Prefrontal cortex oxygenation is preserved and does not contribute to impaired neuromuscular activation during passive hyperthermia

We investigated the role of passive hyperthermia upon motor unit activation and prefrontal cortex oxygenation. Six healthy males were passively heated, using a liquid conditioning garment in a hot environment (35 degrees C, 50% relative humidity). Maximal force output and voluntary activation were examined during a 10 s maximal isometric knee extension. Of the initial 6 subjects, 1 experienced syncope at a rectal temperature (T-re) of 38.0 degrees C and was removed from the study. The remaining 5 subjects completed heating and testing to a T-re of 38.5 degrees C (n = 1), 39.0 degrees C (n = 3), or 39.5 degrees C (n = 1), and then were cooled back to baseline. Force production decreased from 553 +/- 133 to 430 +/- 176 N (p < 0.01) with passive heating, as did voluntary activation (from 90 +/- 5% to 84 +/- 7%). Percent heart rate reserve increased from 8 +/- 5% to 59 +/- 3% before returning to 4 +/- 8% (p < 0.001). Although mean arterial pressure remained unchanged, there were significant decreases in diastolic blood pressure with heating (80 +/- 3 to 63 +/- 8 mm Hg). Passive heating did not alter prefrontal cortex oxygenation, but cooling back to baseline core temperature attenuated cerebral oxygenated and total hemoglobin levels (p < 0.05). Passive heating to the point of voluntary exhaustion elevated cardiovascular and thermal strain and subjective perceptions of thermal discomfort. However, while this resulted in a marked decrement in maximal isometric force production and central voluntary activation, no concomitant changes in cerebral oxygenation were observed, suggesting that overall cerebrovascular regulation was maintained.