Vestibular control of standing balance following 24 h of sleep deprivation.

Sleep deprivation alters cognitive and sensorimotor function, but its effects on the control of standing balance are inconclusive. The vestibular system is critical for standing balance, and is modified by sleep deprivation; however, how sleep deprivation affects vestibular-evoked balance responses is unknown. Thus, this study aimed to examine the effect of 24 h of sleep deprivation on the vestibular control of standing balance. During both a well-rested (i.e., control) and sleep deprivation condition, nine females completed two 90-s trials of bilateral, binaural stochastic electrical vestibular stimulation (EVS) and two 120-s trials of quiet stance on a force plate. Quiet stance performance was assessed by center of pressure displacement parameters. Mediolateral ground reaction force (ML force) and surface electromyography (EMG) of the right medial gastrocnemius (MG) were sampled simultaneously with the EVS signal to quantify vestibular control of balance within the frequency (gain and coherence) and time (cumulant density) domains. Twenty-four hours of sleep deprivation did not affect quiet stance performance. Sleep deprivation also had limited effect on EVS-MG EMG and EVS-ML Force coherence (less than control at 8-10.5 Hz, greater at ~ 16 Hz); however, gain of EVS-MG EMG (< 8, 11-24 Hz) and EVS-ML force (0.5-9 Hz) was greater for sleep deprivation than control. Sleep deprivation did not alter peak-to-peak amplitude of EVS-MG EMG (p = 0.51) or EVS-ML force (p = 0.06) cumulant density function responses. Despite no effect on quiet stance parameters, the observed increase in vestibular-evoked balance response gain suggests 24-h sleep deprivation may lead to greater sensitivity of the central nervous system when transforming vestibular-driven signals for standing balance control.

Effects of sleep deprivation on perceived and performance fatigability in females: An exploratory study.

Sleep deprivation (SD) is prevalent and impairs motor function; however, little is known about its effect on perceived and performance fatigability, especially in females. To examine the effects of 24 h of SD on these attributes of fatigue, nine females completed a 20-min isometric, sustained elbow flexion contraction, followed by 10 min of recovery. The superimposed twitch (SIT) elicited via transcranial magnetic stimulation (TMS) assessed supraspinal drive. Biceps brachii electromyographic data indicated neural excitability in response to stimulation over the motor cortex (motor evoked potential; MEP), corticospinal tract (cervicomedullary motor evoked potential; CMEP), and brachial plexus (maximal M-wave; Mmax). MEPs and CMEPs were recorded during a TMS-induced silent period. At baseline, ratings of perceived effort (RPE; 2.9 vs. 1.6) and fatigue (RPF; 6.9 vs. 2.9), were higher for SD than control. Across the 20-min contraction, RPE increased from 2.2 to 7.6, SIT and MEP/CMEP increased by 284 and 474%, respectively, whereas maximal voluntary isometric contraction (MVC) torque and CMEP/Mmax decreased by 26 and 57%, respectively. No differences were found across conditions for MVC, SIT, Mmax, CMEP/Mmax, or MEP/CMEP prior to, during, and after the fatiguing task. During recovery, RPE (4.9 vs. 3.4), RPF (7.6 vs. 2.8), and perception of task difficulty (5.5 vs. 4.5) were greater for SD than control. Acute SD does not appear to alter performance fatigability development and subsequent recovery; however, it increases perceptions of fatigue, effort, and task difficulty. Thus, the disconnect between perceived and actual neuromuscular capacity following a sustained, submaximal isometric task is exacerbated by SD.HighlightsSleep deprivation did not alter supraspinal drive or neural excitability during and after a 20-min submaximal elbow flexion contractionSleep deprivation increased perceived fatigue and perception of task difficultyThe disconnect between perceived and performance fatigability is exacerbated in a sleep-deprived state.

The influence of reduced foot dorsum cutaneous sensitivity on the vestibular control of balance.

PURPOSE: Foot sole cooling increases vestibular-evoked balance responses, but less is known about foot dorsum temperature alterations. The purpose was to determine whether decreasing cutaneous receptor sensitivity via foot dorsum cooling modulates the vestibular control of balance. METHODS: Eighteen participants (9 males; 9 females) stood quietly on a force plate with feet together, eyes closed, and head rotated leftward during 4, 90-s trials (2 control; 2 cooled) of continuous electrical vestibular stimulation (EVS). Icepacks placed on the dorsum of both feet for 15 min induced cooling and remained throughout the EVS trials. Monofilament testing was performed at multiple locations before and after cooling to determine tactile detection thresholds. T-type thermocouples monitored skin temperature over the tibialis anterior, soleus, foot dorsum and arch of the right leg. Vestibular-evoked balance responses were characterized using time (cumulant density) and frequency (coherence and gain) domain analyses to determine the relationship between the EVS input and motor output (anteroposterior force-AP force; right medial gastrocnemius electromyography-MG EMG). RESULTS: Skin temperature of the foot dorsum and arch decreased ~ 70 and 15%, respectively during cooling (p < 0.05), but was unaltered at other locations (p ≥ 0.10). Detection thresholds for the foot dorsum increased following cooling (p < 0.05). Surprisingly, cooling reduced EVS-AP force and EVS-MG EMG coherence and gain at multiple frequencies, and peak-to-peak amplitude compared to control (p < 0.05). CONCLUSION: Our results indicate that vestibular-driven balance responses are reduced following foot dorsum cooling, likely owing to alterations in cutaneous mechanoreceptor sensitivity and subsequent alterations in the transformation of vestibular cues for balance control.

Neural effects of sleep deprivation on inhibitory control and emotion processing.

Sleep deprivation is commonplace and impairs memory, inhibition, cognitive flexibility and attention. However, little is known about the neurophysiological impact of sleep deprivation in the context of go/no-go (GNG) task performance and emotion processing. To address this knowledge gap, 12 females performed two computerized GNG tasks (shapes; emotional facial expressions) and an object hit and avoid (OHA) task after a night of typical sleep and 24 h without sleep. Electroencephalographic (EEG) recordings were taken during a 3-minute eyes-open resting period as well as during GNG task performance. Resting EEG power in the theta band was 33% higher for the sleep-deprived than control condition (p < 0.05), whereas alpha activity was unchanged. When sleep deprived, participants had ~6% slower response times (go trials) and made ~7% more total errors during GNG tasks (p < 0.05). Reaction time and overall accuracy were ~25% and ~9% worse for the emotional compared to shape GNG task (p < 0.05), respectively, which suggests interference of emotion processing on task performance. Smaller differences in amplitude between go and no-go trials for the N2 and both the N2 and P3 event-related potential components were found during sleep deprivation for the emotional and shape GNG tasks, respectively (p < 0.05). No changes to the N170 component were found. Lastly, participants hit more distractors during the OHA task when sleep deprived (p < 0.05). Altogether, these results indicate sleep deprivation slows neural processing and impairs inhibitory task performance, possibly due to a more bottom-up, stimulus-driven approach to inhibiting motor responses.