To evaluate sarcopenic indices in relation to respiratory muscle strength (RMS) in elderly people.

Muscle strength is highly heritable and predictive for multiple adverse health outcomes including mortality. Here, we present a rare protein-coding variant association study in 340,319 individuals for hand grip strength, a proxy measure of muscle strength. We show that the exome-wide burden of rare protein-truncating and damaging missense variants is associated with a reduction in hand grip strength. We identify six significant hand grip strength genes, KDM5B, OBSCN, GIGYF1, TTN, RB1CC1, and EIF3J. In the example of the titin (TTN) locus we demonstrate a convergence of rare with common variant association signals and uncover genetic relationships between reduced hand grip strength and disease. Finally, we identify shared mechanisms between brain and muscle function and uncover additive effects between rare and common genetic variation on muscle strength.

Photobiomodulation has been shown to improve tissue and cell functions. We evaluated the influence of photobiomodulation, using a B-Cure laser, on: 1) maximal performance, and 2) muscle recovery after resistance exercise. Two separate crossover randomized double-blinded placebo-controlled trials were conducted. Sixty healthy physical education students (28 men, 32 women), aged 20-35, were recruited (30 participants for each trial). Participants performed two interventions for each experiment, with real lasers (GaAlAs, 808 nm) on three quadricep locations in parallel (overall treatment energy of ~150J) or sham (placebo) treatment. In the first experiment muscle total work (TW) and peak torque (PT) were measured by an isokinetic dynamometer in five repetitions of knee extension, and in the second experiment muscle recovery was measured after the induction of muscle fatigue by evaluating TW and PT in five repetitions of knee extension. There were no differences between treatments (real or sham) regarding the TW (F(1,28) = 1.09, p = .31), or PT (F(1,29) = .056, p = .814). In addition, there was no effect of photobiomodulation on muscle recovery as measured by the TW (F(1,27) = .16, p = .69) or PT (F(1,29) = .056, p = .814). Applying photobiomodulation for 10 min immediately before exercise did not improve muscle function or muscle recovery after fatigue.

[Purpose] The purpose of this study was to provide the data for constructing an integrated exercise program to help restore muscle strength and stability through extension strength exercise in adult females with lumbar disc herniation. [Subjects and Methods] An 8-week exercise program for lumbar muscle extension strength and stabilization was performed by 26 females older than 20 with lumbar disc herniation findings. [Results] Significant differences were found in lumbar extension muscle strength at every angle of lumbar flexion after participation in the 8-week stabilization exercise program; but there was no significant difference in the weight distribution index. [Conclusion] An integrated exercise program aiming to strengthen lumbar spine muscles, reduce pain and stabilize the trunk can help to maintain muscle strength and balance. In addition, improvement in extension strength is expected to be helpful in daily life by securing the range of joint motion and improving the strength and stability.

1. In human pennate muscle, changes in anatomical cross-sectional area (CSA) or volume caused by training or inactivity may not necessarily reflect the change in physiological CSA, and thereby in maximal contractile force, since a simultaneous change in muscle fibre pennation angle could also occur. 2. Eleven male subjects undertook 14 weeks of heavy-resistance strength training of the lower limb muscles. Before and after training anatomical CSA and volume of the human quadriceps femoris muscle were assessed by use of magnetic resonance imaging (MRI), muscle fibre pennation angle (theta(p)) was measured in the vastus lateralis (VL) by use of ultrasonography, and muscle fibre CSA (CSA(fibre)) was obtained by needle biopsy sampling in VL. 3. Anatomical muscle CSA and volume increased with training from 77.5 +/- 3.0 to 85.0 +/- 2.7 cm(2) and 1676 +/- 63 to 1841 +/- 57 cm(3), respectively (+/- S.E.M.). Furthermore, VL pennation angle increased from 8.0 +/- 0.4 to 10.7 +/- 0.6 deg and CSA(fibre) increased from 3754 +/- 271 to 4238 +/- 202 microm (2). Isometric quadriceps strength increased from 282.6 +/- 11.7 to 327.0 +/- 12.4 N m. 4. A positive relationship was observed between theta(p) and quadriceps volume prior to training (r = 0.622). Multifactor regression analysis revealed a stronger relationship when theta(p) and CSA(fibre) were combined (R = 0.728). Post-training increases in CSA(fibre) were related to the increase in quadriceps volume (r = 0.749). 5. Myosin heavy chain (MHC) isoform distribution (type I and II) remained unaltered with training. 6. VL muscle fibre pennation angle was observed to increase in response to resistance training. This allowed single muscle fibre CSA and maximal contractile strength to increase more (+16 %) than anatomical muscle CSA and volume (+10 %). 7. Collectively, the present data suggest that the morphology, architecture and contractile capacity of human pennate muscle are interrelated, in vivo. This interaction seems to include the specific adaptation responses evoked by intensive resistance training.

To use isokinetic strength testing system to test and analyze the relationship between changes in muscle strength before and after knee replacement in patients undergoing total knee arthroplasty (TKA).

Muscle soreness after a competition or a training session has been a concern of runners due to its harmful effect on performance. It is not known if stronger individuals present a lower level of muscle soreness after a strenuous physical effort. The aim of this study was to investigate whether the pre-race muscle strength or the V˙O2max level can predict muscle soreness 24, 48 and 72 h after a full marathon in men.

Myostatin, a member of the transforming growth factor-β superfamily, is an attractive target for muscle disease therapy because of its role as a negative regulator of muscle growth and strength. Here, we describe a novel antibody therapeutic approach that maximizes the potential of myostatin-targeted therapy. We generated an antibody, GYM329, that specifically binds the latent form of myostatin and inhibits its activation. Additionally, via "sweeping antibody technology", GYM329 reduces or "sweeps" myostatin in the muscle and plasma. Compared with conventional anti-myostatin agents, GYM329 and its surrogate antibody exhibit superior muscle strength-improvement effects in three different mouse disease models. We also demonstrate that the superior efficacy of GYM329 is due to its myostatin specificity and sweeping capability. Furthermore, we show that a GYM329 surrogate increases muscle mass in normal cynomolgus monkeys without any obvious toxicity. Our findings indicate the potential of GYM329 to improve muscle strength in patients with muscular disorders.

Pulmonary complications, such as atelectasis, pulmonary oedema, pleural effusion, bronchospasm, and pneumonia, have been reported following cardiac surgery. Shallow breathing leading to impaired lung function is the major cause of respiratory complications. Decreases in respiratory muscle strength can be measured using the maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP) produced in the oral cavity. This study aimed to determine the decrease in respiratory muscle strength 8 weeks following cardiac surgery. Moreover, the relationship between lung function and respiratory muscle strength was studied.

Persons with diabetes have accelerated muscle loss compared with their counterparts. The relationship of hyperglycemia per se to declines in muscle function has not been explored yet has implications for developing appropriate intervention strategies to prevent muscle loss.

As individuals with spinal cord injury (SCI) age they report noticeable deficits in muscle strength, endurance and functional capacity when performing everyday tasks. These changes begin at ~45 years. Here we present a cross-sectional analysis of paralyzed thenar muscle and motor unit contractile properties in two datasets obtained from different subjects who sustained a cervical SCI at different ages (≤46 years) in relation to data from uninjured age-matched individuals. First, completely paralyzed thenar muscles were weaker when C6 SCI occurred at an older age. Muscles were also significantly weaker if the injury was closer to the thenar motor pools (C6 vs. C4). More muscles were strong (>50% uninjured) in those injured at a younger (≤25 years) vs. young age (>25 years), irrespective of SCI level. There was a reduction in motor unit numbers in all muscles tested. In each C6 SCI, only ~30 units survived vs. 144 units in uninjured subjects. Since intact axons only sprout 4-6 fold, the limits for muscle reinnervation have largely been met in these young individuals. Thus, any further reduction in motor unit numbers with time after these injuries will likely result in chronic denervation, and may explain the late-onset muscle weakness routinely described by people with SCI. In a second dataset, paralyzed thenar motor units were more fatigable than uninjured units. This gap widened with age and will reduce functional reserve. Force declines were not due to electromyographic decrements in either group so the site of failure was beyond excitation of the muscle membrane. Together, these results suggest that age at SCI is an important determinant of long-term muscle strength, and fatigability, both of which influence functional capacity.

Upper limb muscle strength plays an important role in respiratory and pulmonary function, and limited research focuses on the role of strength and endurance of the elbow extensor and flexor. This study was conducted to accurately assess upper limb muscle function and quantified associations with pulmonary function and respiratory muscle strength in patients with stable chronic obstructive pulmonary disease (COPD).

Sarcopenia, the loss of muscle mass and function with age, is associated with increased morbidity and mortality. Current understanding of the underlying mechanisms is limited. Glucocorticoids (GC) in excess cause muscle weakness and atrophy. We hypothesized that GC may contribute to sarcopenia through elevated circulating levels or increased glucocorticoid receptor (GR) signaling by increased expression of either GR or the GC-amplifying enzyme 11 beta-hydroxysteroid dehydrogenase type 1 (11βHSD1) in muscle.

Skeletal muscle regeneration after injury is essential for maintaining muscle function throughout aging. ARHGEF3, a RhoA/B-specific GEF, negatively regulates myoblast differentiation through Akt signaling independently of its GEF activity in vitro. Here, we report ARHGEF3's role in skeletal muscle regeneration revealed by ARHGEF3-KO mice. These mice exhibit indiscernible phenotype under basal conditions. Upon acute injury, however, ARHGEF3 deficiency enhances the mass/fiber size and function of regenerating muscles in both young and regeneration-defective middle-aged mice. Surprisingly, these effects occur independently of Akt but via the GEF activity of ARHGEF3. Consistently, overexpression of ARHGEF3 inhibits muscle regeneration in a Rho-associated kinase-dependent manner. We further show that ARHGEF3 KO promotes muscle regeneration through activation of autophagy, a process that is also critical for maintaining muscle strength. Accordingly, ARHGEF3 depletion in old mice prevents muscle weakness by restoring autophagy. Taken together, our findings identify a link between ARHGEF3 and autophagy-related muscle pathophysiology.

Fucoidan is a sulfated polysaccharide found in a range of brown algae species. Growing evidence supports the long-term supplementation of fucoidan as an ergogenic aid to improve skeletal muscle performance. The aim of this study was to investigate the effect of fucoidan on the skeletal muscle of mice. Male BL/6 mice (N = 8-10) were administered a novel fucoidan blend (FUC, 400 mg/kg/day) or vehicle (CON) for 4 weeks. Treatment and control experimental groups were further separated into exercise (CON+EX, FUC+EX) or no-exercise (CON, FUC) groups, where exercised groups performed 30 min of treadmill training three times per week. At the completion of the 4-week treatment period, there was a significant increase in cross-sectional area (CSA) of muscle fibers in fucoidan-treated extensor digitorum longus (EDL) and soleus fibers, which was accompanied by a significant increase in tibialis anterior (TA) muscle force production in fucoidan-treated groups. There were no significant changes in grip strength or treadmill time to fatigue, nor was there an effect of fucoidan or exercise on mass of TA, EDL, or soleus muscles. In gastrocnemius muscles, there was no change in mRNA expression of mitochondrial biogenesis markers PGC-1α and Nrf-2 in any experimental groups; however, there was a significant effect of fucoidan supplementation on myosin heavy chain (MHC)-2x, but not MHC-2a, mRNA expression. Overall, fucoidan increased muscle size and strength after 4 weeks of supplementation in both exercised and no-exercised mice suggesting an important influence of fucoidan on skeletal muscle physiology.

Neural drive and contractile properties are well-defined physiological determinants of explosive strength, the influence of muscle architecture and related morphology on explosive strength is poorly understood. The aim of this study was to examine the relationships between Quadriceps muscle architecture (pennation angle [ΘP] and fascicle length [FL]) and size (e.g., volume; QVOL), as well as patellar tendon moment arm (PTMA) with voluntary and evoked explosive knee extension torque in 53 recreationally active young men.

No abstract available

Diabetes-related dementia (DrD), a dementia subgroup associated with specific diabetes mellitus (DM)-related metabolic abnormalities, is clinically and pathophysiologically different from Alzheimer disease (AD) and vascular dementia. We determined whether skeletal muscle strength, quality, and mass decrease in individuals with DrD.

Although the ingestion of total omega-3 fatty acids (omega-3) is positively related with muscular strength in older persons, little is known about the effect of omega-3 plasma levels on muscular function before and after exercise in young men. Moreover, omega-3 supplementation has a positive role in exercise-induced acute muscle damage. This study investigated the relationship between plasma omega-3 in the blood and promotion and preservation of muscle strength after eccentric contractions (ECCs) in young men.

The deleterious impact of concomitant muscle injury on fracture healing and limb function is commonly considered part of the natural sequela of orthopedic trauma. Recent reports suggest that heightened inflammation in the surrounding traumatized musculature is a primary determinant of fracture healing. Relatedly, there are emerging potential therapeutic approaches for severe muscle trauma (e.g., volumetric muscle loss [VML] injury), such as autologous minced muscle grafts (1 mm3 pieces of muscle; GRAFT), that can partially prevent chronic functional deficits and appear to have an immunomodulatory effect within VML injured muscle. The primary goal of this study was to determine if repair of VML injury with GRAFT rescues impaired fracture healing and improves the strength of the traumatized muscle in a male Lewis rat model of tibia open fracture. The most salient findings of the study were: (1) tibialis anterior (TA) muscle repair with GRAFT improved endogenous healing of fractured tibia and improved the functional outcome of muscle regeneration; (2) GRAFT repair attenuated the monocyte/macrophage (CD45+CDllb+) and T lymphocyte (CD3+) response to VML injury; (3) TA muscle protein concentrations of MCP1, IL-10, and IGF-1 were augmented in a proregenerative manner by GRAFT repair; (4) VML injury concomitant with osteotomy induced a heightened systemic presence of alarmins (e.g., soluble RAGE) and leukocytes (e.g., monocytes), and depressed IGF-1 concentration, which GRAFT repair ameliorated. Collectively, these data indicate that repair of VML injury with a regenerative therapy can modulate the inflammatory and regenerative phenotype of the treated muscle and in association improve musculoskeletal healing.