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Background: Effective dissemination of research to health and social care practitioners enhances clinical practice and evidence-based care. Social media use has potential to facilitate dissemination to busy practitioners., Objective: This is a protocol for a systematic review that will quantitatively synthesize evidence of the effectiveness of social media, compared with no social media, for dissemination of research evidence to health and social care practitioners. Social media platforms, formats, and sharing mechanisms used for effective dissemination of research evidence will also be identified and compared., Methods: Electronic database searches (MEDLINE, PsycINFO, CINAHL, ERIC, LISTA, and OpenGrey) will be conducted from January 1, 2010, to January 10, 2023, for studies published in English. Randomized, nonrandomized, pre-post study designs or case studies evaluating the effect of social media on dissemination of research evidence to postregistration health and social care practitioners will be included. Studies that do not involve social media or dissemination or those that evaluate dissemination of nonresearch information (eg, multisource educational materials) to students or members of the public only, or without quantitative data on outcomes of interest, will be excluded. Screening will be carried out by 2 independent reviewers. Data extraction and quality assessment, using either the Cochrane tool for assessing risk of bias or the Newcastle-Ottawa Scale, will be completed by 2 independent reviewers. Outcomes of interest will be reported in 4 domains (reach, engagement, dissemination, and impact). Data synthesis will include quantitative comparisons using narrative text, tables, and figures. A meta-analysis of standardized pooled effects will be undertaken, and subgroup analyses will be applied, if appropriate., Results: Searches and screening will be completed by the end of May 2023. Data extraction and analyses will be completed by the end of July 2023, after which findings will be synthesized and reported by the end of October 2023., Conclusions: This systematic review will summarize the evidence for the effectiveness of social media for the dissemination of research evidence to health and social care practitioners. The limitations of the evidence may include multiple outcomes or methodological heterogeneity that limit meta-analyses, potential risk of bias in included studies, and potential publication bias. The limitations of the study design may include potential insensitivity of the electronic database search strategy. The findings from this review will inform the dissemination practice of health and care research., Trial Registration: PROSPERO CRD42022378793; https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=378793., International Registered Report Identifier (irrid): DERR1-10.2196/45684., (©Sarah F Roberts-Lewis, Helen A Baxter, Gill Mein, Sophia Quirke-McFarlane, Fiona J Leggat, Hannah M Garner, Martha Powell, Sarah White, Lindsay Bearne. Originally published in JMIR Research Protocols (https://www.researchprotocols.org), 12.05.2023.)

Introduction: This short article summarises findings about reduced physical activity of adults with progressive muscle disease as a result of COVID-19 lockdown., Methods: As part of an ongoing longitudinal cohort study, we prospectively and objectively measured physical activity using accelerometry at baseline in 2019 and follow-up in 2020. A subset of 85 participants incidentally had follow-up data collected during the first UK COVID-19 lockdown from 23 March to 4 July 2020. Thus, for this cohort we had activity data from before and during the COVID-19 pandemic and we were able to prospectively and accurately quantify the changes in their physical activity., Results: Our data highlighted reduced overall activity intensity and reduced light activity time in particular., Conclusions: From our findings, we can infer specific evidence-based recommendations about how to redress inactivity secondary to COVID-19 restrictions for adults with progressive muscle diseases. These recommendations are likely to be generalisable to other groups who are vulnerable to functional decline secondary to prolonged inactivity., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.)

Background: Inflammatory neuropathies such as Guillain-Barré syndrome, chronic inflammatory demyelinating polyradiculoneuropathy and paraproteinaemic demyelinating neuropathy are a heterogenous group of peripheral nerve disorders that affect around one to two people per 100,000. Whilst treatments such as intravenous immunoglobulin, plasma exchange and corticosteroids have generally positive results, long-term residual symptoms and associated activity limitations are common. There is currently no standardised care for patients with ongoing activity limitation and participation restriction as a result of inflammatory neuropathy IN but data from observational studies and a randomised controlled trial suggest that exercise either alone or as part of a multidisciplinary rehabilitation programme may be beneficial in improving activity limitation. Tailoring the intervention for participants following physiotherapy assessment and incorporating patient preference for type and location of exercise may be important., Methods/design: The current study is a pragmatic, prospective, parallel observer-blind, randomised controlled trial to evaluate the efficacy and cost-effectiveness of a twelve week tailored home exercise programme versus advice and usual care. Seventy adults with stable immune mediated inflammatory neuropathy IN will be recruited to the study from two main sources: patients attending selected specialist peripheral nerve clinics in the South East and West Midlands of England and people with who access the GAIN charity website or newsletter. Participants will be randomised to receive either advice about exercise and usual care or a 12 week tailored home exercise programme. The primary outcome of activity limitation and secondary outcomes of fatigue, quality of life, self-efficacy, illness beliefs, mood and physical activity will be assessed via self-report questionnaire at baseline, 12 weeks and 12 months post intervention. Cost effectiveness and cost utility will be assessed via interview at baseline and 12 months post intervention. Intention to treat analysis will be our primary model for efficacy analysis. Semi-structured interviews will be conducted with a selected sample of participants in order to explore the acceptability of the intervention and factors affecting adherence to the exercise programme., Discussion: This is the first randomised controlled trial to compare the efficacy and cost-effectiveness of tailored home exercise with advice about exercise and usual care for adults with inflammatory neuropathy., Trial Registration: Current Controlled Trials ISRCTN13311697.

Background: Somatosensory stimulation (SS) is a potential adjuvant to stroke rehabilitation, but the effect on function needs further investigation., Objective: To explore the effect of combining SS with task-specific training (TST) on upper limb function and arm use in chronic stroke survivors and determine underlying mechanisms., Methods: In this double-blinded randomized controlled trial (ISRCTN 05542931), 33 patients (mean 37.7 months poststroke) were block randomized to 2 groups: active or sham SS. They received 12 sessions of 2 hours of SS (active or sham) to all 3 upper limb nerves immediately before 30 minutes of TST. The primary outcome was the Action Research Arm Test (ARAT) score. Secondary outcomes were time to perform the ARAT, Fugl-Meyer Assessment score (FM), Motor Activity Log (MAL), and Goal Attainment Scale (GAS). Underlying mechanisms were explored using transcranial magnetic stimulation stimulus-response curves and intracortical inhibition. Outcomes were assessed at baseline, immediately following the intervention (mean 2 days), and 3 and 6 months (mean 96 and 190 days) after the intervention., Results: The active group (n = 16) demonstrated greater improvement in ARAT score and time immediately postintervention (between-group difference; P < .05), but not at 3- or 6-month follow-ups (P > .2). Within-group improvements were seen for both groups for ARAT and GAS, but for the active group only for FM and MAL (P < .05). Corticospinal excitability did not change., Conclusions: Long-lasting improvements in upper limb function were observed following TST. Additional benefit of SS was seen immediately post treatment, but did not persist and the underlying mechanisms remain unclear., (© The Author(s) 2014.)

The objective of this study was to investigate reliability of transcranial magnetic stimulation (TMS) parameters for three coil systems; hand-held circular and figure-of-eight and navigated figure-of-eight coils. Stimulus response curves, intracortical inhibition (SICI) and facilitation (ICF) were studied in the right first dorsal interosseus muscle of 10 healthy adults. Each coil system was tested twice per subject. Navigation was conducted by a custom built system. Cortical excitability showed moderate-to-good reliability for the hand-held and navigated figure-of-eight coils (Intraclass correlation coefficients (ICCs) 0.55-0.89). The circular coil showed poor reliability for motor evoked potential (MEP) amplitude at 120% resting motor threshold (RMT; MEP(120)) and MEP sum (ICCs 0.09 & 0.48). Reliability for SICI was good for all coil systems when an outlier was removed (ICCs 0.87-0.93), but poor for ICF (ICCs < 0.3). The circular coil had a higher MEP(120) than the navigated figure-of-eight coil (p = 0.004). Figure-of-eight coils can be used confidently to investigate cortical excitability over time. ICF should be interpreted with caution. The navigation device frees the experimenter and enables tracking of the position of the coil and subject. The results help guide the choice of coil system for longitudinal measurements of motor cortex function.

Chronic altitude residence improves muscular performance at altitude, but the effect of intermittent altitude exposures (IAE) on muscular performance at altitude has not been defined. The purpose of this study was to determine the effects of 3 wk of IAE, in combination with rest and cycle training, on muscular performance at altitude. Six lowlanders (23 +/- 2 yr, 77 +/- 6 kg; means +/- SE) completed a cycle time trial and adductor pollicis endurance test at sea level and during a 30-h acute exposure to 4,300 m altitude equivalent (barometric pressure = 446 mmHg) once before (pre-IAE) and once after (post-IAE) a 3-wk period of IAE (4 h/day, 5 days/wk, 4,300 m). During each IAE, three subjects cycled for 45-60 min/day at 60%-70% of maximal O2 uptake and three subjects rested. Cycle training during each IAE did not appear to affect muscular performance at altitude. Thus data from all six subjects were combined. Three weeks of IAE resulted in 1) a 21 +/- 6% improvement (P < 0.05) in cycle time-trial performance (min) from pre-IAE (32.8 +/- 3.7) to post-IAE (24.8 +/- 1.2), 2) a 63 +/- 26% improvement (P < 0.05) in adductor pollicis endurance (min) from pre-IAE (9.2 +/- 2.8) to post-IAE (14.8 +/- 4.2), and 3) a 10 +/- 4% increase (P < 0.05) in resting arterial O2 saturation (%) from pre-IAE (82 +/- 2) to post-IAE (90 +/- 1). These improvements in muscular performance after IAE correlated strongly with increases in resting arterial O2 saturation and were comparable to those reported previously after chronic altitude residence. IAE may therefore be used as an alternative to chronic altitude residence to facilitate improvements in muscular performance in athletes, soldiers, mountaineers, shift workers, and others that are deployed to altitude.

Recently, we reported that, at similar voluntary force development during static submaximal intermittent contractions of the adductor pollicis muscle, fatigue developed more slowly in women than in men under conditions of normobaric normoxia (NN) (Acta Physiol Scand 167: 233-239, 1999). We postulated that the slower fatigue of women was due, in part, to a greater capacity for muscle oxidative phosphorylation. The present study examined whether a gender difference in adductor pollicis muscle performance also exists during acute exposure to hypobaric hypoxia (HH; 4,300-m altitude). Healthy young men (n = 12) and women (n = 21) performed repeated static contractions at 50% of maximal voluntary contraction (MVC) force of rested muscle for 5 s followed by 5 s of rest until exhaustion. MVC force was measured before and at the end of each minute of exercise and at exhaustion. Exhaustion was defined as an MVC force decline to 50% of that of rested muscle. For each gender, MVC force of rested muscle in HH was not significantly different from that in NN. MVC force tended to decline at a faster rate in HH than in NN for men but not for women. In both environments, MVC force declined faster (P < 0.01) for men than for women. For men, endurance time to exhaustion was shorter (P < 0.01) in HH than in NN [6.08 +/- 0.7 vs. 8.00 +/- 0.7 (SE) min]. However, for women, endurance time to exhaustion was similar (not significant) in HH (12.86 +/- 1.2 min) and NN (13.95 +/- 1.0 min). In both environments, endurance time to exhaustion was longer for women than for men (P < 0.01). Gender differences in the impact of HH on adductor pollicis muscle endurance persisted in a smaller number of men and women matched (n = 4 pairs) for MVC force of rested muscle and thus on submaximal absolute force and, by inference, ATP demand in both environments. In contrast to gender differences in the impact of HH on small-muscle (adductor pollicis) exercise performance, peak O(2) uptake during large-muscle exercise was lower in HH than in NN by a similar (P > 0.05) percentage for men and women (-27.6 +/- 2 and -25.1 +/- 2%, respectively). Our findings are consistent with the postulate of a higher adductor pollicis muscle oxidative capacity in women than in men and imply that isolated performance of muscle with a higher oxidative capacity may be less impaired when the muscle is exposed to HH.

Using an exercise device that integrates maximal voluntary static contraction (MVC) of knee extensor muscles with dynamic knee extension, we compared progressive muscle fatigue, i.e., rate of decline in force-generating capacity, in normoxia (758 Torr) and hypobaric hypoxia (464 Torr). Eight healthy men performed exhaustive constant work rate knee extension (21 +/- 3 W, 79 +/- 2 and 87 +/- 2% of 1-leg knee extension O2 peak uptake for normoxia and hypobaria, respectively) from knee angles of 90-150 degrees at a rate of 1 Hz. MVC (90 degrees knee angle) was performed before dynamic exercise and during < or = 5-s pauses every 2 min of dynamic exercise. MVC force was 578 +/- 29 N in normoxia and 569 +/- 29 N in hypobaria before exercise and fell, at exhaustion, to similar levels (265 +/- 10 and 284 +/- 20 N for normoxia and hypobaria, respectively; P > 0.05) that were higher (P < 0.01) than peak force of constant work rate knee extension (98 +/- 10 N, 18 +/- 3% of MVC). Time to exhaustion was 56% shorter for hypobaria than for normoxia (19 +/- 5 vs. 43 +/- 7 min, respectively; P < 0.01), and rate of right leg MVC fall was nearly twofold greater for hypobaria than for normoxia (mean slope = -22.3 vs. -11.9 N/min, respectively; P < 0.05). With increasing duration of dynamic exercise for normoxia and hypobaria, integrated electromyographic activity during MVC fell progressively with MVC force, implying attenuated maximal muscle excitation. Exhaustion, per se, was postulated to related more closely to impaired shortening velocity than to failure of force-generating capacity.

Recently, we described a patient with severe exercise intolerance and episodic myoglobinuria, associated with marked impairment of succinate oxidation and deficient activity of succinate dehydrogenase and aconitase in muscle mitochondria (1). We now report additional enzymatic and immunological characterization of mitochondria. In addition to severe deficiency of complex II, manifested by reduction of succinate dehydrogenase and succinate:coenzyme Q oxidoreductase activities to 12 and 22% of normal, respectively, complex III activity was reduced to 37% and rhodanese to 48% of normal. Furthermore, although complex I activity was not measured, immunoblot analysis of complex I showed deficiency of the 39-, 24-, 13-, and 9-kD peptides with lesser reductions of the 51- and 18-kD peptides. Immunoblots of complex III showed markedly reduced levels of the mature Rieske protein in mitochondria and elevated levels of its precursor in the cytosol, suggesting deficient uptake into mitochondria. Immunoreactive aconitase was also low. These data, together with the previous documentation of low amounts of the 30-kD iron-sulfur protein and the 13.5-kD subunit of complex II, compared to near normal levels of the 70-kD protein suggest a more generalized abnormality of the synthesis, import, processing, or assembly of a group of proteins containing iron-sulfur clusters.

Oxidative metabolism is the major source of energy for muscle activity, and maximal oxygen uptake (VO2max), the product of maximal cardiac output and maximal arteriovenous oxygen difference, indicates individual capacity for oxidative metabolism and performance of exercise by the large muscles. Strength, a function of muscle cross-sectional area, motor-unit recruitment, and neuromuscular coordination, is the ability to develop force in a single, brief, maximal-effort voluntary contraction of rested muscle. Weakness is a diminished ability of rested muscle to exert maximal force. Fatigue is a loss of maximal force-generating capacity that develops during muscular activity, likely originates within muscle itself, and persists until muscle is fully recovered. Individual perception of motor effort can be determined with standardized rating scales. These concepts are discussed in detail, their relevance to the pathophysiology of exercise in chronic fatigue syndrome is analyzed, and a general strategy of exercise evaluation pertinent to chronic fatigue syndrome is presented.

Static exercise in normal humans causes reflex increases in muscle sympathetic nerve activity (MSNA) that are closely coupled to the contraction-induced decrease in muscle cell pH, an index of glycogen degradation and glycolytic flux. To determine if sympathetic activation is attenuated when muscle glycogenolysis is blocked due to myophosphorylase deficiency (McArdle's disease), an inborn enzymatic defect localized to skeletal muscle, we now have performed microelectrode recordings of MSNA in four patients with McArdle's disease during static handgrip contraction. A level of static handgrip that more than doubled MSNA in normal humans had no effect on MSNA and caused an attenuated rise in blood pressure in the patients with myophosphorylase deficiency. In contrast, two nonexercise sympathetic stimuli, Valsalva's maneuver and cold pressor stimulation, evoked comparably large increases in MSNA in patients and normals. The principal new conclusion is that defective glycogen degradation in human skeletal muscle is associated with a specific reflex impairment in sympathetic activation during static exercise.

To determine the effect of relative exercise intensity on organ blood volume and its relation to cardiac function, changes in relative blood volume and cardiac function were monitored with radionuclide techniques in 14 healthy volunteers. After labeling the subject's red cells with technetium 99m, we acquired data at rest, zero-load cycling, and at 50%, 75%, and 100% of maximal oxygen uptake. From rest to zero-load cycling, leg blood volume decreased 32 +/- 2% (mean +/- SEM), whereas relative end-diastolic blood volume increased 9.6 +/- 1.2%, and lung blood volume increased 18 +/- 2%, suggesting that the lungs may act as a blood volume buffer during periods of acutely increased venous return. With relative increasing exercise, leg blood volume stabilized, and then the blood volume in the abdominal organs decreased, further augmenting cardiopulmonary blood volume; leg blood volume and abdominal blood volume decreased by 23 +/- 2% and 19 +/- 2% from baseline, respectively, whereas thoracic blood volume increased 38 +/- 4%. In the abdomen, large decreases in blood volume were observed in the spleen (46 +/- 2%), kidney (24 +/- 4%), and liver (18 +/- 4%). In contrast, lung blood volume increased 50 +/- 4%, with the upper lung fields increasing more than the lower. Blood sampling revealed an increase in the hematocrit level by 4.3 +/- 0.4 units at peak exercise that paralleled the decrease in splenic blood volume (r2 = -0.64, p less than 0.001), suggesting a role for the spleen in augmenting cardiovascular performance by the release of concentrated red blood cells into general circulation. We conclude that upright exercise results in marked blood volume shifts from the legs and abdominal organs to the heart and lungs in a dynamic process correlating closely with oxygen consumption.

Diseases of skeletal muscles (myopathies) produce two major patterns of exercise intolerance. In muscular dystrophies, there is a progressive loss of muscle fibers which results in increasing muscle weakness and reduced VO2max due to the loss of functional muscle mass. In disorders of muscle energy metabolism, muscle bulk and resting strength are preserved, but an imbalance in muscle energy production and utilization in exercise results in exertional muscle pain, cramping, weakness, or fatigue. Isometric exercise is impaired by disorders of anaerobic glycolysis. Dynamic exercise is limited by disorders of oxidative metabolism. Maximal oxygen uptake is low in mitochondrial myopathies which affect pyruvate oxidation and electron transport and in glycolytic disorders which limit the availability of carbohydrate for oxidation during high-intensity exercise. In carnitine palmityl transferase deficiency (under non-fasting conditions) VO2max is normal. Excessive cardiopulmonary responses to exercise occur in some mitochondrial myopathies and in myophosphorylase deficiency and may contribute to exercise intolerance in these diseases.

The disorders of muscle energy metabolism can be classified into degenerative (myopathic) and dynamic syndromes. Four dynamic syndromes are currently recognized: 1) defective carbohydrate utilization, due to block of glycogenolysis or glycolysis; 2) defective lipid utilization, due to deficiency of the mitochondrial translocation of long-chain fatty acids (carnitine palmityltransferase deficiency); 3) lactic acidosis, due to defects of mitochondrial electron transport enzymes and possibly other unidentified defects; and 4) abnormal adenine nucleotide metabolism, exemplified by adenylate deaminase deficiency. The way in which the response to exercise is affected by impaired muscle energy metabolism is dependent on the type of metabolic defect. Defective carbohydrate metabolism severely limits the ability for high-intensity and ischemic exercise. The ability to perform prolonged exercise is markedly impaired in dynamic disorders of lipid metabolism. Other disorders, including those of adenine nucleotide metabolism also may have important implications for our understanding of the metabolic phenomena involved in exercise and recovery.

The study of skeletal muscle disorders is providing potentially important insights into regulatory mechanisms in human exercise and fatigue and information useful for diagnostic and treatment purposes. This review primarily concerned the general metabolic and physiological factors which set upper limits to performance of various types of exercise in patients with a variety of muscle disorders. From the standpoint of exercise performance, skeletal muscle diseases can be classified into three major groups. One group consists of primary disorders of muscle energy metabolism, including defects in muscle carbohydrate and lipid metabolism, disorders of mitochondrial electron transport, and abnormalities of purine nucleotide metabolism. Exercise performance largely reflects the capacity for ATP resynthesis. Oxidative phosphorylation is the dominant quantitative source of energy for ATP resynthesis under most exercise conditions. Consequently, patients with disordered oxidative metabolism (i.e., patients with defects in the availability or utilization of oxidizable substrate, such as those with phosphorylase or PFK deficiency or those with defects in mitochondrial electron transport) typically demonstrate severely impaired exercise performance. Intolerance to sustained exercise and premature fatigability are salient features of muscle oxidative disorders. Maximal oxygen uptake and maximal a-v O2 difference are markedly subnormal related to an attenuated muscle oxygen extraction. Muscle weakness and atrophy are less common. Anaerobic muscle performance is dramatically limited in patients with virtually complete defects of glycogenolysis/glycolysis but appears relatively normal in those with electron transport defects. A second major group of disorders includes patients with decreased muscle mass due to muscle necrosis, atrophy, and replacement of muscle by fat and connective tissue. These disorders are exemplified by the various muscular dystrophies (Duchenne's dystrophy, Becker's dystrophy, LG dystrophy, FSH dystrophy, and myotonic dystrophy) in which exercise performance is severely impaired due to muscle wasting and weakness in spite of largely normal pathways for muscle ATP resynthesis. In muscular dystrophy patients, the degree to which maximal oxygen uptake and anaerobic muscle performance are impaired appears to be a function of the severity of muscle weakness and atrophy. A third group of disorders includes patients with impaired activation of muscle contraction or relaxation. These disorders may be considered in two subcategories. In the first, impaired activation or relaxation of contractile activity is due to intrinsic muscle dysfunction (e.g., diseases associated with myotonia or periodic paralysis). In the second subcategory, there is impaired muscle activation due to a primary abnormality in the central nervous system, motor nerves, or neuromuscular junction.(ABSTRACT TRUNCATED AT 400 WORDS)

This article reviews the research performed to date on the cardiovascular responses to exercise in patients with neuromuscular diseases and lesions affecting the transmission of afferent impulses from skeletal muscle. These studies have provided important information about the roles of central command and reflexes from skeletal muscle afferents in circulatory control. Few animal models of neuromuscular diseases are available. Studies of patients with specific defects in skeletal muscle energy metabolism are particularly valuable because the local metabolic state participates in both systemic and local cardiovascular regulation. In patients with certain muscle metabolic defects (e.g., McArdle's disease, carnitine deficiency) cardiac output is normal at rest but increases excessively in relation to oxygen uptake during exercise. The excessive increase in cardiac output during exercise can be totally or partially normalized by increasing the availability of substrate to exercising muscle. These studies provide unique insights into the specific metabolic factors which are involved in cardiovascular regulation.

A 27-yr-old woman with lifelong severe exercise intolerance manifested by muscle fatigue, lactic acidosis, and prominent symptoms of dyspnea and tachycardia induced by trivial exercise was found to have a skeletal muscle respiratory chain defect characterized by low levels of reducible cytochromes a + a3 and b in muscle mitochondria and marked deficiency of cytochrome c oxidase (complex IV) as assessed biochemically and immunologically. Investigation of the pathophysiology of the exercise response in the patient revealed low maximal oxygen uptake (1/3 that of normal sedentary women) in cycle exercise and impaired muscle oxygen extraction as indicated by profoundly low maximal systemic arteriovenous oxygen difference (5.8 ml/dl; controls = 15.4 +/- 1.4, mean +/- SD). The increases in cardiac output and ventilation during exercise, normally closely coupled to muscle metabolic rate, were markedly exaggerated (more than two- to threefold normal) relative to oxygen uptake and carbon dioxide production accounting for prominent tachycardia and dyspnea at low workloads. Symptoms in our patient are similar to those reported in other human skeletal muscle respiratory chain defects involving complexes I and III, and the exaggerated circulatory response resembles that seen during experimental inhibition of the mitochondrial respiratory chain. These results suggest that impaired oxidative phosphorylation in working muscle disrupts the normal regulation of cardiac output and ventilation relative to muscle metabolic rate in exercise.