Impaired Neural Activity Research Articles

Mechanisms For The Age-related Loss In Power Of The Knee Extensors In Men And Women

The mechanisms for the loss in limb muscle power output in old (60-79 years) and very old adults (≥80 years) and whether these mechanisms differ between older men and women are not well-understood. PURPOSE: Compare peak power output of the knee extensor muscles between young, old, and very old adults and determine the physiological mechanisms for the age-related loss of power in men compared with women. METHODS: 31 young (22.9 ± 3.0 years, 16 men), 83 old (70.4 ± 4.9 years, 44 men), and 16 very old adults (85.8 ± 4.2 years, 7 men) performed maximal isokinetic contractions at 15 different velocities (0 - 450°/s) to identify peak power output across the torque-velocity relationship. Voluntary activation (VA) and contractile properties were assessed with transcranial magnetic stimulation and electrical stimulation of the femoral nerve. RESULTS: Old and very old men and women generated less power than young across all velocities (p < 0.01). Compared with young men (673 ± 41 W), peak power output was ~42% lower in old (399 ± 18 W, p < 0.01) and ~ 67% lower in very old (225 ± 19 W, p < 0.01). For women, peak power output was ~49% lower in old (223 ± 9 W, p < 0.01) and ~ 60% lower in very old (170 ± 15 W) compared with young (428 ± 20 W, p < 0.01). This corresponded with an age-related loss in peak power output of ~6.5 W/year for men (R2 = 0.62, p < 0.01) and ~ 4.2 W/year for women (R2 = 0.77, p < 0.01). Factors within the muscle were the most closely associated variables with peak power for both sexes including; thigh lean tissue mass (men: R2 = 0.53, p < 0.01; women: R2 = 0.34, p < 0.01), potentiated twitch amplitude (men: R2 = 0.60, p < 0.01; women: R2 = 0.55, p < 0.01), and rate of torque development of the potentiated twitch (men: R2 = 0.60, p < 0.01; women: R2 = 0.48, p < 0.01). In contrast, VA was weakly associated with peak power output for women (R2 = 0.13, p = 0.01) but not for men (R2 = 0.03, p = 0.18), and muscle activation (relative EMG amplitude) of the vastus lateralis during the maximal power contraction was not associated with peak power output for either men (R2 = 0.01, p = 0.35) or women (R2 = 0.04, p = 0.11). CONCLUSION: These data suggest that the age-related loss in power of the knee extensor muscles is due primarily to factors within the muscle for both men and women, and that impaired neural activation may play a minor role in the loss in power output for women.

P495. Using Excitation/Inhibition Ratio to Optimize the Classification of Autism Spectrum Disorder and Schizophrenia

Significant genotypic and phenotypic overlap between Autism Spectrum Disorder (ASD) and Schizophrenia (SZ) has been widely documented. Overlap in impaired neural activity, including in excitation/inhibition (E/I) ratio, has also been suggested. Nevertheless, direct comparisons are scarce, which can hinder accurate diagnosis. We used machine learning approaches to assess the potential for differential diagnosis of the E/I ratio, with and without phenotypic measures.

Physical activity, motor performance and skill learning: a focus on primary motor cortex in healthy aging.

Participation in physical activity benefits brain health and function. Cognitive function generally demonstrates a noticeable effect of physical activity, but much less is known about areas responsible for controlling movement, such as primary motor cortex (M1). While more physical activity may support M1 plasticity in older adults, the neural mechanisms underlying this beneficial effect remain poorly understood. Aging is inevitably accompanied by diminished motor performance, and the extent of plasticity may also be less in older adults compared with young. Motor complications with aging may, perhaps unsurprisingly, contribute to reduced physical activity in older adults. While the development of non-invasive brain stimulation techniques have identified that human M1 is a crucial site for learning motor skills and recovery of motor function after injury, a considerable lack of knowledge remains about how physical activity impacts M1 with healthy aging. Reducing impaired neural activity in older adults may have important implications after neurological insult, such as stroke, which is more common with advancing age. Therefore, a better understanding about the effects of physical activity on M1 processes and motor learning in older adults may promote healthy aging, but also allow us to facilitate recovery of motor function after neurological injury. This article will initially provide a brief overview of the neurophysiology of M1 in the context of learning motor skills, with a focus on healthy aging in humans. This information will then be proceeded by a more detailed assessment that focuses on whether physical activity benefits motor function and human M1 processes.

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.

Dose-dependent sensorimotor impairment in human ocular tracking after acute low-dose alcohol administration.

Key points Oculomotor behaviours are commonly used to evaluate sensorimotor disruption due to ethanol (EtOH).The current study demonstrates the dose‐dependent impairment in oculomotor and ocular behaviours across a range of ultra‐low BACs (<0.035%).Processing of target speed and direction, as well as pursuit eye movements, are significantly impaired at 0.015% BAC, suggesting impaired neural activity within brain regions associated with the visual processing of motion.Catch‐up saccades during steady visual tracking of the moving target compensate for the reduced vigour of smooth eye movements that occurs with the ingestion of low‐dose alcohol.Saccade dynamics start to become ‘sluggish’ at as low as 0.035% BAC.Pupillary light responses appear unaffected at BAC levels up to 0.065%. Changes in oculomotor behaviours are often used as metrics of sensorimotor disruption due to ethanol (EtOH); however, previous studies have focused on deficits at blood‐alcohol concentrations (BACs) above about 0.04%. We investigated the dose dependence of the impairment in oculomotor and ocular behaviours caused by EtOH administration across a range of ultra‐low BACs (≤0.035%). We took repeated measures of oculomotor and ocular performance from sixteen participants, both pre‐ and post‐EtOH administration. To assess the neurological impacts across a wide range of brain areas and pathways, our protocol measured 21 largely independent performance metrics extracted from a range of behavioural responses ranging from ocular tracking of radial step‐ramp stimuli, to eccentric gaze holding, to pupillary responses evoked by light flashes. Our results show significant impairment of pursuit and visual motion processing at 0.015% BAC, reflecting degraded neural processing within extrastriate cortical pathways. However, catch‐up saccades largely compensate for the tracking displacement shortfall caused by low pursuit gain, although there still is significant residual retinal slip and thus degraded dynamic acuity. Furthermore, although saccades are more frequent, their dynamics are more sluggish (i.e. show lower peak velocities) starting at BAC levels as low as 0.035%. Small effects in eccentric gaze holding and no effect in pupillary response dynamics were observed at levels below 0.07%, showing the higher sensitivity of the pursuit response to very low levels of blood alcohol, under the conditions of our study.

Microplastic accumulation via trophic transfer: Can a predatory crab counter the adverse effects of microplastics by body defence?

Microplastics are considered detrimental to aquatic organisms due to their potential accumulation along food chains. Thus, it is puzzling why some of them appear unaffected by microplastics. Here, we assessed the contribution of water filtration and food consumption to microplastic accumulation in a predatory marine crab (Charybdis japonica) and examined the associated impacts of microplastics (particle size: 5 μm) following ingestion for one week. Results showed that water filtration and food consumption contributed similarly to the accumulation of microplastics, which were distributed among organs in this order: hepatopancreas > guts > gills > muscles. Yet, biomagnification (i.e. accumulation through consumption of microplastic-contaminated mussels) did not occur possibly due to egestion of microplastics. The crabs upregulated detoxification capacity (EROD) and antioxidant defence (GST) in response to the microplastics accumulated in their tissues. However, these defence mechanisms collapsed when the microplastic concentration in hepatopancreas exceeded ~3 mg g−1, leading to severe hepatic injury (elevated AST and ALT) and impaired neural activity (reduced AChE). Our results suggest that marine organisms have an innate capacity to counter the acute effects of microplastics, but there is a limit beyond which the defence mechanisms fail and hence physiological functions are impaired. As microplastic pollution will deteriorate in the future, the fitness and survival of marine organisms may be undermined by microplastics, affecting the stability and functioning of marine ecosystems.

Metformin Enhances Antidepressant/Antipsychotic Combination Therapy of Schizophrenia With Comorbid Depression in a Murine Model.

Comorbid depressive disorders confound the diagnosis and therapy of schizophrenia. Using a murine model incorporating both MK801 and chronic unpredictable mild stress exposures, we successfully replicated both psychosis and depression. Ex vivo patch clamp recordings and in vivo calcium imaging demonstrated impaired neural activity in the prefrontal cortex (PFC). We then administered triple-drug combinations consisting of two antidepressants (mirtazapine and venlafaxine) plus an antipsychotic (either clozapine or olanzapine), and found improved PFC neuronal activity and performance in behavioral assays. Moreover, the addition of metformin to both psychotropic drug combinations brought further improvements in depressive and schizophrenic-like behaviors and physiological parameters. In summary, our data modeled the neuropathophysiology of schizophrenia with comorbid depression, and may inform drug intervention strategies.

Exposure to valproic acid during middle to late-stage corticogenesis induces learning and social behavioral abnormalities with attention deficit/hyperactivity in adult mice.

Single prenatal exposure to valproic acid (VPA) in rodents is a widely used preclinical model of autism spectrum disorder (ASD). Continuous prenatal VPA exposure has been recently proposed as a new ASD model that closely captures the neuropathological features of ASD, including increases in cerebral cortex volume and the number of cortical upper layer neurons. We investigated the influence of prenatal VPA exposure on the behavior of adult offspring of pregnant dams that received intraperitoneal injections of VPA twice on one day during the genesis of cortical upper layer neurons. Mice exposed to VPA at E14 (E14-VPA) showed typical behavior abnormalities including reduced social interaction, hyperactivity, and poor maze learning due to attention deficit/impulsivity relative to healthy controls. Histological analysis revealed that E14-VPA mice had significantly increased neuronal density and impaired neural activity in the prefrontal cortex, but not the somatosensory area, which is likely linked to the observed abnormalities in social behavior. These results suggest that this VPA exposure method is a good model for gaining new insights into the underlying neuropathology of ASD.

Slow-gamma frequencies are optimally guarded against effects of neurodegenerative diseases and traumatic brain injuries.

We introduce a computational model for the cellular level effects of firing rate filtering due to the major forms of neuronal injury, including demyelination and axonal swellings. Based upon experimental and computational observations, we posit simple phenomenological input/output rules describing spike train distortions and demonstrate that slow-gamma frequencies in the 38-41 Hz range emerge as the most robust to injury. Our signal-processing model allows us to derive firing rate filters at the cellular level for impaired neural activity with minimal assumptions. Specifically, we model eight experimentally observed spike train transformations by discrete-time filters, including those associated with increasing refractoriness and intermittent blockage. Continuous counterparts for the filters are also obtained by approximating neuronal firing rates from spike trains convolved with causal and Gaussian kernels. The proposed signal processing framework, which is robust to model parameter calibration, is an abstraction of the major cellular-level pathologies associated with neurodegenerative diseases and traumatic brain injuries that affect spike train propagation and impair neuronal network functionality. Our filters are well aligned with the spectrum of dynamic memory fields including working memory, visual consciousness, and other higher cognitive functions that operate in a frequency band that is - at a single cell level - optimally guarded against common types of pathological effects. In contrast, higher-frequency neural encoding, such as is observed with short-term memory, are susceptible to neurodegeneration and injury.

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.

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.

Intact neural activity during a Go/No-go task is associated with high global functioning in schizophrenia.

Go/No-go derived event-related potential (ERP) signals have been widely used in schizophrenia research to monitor self-control deficits in this disorder. However, no study to date has associated Go/No-go-related ERP with global functioning. Participants consisted of 21 patients with schizophrenia and 22 healthy controls. We used a visual Go/No-go paradigm to measure Go/No-go-related N2/P3 ERP components by means of a 64-electrode cap for electroencephalogram recording. We used the Global Assessment of Functioning to evaluate global functioning and analyzed the correlation between ERP indices and global functioning scores. N2 amplitudes were reduced in patients with schizophrenia, but not influenced by either of the Go/No-go conditions. P3 amplitudes were influenced by the Go/No-go conditions, but not reduced in patients with schizophrenia. Global functioning was correlated with the No-go P3 amplitudes, but not N2 amplitudes, in patients with schizophrenia. These results indicate that global functioning is associated with intact neural activity rather than impaired neural activity during Go/No-go response inhibition tasks in patients with schizophrenia.

Rumination in major depressive disorder is associated with impaired neural activation during conflict monitoring.

Individuals with major depressive disorder (MDD) often ruminate about past experiences, especially those with negative content. These repetitive thoughts may interfere with cognitive processes related to attention and conflict monitoring. However, the temporal nature of these processes as reflected in event-related potentials (ERPs) has not been well-described. We examined behavioral and ERP indices of conflict monitoring during a modified flanker task and the allocation of attention during an attentional blink (AB) task in 33 individuals with MDD and 36 healthy controls, and whether their behavioral performance and ERPs varied with level of rumination. N2 amplitude elicited by the flanker task was significantly reduced in participants with MDD compared to healthy controls. Level of self-reported rumination was also correlated with N2 amplitude. In contrast, P3 amplitude during the AB task was not significantly different between groups, nor was it correlated with rumination. No significant differences were found in behavioral task performance measures between groups or by rumination levels. These findings suggest that rumination in MDD is associated with select deficits in cognitive control, particularly related to conflict monitoring.

Event-related theta synchronization predicts deficit in facial affect recognition in schizophrenia.

Growing evidence suggests that abnormalities in the synchronized oscillatory activity of neurons in schizophrenia may lead to impaired neural activation and temporal coding and thus lead to neurocognitive dysfunctions, such as deficits in facial affect recognition. To gain an insight into the neurobiological processes linked to facial affect recognition, we investigated both induced and evoked oscillatory activity by calculating the Event Related Spectral Perturbation (ERSP) and the Inter Trial Coherence (ITC) during facial affect recognition. Fearful and neutral faces as well as nonface patches were presented to 24 patients with schizophrenia and 24 matched healthy controls while EEG was recorded. The participants' task was to recognize facial expressions. Because previous findings with healthy controls showed that facial feature decoding was associated primarily with oscillatory activity in the theta band, we analyzed ERSP and ITC in this frequency band in the time interval of 140-200 ms, which corresponds to the N170 component. Event-related theta activity and phase-locking to facial expressions, but not to nonface patches, predicted emotion recognition performance in both controls and patients. Event-related changes in theta amplitude and phase-locking were found to be significantly weaker in patients compared with healthy controls, which is in line with previous investigations showing decreased neural synchronization in the low frequency bands in patients with schizophrenia. Neural synchrony is thought to underlie distributed information processing. Our results indicate a less effective functioning in the recognition process of facial features, which may contribute to a less effective social cognition in schizophrenia.

Muscle size, activation, and coactivation in adults with cerebral palsy

Muscle weakness is present in the paretic limbs of individuals with cerebral palsy (CP). We aimed to determine what neuromuscular factors contribute to weakness in adults with CP during isometric maximal voluntary contractions (iMVCs). Gastrocnemius anatomical cross-sectional area (ACSA) and agonist and antagonist activation were measured in 11 CP and 11 control adult men during plantarflexion iMVC. Plantarflexion iMVC torque of the paretic leg was 42% and 52% less than in the non-paretic and control limbs, respectively. The paretic gastrocnemius ACSA was smaller than in the control group only. Paretic agonist activation was less than the non-paretic and control groups, whereas antagonist coactivation was higher. Multiple regression analysis revealed muscle activation accounted for 57% of variation in paretic plantarflexion iMVC torque. In individuals with CP, muscle weakness in the paretic limb is attributed primarily to impaired neural activation and, to a lesser degree, ACSA.

Individuals With Total Knee Arthroplasty Demonstrate Altered Anticipatory Postural Adjustments Compared With Healthy Control Subjects

Persons with total knee arthroplasty (TKA) have many impairments that may compromise postural control. Most work examining postural control following TKA has focused on static and reactive postural control. The purpose of this study was to (1) compare anticipatory postural adjustments (APAs) between individuals with TKA and healthy controls; and (2) identify possible pre- to postoperative changes in APAs in those undergoing TKA. Ten individuals planning TKA and 10 healthy age- and sex-matched controls were recruited. During a standing reaching task, lower extremity muscle activity was measured using electromyography (EMG) onsets and normalized EMG amplitudes, and center of pressure (COP) excursion was measured via a force platform. Other outcome measures included isometric strength of the knee flexors and extensors. Individuals in the TKA group were tested preoperatively, and at 3 and 6 months postoperatively. Controls were also measured 3 times over 6 months. There were no pre- to postoperative differences in lower extremity EMG onsets, normalized EMG amplitudes, or COP excursion in those with TKA. When compared to controls, individuals with TKA demonstrated lower EMG amplitudes of the vastus lateralis and biceps femoris, whereas EMG onsets and COP excursion did not differ. Individuals with TKA demonstrated lower knee extension torque. It seems that the surgery itself did not alter APAs among individuals with TKA. Potential contributors to the differences in EMG amplitudes in those with TKA compared to controls, such as impaired neural activation or efforts to reduce stress on the involved knee joint, need further investigation.

Intrinsic Properties of the Knee Extensor Muscles After Subacute Stroke

Horstman AM, Gerrits KH, Beltman MJ, Koppe PA, Janssen, TW, de Haan A. Intrinsic properties of the knee extensor muscles after subacute stroke. Objective To characterize muscle properties of paretic lower-limb (PL) and nonparetic lower-limb (NL) knee extensors in patients with subacute stroke. Design Case-control study. Setting Rehabilitation center research laboratory. Participants Patients with subacute stroke (n=14) and able-bodied age-matched control subjects (n=12). Interventions Not applicable. Main Outcome Measures Half relaxation times (HRTs) and maximal rates of torque development (MRTDs) were assessed as indicators of contractile speed using both voluntary and electrically evoked contractions. Moreover, changes in torque were measured during a fatigue protocol (35 electrically evoked intermittent contractions; 1.5s on, 2s off) and recovery. Results No differences among groups were found for normalized MRTDs during electrically evoked contractions ( P=.117). However, during voluntary contractions both PLs (53% of control, P=.022) and NL (71% of control, P<.001) had significantly lower MRTD compared with control. Both PL (134% of control, P=.001) and NL (123% of control, P=.032) had significantly higher HRTs than control, indicating muscle slowing in patients with subacute stroke. PLs fatigued more and faster than control ( P=.011) and both PL and NL recovered slower ( P<.001). Conclusions The changes in HRTs and fatigue suggest adaptations in muscle properties toward slower, more fatigable muscle shortly after stroke. The inability to make use of contractile speed because of impaired neural activation seems the most limiting factor during the initial phase of torque development in PL. Thus, besides strengthening, muscle endurance and speed should also be addressed during rehabilitation.

Parkinson Phenotype in Aged PINK1-Deficient Mice Is Accompanied by Progressive Mitochondrial Dysfunction in Absence of Neurodegeneration

BackgroundParkinson's disease (PD) is an adult-onset movement disorder of largely unknown etiology. We have previously shown that loss-of-function mutations of the mitochondrial protein kinase PINK1 (PTEN induced putative kinase 1) cause the recessive PARK6 variant of PD.Methodology/Principal FindingsNow we generated a PINK1 deficient mouse and observed several novel phenotypes: A progressive reduction of weight and of locomotor activity selectively for spontaneous movements occurred at old age. As in PD, abnormal dopamine levels in the aged nigrostriatal projection accompanied the reduced movements. Possibly in line with the PARK6 syndrome but in contrast to sporadic PD, a reduced lifespan, dysfunction of brainstem and sympathetic nerves, visible aggregates of α-synuclein within Lewy bodies or nigrostriatal neurodegeneration were not present in aged PINK1-deficient mice. However, we demonstrate PINK1 mutant mice to exhibit a progressive reduction in mitochondrial preprotein import correlating with defects of core mitochondrial functions like ATP-generation and respiration. In contrast to the strong effect of PINK1 on mitochondrial dynamics in Drosophila melanogaster and in spite of reduced expression of fission factor Mtp18, we show reduced fission and increased aggregation of mitochondria only under stress in PINK1-deficient mouse neurons.ConclusionThus, aging Pink1−/− mice show increasing mitochondrial dysfunction resulting in impaired neural activity similar to PD, in absence of overt neuronal death.

Muscle function of knee extensors and flexors after stroke is selectively impaired at shorter muscle lengths

To investigate whether muscle strength is selectively more affected at shorter lengths of thigh muscles as result of stroke and to determine whether this is associated with impaired neural activation at shorter muscle lengths. Case-control study. Fourteen patients with sub-acute stroke, and 12 able-bodied controls. In patients (bilaterally) and able-bodied controls torque and activation was measured during maximal voluntary isometric contractions of knee extensors and flexors at 30 degrees , 60 degrees and 90 degrees knee flexion. The paretic knee extensors showed lower normalized maximal torques (73%) and lower normalized activation (71%) compared with control at 30 degrees . The paretic knee flexors showed lower normalized maximal torques at 60 degrees (64%) and 90 degrees (45%) with non-significantly lower normalized activation (~79% and ~67%, respectively). As a result of stroke, lower muscle torque at shorter muscle lengths of the knee extensors is associated with a length-dependent lower voluntary activation, which may also be the case for the flexor muscles, but not with altered co-activation. We recommend investigating the role of specific training of paretic knee extensors and flexors in especially shortened positions to improve recovery of function after stroke.

Acute passive stretching alters the mechanical but not the electrical properties of calf muscles in humans

An acute bout of passive muscle stretching has been shown to diminish maximal force and power output. Two mechanisms have been suggested to explain these findings: a mechanical alteration in the stretched muscle and an impaired neural activation. The aim of the study was to evaluate the stretching-induced changes in the electrical and mechanical properties of the muscle fibres during maximal electrically elicited contractions of the calf muscles. Twelve subjects (age 22±1 years; body mass 75±2 kg; stature 179±2 cm) underwent 6 single twitch electrical stimulations at maximal intensity before and after passive stretching. During contractions, EMG and mechanomyogram (MMG) were simultaneously recorded from the belly of the gastrocnemius muscle, together with the force signal. From the analysis of the 3 signals, after stretching it resulted that: i) the force peak, time-to-peak and the peak rate of force production significantly decreased by 12.6±2.9%, 3.5±1.0% and 13.6±4.9%, respectively; ii) the MMG peak-to-peak also decreased (−3.6±1.3%; p<0.05), iii) the EMG-force and MMG-force delays increased significantly by 8.7±3.1 and 9.7±3.5%, respectively; and iv) no differences were found in EMG parameters. In conclusion, acute passive stretching affected the mechanical but not the electrical properties of the maximally contracting muscles, suggesting an alteration of the musculotendinous stiffness, an impairment of the muscle force generating capacity but not a depression of muscle activation. The study was supported by MURST n. 5059281.