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The effect of breaking up prolonged sitting on paired associative stimulation-induced plasticity.

ABSTRACT: Paired associative stimulation (PAS) can induce plasticity in the motor cortex, as measured by changes in corticospinal excitability (CSE). This effect is attenuated in older and less active individuals. Although a single bout of exercise enhances PAS-induced plasticity in young, physically inactive adults, it is not yet known if physical activity interventions affect PAS-induced neuroplasticity in middle-aged inactive individuals. Sixteen inactive middle-aged office workers participated in a randomized cross-over design investigating how CSE and short-interval intracortical inhibition (SICI) were affected by PAS preceded by 3 h of sitting (SIT), 3 h of sitting interrupted every 30 min by 3 min of frequent short bouts of physical activity (FPA) and 2.5 h of sitting followed by 25 min of moderate-intensity exercise (EXE). Transcranial magnetic stimulation was applied over the primary motor cortex (M1) of the dominant abductor pollicis brevis to induce recruitment curves before and 5 min and 30 min post-PAS. Linear mixed models were used to compare changes in CSE using time and condition as fixed effects and subjects as random effects. There was a main effect of time on CSE and planned within-condition comparisons showed that CSE was significantly increased from baseline to 5 min and 30 min post-PAS, in the FPA condition, with no significant changes in the SIT or EXE conditions. SICI decreased from baseline to 5 min post-PAS, but this was not related to changes in CSE. Our findings suggest that in middle-aged inactive adults, FPAs may promote corticospinal neuroplasticity. Possible mechanisms are discussed.

SUBMITTER: Bojsen-Moller E

PROVIDER: S-EPMC7541377 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature

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The effect of breaking up prolonged sitting on paired associative stimulation-induced plasticity.

Bojsen-Møller E E Ekblom M M MM Tarassova O O Dunstan D W DW Ekblom O O

Experimental brain research 20200828 11

Paired associative stimulation (PAS) can induce plasticity in the motor cortex, as measured by changes in corticospinal excitability (CSE). This effect is attenuated in older and less active individuals. Although a single bout of exercise enhances PAS-induced plasticity in young, physically inactive adults, it is not yet known if physical activity interventions affect PAS-induced neuroplasticity in middle-aged inactive individuals. Sixteen inactive middle-aged office workers participated in a ra ...[more]

PMID: 32860117

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Project description:OBJECTIVE:To determine whether neurophysiological mechanisms indicating cortical excitability, long-term potentiation (LTP)-like plasticity, GABAergic and glutamatergic function are altered in patients with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis and whether they can be helpful as markers of diagnostic assessment, disease progression, and potentially therapy response. METHODS:Neurophysiological characterizations of patients with NMDAR encephalitis (n = 34, mean age: 28 ± 11 years; 30 females) and age/gender-matched healthy controls (n = 27, 28.5 ± 10 years; 25 females) were performed using transcranial magnetic stimulation-derived protocols including resting motor threshold, recruitment curve, intracortical facilitation, short intracortical inhibition, and cortical silent period. Paired associative stimulation (PAS) was applied to assess LTP-like mechanisms which are mediated through NMDAR. Moreover, resting state functional connectivity was determined using functional magnetic resonance imaging. RESULTS:PAS-induced plasticity differed significantly between groups (P = 0.0056). Cortical excitability, as assessed via motor-evoked potentials after PAS, decreased in patients, whereas it increased in controls indicating malfunctioning of NMDAR in encephalitis patients. Lower PAS-induced plasticity significantly correlated with the modified Rankin Scale (mRS) (r = -0.41; P = 0.0031) and was correlated with lower functional connectivity within the motor network in NMDAR encephalitis patients (P < 0.001, uncorrected). Other neurophysiological parameters were not significantly different between groups. Follow-up assessments were available in six patients and demonstrated parallel improvement of PAS-induced plasticity and mRS. INTERPRETATION:Assessment of PAS-induced plasticity may help to determine NMDAR dysfunction and disease severity in NMDAR encephalitis, and might even aid as a sensitive, noninvasive, and well-tolerated "electrophysiological biomarker" to monitor therapy response in the future. CLINICAL TRIAL REGISTRATION:ClinicalTrials.gov: Identifier: NCT01865578.

Project description:PurposeTo identify predictors of favorable changes to postprandial insulin and glucose levels in response to interrupting prolonged sitting time with standing or light-intensity physical activity.MethodsData were combined from four similarly designed randomized acute cross-over trials (n = 129; body mass index [BMI] range, 19.6-44.6 kg·m; South Asian = 31.0%; dysglycemia = 27.1%). Treatments included: prolonged sitting (6.5 h) or prolonged sitting broken-up with either standing or light-intensity physical activity (5 min every 30 min). Time-averaged postprandial responses for insulin and glucose were calculated for each treatment (mean ± 95% confidence interval). Mutually adjusted interaction terms were used to examine whether anthropometric (BMI), demographic (age, sex, ethnicity [white European vs South Asian]) and a cardiometabolic variable (Homeostatic Model Assessment of Insulin Resistance)-modified responses.ResultsPostprandial insulin and glucose were reduced when individuals interrupted prolonged sitting with bouts of light physical activity, but not with standing. Reductions in time-averaged postprandial insulin were more pronounced if individuals were South Asian compared with white European (-18.9 mU·L [-23.5%] vs -8.2 mU·L [-9.3%]), female compared with male (-15.0 mU·L [-21.2%] vs -12.1 mU·L [-17.6%]) or had a BMI ≥27.2 kg·m (-20.9 mU·L [-22.9%] vs -8.7 mU·L [-18.2%]). Similarly, being female (-0.4 mmol·L [-0.6 mmol·L, -0.2 mmol·L], -6.8% vs -0.1 mmol·L [-0.3 mmol·L, 1 mmol·L], -1.7%) or having a BMI ≥27.2 kg·m (-0.4 mmol·L [-0.6 mmol·L, -0.2 mmol·L], -6.7% vs -0.2 mmol·L [-0.4 mmol·L, 0.0 mmol·L], -3.4%) modified the postprandial glucose response. No significant interactions were found for Homeostatic Model Assessment of Insulin Resistance or age.ConclusionsBeing female, South Asian, or having a higher BMI, all predicted greater reductions in postprandial insulin, whereas being female and having a higher BMI predicted greater reductions in postprandial glucose when sitting was interrupted with light physical activity. These results could help to guide personalized interventions in high-risk participants for whom breaking prolonged sitting time with light activity may yield the greatest therapeutic potential.

Project description:Paired associative stimulation is a relatively new non-invasive brain stimulation technique that combines transcranial magnetic stimulation and peripheral nerve stimulation. The effects of paired associative stimulation on the excitability of the cerebral cortex can vary according to the time interval between the transcranial magnetic stimulation and peripheral nerve stimulation. We established a model of cerebral ischemia in rats via transient middle cerebral artery occlusion. We administered paired associative stimulation with a frequency of 0.05 Hz 90 times over 4 weeks. We then evaluated spatial learning and memory using the Morris water maze. Changes in the cerebral ultra-structure and synaptic plasticity were assessed via transmission electron microscopy and a 64-channel multi-electrode array. We measured mRNA and protein expression levels of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1 in the hippocampus using a real-time polymerase chain reaction and western blot assay. Paired associative stimulation treatment significantly improved learning and memory in rats subjected to cerebral ischemia. The ultra-structures of synapses in the CA1 area of the hippocampus in rats subjected to cerebral ischemia were restored by paired associative stimulation. Long-term potentiation at synapses in the CA3 and CA1 regions of the hippocampus was enhanced as well. The protein and mRNA expression of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1 increased after paired associative stimulation treatment. These data indicate that paired associative stimulation can protect cognition after cerebral ischemia. The observed effect may be mediated by increases in the mRNA and protein expression of brain-derived neurotrophic factor and N-methyl-D-aspartate receptor 1, and by enhanced synaptic plasticity in the CA1 area of the hippocampus. The animal experiments were approved by the Animal Ethics Committee of Tongji Medical College, Huazhong University of Science & Technology, China (approval No. TJ-A20151102) on July 11, 2015.

Project description:To compare the acute effects of uninterrupted sitting with sitting interrupted by brief bouts of light-intensity walking on self-reported fatigue, cognition, neuroendocrine biomarkers and cardiometabolic risk markers in overweight/obese adults.Randomised two-condition crossover trial.Laboratory study conducted in Melbourne, Australia.19 overweight/obese adults (45-75 years).After an initial 2 h period seated, participants consumed a meal-replacement beverage and completed (on 2 days separated by a 6-day washout period) each condition over the next 5 h: uninterrupted sitting (sedentary condition) or sitting with 3 min bouts of light-intensity walking every 30 min (active condition).Self-reported fatigue, executive function and episodic memory at 0 h, 4 h and 7 h.Neuroendocrine biomarkers and cardiometabolic risk markers (blood collections at 0 h, 4 h and 7 h, blood pressure and heart rate measured hourly and interstitial glucose measured using a continuous glucose monitoring system).During the active condition, fatigue levels were lower at 4 h (-13.32 (95% CI -23.48 to -3.16)) and at 7 h (-10.73 (95% CI -20.89 to -0.58)) compared to the sedentary condition. Heart rate was higher at 4 h (4.47 (95% CI 8.37 to 0.58)) and at 7 h (4.32 (95% CI 8.21 to 0.42)) during the active condition compared to the sedentary condition. There were no significant differences between conditions by time for other variables. In the sedentary condition, changes in fatigue scores over time correlated with a decrease in heart rate and plasma dihydroxyphenylalanine (DOPA) and an increase in plasma dihydroxyphenylglycol (DHPG).Interrupting prolonged sitting with light-intensity walking breaks may be an effective fatigue countermeasure acutely. Fatigue levels corresponded with the heart rate and neuroendocrine biomarker changes in uninterrupted sitting in this pilot study. Further research is needed to identify potential implications, particularly for the occupational health context.ACTRN12613000137796; Results.

Project description:Background: Cultural, environmental and logistical factors challenge the Qatari population, particularly females, to engage in physical activity, and there is a high prevalence of diabetes in this population. Sedentary behavior is associated with increased cardiometabolic disease risk and early mortality and breaking up sitting can attenuate postprandial cardiometabolic risk markers. However, no studies have evaluated the cardiometabolic response to breaking up sitting in a Qatari population. Purpose: To examine the effects of breaking up sitting with moderate-intensity walking breaks on cardiometabolic disease markers in Qatari females. Methods: Eleven sedentary (sitting ≥ 7 h/day) females completed two experimental conditions in a cross-over randomized design. The two conditions were identical, except participants either remained seated for 5-h (SIT), or interrupted their sitting every 30-min with a 3-min walk (WALK) on a motorized treadmill (rating of perceived exertion 12-14). A fasting venous blood sample was obtained at baseline (-10-min) followed by samples at 0.5-, 1-, 2-, 3-, 3.5-, 4-, and 5-h. Postprandial cardiometabolic variables (insulin, glucose, triglycerides) were calculated as derivatives of total area under the curve [AUC; total (tAUC), net incremental (iAUC) and positive AUC]. Results: Data is reported as effect size; ±90% confidence limit. There was a most likely "moderate" lower tAUC (-0.92 ± 0.26), iAUC (-0.96 ± 0.33), and positive AUC (-0.96 ± 0.33) for insulin in WALK compared to SIT. Additionally, there was a most likely "moderate" lower tAUC (-0.63 ± 0.37), iAUC (-0.91 ± 0.49), and positive AUC (-0.91 ± 0.49) for triglycerides in WALK compared to SIT. Glucose did not differ between conditions. Conclusion: Breaking up prolonged sitting with moderate-intensity walking offers a culturally compatible intervention to acutely improve cardiometabolic risk markers in sedentary Qatari females. Whilst the data offers promise, the long-term chronic effects of breaking up sitting in Qatari adults requires investigation before population level and/or policy recommendations can be made.

Project description:Previous single-site neurostimulation experiments have unsuccessfully attempted to shift decision-making away from habitual control, a fast, inflexible cognitive strategy, towards goal-directed control, a flexible, though computationally expensive strategy. We employed a dual-target neurostimulation approach in 30 healthy participants, using cortico-cortical paired associative stimulation (ccPAS) to target two key nodes: lateral prefrontal cortex (LPFC) and intraparietal sulcus (IPS), to test whether decision-making can be artificially shifted from habitual toward goal-directed control. Participants received three active stimulations, delivered at least six days apart (each involving 100 paired pulses over the IPS and LPFC, varying the interstimulus interval): two interventional, time-relevant ccPAS (10 msec interval) and one control, non-time-relevant ccPAS (100 msec interval). Following stimulation, participants completed a sequential learning task, measuring goal-directed/habitual control, and a working memory task. IPS→LPFC ccPAS (stimulating IPS, then LPFC with a 10 msec interval) shifted decision-making from habitual toward goal-directed control, compared to control ccPAS. There was no effect of LPFC→IPS ccPAS, nor an effect of any PAS condition on working memory. Previous studies have shown ccPAS effects outside the motor domain targeting prefrontal regions on response inhibition, attentional bias, and alpha asymmetry. The present study measures the behavioural effects of parietal-prefrontal PAS, focusing on a highly complex decision-making task and working memory. If confirmed in larger studies, this would be the first instance of neurostimulation successfully shifting decision-making from habitual to goal-directed control, putatively via inducing long-term potentiation between the IPS and LPFC. However, we found no effect in the other direction (LPFC→IPS ccPAS), and no effect on working memory overall. PAS is a relatively new neuromodulatory technique in the cognitive arsenal, and this study could help guide future approaches in healthy and disordered decision-making.

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The effect of breaking up prolonged sitting on paired associative stimulation-induced plasticity.

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The effect of breaking up prolonged sitting on paired associative stimulation-induced plasticity.

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