We investigated 1) the regional distribution of cerebral blood flow (CBF), 2) the influence of end-tidal Pco2 (PetCO2) on CBF, and 3) the potential for an extracranial blood "steal" from the anterior brain region during passive hyperthermia. Nineteen (13 male) volunteers underwent supine passive heating until a steady-state esophageal temperature of 2°C above resting was established. Measurements were obtained 1) during normothermia (Normo), 2) during poikilocapnic hyperthermia (Hyper), and 3) during hyperthermia with PetCO2 and end-tidal Po2 clamped to Normo levels (Hyper-clamp). Blood flow in the internal carotid (Qica), vertebral (QVA), and external carotid (Qeca) arteries (Duplex ultrasound), blood velocity of the middle cerebral (MCAv) and posterior cerebral (PCAv) arteries (transcranial Doppler), and cutaneous vascular conductance on the cheek (cheek CVC; Doppler velocimetry) were measured at each stage. During Hyper, PetCO2 was lowered by 7.0 ± 5.2 mmHg, resulting in a reduction in Qica (-18 ± 17%), Qva (-31 ± 21%), MCAv (-22 ± 13%), and PCAv (-18 ± 10%) compared with Normo (P < 0.05). The reduction in QVA was greater than that in QICA (P = 0.017), MCAv (P = 0.047), and PCAv (P = 0.034). Blood flow/velocity was completely restored in each intracranial vessel (ICA, VA, MCA, and PCA) during Hyper-clamp. Despite a ∼250% increase in QECA and a subsequent increase in cheek CVC during Hyper compared with Normo, reductions in QICA were unrelated to changes in QECA. These data provide three novel findings: 1) hyperthermia attenuates QVA to a greater extent than QICA, 2) reductions in CBF during hyperthermia are governed primarily by reductions in arterial Pco2, and 3) increased QECA is unlikely to compromise QICA during hyperthermia.

Key pointsr Reductions in cerebral blood flow (CBF) may be implicated in the development of neuromuscular fatigue; however, the contribution from hypocapnic-induced reductions (i.e. P ETCO 2 ) in CBF versus reductions in CBF per se has yet to be isolated.r We assessed neuromuscular function while using indomethacin to selectively reduce CBF without changes in P ETCO 2 and controlled hyperventilation-induced hypocapnia to reduce both CBF and P ETCO 2 .r Increased corticospinal excitability appears to be exclusive to reductions in P ETCO 2 but not reductions in CBF, whereas sub-optimal voluntary output from the motor cortex is moderately associated with decreased CBF independent of changes in P ETCO 2 .r These findings suggest that changes in CBF and P ETCO 2 have distinct roles in modulating neuromuscular function.Abstract Although reductions in cerebral blood flow (CBF) may be involved in central fatigue, the contribution from hypocapnia-induced reductions in CBF versus reductions in CBF per se has not been isolated. This study examined whether reduced arterial P CO 2 (P aCO 2 ), independent of concomitant reductions in CBF, impairs neuromuscular function. Neuromuscular function, as indicated by motor-evoked potentials (MEPs), maximal M-wave (M max ) and cortical voluntary activation (cVA) of the flexor carpi radialis muscle during isometric wrist flexion, was assessed in ten males (29 ± 10 years) during three separate conditions: (1) cyclooxygenase inhibition using indomethacin (Indomethacin, 1.2 mg kg −1 ) to selectively reduce CBF by 28.8 ± 10.3% (estimated using transcranial Doppler ultrasound) without changes in end-tidal P CO 2 (P ETCO 2 ); (2) controlled iso-oxic hyperventilation-induced reductions in P aCO 2 (Hypocapnia), P ETCO 2 = 30.1 ± 4.5 mmHg with related reductions in CBF (21.7 ± 6.3%); and (3) isocapnic hyperventilation (Isocapnia) to examine the potential direct influence of hyperventilation-mediated activation of respiratory control centres on CBF and changes in neuromuscular function. Change in MEP amplitude (%M max ) from baseline was greater in Hypocapnia tha in Isocapnia (11.7 ± 9.8%, 95% confidence interval (CI) [2.6, 20.7], P = 0.01) and Indomethacin (13.3 ± 11.3%, 95% CI [2.8, 23.7], P = 0.01) with a large Cohen's effect size (d ࣙ 1.17). Although not statistically significant, cVA was reduced with a moderate effect size in Indomethacin (d = 0.7) and Hypocapnia (d = 0.9) compared to Isocapnia. In summary, increased corticospinal excitability -as reflected by larger MEP amplitude -appears to be exclusive to reduced P aCO 2 , but not reductions in CBF per se. Sub-optimal voluntary output from the motor cortex is moderately associated with decreased CBF, independent of reduced P aCO 2 .

Because the majority of cold exposure studies are constrained to short-term durations of several hours, the long-term metabolic demands of cold exposure, such as during survival situations, remain largely unknown. The present study provides the first estimates of thermogenic rate, oxidative fuel selection, and muscle recruitment during a 24-h cold-survival simulation. Using combined indirect calorimetry and electrophysiological and isotopic methods, changes in muscle glycogen, total carbohydrate, lipid, protein oxidation, muscle recruitment, and whole body thermogenic rate were determined in underfed and noncold-acclimatized men during a simulated accidental exposure to 7.5 °C for 12 to 24 h. In noncold-acclimatized healthy men, cold exposure induced a decrease of ∼0.8 °C in core temperature and a decrease of ∼6.1 °C in mean skin temperature (range, 5.4-6.9 °C). Results showed that total heat production increased by approximately 1.3- to 1.5-fold in the cold and remained constant throughout cold exposure. Interestingly, this constant rise in Ḣprod and shivering intensity was accompanied by a large modification in fuel selection that occurred between 6 and 12 h; total carbohydrate oxidation decreased by 2.4-fold, and lipid oxidation doubled progressively from baseline to 24 h. Clearly, such changes in fuel selection dramatically reduces the utilization of limited muscle glycogen reserves, thus extending the predicted time to muscle glycogen depletion to as much as 15 days rather than the previous estimates of approximately 30-40 h. Further research is needed to determine whether this would also be the case under different nutritional and/or colder conditions.

Improvements in fitness from a brief period of physical training may elicit sufficient physiological adaptations to decrease thermal strain during exercise in the heat. This study tested heat adaptation from short-term endurance (ET) and sprint-interval (SIT) training in moderately fit individuals. The ET group (n = 8) cycled at 65% [Formula: see text] for 8 sessions (4 sessions each at 60 and 90 min, respectively) over two weeks, while the SIT group (n = 8) performed repeated 30-s Wingate sprints (resistance 7.5% body mass; 4 sessions each of 4 and 5 sprints, respectively). [Formula: see text] and heat stress testing (HST; 60 min cycling at 65% [Formula: see text] at 35ºC, 40% relative humidity) were performed pre- and post-training. [Formula: see text]increased by 11% (p = 0.025) and 14% (p = 0.020) for the ET and SIT groups post-training, respectively. Thermal stress was similar pre- and post-training, with no significant difference in the rate of whole-body metabolic heat production (p = 0.106) for either group post-training. Cardiovascular improvement was evident with both ET and SIT, with a significant mean decrease (p = 0.014) in HR for both groups (ET: 146 ± 15 beats·min(-1)pre vs. 142 ± 12 beats·min(-1)post; SIT: 149 ± 15 beats·min(-1)pre vs. 146 ± 12 beats·min(-1)post) during the HST post-training. However, mean sweat loss (p = 0.248) and the rise in core temperature (p = 0. 260) did not change significantly comparing pre- and post-training HST. While short-term ET and SIT both induced significant improvements in aerobic fitness and decreased cardiovascular strain, neither elicited improved thermal responses during exercise in the heat and do not replace heat acclimatization.