 mmol/L), perceived exertion (FI 18 ± 2, SP 16 ± 2), and physiological strain (FI 9.1 ± 0.9, SP 8.3 ± 1.1) were all higher in FI compared to SP at exhaustion/completion. These findings indicate that, when exercise is SP, behavioral modification of metabolic heat production improves the compensability of the thermal environment and reduces thermoregulatory strain. Therefore, under uncompensable heat stress, exercise modality modulates body temperature regulation.

Lower body positive pressure (LBPP) has been used in the treatment of haemorrhagic shock and in offsetting g-force induced fluid shifts. However, the middle cerebral artery blood flow velocity (MCAv) response to supine LBPP is unknown. Fifteen healthy volunteers (mean ± SD: age, 26 ± 5 year; body mass, 79 ± 10 kg; height, 174 ± 9 cm) completed 5 minutes of 20 and 40 mm Hg LBPP, in a randomized order, separated by 5 minutes rest (baseline). Beat-to-beat MCAv and blood pressure, partial pressure of end-tidal carbon dioxide (PET CO2 ) and heart rate were recorded and presented as the change from the preceding baseline. All measures were similar between baseline periods (all P>0·30). Mean arterial pressure (MAP) increased by 7 ± 6 (8 ± 7%) and 13 ± 7 mm Hg (19 ± 11%) from baseline during 20 and 40 mm Hg (P<0·01), respectively. The greater MAP increase at 40 mm Hg (P<0·01 versus 20 mm Hg) was mediated via a greater increase in total peripheral resistance (P<0·01), with heart rate, cardiac output (Model flow) and PET CO2 remaining unchanged (all P>0·05) throughout. MCAv increased from baseline by 3 ± 4 cm s(-1) (5 ± 5%) during 20 mm Hg (P = 0·003), whilst no change (P = 0·18) was observed during 40 mm Hg. Our results indicate a divergent response, in that 20 mm Hg LBPP-induced modest increases in both MCAv and MAP, yet no change in MCAv was observed at the higher LBPP of 40 mm Hg despite a further increase in MAP.

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Acute hypoxia may alter autonomic cardiovascular reflexes during orthostasis. Heart rate variability (HRV), arterial blood pressure (MAP), and respiratory sinus arrhythmia (RSA) were recorded during supine (SUP) and passive head up tilt (HUT) in eight healthy humans, spontaneously breathing either room air or 10% O₂ in N₂. In the time domain, heart rate increased and variability decreased with HUT in both trials, with no difference between trials. In the frequency domain, normalized low frequency HRV increased, and normalized high frequency HRV decreased with HUT in both trials, with no difference between trials. MAP was 74.9 (8.6) and 77.5 (11.7) mmHg when SUP in the room air and hypoxia trials, respectively. A significant increase in MAP occurred with HUT in the room air trial but not in the hypoxia trial. In both trials, end tidal CO₂ decreased with HUT, with no difference between trials. In the room air trial, end tidal O₂ increased with HUT, whereas during the hypoxia trial, end tidal O₂ decreased with HUT. The distribution of heart beats relative to the phase of ventilation (%HBIN and %HBOUT) was similar in both trials: the %HBIN was 43.5 (3.3) % and %HBOUT was 56.5 (4.2) % breathing room air when SUP, and 45.5 (3.0) and 54.5 (3.2) when hypoxic and SUP. For both trials, this distribution did not change with HUT. As both HRV and RSA showed similar responses to HUT when spontaneously breathing either room air or 10% O₂ in N₂, we suggest that autonomic cardiovascular reflexes are preserved during acute hypoxia.