Suppression of cognitive function in hyperthermia; From the viewpoint of executive and inhibitive cognitive processing.

Climate change has had a widespread impact on humans and natural systems. Heat stroke is a life-threatening condition in severe environments. The execution or inhibition of decision making is critical for survival in a hot environment. We hypothesized that, even with mild heat stress, not only executive processing, but also inhibitory processing may be impaired, and investigated the effectiveness of body cooling approaches on these processes using the Go/No-go task with electroencephalographic event-related potentials. Passive heat stress increased esophageal temperature (Tes) by 1.30 ± 0.24 °C and decreased cerebral perfusion and thermal comfort. Mild heat stress reduced the amplitudes of the Go-P300 component (i.e. execution) and No-go-P300 component (i.e. inhibition). Cerebral perfusion and thermal comfort recovered following face/head cooling, however, the amplitudes of the Go-P300 and No-go-P300 components remained reduced. During whole-body cooling, the amplitude of the Go-P300 component returned to the pre-heat baseline, whereas that of the No-go-P300 component remained reduced. These results suggest that local cooling of the face and head does not restore impaired cognitive processing during mild heat stress, and response inhibition remains impaired despite the return to normothermia.

Effects of aerobic exercise under different thermal conditions on human somatosensory processing.

The present study aimed to investigate the effects of aerobic exercise on human somatosensory processing recorded by somatosensory evoked potentials (SEPs) under temperate [TEMP, 20°C and 40% relative humidity (RH)] and hot (HOT, 35°C and 30% RH) environments. Fifteen healthy subjects performed 4 × 15-min bouts of a moderate cycling exercise [mean power output: 156.5 ± 7.7 (SE) W], with a 10-min rest period and received a posterior tibial nerve stimulation at the left ankle before and after each exercise bout; SEPs were recorded in five sessions; 1st (pre), 2nd (post-1st exercise bout), 3rd (post-2nd exercise bout), 4th (post-3rd exercise bout), and 5th (post-4th exercise bout). The peak latencies and amplitudes of the P37, N50, P60, and N70 components at Cz were evaluated. The latencies of P37, N50, P60, and N70 were significantly shorter with the repetition of aerobic exercise, and these shortened latencies were significantly greater in the HOT condition than in the TEMP condition (P37: 3rd, P < 0.05, and 5th, P < 0.01; P60: 4th, P < 0.05, and 5th, P < 0.01; N70: 4th, P < 0.05, and 5th, P < 0.001). No significant differences were observed in the amplitudes of any SEP component under either thermal condition. These results suggest that the conduction velocity of the ascending somatosensory input was accelerated by increases in body temperature, and aerobic exercise did not alter the strength of neural activity in cortical somatosensory processing.

The effect of elevations in internal temperature on event-related potentials during a simple cognitive task in humans.

The effect of hyperthermia on cognitive function remains equivocal, perhaps because of methodological discrepancy. Using electroencephalographic event-related potentials (ERPs), we tested the hypothesis that a passive heat stress impairs cognitive processing. Thirteen volunteers performed repeated auditory oddball paradigms under two thermal conditions, normothermic time control and heat stress, on different days. For the heat stress trial, these paradigms were performed at preheat stress (i.e., normothermic) baseline, when esophageal temperature had increased by ∼0.8°C, when esophageal temperature had increased by ∼2.0°C, and during cooling following the heat stress. The reaction time and ERPs were recorded in each session. For the time control trial, subjects performed the auditory oddball paradigms at approximately the same time interval as they did in the heat stress trial. The peak latency and amplitude of an indicator of auditory processing (N100) were not altered regardless of thermal conditions. An indicator of stimulus classification/evaluation time (latency of P300) and the reaction time were shortened during heat stress; moreover an indicator of cognitive processing (the amplitude of P300) was significantly reduced during severe heat stress (8.3 ± 1.3 µV) relative to the baseline (12.2 ± 1.0 µV, P < 0.01). No changes in these indexes occurred during the time control trial. During subsequent whole body cooling, the amplitude of P300 remained reduced, and the reaction time and latency of P300 remained shortened. These results suggest that excessive elevations in internal temperature reduce cognitive processing but promote classification time.

Effects of passive heat stress on human somatosensory processing.

Herein, we investigated the effects of passive heat stress on human somatosensory processing recorded by somatosensory-evoked potentials (SEPs). Fifteen healthy subjects received a median nerve stimulation at the left wrist under two thermal conditions: Heat Stress and normothermic Time Control. The latencies and amplitudes of P14, N20, P25, N35, P45, and N60 at C4' and P14, N18, P22, and N30 at Fz were evaluated. Under the Heat Stress condition, SEPs were recorded at normothermic baseline (1st), early in heat stress (2nd), when esophageal temperature had increased by ~1.0°C (3rd) and ~2.0°C (4th), and after heat stress (5th). In the Time Control condition, SEPs were measured at the same time intervals as those in the Heat Stress condition. The peak latencies and amplitudes of SEPs did not change early in heat stress. However, the latencies of P14, N20, and N60 at C4' and P14, N18, and P22 at Fz were significantly shorter in the 4th session than in the 1st session. Furthermore, the peak amplitudes of P25 and N60 at C4', and P22 and N30 at Fz decreased with increases in body temperature. On the other hand, under the Time Control condition, no significant differences were observed in the amplitudes or latencies of any component of SEPs. These results suggested that the conduction velocity of the ascending somatosensory input was accelerated by increases in body temperature, and hyperthermia impaired the neural activity of cortical somatosensory processing.