Recovery Of Muscle Atrophy Research Articles

Exercise Training’s Impact on Multifidus Muscle Thickness in Patients with Lower Back Pain: A Systematic Review

Various previous studies showed that there is involvement of multifidus muscle in lower back pain patients. Atrophy of lumbar multifidus is commonly witnessed among LBP patients. However, there is a lack of scientific findings regarding the training of this muscle. It is still unknown what changes are caused in the multifidus by such training methods. Therefore, the aim of this review is to explore the impact of various training techniques on the thickness of the multifidus muscle in patients with chronic or nonspecific back pain. Various international databases like Google Scholar, Scopus Elsevi¬er, Web of Science, and PubMed were searched by using a combination of keywords like “Exercise”, “Multifidus”, “Thickness” and “Lower Back Pain”. PEDro scoring was used for the assessment of the quality of included RCTs in the present review. It was found that there are few studies that showed improvement in the thickness of lumbar muscles due to different types of training but without investigating lumbar multifidus specifically. Isokinetic training and core stabilization exercises have been found to improve the thickness and symmetry of the multifidus muscle, as well as aid in muscle atrophy recovery. Isokinetic exercises and core-strengthening routines have been shown to enhance the multifidus muscle’s thickness and symmetry, and also assist in reversing muscle atrophy. It can be used to improve the knowledge of physical therapists and LBP patients who are suffering from chronic or nonspecific back pain.

The Effects of Reconditioning Exercises Following Prolonged Bed Rest on Lumbopelvic Muscle Volume and Accumulation of Paraspinal Muscle Fat

Reduced muscle size and accumulation of paraspinal muscle fat content (PFC) have been reported in lumbopelvic muscles after spaceflights and head-down tilt (HDT) bed rest. While some information is available regarding reconditioning programs on muscle atrophy recovery, the effects on the accumulation of PFC are unknown. Recently, a device (the Functional Re-adaptive Exercise Device—FRED) has been developed which aims to specifically recruit lumbopelvic muscles. This study aimed to investigate the effects of a standard reconditioning (SR) program and SR program supplemented by FRED (SR + FRED) on the recovery of the lumbopelvic muscles following 60-day HDT bed rest. Twenty-four healthy participants arrived at the facility for baseline data collection (BDC) before the bed rest period. They remained in the facility for 13-day post-HDT bed rest and were randomly allocated to one of two reconditioning programs: SR or SR + FRED. Muscle volumes of the lumbar multifidus (LM), lumbar erector spinae (LES), quadratus lumborum (QL), and psoas major (PM) muscles were measured from axial T1-weighted magnetic resonance imaging (MRI) at all lumbar intervertebral disc levels. PFC was determined using a chemical shift-based lipid/water Dixon sequence. Each lumbopelvic muscle was segmented into four equal quartiles (from medial to lateral). MRI of the lumbopelvic region was conducted at BDC, Day-59 of bed rest (HDT59), and Day-13 after reconditioning (R13). Comparing R13 with BDC, the volumes of the LM muscle at L4/L5 and L5/S1, LES at L1/L2, and QL at L3/L4 had not recovered (all—p < 0.05), and the PM muscle remained larger at L1/L2 (p = 0.001). Accumulation of PFC in the LM muscle at the L4/L5 and L5/S1 levels remained higher in the centro-medial regions at R13 than BDC (all—p < 0.05). There was no difference between the two reconditioning programs. A 2-week reconditioning program was insufficient to fully restore all volumes of lumbopelvic muscles and reverse the accumulation of PFC in the muscles measured to BDC values, particularly in the LM muscle at the lower lumbar levels. These findings suggest that more extended reconditioning programs or alternative exercises may be necessary to fully restore the size and properties of the lumbopelvic muscles after prolonged bed rest.

Recovery of Muscle Atrophy and Fatty Infiltration in Patients With Acetabular Dysplasia After Total Hip Arthroplasty.

Hip osteoarthritis (OA) with acetabular dysplasia negatively affects pelvic alignment and muscle function. We aimed to investigate the changes in muscle atrophy and fatty infiltration of the hip and trunk muscles 1 year after total hip arthroplasty (THA) in patients with hip OA with acetabular dysplasia. This study included 51 female patients who underwent THA for unilateral hip OA with acetabular dysplasia. The cross-sectional area (CSA) and muscle density of the gluteus maximus, gluteus medius, gluteus minimus, piriformis, iliopsoas, rectus abdominis, and abdominal oblique muscles using computer tomography and pelvic inclination angle using radiographs were assessed before and 1 year after THA. At the 1-year follow-up, the CSA and muscle density of the gluteus medius (2,078 to 2,522 mm2 and 30.3 to 39.4 hounsfield units [HU]), iliopsoas (715 to 901 mm2 and 40.3 to 50.8 HU), and rectus abdominis (336 to 363 mm2 and 28.6 to 30.6 HU) of the affected limb had increased significantly (P < 0.05). The CSA and muscle density of the gluteus maximus (2,429 versus 2,884 mm2 and 23.7 versus 32.6 HU), gluteus minimus (636 versus 785 mm2 and 14.3 versus 37.1 HU), piriformis (505 versus 607 mm2 and 23.4 versus 31.6 HU), and iliopsoas (901 versus 997 mm2 and 50.8 versus 54.5 HU) in the affected limb were lower than those in the unaffected limb (P < 0.01). Postoperatively, the CSA and muscle density of the rectus abdominis were not significantly different between the limbs, and the pelvic inclination angle (35.2° to 32.1°, P < 0.01) was significantly decreased. Compared with the nonoperated limb, substantial atrophy and fatty infiltration of most hip muscles persisted in the operated limb 1 year after THA in patients with acetabular dysplasia; asymmetry in the rectus abdominis muscle fully resolved. In patients with acetabular dysplasia, the surgical technique and postoperative rehabilitation should be further considered to optimize hip muscle recovery.

Platelet-rich fibrin membrane nerve guidance conduit: a potentially promising method for peripheral nerve injuries.

Platelet-rich fibrin membrane nerve guidance conduit: a potentially promising method for peripheral nerve injuries.

Panax ginseng Total Protein Facilitates Recovery from Dexamethasone-Induced Muscle Atrophy through the Activation of Glucose Consumption in C2C12 Myotubes.

Background The clinical anti-inflammatory drug dexamethasone (DEX) can cause many side effects such as muscle atrophy for long-term use. Muscle atrophy induced by DEX may be caused by decrease of glucose consumption. Panax ginseng C.A. Meyer was previously considered to be an antiatrophic agent for glucocorticoid- (GC-) treated therapies. As one of the main components, it remains unclear whether ginseng total protein (GP) facilitates recovery from muscle atrophy induced by DEX. Methods In this study, GP was extracted and purified with Sephadex-G50. C2C12 myoblasts was induced with 2% horse serum to differentiate into C2C12 myotubes. Cell viability was analyzed by the MTT assay, and Ca2+ concentration was analyzed by a flow cytometer. The release of lactic dehydrogenase (LDH) and the glucose consumption were analyzed by spectrophotometry. The phosphorylation of AMP-activated protein kinase (AMPK), phosphoinositide 3-kinase (PI3K), and protein kinase B (Akt) and the expression of glucose transporter 4 (GLUT4) were analyzed by Western blotting. The phosphorylation of AS160 was quantified by Immunofluorescence staining. Results We found that GP increased cell viability and increased myotube diameter in high-dose DEX-treated C2C12 myotubes for 24 h, but this activity was not found in the enzymatic hydrolyzed GP group. GP reduced muscle atrophy by decreasing the expression of key proteins such as muscle RING-finger protein-1 and muscle atrophy F-box, reducing the Ca2+ concentration, and decreasing the release of LDH in DEX-injured C2C12 myotubes. Moreover, GP improved glucose consumption and increased the phosphorylation of AMPK, PI3K, Akt, and AS160 and the expression of GLUT4 in DEX-treated C2C12 myotubes. Conclusion The results of this study suggest that GP has effects on recovering DEX-induced muscle atrophy and cell injury, which may improve glucose consumption via the AMPK and PI3K/Akt pathways in high-dose DEX-treated C2C12 myotubes. This study provides in vitro mechanistic insights into the recovery of muscle atrophy with GP treatment.

Suprascapular nerve: is it important in cuff pathology?

Suprascapular nerve and rotator cuff function are intimately connected. The incidence of suprascapular neuropathy has been increasing due to improved understanding of the disease entity and detection methods. The nerve dysfunction often results from a traction injury or compression, and a common cause is increased tension on the nerve from retracted rotator cuff tears. Suprascapular neuropathy should be considered as a diagnosis if patients exhibit posterosuperior shoulder pain, atrophy or weakness of supraspinatus and infraspinatus without rotator cuff tear, or massive rotator cuff with retraction. Magnetic resonance imaging and electromyography studies are indicated to evaluate the rotator cuff and function of the nerve. Fluoroscopically guided injections to the suprascapular notch can also be considered as a diagnostic option. Nonoperative treatment of suprascapular neuropathy can be successful, but in the recent decade there is increasing evidence espousing the success of surgical treatment, in particular arthroscopic suprascapular nerve decompression. There is often reliable improvement in shoulder pain, but muscle atrophy recovery is less predictable. More clinical data are needed to determine the role of rotator cuff repair and nerve decompression in the same setting.

Postural muscle atrophy prevention and recovery and bone remodelling through high frequency proprioception for astronauts

The difficulty in applying active exercises during space flights increases the importance of passive countermeasures, but coupling load and instability remains indispensable for generating high frequency (HF) proprioceptive flows and preventing muscle atrophy and osteoporosis. The present study, in microgravity conditions during a parabolic flight, verified whether an electronic system, composed of a rocking board, a postural reader and a bungee-cord loading apparatus creates HF postural instability comparable to that reachable on the Earth. Tracking the subject, in single stance, to real-time visual signals is necessary to obtain HF instability situations. The bungee-cord loading apparatus allowed the subject to manage the 81.5% body weight load (100% could easily be exceeded). A preliminary training programme schedule on the Earth and in space is suggested. Comparison with a pathological muscle atrophy is presented. The possibility of generating HF proprioceptive flows could complement current countermeasures for the prevention and recovery of muscle atrophy and osteoporosis in terrestrial and space environments. These exercises combine massive activation of spindles and joint receptors, applying simultaneously HF variations of pressure to different areas of the sole of the foot. This class of exercises could improve the effectiveness of current countermeasures, reducing working time and fatigue.

Recovery of muscle atrophy and bone loss from 90 days bed rest: Results from a one-year follow-up

Earlier studies found the recovery of bone loss after clinical immobilization to be incomplete. It has been argued that this is due to the human skeleton's inability to accrue bone mass once peak bone mass has been attained. However, recent studies suggest that bone losses can fully recover when complete functional rehabilitation is achieved. Accordingly, we hypothesized that bone losses by experimental bed rest would recover within one-year of follow-up. Twenty-five men (mean age 32 years, SD 4.2) were randomly assigned to either bed rest only (Ctrl), resistive flywheel exercise (FW), or to a group receiving 60 mg. i.v pamidronate prior to bed rest (Pam). Calf muscle cross sectional area and bone mineral content of the tibia was measured by peripheral quantitative computed tomography. Calcium, PTH and alkaline phosphatase blood levels were assessed along with urinary desoxypyridinoline excretion. Physical activity was assessed by the Freiburg questionnaire. In Pam and FW, diaphyseal bone losses were completely recovered at a 180-day follow-up, and there was even a small surplus after 1 year ( p = 0.016). Epiphyseal bone losses were largely, although not completely recovered after 1 year, when they still amounted to − 0.6% (SD 1.3%, p = 0.034, averaged over all groups). Bone formation and resorption markers had returned to baseline values at this time. However, epiphyseal recovery may still have been on-going, and fitting an exponential model yielded full recovery of the epiphysis within 2 years. Importantly, recovery of calf muscle cross-section and resumption of impact sport activities seemed to precede bone recovery, and bone accrual was closely matching the prior losses on an individual basis. No relationship was found between the epiphyseal BMC deficit at one-year follow-up and the participants' age. Results demonstrate recovery of bed rest induced bone losses in healthy adults. The initial re-accrual rate was remarkably high and is comparable to the accrual of bone mass during the pubertal growth spurt. This and the fact that the recovery of bone appeared to be tightly regulated, and generally followed neuromuscular recovery underline the adult skeleton's capability to adapt to mechanical stimuli.

Progesterone modulates brain-derived neurotrophic factor and choline acetyltransferase in degenerating Wobbler motoneurons

Progesterone (PROG) shows neuroprotective effects in nervous system diseases. The Wobbler mouse, a model of motoneuron degeneration, suffers a mutation of the Vsp154 gene on chromosome 11 leading to motoneuron vacuolation and astrocytosis of the spinal cord. Previous work has demonstrated beneficial effects of PROG in the Wobbler mouse. As an extension of this work, we now studied steroid effects on neuronal brain-derived neurotrophic factor (BDNF) mRNA and protein, on choline acetyltransferase (ChAT) immunoreactivity (IR) and activity in the spinal cord, and on recovery of muscle atrophy. Wobbler mice received implants of PROG pellets (20 mg) at 6 and 10 weeks of age and were killed at 14 weeks. In situ hybridization for BDNF mRNA demonstrated that grain density in large (> 600 μm 2) and medium size (< 600 μm 2) ventral horn neurons was decreased in untreated Wobblers, whereas PROG treatment increased BDNF mRNA in both neuronal types. PROG also induced a subcellular redistribution of BDNF protein, which in controls and steroid-naive Wobblers showed a predominant perinuclear and nucleolar location, whereas after PROG treatment, it was detected in cytoplasmic aggregates. ChAT activity was reduced by 55.3% in muscles of untreated Wobbler mice, whereas a significant increment was obtained after PROG treatment. Wobblers also showed reduced number of ChAT positive motoneurons, but this number was restored to normal by PROG. Finally, the pronounced biceps atrophy of steroid-naive Wobbler mice was slightly but significantly increased by PROG-treatment. Considering the important role played by neurotrophins on neuronal function, changes in BDNF might be part of the PROG activated-pathways to provide neuroprotection and re-establish neurotransmission and neuromuscular function in this degeneration model.