Effects of passive heat stress on human somatosensory processing

Abstract

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.

Effects of face/head and whole body cooling during passive heat stress on human somatosensory processing

“…To record SEPs, the electric stimulus used was a constant current square-wave pulse delivered to the left median nerve at a rate of 3 Hz (22)(23)(24). The stimulus duration was 0.2 ms, and stimulus intensity was sufficient to produce a slight but definite twitch of the thumb.…”

“…For example, the amplitude of N35 is easily affected by the amplitude of P25, and N35 often shows a positive rather than negative potential when the baseline-to-peak measurement is used. We employed the same analysis methods as those reported previously (12,(22)(23)(24)37). The peak amplitudes and latencies for the individual SEP components were assessed using a measuring scale on the Neuropack system with visual inspection.…”

“…The P22 and N30 components are recorded at the frontal electrodes and are generated from the primary motor cortex, premotor area, and prefrontal cortex (9,16,35). Our previous study using median nerve stimulation demonstrated that the peak latencies of some SEP components were shortened, but these peak amplitudes were reduced in subjects with increases in body temperature (24). We also reported 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 (25).…”

Cortical Somatosensory Excitability Is Modulated in Response to Several Days of Muscle Soreness

“…The main SEP components affected in the present study was centro-parietal P45 (centro-parietal recording sites), suggesting that the parietal cortex was mainly affected by muscle soreness. attenuation of SEPs has been described during active and passive movement [40], tactile stimulation [20], water immersion [41], passive heat stress conditions [31], 1Hz repetitive TMS [12] and continuous theta burst stimulation [18], whereas enhancement of SEPs has been described in response to motor learning [30], attention [14], anestetics blocks [53], paired associative stimulation [61] and intermittent theta burst stimulation [19]. These results suggest that the excitability of the sensory cortex can be modulated through several different interventions and a challenge for future research is to use and/or develop different therapeutic interventions able to reverse or modulate sensory cortex adaptations provoked by muscle pain.…”

Residual heat stress improves spatial rotation function, but does not modify attention

“…Studies with functional imaging techniques demonstrate that during intense emotional states (for example stress) neural activity in some cognitive-processing areas could be suppressed (Drevets & Raichle, 1998). Some studies suggest that the conduction velocity of the ascending somatosensory input (Nakata, Oshiro, Namba, & Shibasaki, 2015) and reaction time (Shibasaki et al, 2016) is accelerated under increased body temperature or may reduce neural activity in particular brain regions (Shibasaki et al, 2017). Stressors activate the hypothalamopituitary-adrenocortical and the sympatho-adrenal medullary axis, and increase in concentration of cortisol, adrenaline and noradrenaline is observing (McMorris et al, 2006;Minton, 1994).…”