Skeletal Muscle Structure Research Articles

4D biofabrication of skeletal muscle microtissues

Skeletal muscle is one of the most abundant tissues in the body. Although it has a relatively good regeneration capacity, it cannot heal in the case of disease or severe damage. Many current tissue engineering strategies fall short due to the complex structure of skeletal muscle. Biofabrication techniques have emerged as a popular set of methods for increasing the complexity of tissue-like constructs. In this paper, 4D biofabrication technique is introduced for fabrication of the skeletal muscle microtissues. To this end, a bilayer scaffold consisting of a layer of anisotropic methacrylated alginate fibers (AA-MA) and aligned polycaprolactone (PCL) fibers were fabricated using electrospinning and later induced to self-fold to encapsulate myoblasts. Bilayer mats undergo shape-transformation in an aqueous buffer, a process that depends on their overall thickness, the thickness of each layer and the geometry of the mat. Proper selection of these parameters allowed fabrication of scroll-like tubes encapsulating myoblasts. The myoblasts were shown to align along the axis of the anisotropic PCL fibers and further differentiated into aligned myotubes that contracted under electrical stimulation. Overall the significance of this approach is in the fabrication of hollow tubular constructs that can be further developed for the formation of a vascularized and functional muscle.

Micro-dystrophin Gene Therapy Partially Enhances Exercise Capacity in Older Adult mdx Mice

Micro-dystrophin (μDys) gene therapeutics can improve striated muscle structure and function in different animal models of Duchenne muscular dystrophy. Most studies, however, used young mdx mice that lack a pronounced dystrophic phenotype, short treatment periods, and limited muscle function tests. We, therefore, determined the relative efficacy of two previously described μDys gene therapeutics (rAAV6:μDysH3 and rAAV6:μDys5) in 6-month-old mdx mice using a 6-month treatment regimen and forced exercise. Forelimb and hindlimb grip strength, metabolic rate (VO2 max), running efficiency (energy expenditure), and serum creatine kinase levels similarly improved in mdx mice treated with either vector. Both vectors produced nearly identical dose-responses in all assays. They also partially prevented the degenerative effects of repeated high-intensity exercise on muscle histology, although none of the metrics examined was restored to normal wild-type levels. Moreover, neither vector had any consistent effect on respiration while exercising. These data together suggest that, although μDys gene therapy can improve isolated and systemic muscle function, it may be only partially effective when dystrophinopathies are advanced or when muscle structure is significantly challenged, as with high-intensity exercise. This further suggests that restoring muscle function to near-normal levels will likely require ancillary or combinatorial treatments capable of enhancing muscle strength.

NMR: From Molecular Mechanism to its Application in Medical Care.

Nuclear Magnetic Resonance (NMR) spectroscopy is a systematic science strategy utilized in pharmaceutical research, development, quality control, and research to decide the content and purity of a sample as well as its sub-atomic structure. There are several parameters working for better execution of NMR which can include chemical shifts, spin multiplicity, pH dependence, heteronuclear and homonuclear covalent network, and the atomic overhauser impact. NMR imaging offers an extensive scope of potential outcomes for the portrayal of skeletal muscle structure, function and metabolism. 1H additionally has the most noteworthy NMR affectability of any nucleus. The principle of NMR depends on the spins of atomic nuclei. The magnetic estimations rely on an unpaired electron, while NMR estimates attractive impact brought about by the turn of protons and neutrons. The nucleons have intrinsic angular momenta or spins, which is considered as basic magnet. The presence of atomic attraction was uncovered in the hyperfine structure of spectral lines. If the nucleus magnetic moment is put in the magnetic field, the phenomenon of space quantization can be observed and each allowed direction will have a marginally unique energy level. Invitro, high-resolution NMR spectroscopy helps to assess tumor metabolism by the investigation of body liquids like urine, blood and removed tissue specimens. In-cell NMR is a powerful technique to assess strong compounds in medication improvement to spare exploratory expenses.

Mammalian muscle fibers may be simple as well as slow.

Squire and Luther consider new evidence for a simple lattice structure in mammalian skeletal muscle.

Protein and amino acids for skeletal muscle health in aging.

Proteins and its building blocks, amino acids, have many physiological roles in the body. While some amino acids can be synthesized endogenously, exogenous protein and amino acids are necessary to maintain homeostasis. Because skeletal muscle contains a large portion of endogenous protein and plays important roles in movement, regulation, and metabolism, imbalanced protein and amino acid availability may result in clinical conditions including skeletal muscle atrophy, impaired muscle growth or regrowth, and functional decline. Aging is associated with changes in protein metabolism and multiple physiological and functional alterations in the skeletal muscle that are accentuated by decreased dietary protein intake and impaired anabolic responses to stimuli. Inactivity and chronically elevated inflammation of the skeletal muscle can initiate and/or augment pathological remodeling of the tissue (i.e., increase of fat and fibrotic tissues and atrophy of the muscle). Defining an adequate amount of dietary protein that is appropriate to maintain the availability of amino acids for biological needs is necessary but is still widely debated for older adults. This chapter will provide (i) an overview of dietary protein and amino acids and their role in skeletal muscle health; (ii) an overview of skeletal muscle structure and function and the deterioration of muscle that occurs with advancing age; (iii) a discussion of the relationship between protein/amino acid metabolism and skeletal muscle decline with aging; and (iv) a brief discussion of optimal protein intakes for older adults to maintain skeletal muscle health in aging.

Long-term Effects of Hypothermic Ex Situ Perfusion on Skeletal Muscle Metabolism, Structure, and Force Generation After Transplantation.

Hypothermic ex situ perfusion (HESP) systems are used to prolong allograft survival in solid organ transplantations and have been shown to be superior to static cold storage (SCS) methods. However, the effect of this preservation method on limb allograft survival and long-term function has not yet been tested. In this study, we investigated the long-term effects of the HESP on skeletal muscle metabolism, structure, and force generation and compared it with the current standard of preservation. Forty male Lewis rats (250 ± 25 g) were divided into 5 groups, including naive control, sciatic nerve transection or repair, immediate transplantation, SCS, and HESP. For the SCS group, limbs were preserved at 4°C for 6 hours. In the HESP group, limbs were continuously perfused with oxygenated histidine-tryptophan-ketoglutarate (HTK) solution at 10-15°C for 6 hours. Hemodynamic and biochemical parameters of perfusion were recorded throughout the experiment. At 12 weeks, electromyography and muscle force measurements (maximum twitch and tetanic forces) were obtained along with muscle samples for histology and metabolomics analysis. Histology demonstrated 48% myocyte injury in the HESP group compared with 49% in immediate transplantation (P = 0.96) and 74% in the SCS groups (P < 0.05). The maximum twitch force measurement revealed a significantly higher force in the HESP group compared with the SCS group (P = 0.029). Essential amino acid levels of the gastrocnemius muscle did not reach significance, with the exception of higher proline levels in the HESP group. HESP using HTK protects viability of the limb but fails to restore muscle force in the long term.

The Role of the Molecular Clock in Promoting Skeletal Muscle Growth and Protecting against Sarcopenia.

The circadian clock has a critical role in many physiological functions of skeletal muscle and is essential to fully understand the precise underlying mechanisms involved in these complex interactions. The importance of circadian expression for structure, function and metabolism of skeletal muscle is clear when observing the muscle phenotype in models of molecular clock disruption. Presently, the maintenance of circadian rhythms is emerging as an important new factor in human health, with disruptions linked to ageing, as well as to the development of many chronic diseases, including sarcopenia. Therefore, the aim of this review is to present the latest findings demonstrating how circadian rhythms in skeletal muscle are important for maintenance of the cellular physiology, metabolism and function of skeletal muscle. Moreover, we will present the current knowledge about the tissue-specific functions of the molecular clock in skeletal muscle.

Genetic Markers Associated with Power Athlete Status.

Athletic performance is a multifactorial phenotype influenced by environmental factors as well as multiple genetic variants. Different genetic elements have a great influence over components of athletic performance such as endurance, strength, power, flexibility, neuromuscular coordination, psychological traits and other features important in sport. The current literature review revealed that to date more than 69 genetic markers have been associated with power athlete status. For the purpose of the present review we have assigned all genetic markers described with reference to power athletes status to seven main groups: 1) markers associated with skeletal muscle structure and function, 2) markers involved in the inflammatory and repair reactions in skeletal muscle during and after exercise, 3) markers involved in blood pressure control, 4) markers involved in modulation of oxygen uptake, 5) markers that are regulators of energy metabolism and cellular homeostasis, 6) markers encoding factors that control gene expression by rearrangement of chromatin fibers and mRNA stability, and 7) markers modulating cellular signaling pathways. All data presented in the current review provide evidence to support the notion that human physical performance may be influenced by genetic profiles, especially in power sports. The current studies still represent only the first steps towards a better understanding of the genetic factors that influence power-related traits, so further analyses are necessary before implementation of research findings into practice.

Skeletal muscle: A review of molecular structure and function, in health and disease.

Decades of research in skeletal muscle physiology have provided multiscale insights into the structural and functional complexity of this important anatomical tissue, designed to accomplish the task of generating contraction, force and movement. Skeletal muscle can be viewed as a biomechanical device with various interacting components including the autonomic nerves for impulse transmission, vasculature for efficient oxygenation, and embedded regulatory and metabolic machinery for maintaining cellular homeostasis. The “omics” revolution has propelled a new era in muscle research, allowing us to discern minute details of molecular cross‐talk required for effective coordination between the myriad interacting components for efficient muscle function. The objective of this review is to provide a systems‐level, comprehensive mapping the molecular mechanisms underlying skeletal muscle structure and function, in health and disease. We begin this review with a focus on molecular mechanisms underlying muscle tissue development (myogenesis), with an emphasis on satellite cells and muscle regeneration. We next review the molecular structure and mechanisms underlying the many structural components of the muscle: neuromuscular junction, sarcomere, cytoskeleton, extracellular matrix, and vasculature surrounding muscle. We highlight aberrant molecular mechanisms and their possible clinical or pathophysiological relevance. We particularly emphasize the impact of environmental stressors (inflammation and oxidative stress) in contributing to muscle pathophysiology including atrophy, hypertrophy, and fibrosis.This article is categorized under:Physiology > Mammalian Physiology in Health and DiseaseDevelopmental Biology > Developmental Processes in Health and DiseaseModels of Systems Properties and Processes > Cellular Models

Abstract 273: The Role of Estrogen in Protection of Skeletal Muscle Function in Diastolic Dysfunction

Diastolic dysfunction (DD) is prevalent in elderly post-menopausal women. In addition to impaired cardiac relaxation and output, DD is associated with loss of skeletal muscle mass, muscle strength and function, and exercise capacity. Understanding the mechanisms of estrogen (E2)-mediated regulation of skeletal muscle structure and function in DD can have broader implications in understanding the progression of heart disease in post-menopausal women. In muscle, E2 regulates autophagy and mitophagy, processes that orchestrate degradation and recycling of damaged cellular components to maintain healthy tissue and conserve energy. However, this role of E2 under a physiological stress such as DD, is largely unknown. Our study aimed to understand the relationship between E2, autophagy/mitophagy and muscle function in DD. We hypothesized that estrogen receptor (ER) signaling plays a direct role in regulation of autophagy and mitophagy-mediated maintenance of muscle mass and muscle mitochondrial function in DD. Sham or ovariectomy (OVX) surgeries were performed to induce E2-deficiency, followed by induction of DD by administering hypertension agents L-NAME and angiotensin II. NMR analysis revealed significantly reduced total lean mass in OVX mice with DD, further confirmed by direct measurement of gastrocnemius muscle mass. Expression of ERα target-genes PDK4 and STAT3 were reduced in muscle of OVX mice with DD. DD significantly reduced LC3B II/I ratio in muscle, indicative of reduced autophagy. Consistent with this, expression of transcription factor FoxO3, a master-regulator of multiple autophagy and mitophagy genes, was reduced in OVX mice with DD compared to sham control mice. Expression of SDHA gene coding for mitochondrial respiratory chain subunit II, was reduced in sham and OVX mice with DD compared to sham control mice. Mitochondrial respiratory function measured from isolated muscle mitochondria, was reduced in sham and OVX mice with DD compared to sham control mice, and in OVX mice with DD compared to OVX control mice, indicating compromised skeletal muscle mitochondrial function. Our findings indicate that OVX-induced E2-deficiency and DD leads to muscle impairments, including defects in mitochondrial function.

PGC-1α regulates mitochondrial properties beyond biogenesis with aging and exercise training.

Impaired mitochondrial function has been implicated in the pathogenesis of age-associated metabolic diseases through regulation of cellular redox balance. Exercise training is known to promote mitochondrial biogenesis in part through induction of the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). Recently, mitochondrial ADP sensitivity has been linked to reactive oxygen species (ROS) emission with potential impact on age-associated physiological outcomes, but the underlying molecular mechanisms remain unclear. Therefore, the present study investigated the effects of aging and exercise training on mitochondrial properties beyond biogenesis, including respiratory capacity, ADP sensitivity, ROS emission, and mitochondrial network structure, in myofibers from inducible muscle-specific PGC-1α-knockout mice and control mice. Aged mice displayed lower running endurance and mitochondrial respiratory capacity than young mice. This was associated with intermyofibrillar mitochondrial network fragmentation, diminished submaximal ADP-stimulated respiration, increased mitochondrial ROS emission, and oxidative stress. Exercise training reversed the decline in maximal respiratory capacity independent of PGC-1α, whereas exercise training rescued the age-related mitochondrial network fragmentation and the impaired submaximal ADP-stimulated respiration in a PGC-1α-dependent manner. Furthermore, lack of PGC-1α was associated with altered phosphorylation and carbonylation of the inner mitochondrial membrane ADP/ATP exchanger adenine nucleotide translocase 1. In conclusion, the present study provides evidence that PGC-1α regulates submaximal ADP-stimulated respiration, ROS emission, and mitochondrial network structure in mouse skeletal muscle during aging and exercise training.

Changes in Musculoskeletal System and Metabolism in Osteoporotic Rats Treated With Urocortin.

Objective: In aging population, postmenopausal osteoporosis and decline of musculoskeletal function, referred to as “frailty syndrome” lead to loss of bone and muscle, causing falls, and fall-related injuries. To limit the impact of this portentous duo, simultaneous treatment of both is needed. Urocortin (UCN) has been reported to improve osteoporotic bone properties while its effect on muscle has not been addressed yet.Design and Methods: We aimed to investigate the effect of urocortin in vivo on skeletal muscle structure in osteopenic rats. Sixty Sprague-Dawley rats were divided into five groups: four were ovariectomized (OVX) and one underwent sham operation (SHAM). One ovariectomized group was left untreated (OVX), while one was treated with urocortin s.c. in 3 μg/kg body weight (bw) (OVX+UCN low), one with 30 μg/kg (OVX+UCN high), while one group was treated with estradiol orally (OVX+E: 0.2 mg/kg bw), each for 35 days. Mm. gastrocnemius, longissimus, and soleus were isolated and capillary density as well as diameters of type I and II fibers were measured. In addition, we examined the effect of UCN on tibia using biomechanical, micro-CT and ashing analysis and investigated the blood serum.Results: We demonstrated a positive effect of UCN on M. soleus, in which fiber diameter was positively influenced. The biomechanical and structural parameters of bone were not changed in UCN treated rats. The higher cholesterol, glucose and triglyceride levels in the “UCN high” group raise concern about this treatment.Conclusions: Our results portray urocortin as a substance that can be assessed for future therapeutic treatments of estrogen deficiency.New and Noteworthy: Urocortin has a positive effect on M. soleus (diameter). Urocortin raises serum cholesterol and triglyceride levels. Bone tissue was not affected by UCN.

Tissue Engineering for Clean Meat Production

Increasing public awareness of foodborne illnesses, factory farming and the ecological footprint of the meat industry, has generated the need for animal-free meat alternatives. In the last decade, scientists have begun to leverage the knowledge and tools accumulated in the fields of stem cells and tissue engineering towards the development of cell-based meat (i.e., clean meat). In tissue engineering, the physical and biochemical features of the native tissue can be mimicked; cells and biomaterials are integrated under suitable culture conditions to form mature tissues. More specifically, in skeletal muscle tissue engineering, a plurality of cell types can be co-cultured on a 3D scaffold to generate muscle fibers, blood vessels and a dense extracellular matrix (ECM). This review focuses on tissue engineering of skeletal muscle and the adjustments needed for clean meat development. We discuss the skeletal muscle structure and composition, and elaborate on cell types from farm animals that have the potential to recapitulate the muscle ECM, blood vessels, muscle fibers and fat deposits. We also review relevant biomaterials, primarily for fabricating scaffolds that can mimic the intramuscular connective tissues, as well as gene expression studies on the biological pathways that influence meat quality.

The role of SIRT1 in skeletal muscle function and repair of older mice.

BackgroundSirtuin 1 (SIRT1) is a NAD+ sensitive deacetylase that has been linked to longevity and has been suggested to confer beneficial effects that counter aging‐associated deterioration. Muscle repair is dependent upon satellite cell function, which is reported to be reduced with aging; however, it is not known if this is linked to an aging‐suppression of SIRT1. This study tested the hypothesis that Sirtuin 1 (SIRT1) overexpression would increase the extent of muscle repair and muscle function in older mice.MethodsWe examined satellite cell dependent repair in tibialis anterior, gastrocnemius, and soleus muscles of 13 young wild‐type mice (20–30 weeks) and 49 older (80+ weeks) mice that were controls (n = 13), overexpressed SIRT1 in skeletal muscle (n = 14), and had a skeletal muscle SIRT1 knockout (n = 12) or a satellite cell SIRT1 knockout (n = 10). Acute muscle injury was induced by injection of cardiotoxin (CTX), and phosphate‐buffered saline was used as a vector control. Plantarflexor muscle force and fatigue were evaluated before or 21 days after CTX injection. Satellite cell proliferation and mitochondrial function were also evaluated in undamaged muscles.ResultsMaximal muscle force was significantly lower in control muscles of older satellite cell knockout SIRT1 mice compared to young adult wild‐type (YWT) mice (P < 0.001). Mean contraction force at 40 Hz stimulation was significantly greater after recovery from CTX injury in older mice that overexpressed muscle SIRT1 than age‐matched SIRT1 knockout mice (P < 0.05). SIRT1 muscle knockout models (P < 0.05) had greater levels of p53 (P < 0.05 MKO, P < 0.001 OE) in CTX‐damaged tissues as compared to YWT CTX mice. SIRT1 overexpression with co‐expression of p53 was associated with increased fatigue resistance and increased force potentiation during repeated contractions as compared to wild‐type or SIRT1 knockout models (P < 0.001). Muscle structure and mitochondrial function were not different between the groups, but proliferation of satellite cells was significantly greater in older mice with SIRT1 muscle knockout (P < 0.05), but not older SIRT1 satellite cell knockout models, in vitro, although this effect was attenuated in vivo after 21 days of recovery.ConclusionsThe data suggest skeletal muscle structure, function, and recovery after CTX‐induced injury are not significantly influenced by gain or loss of SIRT1 abundance alone in skeletal muscle; however, muscle function is impaired by ablation of SIRT1 in satellite cells. SIRT1 appears to interact with p53 to improve muscle fatigue resistance after repair from muscle injury.

Short Communication: Optimazing culture and differentiation L6 cell, C2C12 cell and primary myoblast cells culture

Abstract. Lesmana R, Goenawan H, Tarawan VM, Setiawan I, Hidayat A, Supratman U. 2018. Short Communication: Optimizing culture and differentiation of L6 cell, C2C12 cell, and primary myoblast cells culture. Cell Biol Dev 2: 51-54. Alteration in skeletal muscle function and structure could result from many chronic diseases, drug treatment, or physical activity. Therefore, understanding the molecular mechanism of skeletal muscle diseases or the adaptation process will be very important and beneficial. In most cases, for example, during aging, the imbalance between anabolic and catabolic processes could initiate a decreased muscle mass and change its fiber structure. Unfortunately, there is no suitable animal model for study, and animal model development is time-consuming at some point. Next, it is good to study and elaborate a model on disease mechanisms, drug targets, and hormonal effects in skeletal muscle, which is not easy and tricky. Finally, the promising methods to study molecular biology properties of muscle are using in vitro systems utilizing 2 cell lines derived from mouse (C2C12 myoblast cells) and rat (L6 myoblast. Another establishment technique is using mixed and isolated single fiber primary myocytes culture.

Higher Protein Diets Oppose Changes in Skeletal Muscle Transcriptome with Age (OR18-03-19)

ObjectivesAdvancing age during adulthood is associated with deterioration of skeletal muscle (SkM) structure and function (i.e., sarcopenia). Currently, high-protein diets are one of the few recommended therapies to attenuate sarcopenia. However, the mechanisms by which high-protein diets may improve SkM health are not fully understood. The objective of this study was to compare changes in the SkM transcriptome that occur with age (AGE: old vs. young adults) to changes in the SkM transcriptome of older adults in response to protein diets (PROTEIN: high protein vs. low protein diet). MethodsTwo previously published microarray datasets were used for this analysis. The AGE dataset included SkM transcriptomic data from 15 young (25 ± 1 years) and 21 older (78 ± 1 years) adults. The PROTEIN dataset included SkM transcriptomic data obtained from 10 older (72 ± 6 years) adults who consumed either a high (1.0 g protein x kg body wt–1x d–1) or a low (0.5 g protein x kg body wt–1x d–1) protein diet for 18 days. For both studies, morning fasting SkM biopsies were obtained from the vastus lateralis. RNA was extracted, and RNA quality and quantity was checked prior to microarray analysis. A False Discovery Rate correction was used to adjust for multiple comparisons. Differentially expressed genes were uploaded into Ingenuity Pathway Analysis (IPA), and upstream regulators, canonical pathways, and cellular and molecular functions were compared between the AGE and PROTEIN. ResultsThere were 11 common upstream regulators between the AGE and PROTEIN, including TGFB1, CREB1, TP53, ATF4, and FOXO1 that had opposing differences in regulation with the higher protein diet (Table 1). Similarly, there were 4 common canonical pathways between AGE and PROTEIN. Three of the four pathways had opposing changes in regulation including the Sirtuin Signaling, Nucleotide Excision Repair, and Integrin Signaling pathways. Lastly, there were three common Cellular and Molecular Functions (Organismal Death, Apoptosis, Cell Movement), all of which had opposing changes AGE vs. PROTEIN. ConclusionsThese results suggest that high protein diets alter the SkM transcriptome in older adults and may oppose age-related changes in the SkM, particularly those of tissue remodeling, nutrient sensing, and inflammation. Additionally, inadequate protein intake may promote age-related changes in SkM. Funding SourcesNA Supporting Tables, Images and/or Graphs▪

Optimization of Exercise Countermeasures for Human Space Flight: Operational Considerations for Concurrent Strength and Aerobic Training.

The physiological challenges presented by space flight and in microgravity (μG) environments are well documented. μG environments can result in declines muscle mass, contractile strength, and functional capabilities. Previous work has focused on exercise countermeasures designed to attenuate the negative effects of μG on skeletal muscle structure, function, and contractile strength and aerobic fitness parameters. Exposure to μG environments influences both strength and aerobic type physical qualities. As such, the current exercise recommendations for those experiencing μG involve a combination of strength and aerobic training or “concurrent training.” Concurrent training strategies can result in development and maintenance of both strength and aerobic capabilities. However, terrestrial research has indicated that if concurrent training strategies are implemented inappropriately, strength development can be inhibited. Previous work has also demonstrated that the aforementioned inhibition of strength development is dependent on the frequency of aerobic training, modality of aerobic training, the relief period between strength and aerobic training, and the intra-session sequencing of strength and aerobic training. While time constraints and feasibility are important considerations for exercise strategies in μG, certain considerations could be made when prescribing concurrent strength and aerobic training to those experiencing human space flight. If strength and aerobic exercise must be performed in close proximity, strength should precede aerobic stimulus. Eccentric strength training methods should be considered to increase mechanical load and reduce metabolic cost. For aerobic capacity, maintenance cycle and/or rowing-based high-intensity intermittent training (HIIT) should be considered and cycle ergometry and/or rowing may be preferable to treadmill running.

THE CORELATION BETWEEN GRIP MUSCLES’ STRENTGH AND A LEVEL OF FUNCTIONAL ABILITY AMONG THE ELDERLY WOMEN IN TISTA KERAMBITAN, TABANAN

The aging process affects the skeletal muscle structure and disability of the musculoskeletal system which resulted in limited and slowed motion. One characteristic of the aging process is a decrease in muscle strength. Muscle strength affects almost all daily activity. Decreased muscle strength can lead to limitations in daily activities, independence and quality of life. This study aims to determine the relationship between handgrip muscles’ strength and level of functional ability among elderly women in Tista, Kerambitan Tabanan. To assess the strength of the relationship and assess the direction of the relationship between the variables. The research design was used cross sectional study with Simple Random Sampling and got 73 samples. The strength of handgrip muscles was measured using Hand-grip dynamometer, while the functional independence level was assessed by Intermediate Activity Daily Living (IADL) questionnaire interview. Result of research by using Spearman correlation test got value P = 0,000 (P &lt;0,05) and Coefficient correlation value equal to 0,489 indicate that there is a significant correlation between handgrip muscles’ strength with functional ability independence level, this relation is positive and medium. In conculsion that handgrip muscles’s strength and level of functional ability are positively correlated and medium. The stronger the muscle strength of the handgrip, the higher the level of functional ability independence and vice versa. Therefore, handgrip muscle’s strength can be used in identifying disabilities in the elderly.&#x0D; Keywords: elderly, handgrip muscles’ strength, functional capabilities, disability.

Echogenicity Is Related to Skeletal Muscle Strength in Patients With Acute Respiratory Failure.

Patients with acute respiratory failure (ARF) show changes in skeletal muscle structure and strength. The purpose of this study was to examine the relationship between muscle thickness, echogenicity, and strength in patients with ARF. Thirteen (6 females, 7 males) patients with ARF participated in the study. Knee extensor strength was measured via a handheld dynamometer and quadriceps images were obtained via ultrasonography at hospital discharge. The ultrasonograms were used to obtain muscle thickness and both mean ± SD echogenicity of the rectus femoris, vastus lateralis, and vastus medialis. Partial correlations, controlling for age, body mass index, and fluid intake were used to describe the relationships among knee extensor strength and echogenicity and muscle thickness. Knee extensor strength and vastus lateralis SD echogenicity were significantly correlated when controlling for age, body mass index, and fluid intake (r = 0.69, P = .029). Knee extensor strength and vastus lateralis echogenicity were 19.1 ± 8.0 kg and 19.8 ± 5.4 units, respectively. No other correlations between strength and ultrasound measures were found to be significant. These results show skeletal muscle echogenicity to be significantly correlated with skeletal muscle strength in patients with ARF. As such, it may be useful in identifying muscle weakness in these patients when they are unable or unwilling to perform voluntary strength testing.

The Effect of Low Dose Statin Combined with Grapefruit on Skeletal Muscle Structure and the Possible Protective Role of Mesenchymal Stem Cells

The Effect of Low Dose Statin Combined with Grapefruit on Skeletal Muscle Structure and the Possible Protective Role of Mesenchymal Stem Cells