Observations of cold-induced vasodilation in persons with spinal cord injuries.

STUDY DESIGN: Acute experimental study. OBJECTIVES: Cold-induced vasodilation is a local mechanism of protection against frostbite in non-injured persons. We assessed whether an increase in skin blood flow (SkBF) during local cooling (LC) was observed in individuals with spinal cord injuries (SCIs) and if the response patterns differed between region levels or sites. SETTING: Laboratory of Wakayama Medical University and the affiliated clinics, Japan. METHODS: A local cooler device (diameter 4 cm) was placed on the chest (sensate) and right thigh (non-sensate) in persons with cervical (SCIC; n = 9) and thoracolumbar SCIs (SCITL; n = 9). After the surface temperature under the device was controlled at 33 °C for 10 min (baseline), LC (-0.045 °C/s) was applied and the skin temperature was maintained at 15 and 8 °C for 15 min of each stage. SkBF (laser Doppler flowmetry) was monitored using a 1-mm needle-type probe inserted into its center. RESULTS: The percent change in SkBF (%ΔSkBF) on the chest remained unchanged until the end of 15 °C stage; thereafter, it increased to a level at least 70% greater than the baseline during the 8 °C stage in both groups. The %ΔSkBF on the thigh in both SCIC and SCITL notably increased from 8 and 6 min respectively, during the 8°C stage, compared to 1 min before the stage; however, it did not exceed the baseline level. CONCLUSIONS: An increase in SkBF during LC was observed both in the sensate and non-sensate areas in SCIs, although the magnitude was larger in the sensate area.

Synesthesia has specific cognitive processing during Go/No-go paradigms.

Grapheme-color synesthesia is a consistent and automatic perception of non-physical color when presented with a grapheme. Many previous studies focused on the synesthetic visual system, but other cognitive functions in grapheme-color synesthetes have remained unclear. Therefore, the objective of the present study was to investigate the characteristics of cognitive processing for motor execution and inhibition during Go/No-go paradigms in grapheme-color synesthesia using event-related potentials (ERPs). Six grapheme-color synesthetes and 24 non-synesthetes performed visual, auditory, and somatosensory Go/No-go paradigms. Omission errors were higher in grapheme-color synesthetes than non-synesthetes. Group-trial interactions (i.e., synesthetes-non-synesthetes × Go-No-go) were observed for the latency of the visual N2 component and amplitude of the somatosensory N2 component. Latencies of auditory and somatosensory P3 components were shorter in grapheme-color synesthetes than non-synesthetes. These findings suggest that grapheme-color synesthetes have specific cognitive processing in motor execution and inhibition as well as synesthetic color perception. Our data advance understanding of cognitive processing in grapheme-color synesthesia.

Quantification of catecholamine neurotransmitters released from cutaneous vasoconstrictor nerve endings in men with cervical spinal cord injury.

Control of cutaneous circulation is critically important to maintain thermoregulation, especially in individuals with cervical spinal cord injury (CSCI) who have no or less central thermoregulatory drive. However, the peripheral vasoconstrictor mechanism and capability have not been fully investigated after CSCI. Post- and presynaptic sensitivities of the cutaneous vasoconstrictor system were investigated in 8 CSCI and 7 sedentary able-bodied (AB) men using an intradermal microdialysis technique. Eight doses of norepinephrine (NE, 10-8 to 10-1 M) and five doses of tyramine (TY, 10-8, 10-5 to 10-2 M) were administered into the anterior right and left thigh, respectively. Endogenous catecholamines, noradrenaline, and dopamine, collected at the TY site, were determined by high-performance liquid chromatography with electrochemical detection. Regardless of vasoconstrictor agents, cutaneous vascular conductance decreased dose-dependently and responsiveness was similar between the groups (NE: Group P = 0.255, Dose P = 0.014; TY: Group P = 0.468, Dose P < 0.001), whereas the highest dose of each drug induced cutaneous vasodilation. Administration of TY promoted the release of noradrenaline and dopamine in both groups. Notably, the amount of noradrenaline released was similar between the groups (P = 0.819), although the concentration of dopamine was significantly greater in individuals with CSCI than in AB individuals (P = 0.004). These results suggest that both vasoconstrictor responsiveness and neural functions are maintained after CSCI, and dopamine in the skin is likely to induce cutaneous vasodilation.

Effects of hypocapnia and hypercapnia on human somatosensory processing.

The present study investigated the effects of hypocapnia and hypercapnia on human somatosensory processing by utilizing somatosensory evoked magnetic fields (SEFs) with magnetoencephalography (MEG). Thirteen volunteers participated in two experiments separately to measure respiratory and cardiovascular data and SEFs. Both experiments consisted of a combination of normal and rapid respiratory rhythms and two inspiratory gas conditions (air and a hypercapnic gas); normal breathing with air (NB), rapid breathing with air (RB), normal breathing with the hypercapnic gas (NB+Gas), and rapid breathing with gas (RB+Gas). Partial pressures of end-tidal CO2 (PETCO2) increased during inhaling the hypercapnic gas and decreased during RB, but the RB+Gas condition continued to cause elevated PETCO2 compared with the baseline. Subsequently, middle cerebral artery blood (MCA) velocity using transcranial Doppler changed as well, while mean MCA velocity increased under the RB+Gas condition. The peak amplitude of the M60 component in SEFs was also significantly larger under with-gas than without-gas conditions, irrespective of the respiratory frequency. These results suggest that there is a close relationship between cerebral blood flow and neural activity of the M60 component in SEFs. This study provides evidence to further understanding on one of the neural mechanisms of hypercapnia.

Altered cardiac ß1 responsiveness in hyperthermic older adults.

Compared with younger adults, passive heating induced increases in cardiac output are attenuated by ∼50% in older adults. This attenuated response may be associated with older individuals' inability to maintain stroke volume through ionotropic mechanisms and/or through altered chronotropic mechanisms. The purpose of this study was to identify the interactive effect of age and hyperthermia on cardiac responsiveness to dobutamine-induced cardiac stimulation. Eleven young (26 ± 4 yr) and 8 older (68 ± 5 yr) participants underwent a normothermic and a hyperthermic (baseline core temperature +1.2°C) trial on the same day. In both thermal conditions, after baseline measurements, intravenous dobutamine was administered for 12 min at 5 µg/kg/min, followed by 12 min at 15 µg/kg/min. Primary measurements included echocardiography-based assessments of cardiac function, gastrointestinal and skin temperatures, heart rate, and mean arterial pressure. Heart rate responses to dobutamine were similar between groups in both thermal conditions (P > 0.05). The peak systolic mitral annular velocity (S'), i.e., an index of left ventricular longitudinal systolic function, was similar between groups for both thermal conditions at baseline. While normothermic, the increase in S' between groups was similar with dobutamine administration. However, while hyperthermic, the increase in S' was attenuated in the older participants with dobutamine (P < 0.001). Healthy, older individuals show attenuated inotropic, but maintained chronotropic responsiveness to dobutamine administration during hyperthermia. These data suggest that older individuals have a reduced capacity to increase cardiomyocyte contractility, estimated by changes in S', via ß1-adrenergic mechanisms while hyperthermic.

Modality differences in ERP components between somatosensory and auditory Go/No-go paradigms in prepubescent children.

We investigated modality differences in the N2 and P3 components of event-related potentials (ERPs) between somatosensory and auditory Go/No-go paradigms in eighteen healthy prepubescent children (mean age: 125.9±4.2 months). We also evaluated the relationship between behavioral responses (reaction time, reaction time variability, and omission and commission error rates) and amplitudes and latencies of N2 and P3 during somatosensory and auditory Go/No-go paradigms. The peak latency of No-go-N2 was significantly shorter than that of Go-N2 during somatosensory paradigms, but not during auditory paradigms. The peak amplitude of P3 was significantly larger during somatosensory than auditory paradigms, and the peak latency of P3 was significantly shorter during somatosensory than auditory paradigms. Correlations between behavioral responses and the P3 component were not found during somatosensory paradigms. On the other hand, in auditory paradigms, correlations were detected between the reaction time and peak amplitude of No-go-P3, and between the reaction time variability and peak latency of No-go-P3. A correlation was noted between commission error and the peak latency of No-go-N2 during somatosensory paradigms. Compared with previous adult studies using both somatosensory and auditory Go/No-go paradigms, the relationships between behavioral responses and ERP components would be weak in prepubescent children. Our data provide findings to advance understanding of the neural development of motor execution and inhibition processing, that is dependent on or independent of the stimulus modality.

Effects of passive heat stress and recovery on human cognitive function: An ERP study.

Using event-related potentials (ERPs), we investigated the effects of passive heat stress and recovery on the human cognitive function with Flanker tasks, involving congruent and incongruent stimuli. We hypothesized that modulation of the peak amplitude and latency of the P300 component in ERP waveforms would differ with task difficulty during passive heat stress and recovery. Subjects performed the Flanker tasks before (Pre), at the end of whole body heating (Heat: internal temperature increase of ~1.2°C from the pre-heat baseline), and after the internal temperature had returned to the pre-heat baseline (Recovery). The internal temperature was regulated by a tube-lined suit by perfusing 50°C water for heat stress and 25°C water for recovery immediately after the heat stress. Regardless of task difficulty, the reaction time (RT) was shortened during Heat rather than Pre and Recovery, and standard deviations of RT (i.e., response variability) were significantly smaller during Heat than Pre. However, the peak amplitudes of the P300 component in ERPs, which involved selective attention, expectancy, and memory updating, were significantly smaller during Heat than during Pre, suggesting the impairment of neural activity in cognitive function. Notably, the peak amplitudes of the P300 component were higher during Recovery than during Heat, indicating that the impaired neural activity had recovered after sufficient whole-body cooling. An indicator of the stimulus classification/evaluation time (peak latency of P300) and the RT were shortened during Heat stress, but such shortening was not noted after whole-body cooling. These results suggest that hyperthermia affects the human cognitive function, reflected by the peak amplitude and latency of the P300 component in ERPs during the Flanker tasks, but sufficient treatment such as whole-body cooling performed in this study can recover those functions.

The relationship between cognitive style and sensory gating during auditory and somatosensory tasks.

Cognitive styles such as field dependence/independence and empathizing influence individual personalities. Sensory gating is conceptualized as an automatic inhibitory function related to human higher cognitive processing. The present study investigated the relationship between cognitive styles and the automatic inhibitory function using electroencephalographic evoked potentials (EPs) during auditory and somatosensory tasks with a paired stimulus. The Embedded-Figures Test (EFT) and Empathy Questionnaire (EQ) were performed to assess the cognitive styles (field dependence: FD; field independence: FI; empathizing: EM; non-empathizing: Non-EM). Sensory gating was evaluated as an amplitude ratio of EP responses to the second stimulus (S2) over responses to the first stimulus (S1). Subjects were divided into two groups based on EFT scores (FD vs. FI) or EQ scores (EM vs. Non-EM). The S2/S1 amplitude ratio of the auditory long-latency component was significantly smaller in the FD than FI group, while the S2/S1 amplitude ratio of a somatosensory long-latency component was significantly smaller in the FI than FD group. In contrast, these differences in the S2/S1 amplitude ratios of any auditory and somatosensory components were not observed between EM and Non-EM groups. Our results suggest that sensory gating conceptualized as an automatic inhibitory function is related to FD and FI cognitive styles.

An assessment of hypercapnia-induced elevations in regional cerebral perfusion during combined orthostatic and heat stresses.

We investigated that the effects of hypercapnia-induced elevations in cerebral perfusion during a heat stress on global cerebrovascular responses to an orthostatic challenge. Seven volunteers completed a progressive lower-body negative pressure (LBNP) challenge to presyncope during heat stress, with or without breathing a hypercapnic gas mixture. Administration of the hypercapnic gas mixture increased the partial pressure of end-tidal CO2 greater than pre-heat stress alone, and increased both internal carotid artery (ICA) and vertebral artery (VA) blood flows (P < 0.05). During LBNP, both ICA and VA blood flows with the hypercapnic gas mixture remained elevated relative to the control trial (P < 0.05). However, at the end of LBNP due to pre-syncopal symptoms, both ICA and VA blood flows decreased to similar levels between trials. These findings suggest that hypercapnia-induced cerebral vasodilation is insufficient to maintain cerebral perfusion at the end of LBNP due to pre-syncope in either the anterior or posterior vascular beds.

Differences in characteristics of somatosensory evoked potentials between children and adults.

The present study examined the characteristics of somatosensory processing in healthy prepubescent children (mean age: 124.9 ± 3.8 months) compared with young adults. Somatosensory evoked potentials at the frontal (Fz) and centroparietal (C3') electrodes were recorded by delivering an electrical stimulus to the right median nerve at a rate of 3 Hz. The characteristics of somatosensory evoked potential waveforms at C3' were markedly different between the two groups, while those at Fz were similar. Specifically, the waveforms at C3' in the children involved not only standard P12, N18, P22, N27, P45, and N60 components, but also additional positive (P3) and negative (N3) components between N27 and P45, which were not found in adults. The amplitude of P22 at C3' was significantly larger in the children than adults, indicating hyper-excitability/responsiveness of neural activity on somatosensory processing. In contrast, the amplitudes of N15 at Fz and N27 at C3' were smaller in the children than adults, suggesting an immature somatosensory system in the children. The peak latencies of P12, N15, and P18 at Fz, and P12 and N18 at C3' were significantly shorter in the children than adults, which was dependent on the height. These results indicate the developing somatosensory processing with hyper- and hypo-excitability of neural activity in prepubescent children.

Effects of whole body skin cooling on human cognitive processing: a study using SEPs and ERPs.

The present study investigated the effect of whole body skin cooling on somatosensory ascending processing by utilizing somatosensory-evoked potentials (SEPs) and motor execution, as well as inhibitory processing by event-related potentials (ERPs). Fourteen healthy participants wearing a water-perfused suit performed two sessions (sessions 1 and 2) consisting of SEPs and ERPs with somatosensory Go/No-go paradigms under two conditions (cold stress and control) on different days. In session 2, under the cold stress condition, whole body skin cooling was achieved by circulating 20°C water through the suit for 40 min, whereas 34°C water was perfused in the other sessions. The mean skin temperature decreased from 35.0 ± 0.5°C (session 1) to 30.4 ± 0.9°C (session 2) during whole body skin cooling, but the internal temperature was maintained. Whole body skin cooling delayed the peak latencies of N20, P25, and P45 components at C4' of SEPs (all: P < 0.05). Moreover, the peak latencies of P14, N18, and P22 components at Fz of SEPs and the Go-P300 component of ERPs were delayed (all: P < 0.05). In contrast, the peak amplitudes of all individual components of SEPs as well as N140 and P300 of ERPs remained unchanged. These results suggest that passive whole body skin cooling delays neural activities on somatosensory processing and higher cognitive function.

Effects of repetitive exercise and thermal stress on human cognitive processing.

Cognitive performances may improve after acute moderate exercise, but not after prolonged and/or heavy exercise. The present study aimed to investigate the effects of environmental temperature during exercise on human cognitive processing. Fifteen healthy males performed four bouts of a 15-min cycling exercise with a 10-min rest between each bout, and event-related potentials (ERPs) were recorded in five sessions during somatosensory Go/No-go paradigms (i.e., Pre, post-first exercise bout, post-second exercise bout, post-third exercise bout, and post-fourth exercise bout) in an environmental chamber with temperature controlled at 20°C (Temperate) and 35°C (Hot). Increases in external canal temperature and heart rate were greater under the 35°C condition than under the 20°C condition. Regardless of thermal conditions, reaction times (RT) and error rates were not affected by the repetition of moderate exercise, whereas the peak amplitude of the N140 component, which is mainly related to somatosensory processing, was significantly reduced with the repetition of the exercise. However the peak amplitude of P300, which is linked to cognitive processes of context updating, context closure, and event-categorization, was significantly smaller in post-third and post-fourth exercise bouts under the 35°C condition than under the 20°C condition, and this decrease was more prominent in No-go trials under the 35°C condition. These results suggest that executive function, which is based on RTs and error rates, is not affected by prolonged exercise and different thermal conditions, whereas the exercise in a hot environment impairs human cognitive processing, particularly response inhibition.

Differences in serum IL-6 response after 1 °C rise in core body temperature in individuals with spinal cord injury and cervical spinal cord injury during local heat stress.

OBJECTIVES: Passive rise in core body temperature achieved by head-out hot water immersion (HHWI) results in acute increases in serum interleukin (IL)-6 but no change in plasma adrenaline in patients with cervical spinal cord injury (CSCI). The purpose of the present study was to determine the mechanism of heat stress-induced increase in serum IL-6. SETTING: A cross-sectional study. METHODS: The study subjects were nine with CSCI, ten with thoracic and lumbar spinal cord injury (TLSCI) and eight able-bodied (AB) subjects. Time since injury was 16.1 ± 3.4 years in TLSCI and 16.4 ± 4.1 years in CSCI. Subjects were subjected to lower-body heat stress (LBH) by wearing a hot water-perfused suit until 1 °C increase in core temperature. The levels of serum IL-6, plasma adrenaline, tumour necrosis factor (TNF)-α, C-reactive protein (CRP), and counts of blood cells were measured at normothermia and after LBH. RESULTS: Serum IL-6 concentrations increased significantly immediately after LBH in all the three groups. ΔIL-6% was lower in CSCI subjects compared with AB subjects. Plasma adrenaline concentrations significantly increased after LBH in AB and TLSCI subjects, but did not change throughout the study in CSCI subjects. Cardiac output and heart rate increased at the end of LBH in all three groups. CONCLUSIONS: Under a similar increase in core temperature, ΔIL-6% was lower in the CSCI group compared with the AB group. These findings suggest that the observed rise in IL-6 during hyperthermia is mediated, at least in part, by plasma adrenaline.

Dynamic cerebral autoregulation during cognitive task: effect of hypoxia.

Changes in cerebral blood flow (CBF) subsequent to alterations in the partial pressures of oxygen and carbon dioxide can modify dynamic cerebral autoregulation (CA). While cognitive activity increases CBF, the extent to which it impacts CA remains to be established. In the present study we determined whether dynamic CA would decrease during a cognitive task and whether hypoxia would further compound impairment. Fourteen young healthy subjects performed a simple Go/No-go task during normoxia and hypoxia (inspired O2 fraction = 12%), and the corresponding relationship between mean arterial pressure (MAP) and mean middle cerebral artery blood velocity (MCA Vmean) was examined. Dynamic CA and steady-state changes in MCA V in relation to changes in arterial pressure were evaluated with transfer function analysis. While MCA Vmean increased during the cognitive activity ( P < 0.001), hypoxia did not cause any additional changes ( P = 0.804 vs. normoxia). Cognitive performance was also unaffected by hypoxia (reaction time, P = 0.712; error, P = 0.653). A decrease in the very low- and low-frequency phase shift (VLF and LF; P = 0.021 and P = 0.01) and an increase in LF gain were observed ( P = 0.037) during cognitive activity, implying impaired dynamic CA. While hypoxia also increased VLF gain ( P < 0.001), it failed to cause any additional modifications in dynamic CA. Collectively, our findings suggest that dynamic CA is impaired during cognitive activity independent of altered systemic O2 availability, although we acknowledge the interpretive complications associated with additional competing, albeit undefined, inputs that could potentially distort the MAP-MCA Vmean relationship. NEW & NOTEWORTHY During normoxia, cognitive activity while increasing cerebral perfusion was shown to attenuate dynamic cerebral autoregulation (CA) yet failed to alter reaction time, thereby questioning its functional significance. No further changes were observed during hypoxia, suggesting that impaired dynamic CA occurs independently of altered systemic O2 availability. However, impaired dynamic CA may reflect a technical artifact, given the confounding influence of additional inputs that could potentially distort the mean arterial pressure-mean middle cerebral artery blood velocity relationship.

A comparison of static and dynamic cerebral autoregulation during mild whole-body cold stress in individuals with and without cervical spinal cord injury: a pilot study.

STUDY DESIGN: Experimental study. OBJECTIVES: To characterize static and dynamic cerebral autoregulation (CA) of individuals with cervical spinal cord injury (SCI) compared to able-bodied controls in response to moderate increases in mean arterial pressure (MAP) caused by mild whole-body cold stress. SETTING: Japan METHODS: Five men with complete autonomic cervical SCI (sustained > 5 y) and six age-matched able-bodied men participated in hemodynamic, temperature, catecholamine and respiratory measurements for 60 min during three consecutive stages: baseline (10 min; 33 °C water through a thin-tubed whole-body suit), mild cold stress (20 min; 25 °C water), and post-cold recovery (30 min; 33 °C water). Static CA was determined as the ratio between mean changes in middle cerebral artery blood velocity and MAP, dynamic CA as transfer function coherence, gain, and phase between spontaneous changes in MAP to middle cerebral artery blood velocity. RESULTS: MAP increased in both groups during cold and post-cold recovery (mean differences: 5-10 mm Hg; main effect of time: p = 0.001). Static CA was not different between the able-bodied vs. the cervical SCI group (mean (95% confidence interval (CI)) of between-group difference: -4 (-11 to 3) and -2 (-5 to 1) cm/s/mm Hg for cold (p = 0.22) and post-cold (p = 0.24), respectively). At baseline, transfer function phase was shorter in the cervical SCI group (mean (95% CI) of between-group difference: 0.6 (0.2 to 1.0) rad; p = 0.006), while between-group differences in changes in phase were not different in response to the cold stress (interaction term: p = 0.06). CONCLUSIONS: This pilot study suggests that static CA is similar between individuals with cervical SCI and able-bodied controls in response to moderate increases in MAP, while dynamic CA may be impaired in cervical SCI because of disturbed sympathetic control.

Effect of increases in cardiac contractility on cerebral blood flow in humans.

The effect of acute increases in cardiac contractility on cerebral blood flow (CBF) remains unknown. We hypothesized that the external carotid artery (ECA) downstream vasculature modifies the direct influence of acute increases in heart rate and cardiac function on CBF regulation. Twelve healthy subjects received two infusions of dobutamine [first a low dose (5 µg·kg-1·min-1) and then a high dose (15 µg·kg-1·min-1)] for 12 min each. Cardiac output, blood flow through the internal carotid artery (ICA) and ECA, and echocardiographic measurements were performed during dobutamine infusions. Despite increases in cardiac contractility, cardiac output, and arterial pressure with dobutamine, ICA blood flow and conductance slightly decreased from resting baseline during both low- and high-dose infusions. In contrast, ECA blood flow and conductance increased appreciably during both low- and high-dose infusions. Greater ECA vascular conductance and corresponding increases in blood flow may protect overperfusion of intracranial cerebral arteries during enhanced cardiac contractility and associated increases in cardiac output and perfusion pressure. Importantly, these findings suggest that the acute increase of blood perfusion attributable to dobutamine administration does not cause cerebral overperfusion or an associated risk of cerebral vascular damage.NEW & NOTEWORTHY A dobutamine-induced increase in cardiac contractility did not increase internal carotid artery blood flow despite an increase in cardiac output and arterial blood pressure. In contrast, external carotid artery blood flow and conductance increased. This external cerebral blood flow response may assist with protecting from overperfusion of intracranial blood flow.

Effects of acute hypoxia on human cognitive processing: a study using ERPs and SEPs.

Although hypoxia has the potential to impair the cognitive function, the effects of acute hypoxia on the high-order brain function (executive and/or inhibitory processing) and somatosensory ascending processing remain unknown. We tested the hypothesis that acute hypoxia impairs both motor executive and inhibitory processing and somatosensory ascending processing. Fifteen healthy subjects performed two sessions (sessions 1 and 2), consisting of electroencephalographic event-related potentials with somatosensory Go/No-go paradigms and somatosensory-evoked potentials (SEPs) under two conditions (hypoxia and normoxia) on different days. On 1 day, participants breathed room air in the first and second sessions of the experiment; on the other day, participants breathed room air in the first session, and 12% O2 in the second session. Acute hypoxia reduced the peak amplitudes of Go-P300 and No-go-P300, and delayed the peak latency of Go-P300. However, no significant differences were observed in the peak amplitude or latency of N140, behavioral data, or the amplitudes and latencies of individual SEP components between the two conditions. These results suggest that acute hypoxia impaired neural activity in motor executive and inhibitory processing, and delayed higher cognitive processing for motor execution, whereas neural activity in somatosensory processing was not affected by acute hypoxia.NEW & NOTEWORTHY Hypoxia has the potential to impair the cognitive function, but the effects of acute hypoxia on the cognitive function remain debatable. We investigated the effects of acute hypoxia on human cognitive processing using electroencephalographic event-related potentials and somatosensory-evoked potentials. Acute normobaric hypoxia impaired neural activity in motor executive and inhibitory processing, but no significant differences were observed in neural activity in somatosensory processing.

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

We herein investigated the effects of face/head and whole body cooling during passive heat stress on human somatosensory processing recorded by somatosensory-evoked potentials (SEPs) at C4' and Fz electrodes. Fourteen healthy subjects received a median nerve stimulation at the left wrist. SEPs were recorded at normothermic baseline (Rest), when esophageal temperature had increased by ~1.2°C (heat stress: HS) during passive heating, face/head cooling during passive heating (face/head cooling: FHC), and after HS (whole body cooling: WBC). The latencies and amplitudes of P14, N20, P25, N35, P45, and N60 at C4' and P14, N18, P22, and N30 at Fz were evaluated. Latency indicated speed of the subcortical and cortical somatosensory processing, while amplitude reflected the strength of neural activity. Blood flow in the internal and common carotid arteries (ICA and CCA, respectively) and psychological comfort were recorded in each session. Increases in esophageal temperature due to HS significantly decreased the amplitude of N60, psychological comfort, and ICA blood flow in the HS session, and also shortened the latencies of SEPs (all, P < 0.05). While esophageal temperature remained elevated, FHC recovered the peak amplitude of N60, psychological comfort, and ICA blood flow toward preheat baseline levels as well as WBC. However, the latencies of SEPs did not recover in the FHC and WBC sessions. These results suggest that impaired neural activity in cortical somatosensory processing during passive HS was recovered by FHC, whereas conduction velocity in the ascending somatosensory input was accelerated by increases in body temperature.

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.