Changes In Muscle Structure Research Articles

Changes to muscle and fascia tissue after eighteen days of ankle immobilization post-ankle sprain injury: an MRI case study

BackgroundAnkle sprains often result in muscle atrophy and reduced range of motion, which can cause long-term ankle instabilities. Understanding the changes to muscle—such as atrophy—and concomitant changes to deep fascia—which may thicken alongside muscle loss—after ankle sprain injury is important to understanding structural changes about the joint and how they might contribute to longer-term impairments. Here, we employ advanced MRI to investigate skeletal muscle and fascial structural changes during the recovery period of one patient undergoing immobilization after ankle sprains.Material and methodsIn this case study, a participant who suffered an ankle sprain underwent initial MRI scans and, after 21 days (18 of which included immobilization), a follow-up MRI. Techniques used included proton density, 3D stack of spirals, and diffusion tensor imaging to analyse muscle and fascia changes pre- and post-injury.ResultsResults showed muscle atrophy in most shank muscles, with volume loss ranging from no change in the lateral gastrocnemius to 12.11% in the popliteus. Thigh muscles displayed hypertrophy of 6% in the hamstrings, while the quadriceps atrophied by 2.5%. Additionally, fascia thickness increased from 0.94 mm to 1.03 mm. Diffusion tensor imaging indicated that the biceps femoris experienced the most significant changes in physiological cross-sectional area, while the rectus femoris showed minimal change.ConclusionThe findings highlight the variable responses of muscles and a notable thickening of deep fascia post-injury, underscoring its role in recovery from ankle sprains.

Consistent use injectable and oral chondroprotectors in patients with osteoarthritis and lower back pain. Case report

Osteoarthritis (OA) is a disease of the entire joint, including structural changes in hyaline articular cartilage, subchondral bone, ligaments, capsule, synovial membrane and periarticular muscles. One of the causes of the development of nonspecific chronic lower back pain (LBP) is OA of the facet joints. In the treatment of OA and LBP against the background of OA facet joints, the chondroprotective agents are widely used: chondroitin sulfate (CS), glucosamine sulfate, undenatured type II collagen and their combinations. The aim of the article is to systematize the possibilities of practical application of Chondroguard TRIO® in patients with OA of different phenotypes and different localization. The experience of sequential administration of CS in patients (n=11) with OA and LBP with comorbid diseases is presented. At the initial stage of therapy, CS (Chondroguard®) was prescribed intramuscularly according to the scheme, then CS was prescribed perorally as part of a pharmaconutraceutical (Chondroguard® TRIO). The original pharmaconutraceutical Chondroguard® TRIO contains recommended doses of CS (1200 mg), glucosamine sulfate (1500 mg), undenatured type II collagen (40 mg). Clinical cases of the use of sequential administration of chondroprotectors (stage 1 – intramuscularly Chondroguard®, stage 2 – perorally Chondroguard® TRIO) demonstrate the clinical effectiveness of the proposed treatment regimen in patients of different age groups and OA phenotypes (posttraumatic, metabolic).

Immersion frozen storage combined with silver carp muscle hydrolysate: Effects on freshness, protein properties and microstructure of cryopreserved grass carp

This study highlighted the combined effects of immersion frozen storage (IFS) and silver carp muscle hydrolysate (SCMH) on the quality of cryopreserved grass carp. The fish fillets were pretreated with SCMH and stored at −18 °C using an indirect IFS method (SCMH + IFS), which offered rapid freezing and reduced temperature fluctuations (±0.4 °C), and changes in freshness, protein properties and muscle structure were evaluated over a 60-day storage period. Compared to IFS alone or traditional air frozen storage (AFS), samples treated with SCMH + IFS showed lower increases in K value (from 10.4% to 33.9%), TVB-N (from 7.3 mg/100g to 15.1 mg/100g), as well as retarded changes in the solubility, Ca2+-ATPase activity, surface hydrophobicity, and sulfhydryl content of myofibrillar protein. Furthermore, the ice formation and recrystallization as well as the physical damages to fish muscle myofibril structure were markedly mitigated in the SCMH + IFS samples. Therefore, SCMH + IFS was a promising approach for enhancing the quality of cryopreserved fish products.

Advanced quantitative magnetic resonance imaging of lower extremity muscle microtrauma after marathon: a mini review.

This article reviews the existing literature and outlines recent advances in quantitative Magnetic Resonance Imaging (MRI) techniques for the assessment of lower extremity muscle microtrauma following a marathon. Single-modality quantitative MRI techniques include T2 mapping to assess the dynamics of muscle inflammatory edema and variability at the site of injury, Diffusion Tensor Imaging (DTI) to detect subclinical changes in muscle injury, Intravoxel Incoherent Motion (IVIM) imaging to provide simultaneous information on perfusion and diffusion in muscle tissue without the need for intravenous contrast, and Magnetic Resonance Spectroscopy (MRS) to noninvasively detect intramyocellular lipid (IMCL)content in muscle before and after marathon exercise to explain the use of fatty acids as an energy source in skeletal muscle during long-distance running. As well as Chemical Exchange Saturation Transfer (CEST) is particularly suitable for detecting changes in free creatine, pH values and lactate concentrations in muscles before and after exercise, providing a more detailed picture of muscle physiology and chemistry. These metabolic MRI methods enhance the understanding of biochemical alterations occurring in muscles pre- and post-exercise. Multimodal techniques combine different modalities to provide a comprehensive evaluation of muscle structural and functional changes. These advanced techniques aim to better assess microtrauma and guide clinical treatment, though further validation with larger studies is needed to establish their potential over traditional qualitative methods.

The Use of Grayscale Muscle Ultrasound to Indicate Muscle Recovery After Peripheral Nerve Reconstruction.

This study aimed to validate the use of grayscale muscle ultrasound by measuring echo intensity to longitudinally evaluate functional muscle reinnervation in a rabbit peroneal nerve defect model. Eighteen New Zealand White rabbits underwent a 30-mm peroneal nerve reconstruction with autografts or decellularized allografts. Ultrasound measurements of tibialis anterior muscles were performed before surgery and at 4, 8, 12, 16, 20, and 24 weeks postoperatively and included cross-sectional muscle area, mean gray value (MGV), and mean gray value normalized for area (MGVA). At 24 weeks, functional motor recovery was evaluated with isometric tetanic force (ITF) and compound muscle action potential (CMAP). MGVA data was compared with ITF and CMAP measurements by calculating the Spearman correlation coefficient. Muscle area (Left/Right Ratio (L/R)) of autografts was superior to allografts at 4, 12, 16, 20 and 24 weeks (p<0.03 for all comparisons). MGVs of the operated side were significantly higher for autografts at 4, 8, and 12 weeks and at 12, 16, 20, and 24 weeks for allografts (p<0.01 for all comparisons), compared to their unoperated sides. Similar patterns were seen in both groups for MGVA (operated versus control side). MGVA (L/R) demonstrated a strong correlation with ITF (L/R) for autografts (ρ = -0.7) and allografts (ρ = -0.87), but inconsistent with CMAPs (L/R). Quantitative muscle ultrasound demonstrated a reliable, non-invasive tool for evaluating motor recovery in a rabbit peroneal nerve reconstruction model. Clinical translation could provide valuable insights into muscle health and structural changes following nerve reconstruction.

Pelvic floor muscle electrical coupling in chronic pelvic pain: Insights into pathophysiology and botulinum toxin treatment effects

This study aimed to assess the electrical coupling between both pelvic floor muscle (PFM) sides (two-sided coupling) and within individual PFM sides (one-sided coupling) in chronic pelvic pain (CPP) before and after botulinum neurotoxin type A (BoNT/A) treatment. Surface electromyographic (sEMG) signals were recorded from the left and right PFM of 24 patients (P) with CPP before and after being treated with BoNT/A (Weeks 0,8,12,24). Recordings were also made in 24 healthy women (H). PFM two-sided and one-sided coupling was evaluated during contractions by the cross-correlation (CC) and the imaginary part of coherency (iCOH) of their sEMG signals. Significant differences between their values were assessed comparing P(0) vs. P(8,12,24) and H vs. P(0,8,12,24). This study showed that PFM two-sided coupling is similar across groups before treatment, while PFM one-sided coupling on the patients’ most painful side is deranged before and also after BoNT/A treatment: amplitude coupling is lower (<CC) and phase difference is greater (>iCOH) than healthy women’s. This could be justified by altered neuromotor control strategies developed as an adaptation to muscle pain, structural and electrical changes in PFM, and alterations in their innervation pattern, which may influence the onset, perpetuation, or recurrence of CPP after treatment.

Structural and Functional Alterations of the Deltoid Muscle After Arthroscopic Rotator Cuff Repair: A 2-Year Longitudinal Observation Study.

Deltoid muscle detachment and atrophy have been reported to occur after shoulder surgery. To investigate the 2-year changes in deltoid muscle structure and function after arthroscopic rotator cuff repair (ARCR) using magnetic resonance imaging (MRI) and electrophysical examination. Case series; Level of evidence, 4. A total of 72 patients (72 shoulders) who underwent ARCR between 2015 and 2020 were enrolled. Whole deltoid muscle volume and regional (anterior, lateral, and posterior) muscle thicknesses were determined on T2-weighted MRI scans of both shoulders taken preoperatively and at 1, 3, 6, 12, and 24 months postoperatively, and their correlations with compound muscle action potentials (CMAPs), shoulder abduction muscle strength, and Constant scores were investigated. Comparison between groups was performed using paired or Student t tests, and the relationship between deltoid muscle volume and various factors was determined using Pearson correlation analysis. The volume of the deltoid muscle on the affected side decreased from 44,369 ± 12,371 mm3 preoperatively to 38,139 ± 10,615 mm3 at 1 month postoperatively (P < .05), representing a 14% decrease. The deltoid muscle volume of the contralateral side also significantly decreased during the same time frame, from 43,278 ± 12,248 to 40,273 ± 11,464 mm3 (P < .05), representing a 7% decrease at 1 month postoperatively. Subsequently, the deltoid muscle volume on both sides recovered to preoperative levels at 12 months and was maintained at 24 months. Only the thickness of the anterior part of the deltoid was markedly decreased, from 13.9 ± 3.7 mm preoperatively to 12.0 ± 3.2 mm at 1 month postoperatively (P < .05), representing a 14% reduction. The CMAP amplitude showed a significant decrease at 1 month postoperatively; however, no significant difference was observed after 12 months when compared with the preoperative values or the values on the contralateral side. Positive correlations were found between deltoid muscle volume and CMAP amplitude at 24 months as well as between deltoid muscle volume and shoulder abduction muscle strength (R 2 = 0.698; P < .05) and Constant score (R 2 = 0.133; P < .05). Our study demonstrated that the early structural and functional decline of the deltoid muscle after ARCR was fully recovered within 1 year, confirming that this procedure does not negatively affect the deltoid muscle.

Changes in masseter muscle structure, membrane lipid peroxidation and Ca-ATPase activity as effects of different local anesthetics.

Local anesthetics (LA) can cause undesired effects such as sustained contraction of skeletal muscles as a result of structural and functional changes. Proper skeletal muscle function is controlled by intracellular Ca2+ concentration and efficient energy (ATP) production, which is closely related to cell ultrastructure. Aim: The aim of this study was to identify the structural and functional changes caused by LAs. Materials and Method: Male Wistar rats weighing 200 to 250g were used (n:49). They were divided into seven groups. One group was not anesthetized or treated (Control). The other six groups underwent intramuscular (IM) anesthesia with xylazine 2% (0.05 ml) and ketamine 50 mg/ml (0.1 ml/100g rat weight), and one of the following was applied to the masseter muscle (MM): no further treatment (Anesthetic Control group, CA); 0.1ml physiological saline solution (group SF); Carrageenin (group Carr) 1% as positive control group; prilocaine (group Pri), mepivacaine (group Mepi); or articaine (group Arti) 0.3M, IM. The animals were euthanized by cervical dislocation one hour after treatment. The effects of the different anesthetics on the MM were evaluated histologically and by electronic microscopy (EM). Ca-ATPase and membrane lipid peroxidation (LPX) were evaluated in muscle homogenates under the same conditions as those used to prepare the histological sections. Results: In general, structural damage and increased muscle contraction were observed in tissues treated with anesthetics. The most extreme values of Ca-ATPase activity and LPX were observed in the positive control group (carrageenin). Results were analyzed by one-way ANOVA for multiple comparisons and Tukey's test (p < 0.05). Conclusions: The results suggest that in the short term, local anesthetics affect the muscle function and are associated to structural changes.

Structural Changes in Pharyngeal and Tongue Muscles as a Potential Contributor to Dysphagia in Alzheimer Disease Rat Model

Structural Changes in Pharyngeal and Tongue Muscles as a Potential Contributor to Dysphagia in Alzheimer Disease Rat Model

Changes in masseter muscle structure, membrane lipid peroxidation and Ca-ATPase activity as effects of different local anesthetics

Local anesthetics (LA) can cause undesired effects such as sustained contraction of skeletal muscles as a result of structural and functional changes. Proper skeletal muscle function is controlled by intracellular Ca2+ concentration and efficient energy (ATP) production, which is closely related to cell ultrastructure. Aim: The aim of this study was to identify the structural and functional changes caused by LAs. Materials and Method: Male Wistar rats weighing 200 to 250g were used (n:49). They were divided into seven groups. One group was not anesthetized or treated (Control). The other six groups underwent intramuscular (IM) anesthesia with xylazine 2% (0.05 ml) and ketamine 50 mg/ ml (0.1 ml/100g rat weight), and one of the following was applied to the masseter muscle (MM): no further treatment (Anesthetic Control group, CA); 0.1ml physiological saline solution (group SF); Carrageenin (group Carr) 1% as positive control group; prilocaine (group Pri), mepivacaine (group Mepi); or articaine (group Arti) 0.3M, IM. The animals were euthanized by cervical dislocation one hour after treatment. The effects of the different anesthetics on the MM were evaluated histologically and by electronic microscopy (EM). Ca-ATPase and membrane lipid peroxidation (LPX) were evaluated in muscle homogenates under the same conditions as those used to prepare the histological sections. Results: In general, structural damage and increased muscle contraction were observed in tissues treated with anesthetics. The most extreme values of Ca-ATPase activity and LPX were observed in the positive control group (carrageenin). Results were analyzed by one-way ANOVA for multiple comparisons and Tukey’s test (p &lt; 0.05). Conclusions: The results suggest that in the short term, local anesthetics affect the muscle function and are associated to structural changes.

Subclinical Ocular Motility Dysfunction and Extraocular Muscle Changes in Inactive Graves' Orbitopathy.

This study aimed to investigate the presence of structural and functional changes in extraocular muscles (EMs) among patients with inactive Graves' orbitopathy (GO) classified according to the Clinical Activity Score (CAS). Sixty-seven patients with Graves' disease (GD) and inactive GO were included. The data collected included clinical parameters, thyroid function, autoantibody levels, EOM morphology via orbital ultrasound (US), and ocular motility. Patients were stratified into Red Filter Test (RFT)-positive or RFT-negative groups based on the presence or absence of latent diplopia during the RFT examination. Thirty-three patients (49.25%) exhibited latent diplopia on the RFT, despite not reporting double vision during standard ocular motility tests. Significant differences were observed between the two groups in terms of age, disease duration, intraocular pressure (IOP) elevation in up-gaze, and medial rectus muscle thickness (p < 0.05). No significant differences were found in thyroid status, TRAb and ATA levels, CASs, exophthalmos, or lateral rectus thickness between the two groups. This study revealed that in inactive GO, subclinical EM dysfunction and morphological changes may be present, which might not be apparent through routine ocular examinations. The RFT is effective in detecting latent diplopia, highlighting its utility in identifying subtle ocular motility issues and subclinical muscle involvement. Comprehensive evaluations combining functional tests like the RFT and imaging are essential for early detection of GO-related abnormalities, enabling tailored and prompt management and improving patient outcomes.

Impact of Muscle Changes Assessed by Ultrasonography on Muscle Strength and Functioning after ICU Discharge: A Systematic Review with Meta-Analysis.

Ultrasonography has been used to identify structural, quantitative, and qualitative muscle changes. These changes have been assessed in different muscles during ICU stays; however, it is unclear if it can predict functioning after ICU discharge. To analyze the relationship between muscle changes assessed by ultrasonography and the strength and functioning of ICU survivors. A systematic review with a meta-analysis was performed according to the MOOSE guidelines and registered in PROSPERO. Searches of the following databases were performed by two of the authors: PubMed, Cinahl, Embase, Scopus, LILACS, Web of Science, and Science Direct. Qualitative analysis was performed using NOS and AHRQ scales. Meta-analysis was performed using the "R", "metafor" package. Heterogeneity was assessed by I2 and Cochran's Q test. Meta-regression analyses were performed to verify the moderators, and funnel plots and Egger's regression intercept test were used to analyze the publication bias. Sixteen articles were included in the qualitative assessment, and nine were used in the quantitative assessment. There is evidence of correlations between MT and muscle strength (r = 0.20 [0.11; 0.27]; p < 0.0001), and MT (r = 0.35 [0.19; 0.49]; p < 0.0001), CSA (r = 0.30 [0.10; 0.47]; p = 0.0038), EI (r = -0.29 [-0.53; -0.01]; p = 0.043) and mobility. In the subgroup analyses, some evidence of a correlation between specific muscles and strength and mobility were found. There is evidence for the correlation between muscle characteristics assessed by US and functioning outcomes.

Noninvasive analysis of overactive muscle structure and elasticity after botulinum toxin type A injection: a systematic review and meta-analysis.

Injections of botulinum toxin type A (BoNT-A) are the first-line treatment for spastic muscle overactivity (MO). Some authors observed that BoNT-A injections lead to changes in muscle structure and muscle elasticity that are probably not completely reversible. This possible effect is critical, as it could lead to negative impacts on the effectiveness of BoNT-A interventions. Our study aimed to evaluate the current literature regarding changes in muscle elasticity and structure after BoNT-A injection, by diagnostic imaging, in neurological populations with MO. Our second objective was to pool all articles published on this topic in order to provide a quantitative synthesis of the data. A systematic search was conducted between October 2021 and April 2023 using different databases in accordance with PRISMA guidelines. Two independent reviewers screened articles for inclusion, extracted data, and evaluated methodological quality of the studies. A meta-analysis was performed to compare muscle elasticity and structure before and after BoNT-A injections. A sample of 34 studies was selected for qualitative review and 19 studies for quantitative review. Meta-analysis of pre-post studies demonstrated significant improvement with a medium effect size (standardized mean difference=0.74; 95% CI 0.46-1.02; P<0.001) of muscle elasticity assessed by ultrasound elastography (USE) 4 weeks after BoNT-A injection. No statistically significant difference was found for muscle thickness, pennation angle, and muscle echo-intensity assessed by magnetic resonance imaging and/or ultrasonography at short-term. On the other hand, normalized muscle volume decreased with a small effect size (standardized mean difference = -0.17; 95% CI -0.25 - -0.09; P<0.001) 6 months after BoNT-A injection. Muscle elasticity measured by USE improves with a temporary effect at short-term following BoNT-A injections. Synthesis of studies that assesses muscle structure is hindered by methodological differences between studies. However, based on a small amount of data, normalized muscle volume seems to decrease at long-term after BoNT-A injections in children with CP suggesting that the timing of re-injection should be considered with caution in this population. Further work should focus on the long-term effect of repeated injections on muscle structure and elasticity in neurological populations.

Comparative study of functional and structural muscle changes in peripheral artery disease: rubidium-82 positron emission tomography and histological correlation

Comparative study of functional and structural muscle changes in peripheral artery disease: rubidium-82 positron emission tomography and histological correlation

Zebrafish as a Human Muscle Model for Studying Age-Dependent Sarcopenia and Frailty.

Currently, there is an increase in the aging of the population, which represents a risk factor for many diseases, including sarcopenia. Sarcopenia involves progressive loss of mass, strength, and function of the skeletal muscle. Some mechanisms include alterations in muscle structure, reduced regenerative capacity, oxidative stress, mitochondrial dysfunction, and inflammation. The zebrafish has emerged as a new model for studying skeletal muscle aging because of its numerous advantages, including histological and molecular similarity to human skeletal muscle. In this study, we used fish of 2, 10, 30, and 60 months of age. The older fish showed a higher frailty index with a value of 0.250 ± 0.000 because of reduced locomotor activity and alterations in biometric measurements. We observed changes in muscle structure with a decreased number of myocytes (0.031 myocytes/μm2 ± 0.004 at 60 months) and an increase in collagen with aging up to 15% ± 1.639 in the 60-month group, corresponding to alterations in the synthesis, degradation, and differentiation pathways. These changes were accompanied by mitochondrial alterations, such as a nearly 50% reduction in the number of intermyofibrillar mitochondria, 100% mitochondrial damage, and reduced mitochondrial dynamics. Overall, we demonstrated a similarity in the aging processes of muscle aging between zebrafish and mammals.

Disuse-Induced Muscle Fatigue: Facts and Assumptions.

Skeletal muscle unloading occurs during a wide range of conditions, from space flight to bed rest. The unloaded muscle undergoes negative functional changes, which include increased fatigue. The mechanisms of unloading-induced fatigue are far from complete understanding and cannot be explained by muscle atrophy only. In this review, we summarize the data concerning unloading-induced fatigue in different muscles and different unloading models and provide several potential mechanisms of unloading-induced fatigue based on recent experimental data. The unloading-induced changes leading to increased fatigue include both neurobiological and intramuscular processes. The development of intramuscular fatigue seems to be mainly contributed by the transformation of soleus muscle fibers from a fatigue-resistant, "oxidative" "slow" phenotype to a "fast" "glycolytic" one. This process includes slow-to-fast fiber-type shift and mitochondrial density decline, as well as the disruption of activating signaling interconnections between slow-type myosin expression and mitochondrial biogenesis. A vast pool of relevant literature suggests that these events are triggered by the inactivation of muscle fibers in the early stages of muscle unloading, leading to the accumulation of high-energy phosphates and calcium ions in the myoplasm, as well as NO decrease. Disturbance of these secondary messengers leads to structural changes in muscles that, in turn, cause increased fatigue.

Differences in thick filament activation in fast rodent skeletal muscle and slow porcine cardiac muscle.

There is a growing appreciation that regulation of muscle contraction requires both thin filament and thick filament activation in order to fully activate the sarcomere. The prevailing mechano-sensing model for thick filament activation was derived from experiments on fast-twitch muscle. We address the question whether, or to what extent, this mechanism can be extrapolated to the slow muscle in the hearts of large mammals, including humans. We investigated the similarities and differences in structural signatures of thick filament activation in porcine myocardium as compared to fast rat extensor digitorum longus (EDL) skeletal muscle under relaxed conditions and sub-maximal contraction using small angle X-ray diffraction. Thick and thin filaments were found to adopt different structural configurations under relaxing conditions, and myosin heads showed different changes in configuration upon sub-maximal activation, when comparing the two muscle types. Titin was found to have an X-ray diffraction signature distinct from those of the overall thick filament backbone, and its spacing change appeared to be positively correlated to the force exerted on the thick filament. Structural changes in fast EDL muscle were found to be consistent with the mechano-sensing model. In porcine myocardium, however, the structural basis of mechano-sensing is blunted suggesting the need for additional activation mechanism(s) in slow cardiac muscle. These differences in thick filament regulation can be related to their different physiological roles where fast muscle is optimized for rapid, burst-like, contractions, and the slow cardiac muscle in large mammalian hearts adopts a more finely tuned, graded response to allow for their substantial functional reserve. KEY POINTS: Both thin filament and thick filament activation are required to fully activate the sarcomere. Thick and thin filaments adopt different structural configurations under relaxing conditions, and myosin heads show different changes in configuration upon sub-maximal activation in fast extensor digitorum longus muscle and slow porcine cardiac muscle. Titin has an X-ray diffraction signature distinct from those of the overall thick filament backbone and this titin reflection spacing change appeared to be directly proportional to the force exerted on the thick filament. Mechano-sensing is blunted in porcine myocardium suggesting the need for additional activation mechanism(s) in slow cardiac muscle. Fast skeletal muscle is optimized for rapid, burst-like contractions, and the slow cardiac muscle in large mammalian hearts adopts a more finely tuned graded response to allow for their substantial functional reserve.

Impact of hindlimb length variation on jumping dynamics in the Longshanks mouse.

Distantly related mammals (e.g. jerboa, tarsiers, kangaroos) have convergently evolved elongated hindlimbs relative to body size. Limb elongation is hypothesized to make these species more effective jumpers by increasing their kinetic energy output (through greater forces or acceleration distances), thereby increasing take-off velocity and jump distance. This hypothesis, however, has rarely been tested at the population level, where natural selection operates. We examined the relationship between limb length, muscular traits and dynamics using Longshanks mice, which were selectively bred over 22 generations for longer tibiae. Longshanks mice have approximately 15% longer tibiae and 10% longer femora compared with random-bred Control mice from the same genetic background. We collected in vivo measures of locomotor kinematics and force production, in combination with behavioral data and muscle morphology, to examine how changes in bone and muscle structure observed in Longshanks mice affect their hindlimb dynamics during jumping and clambering. Longshanks mice achieved higher mean and maximum lunge-jump heights than Control mice. When jumping to a standardized height (14 cm), Longshanks mice had lower maximum ground reaction forces, prolonged contact times and greater impulses, without significant differences in average force, power or whole-body velocity. While Longshanks mice have longer plantarflexor muscle bodies and tendons than Control mice, there were no consistent differences in muscular cross-sectional area or overall muscle volume; improved lunge-jumping performance in Longshanks mice is not accomplished by simply possessing larger muscles. Independent of other morphological or behavioral changes, our results point to the benefit of longer hindlimbs for performing dynamic locomotion.

Reduced exercise capacity occurs before intrinsic skeletal muscle dysfunction in experimental rat models of pulmonary hypertension.

Reduced exercise capacity in pulmonary hypertension (PH) significantly impacts quality of life. However, the cause of reduced exercise capacity in PH remains unclear. The objective of this study was to investigate whether intrinsic skeletal muscle changes are causative in reduced exercise capacity in PH using preclinical PH rat models with different PH severity. PH was induced in adult Sprague-Dawley (SD) or Fischer (CDF) rats with one dose of SU5416 (20 mg/kg) injection, followed by 3 weeks of hypoxia and additional 0-4 weeks of normoxia exposure. Control s rats were injected with vehicle and housed in normoxia. Echocardiography was performed to assess cardiac function. Exercise capacity was assessed by VO2 max. Skeletal muscle structural changes (atrophy, fiber type switching, and capillary density), mitochondrial function, isometric force, and fatigue profile were assessed. In SD rats, right ventricular systolic dysfunction is associated with reduced exercise capacity in PH rats at 7-weektimepoint in comparison to control rats, while no changes were observed in skeletal muscle structure, mitochondrial function, isometric force, or fatigue profile. CDF rats at 4-weektimepoint developed a more severe PH and, in addition to right ventricular dysfunction, the reduced exercise capacity in these rats is associated with skeletal muscle atrophy; however, mitochondrial function, isometric force, and fatigue profile in skeletal muscle remain unchanged. Our data suggest that cardiopulmonary impairments in PH are the primary cause of reduced exercise capacity, which occurs before intrinsic skeletal muscle dysfunction.

Effects of intra-articular injection of platelet-rich plasma on the inflammatory process and histopathological characteristics of cartilage and synovium in animals with osteoarthritis: a systematic review with meta-analysis

BackgroundOsteoarthritis (OA) affects the entire joint, causing structural changes in articular cartilage, subchondral bone, ligaments, capsule, synovial membrane, and periarticular muscles that afflicts millions of people globally, leading to persistent pain and diminished quality of life. The intra-articular use of platelet-rich plasma (PRP) is gaining recognition as a secure therapeutic approach due to its potential regenerative capabilities. However, there is controversial clinical data regarding efficacy of PRP for OA treatment. In this context, gathering scientific evidence on the effects of PRP in treating OA in animal models could provide valuable insights into understanding its impact on aspects like cartilage health, synovial tissue integrity, and the inflammatory process in affected joints. Thus, the objective of this study was to assess the effects of PRP injections on inflammation and histopathological aspects of cartilage and synovium in animal models of OA through a comprehensive systematic review with meta-analysis.MethodsA electronic search was conducted on Medline, Embase, Web of Science, The Cochrane Library, LILACS, and SciELO databases for relevant articles published until June 2022. A random-effects meta-analysis was employed to synthesize evidence on the histological characteristics of cartilage and synovium, as well as the inflammatory process. The GRADE approach was utilized to categorize the quality of evidence, and methodological quality was assessed using SYRCLE’s RoB tool.ResultsTwenty-one studies were included in the review, with twelve of them incorporated into the meta-analysis. PRP treatment demonstrated superior outcomes compared to the control group in terms of cartilage histology (very low quality; p = 0.0002), synovium histology (very low quality; p < 0.0001), and reductions in proinflammatory markers, including IL-1 (low quality; p = 0.002), IL-6 (very low quality; p < 0.00001), and TNF-α (very low; p < 0.00001). However, PRP treatment did not yield a significant impact on PDGF-A levels (very low quality; p = 0.81).ConclusionPRP appears capable of reducing proinflammatory markers (IL-1, IL-6, TNF-α) and mitigating cartilage and synovium damage in animals with OA. However, the levels of evidence of these findings are low to very low. Therefore, more rigorous studies with larger samples are needed to improve the quality of evidence.PROSPERO registrationCRD42022250314