Four hours of normobaric hypoxia reduces Achilles tendon reflex inhibition.

Acute exposure to hypoxia increases postural sway, but the underlying neurophysiological factors are unclear. Golgi tendon organs (GTOs), located within the musculotendinous junction (MTJ), provide inhibitory signals to plantar flexor muscles that are important for balance control; however, it is uncertain if GTO function is influenced by hypoxia. The aim of this study was to determine how normobaric hypoxia influences lower limb tendon-evoked inhibitory reflexes during upright stance. We hypothesized that tendon-evoked reflex area and duration would decrease during hypoxia, indicating less inhibition of postural muscles compared to normoxia. At baseline (BL; 0.21 fraction of inspired oxygen, FIO2) and at ~2 (H2) and 4 (H4) hours of normobaric hypoxia (0.11 FIO2) in a normobaric hypoxic chamber, sixteen healthy participants received electrical musculotendinous stimulation (MTstim) to the MTJ of the left Achilles tendon. The MTstim was delivered as two sets of 50 stimuli while the participant stood on a force plate with their feet together. Tendon-evoked inhibitory reflexes were recorded from the surface electromyogram of the ipsilateral medial gastrocnemius, and center of pressure (CoP) variables were recorded from the force plate. Normobaric hypoxia increased CoP velocity (p ≤ 0.002) but not CoP standard deviation (p ≥0.12). Compared to BL, normobaric hypoxia reduced tendon-evoked inhibitory reflex area by 45% at H2 and 53% at H4 (p ≤ 0.002). In contrast, reflex duration was unchanged during hypoxia. The reduced inhibitory feedback from the GTO pathway could likely play a role in the increased postural sway observed during acute exposure to hypoxia.

Differential Modulation of Motor Unit Behaviour when a Fatiguing Contraction is Matched for Torque versus EMG.

INTRODUCTION: When an isometric contraction is sustained at a submaximal torque, activation of the motoneuron pool increases, making it difficult to measure neural excitability alterations. Thus, more recently, isometric contractions with maintained electromyographic activity (matched-EMG) are being used to induce fatigue; however, little is known about the neurophysiological adjustments that occur to satisfy the requirements of the task. METHODS: For our study, 16 participants performed a 10-min sustained isometric elbow flexion contraction at 20% maximal voluntary contraction (MVC) torque or the level of integrated biceps brachii EMG recorded at 20% MVC torque. Surface EMG was used to assess global median frequency, and four fine-wire electrode pairs were used to obtain motor unit (MU) discharge rate from biceps brachii. Torque or EMG steadiness was also assessed throughout the fatiguing contractions. RESULTS: MU discharge rate increased and torque steadiness decreased during the matched-torque contraction; however, MU discharge rate decreased during the matched-EMG contraction and no changes occurred for EMG steadiness. Data pooled for the two contractions revealed a decrease of global median frequency. Lastly, a greater loss of MVC torque was observed immediately after the matched-torque compared to matched-EMG contraction. CONCLUSIONS: These findings indicate that, during a matched-torque fatiguing contraction, the nervous system increases MU discharge rates at the cost of poorer steadiness in order to maintain the requisite torque. In contrast, during a matched-EMG fatiguing contraction, a reduction of MU discharge rates allows for a maintenance of EMG steadiness.

Normobaric hypoxia does not influence the sural nerve cutaneous reflex during standing.

Hypoxia increases postural sway compared to normoxia, but the underlying sensorimotor factors remain unclear. An important contributor to balance control is cutaneous feedback arising from the feet, which can be partially characterized by electrically evoking a reflex from a purely cutaneous nerve (i.e., sural) and sampling the subsequent motor activity of a muscle. The purpose of the present study was to determine how normobaric hypoxia influences sural nerve reflex parameters during a standing posture. It was hypothesized that normobaric hypoxia would reduce cutaneous reflex area compared to normoxia. Participants (n = 16; 5 females, 11 males) stood with their feet together while receiving two trials of 50 sural nerve stimulations (200-Hz, 5-pulse train, presented randomly every 3-6 s) at baseline (BL; normoxia), and at 2 (H2) and 4 (H4) h of normobaric hypoxia (~ 0.11 fraction of inspired oxygen in a hypoxic chamber). The sural nerve reflex was recorded using surface electromyography from the left medial gastrocnemius, and characterized by area and duration of the initial positive and negative peaks of the response. When normalized to pre-stimulus electromyography, the area of the peak-to-peak cutaneous reflex was not different than BL (p ≥ 0.14) for up to 4 h of normobaric hypoxia (BL: 0.26 ± 0.22, H2: 0.19 ± 0.19, H4: 0.22 ± 0.20 A.U.). Furthermore, the duration of the response was not different during hypoxia (BL: 73.2 ± 42.4; H2: 75.2 ± 47.0; H4: 77.6 ± 54.6 ms; p ≥ 0.13) than BL. Thus, reflexes arising from cutaneous afferents of the lateral border of the foot are resilient to at least 4 h of normobaric hypoxia.

Voluntary activation does not differ when using two different methods to determine transcranial magnetic stimulator output.

According to current guidelines, when measuring voluntary activation (VA) using transcranial magnetic stimulation (TMS), stimulator output (SO) should not exceed the intensity that, during a maximal voluntary contraction (MVC), elicits a motor evoked potential (MEP) from the antagonist muscle >15%-20% of its maximal M-wave amplitude. However, VA is based on agonist evoked-torque responses [i.e., superimposed twitch (SIT) and estimated resting twitch (ERT)], which means limiting SO based on electromyographic (EMG) responses will often lead to a submaximal SIT and ERT, possibly underestimating VA. Therefore, the purpose of this study was to compare elbow flexor VA calculated using the original method (i.e., intensity based on MEP size; SOMEP) and a method based solely on eliciting the largest SIT at 50% MVC torque (SOSIT), regardless of triceps brachii MEP size. Fifteen healthy, young participants performed 10 sets of brief contractions at 100%, 75%, and 50% MVC torque, with TMS delivered at SOMEP (73.0 ± 13.5%) or SOSIT (92.0 ± 10.8%) for five sets each. Although the mean ERT torque was greater using SOSIT (15.2 ± 4.8 Nm) compared with SOMEP (13.0 ± 3.7 Nm; P = 0.031), the SIT amplitude at 100% MVC torque was not different (SOMEP: 0.69 ± 0.49 Nm vs. SOSIT: 0.74 ± 0.52 Nm; P = 0.604). Despite the ERT disparity, VA scores were not different between SOMEP (94.6 ± 3.5%) and SOSIT (95.0 ± 3.3%; P = 0.572). Even though SOSIT did not lead to a higher VA score than the SOMEP method, it has the benefit of yielding the same result without the need to record antagonist EMG or perform MVCs when determining SO, which can induce fatigue before measuring VA.NEW & NOTEWORTHY When using transcranial magnetic stimulation (TMS) to determine voluntary activation (VA) of the elbow flexors, we hypothesized that a stimulator output designed to limit antagonist muscle activity would evoke submaximal agonist superimposed twitch amplitudes, thus underestimating VA. Contrary to our hypothesis, VA was not greater with an output based on maximal superimposed twitch amplitude. Nevertheless, our findings advance methodological practices by simplifying the equipment and minimizing the time required to determine VA using TMS.

Increased corticospinal inhibition following brief maximal and submaximal contractions in humans.

A potentiating conditioning contraction (CC) has been shown to increase silent period duration, an index of corticospinal inhibition; however, it is unknown if the CC must induce potentiation for corticospinal inhibition to increase. Ten healthy, young adults (four females) completed this study to assess potentiation and silent period (SP) duration before and after four types of CCs: voluntary and electrically evoked maximal CCs to optimize potentiation, and voluntary and electrically evoked submaximal CCs (∼40% of maximal voluntary force) that induced minimal potentiation. Stimulation was applied to the ulnar nerve to evoke twitches for the assessment of potentiation and to evoke tetanic CCs of the first dorsal interosseous muscle. The SP was elicited by applying transcranial magnetic stimulation to the motor cortex during brief contractions at 25% of maximal voluntary force. Changes to twitch force and SP duration were not different for voluntary and tetanic contractions, so data were pooled. Twitch force increased by 81.2 ± 35.7% (P < 0.001) and 3.2 ± 6.5% (P = 0.039) following maximal and submaximal CCs, respectively. The SP was prolonged following maximal (12.6 ± 6.3%; P < 0.001) and submaximal (4.8 ± 4.9%; P < 0.001) CCs. Correlations between post-CC twitch force and SP duration were not significant for maximal or submaximal conditions (r = -0.068; r = 0.067; P ≥ 0.780, respectively). Duration of the SP increased not only following maximal-intensity CCs but also after submaximal-intensity CCs that induced virtually no potentiation (∼3%). Thus, we suggest that corticospinal inhibition is not directly related to mechanisms of muscle potentiation per se, but, rather, the level of muscle contraction likely mediates feedback from large diameter afferents that affect the SP.NEW & NOTEWORTHY The transcranial magnetic stimulation-induced silent period reflects a transient state of corticospinal inhibition that is influenced by recent history of muscle activation, which may include an effect of potentiation. We demonstrate that silent period duration increases following both voluntary and electrically evoked maximal and submaximal conditioning contractions, even though the latter intensity produced virtually no muscle potentiation. Feedback from group Ia and Ib muscle afferents is proposed as the cause of the increased corticospinal inhibition.

A violation of Fitts' Law occurs when a target range is presented before and during movement.

According to Fitts' Law, the time to reach a target (movement time, MT) increases with distance. A violation of Fitts' Law occurs when target positions are outlined before and during movement, as MTs are not different when reaching to the farthest and penultimate targets. One hypothesis posits that performers cognitively process the edges of a target array before the center, allowing for corrective movements to be completed more quickly when moving to edge targets compared to middle targets. The objective of this study was to test this hypothesis by displaying a target range rather than outlines of individual targets in an effort to identify the effects of array edges. Using a touch-screen laptop, participants (N = 24) were asked to reach to one of three targets which would appear within a presented range. Separately, targets were also presented without a range to determine if the display protocol could evoke Fitts' Law. Movements were assessed with the touch screen and optical position measurement. A main effect was found for relative position within a range (touch: F2,44 = 15.4, p < 0.001, η2p = 0.412; position: F2,40 = 15.6, p < 0.001, η2p = 0.439). As hypothesised, MT to the farthest target in a range was not significantly different than MT to the middle target (touch: p = 0.638, position: p = 0.449). No violation was found when a target range was not presented (touch: p = 0.003, position: p = 0.001). Thus, a target range reproduces the Fitts' Law violation previously documented with individually outlined targets, which supports and extends the discussed hypothesis.

The orderly recruitment of motor units may be modified when a muscle is acting as an antagonist.

Despite the perceived importance of antagonist muscle activity, it is unknown if motor unit (MU) behavior at recruitment differs when a muscle acts as an antagonist versus agonist. Fourteen healthy participants performed ramped, isometric elbow flexor or extensor contractions to 50% or 100% maximal voluntary contraction (MVC) torque. Surface and fine-wire intramuscular electromyographic (EMG) recordings were sampled from biceps and triceps brachii. During agonist contractions, low-threshold MUs (recruited at <10% MVC torque) were sampled in all participants, with a total of 107 and 90 for biceps and triceps brachii, respectively. For ramped MVCs, antagonist surface EMG coactivation (% amplitude during agonist MVC) was 8.3 ± 6.6% for biceps and 15.2 ± 7.3% for triceps brachii. However, antagonist single MU activity was recorded from only four participants, with only one of these individuals having antagonist MUs recorded from both muscles. All antagonist MUs were successfully detected during agonist contractions, but many (∼40%) had a recruitment threshold >10% MVC torque. For MUs recorded during both agonist and antagonist contractions, discharge rate at recruitment was seemingly lower for antagonist than agonist contractions. Coexistence of typical levels of surface EMG-derived coactivation with scant antagonist MU recordings suggests that coactivation in these muscles is primarily the result of cross talk. Based on the limited antagonist MU data detected, MUs recruited early during an agonist contraction are not necessarily among those first recruited during an antagonist contraction. These findings highlight the possibility of a modification of orderly recruitment when a motoneuron pool is acting as an antagonist.NEW & NOTEWORTHY Modest levels of coactivation are widely considered essential for appropriate motor control; however, minimal attention has been given to recruitment patterns of motor units (MUs) from antagonist muscles. Despite the successful recording of many low-threshold MUs during agonist contractions, we recorded no antagonist MUs in most participants. Of the units recorded, only ∼60% matched those recruited at <10% of maximal torque when the muscle acted as an agonist, which suggests a modified recruitment order for antagonist MUs.

Electrical stimulation for investigating and improving neuromuscular function in vivo: Historical perspective and major advances.

This historical review summarizes the major advances - particularly from the last 50 years - in transcutaneous motor-level electrical stimulation, which can be used either as a tool to investigate neuromuscular function and its determinants (electrical stimulation for testing; EST) or as a therapeutic/training modality to improve neuromuscular and physical function (neuromuscular electrical stimulation; NMES). We focus on some of the most important applications of electrical stimulation in research and clinical settings, such as the investigation of acute changes, chronic adaptations and pathological alterations of neuromuscular function with EST, as well as the enhancement, preservation and restoration of muscle strength and mass with NMES treatment programs in various populations. For both EST and NMES, several major advances converge around understanding and optimizing motor unit recruitment during electrically-evoked contractions, also taking into account the influence of stimulation site (e.g., muscle belly vs nerve trunk) and type (e.g., pulse duration, frequency, and intensity). This information is equally important both in the context of mechanistic research of neuromuscular function as well as for clinicians who believe that improvements in neuromuscular function are required to provide health-related benefits to their patients.

Lower-limb resistance training reduces exertional dyspnea and intrinsic neuromuscular fatigability in individuals with chronic obstructive pulmonary disease.

Skeletal muscle atrophy, dysfunction, and fatigue are important complications of chronic obstructive pulmonary disease (COPD). Greater reliance on glycolytic metabolism and increased type III/IV muscle afferent activity increase ventilatory drive, promote ventilatory constraint, amplify exertional dyspnea, and limit exercise tolerance. To investigate whether muscular adaptation with resistance training (RT) could improve exertional dyspnea, exercise tolerance, and intrinsic neuromuscular fatigability in individuals with COPD (n = 14, FEV1 = 62 ± 21% predicted), we performed a proof-of-concept single-arm efficacy study utilizing 4 wk of individualized lower-limb RT (3 times/wk). At baseline, dyspnea (Borg scale), ventilatory parameters, lung volumes (inspiratory capacity maneuvers), and exercise time were measured during a constant-load test (CLT) at 75% maximal workload to symptom limitation. On a separate day, fatigability was assessed using 3 min of intermittent stimulation of the quadriceps (initial output of ∼25% maximal voluntary force). Following RT, the CLT and fatigue protocols were repeated. Compared with baseline, isotime dyspnea was reduced (5.9 ± 2.4 vs. 4.5 ± 2.4 Borg units, P = 0.02) and exercise time increased (437 ± 405 s vs. 606 ± 447 s, P < 0.01) following RT. Isotime tidal volume increased (P = 0.01), whereas end-expiratory lung volumes (P = 0.02) and heart rate (P = 0.03) decreased. Quadriceps force, relative to initial force, was higher at the end of the stimulation protocol posttraining (53.2 ± 9.1 vs. 46.8 ± 11.9%, P = 0.04). This study provides evidence that 4 wk of RT attenuates exertional dyspnea and improves exercise tolerance in individuals with COPD, which in part, is likely due to delayed ventilatory constraint and reduced intrinsic fatigability. A pulmonary rehabilitation program beginning with individualized lower-limb RT may help mitigate dyspnea before performing aerobic training in individuals with COPD.NEW & NOTEWORTHY This study presents the novel finding that 4-wk resistance training (RT) focused specifically on the lower limbs can reduce exertional dyspnea during constant-load cycling, improve exercise tolerance, and reduce intrinsic fatigability of the quadriceps in individuals with COPD.

UBC-Nepal Expedition: Motor Unit Characteristics in Lowlanders Acclimatized to High Altitude and Sherpa.

INTRODUCTION: With acclimatization to high altitude (HA), adaptations occur throughout the nervous system and at the level of the muscle, which may affect motor unit (MU) characteristics. However, despite the importance of MUs as the final common pathway for the control of voluntary movement, little is known about their adaptations with acclimatization. METHODS: Ten lowlanders and Sherpa participated in this study 7 to 14 d after arrival at HA (5050 m), with seven lowlanders repeating the experiment at sea level (SL), 6 months after the expedition. The maximal compound muscle action potential (M max ) was recorded from relaxed biceps brachii. During isometric elbow flexions at 10% of maximal torque, a needle electrode recorded the MU discharge rate (MUDR) and MU potential (MUP) characteristics of single biceps brachii MUs. RESULTS: Compared with SL, acclimatized lowlanders had ~10% greater MUDR, ~11% longer MUP duration, as well as ~18% lower amplitude and ~6% greater duration of the first phase of the M max (all P < 0.05). No differences were noted between SL and HA for variables related to MUP shape (e.g., jitter, jiggle; P > 0.08). Apart from lower near-fiber MUP area for Sherpa than acclimatized lowlanders ( P < 0.05), no M max or MU data were different between groups ( P > 0.10). CONCLUSIONS: Like other components of the body, MUs in lowlanders adapt with acclimatization to HA. The absence of differences between acclimatized lowlanders and Sherpa suggests that evolutionary adaptations to HA are smaller for MUs than components of the cardiovascular or respiratory systems.

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.

Critical considerations of the contribution of the corticomotoneuronal pathway to central fatigue.

Neural drive originating in higher brain areas reaches exercising limb muscles through the corticospinal-motoneuronal pathway, which links the motor cortex and spinal motoneurones. The properties of this pathway have frequently been observed to change during fatiguing exercise in ways that could influence the development of central fatigue (i.e. the progressive reduction in voluntary muscle activation). However, based on differences in motor cortical and motoneuronal excitability between exercise modalities (e.g. single-joint vs. locomotor exercise), there is no characteristic response that allows for a categorical conclusion about the effect of these changes on functional impairments and performance limitations. Despite the lack of uniformity in findings during fatigue, there is strong evidence for marked 'inhibition' of motoneurones as a direct result of voluntary drive. Endogenous forms of neuromodulation, such as via serotonin released from neurones, can directly affect motoneuronal output and central fatigue. Exogenous forms of neuromodulation, such as brain stimulation, may achieve a similar effect, although the evidence is weak. Non-invasive transcranial direct current stimulation can cause transient or long-lasting changes in cortical excitability; however, variable results across studies cast doubt on its claimed capacity to enhance performance. Furthermore, with these studies, it is difficult to establish a cause-and-effect relationship between brain responsiveness and exercise performance. This review briefly summarizes changes in the corticomotoneuronal pathway during various types of exercise, and considers the relevance of these changes for the development of central fatigue, as well as the potential of non-invasive brain stimulation to enhance motor cortical excitability, motoneuronal output and, ultimately, exercise performance.

Cognition and brain iron deposition in whole grey matter regions and hippocampal subfields.

Regional brain iron accumulation is observed in many neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease, and is associated with cognitive decline. We explored associations between age, cognition and iron content in grey matter regions and hippocampal subfields in 380 participants of the Aberdeen children of the 1950s cohort and their first-generation relatives (aged 26-72 years). Participants underwent cognitive assessment at the time of MRI scanning. Quantitative susceptibility mapping of these MRI data was used to assess iron content in grey matter regions and in hippocampal subfields. Principle component analysis was performed on cognitive test scores to create a general cognition score. Spline analysis was used with the Akaike information criterion to determine if order 1, 2 or 3 natural splines were optimal for assessing non-linear relationships between regional iron and age. Multivariate linear models were used to assess associations between regional iron and cognition. Higher iron correlated with older age in the left putamen across all ages and in the right putamen of only participants over 58. Whereas a decrease in iron with older age was observed in the right thalamus and left pallidum across all ages. Right amygdala iron levels were associated with poorer general cognition scores and poorer immediate recall scores. Iron was not associated with any measures of cognitive performance in other regions of interest. Our results suggest that, whilst iron in some regions was associated with cognitive performance, there is an overall lack of association between regional iron content and cognitive ability in cognitively healthy individuals.

Age-related performance fatigability: a comprehensive review of dynamic tasks.

Adult aging is associated with a myriad of changes within the neuromuscular system, leading to reductions in contractile function of old adults. One of the consequences of these age-related neuromuscular adaptations is altered performance fatigability, which can limit the ability of old adults to perform activities of daily living. Whereas age-related fatigability during isometric tasks has been well characterized, considerably less is known about fatigability of old adults during dynamic tasks involving movement about a joint, which provides a more functionally relevant task compared with static contractions. This review provides a comprehensive summary of age-related fatigability during dynamic contractions, where the importance of task specificity is highlighted with a brief discussion of the potential mechanisms responsible for differences in fatigability between young and old adults. The angular velocity of the task is critical for evaluating age-related fatigability, as tasks that constrain angular velocity (i.e., isokinetic) produce equivocal age-related differences in fatigability, whereas tasks involving unconstrained velocity (i.e., isotonic-like) consistently induce greater fatigability for old compared with young adults. These unconstrained velocity tasks, which are more closely associated with natural movements, offer an excellent model to uncover the underlying age-related mechanisms of increased fatigability. Future work evaluating the mechanisms of increased age-related fatigability during dynamic tasks should be evaluated using contraction modes that are specific to the task (i.e., dynamic), rather than isometric, particularly for the assessment of spinal and supra spinal components. Advancing our understanding of age-related fatigability is likely to yield novel insights and approaches for improving mobility limitations in old adults.

Post-fatigue ability to activate muscle is compromised across a wide range of torques during acute hypoxic exposure.

The purpose of this study was to assess how severe acute hypoxia alters the neural mechanisms of muscle activation across a wide range of torque output in a fatigued muscle. Torque and electromyography responses to transcranial and motor nerve stimulation were collected from 10 participants (27 years ± 5 years, 1 female) following repeated performance of a sustained maximal voluntary contraction that reduced torque to 60% of the pre-fatigue peak torque. Contractions were performed after 2 h of hypoxic exposure and during a sham intervention. For hypoxia, peripheral blood oxygen saturation was titrated to 80% over a 15-min period and remained at 80% for 2 h. Maximal voluntary torque, electromyography root mean square, voluntary activation and corticospinal excitability (motor evoked potential area) and inhibition (silent period duration) were then assessed at 100%, 90%, 80%, 70%, 50% and 25% of the target force corresponding to the fatigued maximal voluntary contraction. No hypoxia-related effects were identified for voluntary activation elicited during motor nerve stimulation. However, during measurements elicited at the level of the motor cortex, voluntary activation was reduced at each torque output considered (P = .002, ηp 2  = .829). Hypoxia did not impact the correlative linear relationship between cortical voluntary activation and contraction intensity or the correlative curvilinear relationship between motor nerve voluntary activation and contraction intensity. No other hypoxia-related effects were identified for other neuromuscular variables. Acute severe hypoxia significantly impairs the ability of the motor cortex to voluntarily activate fatigued muscle across a wide range of torque output.

Sexual dimorphism in the relationship between brain complexity, volume and general intelligence (g): a cross-cohort study.

Changes in brain morphology have been reported during development, ageing and in relation to different pathologies. Brain morphology described by the shape complexity of gyri and sulci can be captured and quantified using fractal dimension (FD). This measure of brain structural complexity, as well as brain volume, are associated with intelligence, but less is known about the sexual dimorphism of these relationships. In this paper, sex differences in the relationship between brain structural complexity and general intelligence (g) in two diverse geographic and cultural populations (UK and Indian) are investigated. 3D T1-weighted magnetic resonance imaging (MRI) data and a battery of cognitive tests were acquired from participants belonging to three different cohorts: Mysore Parthenon Cohort (MPC); Aberdeen Children of the 1950s (ACONF) and UK Biobank. We computed MRI derived structural brain complexity and g estimated from a battery of cognitive tests for each group. Brain complexity and volume were both positively corelated with intelligence, with the correlations being significant in women but not always in men. This relationship is seen across populations of differing ages and geographical locations and improves understanding of neurobiological sex-differences.

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.

Volleyball Competition on Consecutive Days Modifies Jump Kinetics but Not Height.

PURPOSE: In volleyball, jump execution is critical for the match outcome. Game-play-related neuromuscular impairments may manifest as decreased jump height (JH) or increased jump total duration, both of which are pivotal for performance. To investigate changes in JH and kinetics with game play, the authors conducted a prospective exploratory analysis using minimal-effect testing (MET) and equivalence testing with the 2 one-sided tests procedure, univariate, and bivariate functional principal component analysis, respectively. METHODS: Twelve male varsity athletes completed 3-set matches on 2 consecutive days. Countermovement jumps were performed on a force platform immediately prematch and postmatch on days 1 and 2 and once on days 3 and 4. RESULTS: Across sessions, JH was equivalent (P < .022, equivalence test), while total duration reported inconclusive changes (P > .227). After match 2, MET indicated that relative force at zero velocity (P = .036) decreased, while braking duration (P = .040) and time to peak force (P = .048) increased compared with baseline. With the first and second functional principal components, these alterations, together with decreased relative braking rate of force development (P = .092), were already evident after match 1. On day 4, MET indicated that relative peak force (P = .049), relative force at zero velocity (P = .023), and relative braking rate of force development (P = .021) decreased, whereas braking duration (P = .025) increased from baseline. CONCLUSIONS: Impairments in jump kinetics were evident from variables related to the countermovement-jump braking phase, while JH was equivalent. In addition to these experimental findings, the present research provides information for the choice of sample size and smallest effect size of interest when using MET and 1- and 2-dimensional analyses for countermovement-jump height and kinetics.