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Results for “Muscle atrophy”

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PubMed2003

Muscle atrophy in patients receiving hemodialysis: effects on muscle strength, muscle quality, and physical function.

BACKGROUND: Dialysis patients are less active and have reduced functional capacity compared to individuals with normal renal function. Muscle atrophy and weakness may contribute to these problems. This investigation was undertaken to quantify the extent of atrophy in the lower extremity muscles, to determine whether defects in muscle specific strength (force per unit mass) or central nervous system (CNS) activation are present, and to assess the relationship between muscle size and physical performance in a group of patients on hemodialysis. METHODS: Thirty-eight dialysis subjects (aged 55 +/- 15 years) and nineteen healthy sedentary controls (aged 55 +/- 13 years) were enrolled. Magnetic resonance imaging of the lower leg was used to determine the total cross-sectional area (CSA) and the area of contractile and non-contractile tissue of the ankle dorsiflexor muscles. Isometric dorsiflexor strength was measured during a maximal voluntary contraction with and without superimposed tetanic stimulation (N = 22 for dialysis subjects, N = 12 for controls). Physical activity was measured by accelerometry, and gait speed was recorded as a measure of physical performance. RESULTS: Dialysis subjects were weaker, less active, and walked more slowly than controls. Total muscle compartment CSA was not significantly different between dialysis subjects and controls, but the contractile CSA was smaller in the dialysis patients even after adjustment for age, gender, and physical activity. Central activation and specific strength were normal. Gait speed was correlated with contractile CSA. CONCLUSIONS: Significant atrophy and increased non-contractile tissue are present in the muscle of patients on hemodialysis. The relationship between contractile area and strength is intact in this population. Muscle atrophy is associated with poor physical performance. Thus, interventions to increase physical activity or otherwise address atrophy may improve performance and quality of life.

Adult↗

PubMed2006

The effect of glutamine on prevention of glucocorticoid-induced skeletal muscle atrophy is associated with myostatin suppression.

Excess glucocorticoids (GCs) cause muscle atrophy. Glucocorticoid-induced muscle atrophy is associated with increased intramuscular myostatin expression. Myostatin is a negative regulator of skeletal muscle mass. Glutamine prevents GC-induced muscle atrophy. We hypothesized that glutamine effect on reversal of GC-induced muscle atrophy is mediated in part by suppression of myostatin. We administered daily to male Sprague-Dawley rats dexamethasone, dexamethasone plus glutamine, saline or saline plus glutamine, all pair-fed. Animals were killed on day 5. Body weight and weights of gastrocnemius muscles were measured. Myostatin expression was measured by Northern and Western blots, and was compared with glyceraldehyde-3-phosphate dehydrogenase. Myoblast C2C12 cells were exposed to dexamethasone, or dexamethasone and glutamine, and their myostatin messenger RNA and protein expression compared with glyceraldehyde-3-phosphate dehydrogenase. Myostatin promoter activity was measured by luciferase activity of transfected C2C12 cells, grown in medium including dexamethasone, or dexamethasone plus glutamine. Rats that received dexamethasone showed significant body and muscle weight loss accompanied by an increase in intramuscular myostatin expression, compared with their saline-treated controls. Pair-fed rats given dexamethasone plus glutamine had significantly less reduction in body and muscle weights and lower myostatin expression when compared with those treated with dexamethasone alone. In C2C12 myoblast cells, addition of glutamine to dexamethasone prevented the hyperexpression of myostatin induced by dexamethasone. Myostatin promoter activity increased in cells exposed to dexamethasone, but this increase was partially blocked by addition of the glutamine. Administration of glutamine partially prevents GC-induced myostatin expression and muscle atrophy, providing a potential mechanism for the prevention of muscle atrophy induced by glucocorticoids.

Animals↗

PubMedDate not supplied

Infraspinatus muscle atrophy in professional baseball players.

BACKGROUND: Infraspinatus muscle atrophy has been observed in athletes who stress their upper extremities in an overhead fashion. The majority of such case reports have been in volleyball players, with far fewer cases reported in baseball players. HYPOTHESIS: Infraspinatus muscle atrophy occurs to a notable degree in professional baseball players. STUDY DESIGN: Retrospective cohort study. METHODS: At the end of the 1999 baseball season, data were collected from all Major League Baseball teams in regards to players affected with infraspinatus muscle atrophy. RESULTS: Twelve of the 1491 major league professional baseball players were identified as having appreciable infraspinatus muscle atrophy. There was an increased prevalence of the muscle atrophy in professional pitchers (10 of 494, 4%) compared to position players (2 of 997, 0.2%) (P <0.001). Among affected pitchers, the atrophy was identified more frequently in starting pitchers (8 of 10) compared to relief pitchers (2 of 10) (P = 0.036), pitchers who had played for more years at the major league level (8.7 +/- 4.9 versus 5.2 +/- 4.0) (P = 0.017), and pitchers who had thrown for more innings at the major league level (971.4 +/- 784.4 versus 485.0 +/- 594.6) (P <0.001). CONCLUSION: Infraspinatus atrophy was identified in 4.4% of major league starting pitchers and occurred in those pitchers who pitched for more years and innings during their major league career.

Adult↗

PubMed1997

Chronic neck pain, standing balance, and suboccipital muscle atrophy--a pilot study.

OBJECTIVE: To study the relationship between chronic neck pain, standing balance and suboccipital muscle atrophy. We hypothesize that patients with chronic neck pain have more somatic dysfunction in the cervical spine than control subjects without neck pain. We also hypothesize that patients with chronic neck pain and somatic dysfunction exhibit more atrophy of suboccipital muscles. Lastly, because suboccipital muscles have a high density of proprioceptors, we hypothesize that chronic pain patients exhibit a loss in standing balance. DESIGN: Randomized, controlled, partially blind study examining chronic neck pain patients and control subjects for differences in degree of upper cervical somatic dysfunction, standing balance and suboccipital muscle atrophy. SETTING: Subjects were recruited from a clinical practice at Michigan State University; controls were recruited from the faculty, staff and students. PARTICIPANTS: Seven chronic neck pain patients and seven asymptomatic control subjects. MAIN OUTCOME MEASURES: Palpation was used to diagnose somatic dysfunction in the upper cervical spine. Balance parameters were calculated using a force platform; muscle atrophy was judged with magnetic resonance images. RESULTS: Chronic neck pain patients had almost twice as many somatic dysfunctions as controls (p = .028). Force platform results showed a decrease in standing balance in patients compared with control subjects (p = .004). MRI showed that chronic neck pain subjects had marked atrophy of the rectus capitis posterior major and minor muscles, including fatty infiltration. CONCLUSIONS: This study suggests that there is a relationship between chronic pain, somatic dysfunction, muscle atrophy and standing balance. We hypothesize a cycle initiated by chronic somatic dysfunction, which may result in muscle atrophy, which can be further expected to reduce proprioceptive output from atrophied muscles. The lack of proprioceptive inhibition of nociceptors at the dorsal horn of the spinal cord would result in chronic pain and a loss of standing balance.

Adult↗

PubMed1984

Further studies on 6-mercaptopurine-induced muscle atrophy in rats, mice, and hamsters treated as neonates.

In previous studies, we found that Sprague-Dawley rats injected with 6-mercaptopurine monohydrate (6-MP) at 2 mg base/kg sc daily from 2 to 22 days of age had atrophy of thigh and sublumbar muscles when killed at 16 months of age. The first sign of this muscle atrophy was detected grossly (flattened croup with or without paresis) at 12 months of age. In one experiment of the present work, using the same treatment in rats as above, we found that the earliest onset of muscle atrophy observed by light microscopy occurred at 2 months of age. By 4 months the atrophy could be detected grossly. The atrophy did not uniformly involve all muscles of the hindquarters; the thigh (especially the semitendinosus), leg (soleus but not the extensor carpi group), and lumbar vertebral (including the psoas) muscles were involved. Foreleg (biceps), intercostal, and tongue muscles as well as the sciatic nerve and internal organs appeared unaffected. In another experiment, weanling Sprague-Dawley rats given large daily doses of 6-MP from 25 to 45 days of age had normal muscles when killed at 8 months. In a third experiment, Wistar rats injected with 6-MP (2 mg base/kg sc) daily from 2 to 22 days of age and killed at 6 months had muscle atrophy similar to that seen in Sprague-Dawley rats. In the last experiment, mice and hamsters given large daily doses of 6-MP from 2 to 22 days of age had normal muscles when killed at 10 months. It appears from these results that the 6-MP-induced muscle atrophy occurs only after treatment during the neonatal period and that the atrophy may be species specific.

Animals↗

PubMed2005

Attenuation of skeletal muscle atrophy via protease inhibition.

Skeletal muscle atrophy in response to a number of muscle wasting conditions, including disuse, involves the induction of increased protein breakdown, decreased protein synthesis, and likely a variable component of apoptosis. The increased activation of specific proteases in the atrophy process presents a number of potential therapeutic targets to reduce muscle atrophy via protease inhibition. In this study, mice were provided with food supplemented with the Bowman-Birk inhibitor (BBI), a serine protease inhibitor known to reduce the proteolytic activity of a number of proteases, such as chymotrypsin, trypsin, elastase, cathepsin G, and chymase. Mice fed the BBI diet were suspended for 3-14 days, and the muscle mass and function were then compared with those of the suspended mice on a normal diet. The results indicate that dietary supplementation with BBI significantly attenuates the normal loss of muscle mass and strength following unloading. Furthermore, the data reveal the existence of yet uncharacterized serine proteases that are important contributors to the evolution of disuse atrophy, since BBI inhibited serine protease activity that was elevated following hindlimb unloading and also slowed the loss of muscle fiber size. These results demonstrate that targeted reduction of protein degradation can limit the severity of muscle mass loss following hindlimb unloading. Thus BBI is a candidate therapeutic agent to minimize skeletal muscle atrophy and loss of strength associated with disuse, cachexia, sepsis, weightlessness, or the combination of age and inactivity.

Animals↗

PubMed2006

Intracellular signaling during skeletal muscle atrophy.

A variety of conditions lead to skeletal muscle atrophy including muscle inactivity or disuse, multiple disease states (i.e., cachexia), fasting, and age-associated atrophy (sarcopenia). Given the impact on mobility in the latter conditions, inactivity could contribute in a secondary manner to muscle atrophy. Because different events initiate atrophy in these different conditions, it seems that the regulation of protein loss may be unique in each case. In fact differences exist between the regulation of the various atrophy conditions, especially sarcopenia, as evidenced in part by comparisons of transcriptional profiles as well as by the unique triggering molecules found in each case. By contrast, recent studies have shown that many of the intracellular signaling molecules and target genes are similar, particularly among the atrophies related to inactivity and cachexia. This review focuses on the most recent findings related to intracellular signaling during muscle atrophy. Key findings are discussed that relate to signaling involving muscle ubiquitin ligases, the IGF/PI3K/Akt pathway, FOXO activity, caspase-3 activity, and NF-kappaB signaling, and an attempt is made to construct a unifying picture of how these data can be connected to better understand atrophy. Once more detailed cellular mechanisms of the atrophy process are understood, more specific interventions can be designed for the attenuation of protein loss.

Animals↗

PubMed2005

Mechanisms of disuse muscle atrophy: role of oxidative stress.

Prolonged periods of skeletal muscle inactivity lead to a loss of muscle protein and strength. Advances in cell biology have progressed our understanding of those factors that contribute to muscle atrophy. To this end, abundant evidence implicates oxidative stress as a potential regulator of proteolytic pathways leading to muscle atrophy during periods of prolonged disuse. This review will address the role of reactive oxygen species and oxidative stress as potential contributors to the process of disuse-mediated muscle atrophy. The first section of this article will discuss our current understanding of muscle proteases, sources of reactive oxygen in muscle fibers, and the evidence linking oxidative stress to disuse muscle atrophy. The second section of this review will highlight gaps in our knowledge relative to the specific role of oxidative stress in the regulation of disuse muscle atrophy. By discussing unresolved issues and suggesting topics for future research, it is hoped that this review will serve as a stimulus for the expansion of knowledge in this exciting field.

Animals↗

PubMed1995

Polyubiquitin in crustacean striated muscle: increased expression and conjugation during molt-induced claw muscle atrophy.

The claw muscles of decapod crustaceans undergo a molt-induced atrophy to facilitate withdrawal of the claws at ecdysis. Polyubiquitin expression, as well as the levels of ubiquitin conjugates, a ubiquitin-conjugating enzyme involved in the ATP/ubiquitin-dependent proteolytic pathway (crustacean E2(16 kDa) homolog of Drosophila UbcD1), and proteasome, were examined to determine the role of ATP/ubiquitin-dependent proteolysis in the enhanced degradation of myofibrillar proteins during muscle atrophy. A partial-length clone (1.7 kb) of polyubiquitin was isolated from a lobster muscle cDNA library; the 5' end lacked the 5' untranslated region (UTR) and the beginning of the first ubiquitin monomer, while the 3' end contained the terminal ubiquitin monomer and 3' UTR. The deduced amino acid sequence was 100% identical with that from Manduca, Drosophila, and human. In land crab claw muscle, the polyubiquitin mRNA (2.7 kb) increased about 5-fold and ubiquitin-protein conjugates (> 200 kDa) increased about 8-fold during atrophy. In contrast, the level of a ubiquitin-conjugating enzyme (E2(16 kDa)) remained unchanged. The proteasome, which constitutes the catalytic core of the ATP/ubiquitin-dependent proteinase complex, increased about 2-fold during proecdysis, reaching its highest level immediately before ecdysis. These results suggest that the ATP/ubiquitin-dependent proteolytic pathway contributes to the changes in protein metabolism that occur during molt-induced muscle atrophy.

Amino Acid Sequence↗

PubMed2001

Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo.

Skeletal muscles adapt to changes in their workload by regulating fibre size by unknown mechanisms. The roles of two signalling pathways implicated in muscle hypertrophy on the basis of findings in vitro, Akt/mTOR (mammalian target of rapamycin) and calcineurin/NFAT (nuclear factor of activated T cells), were investigated in several models of skeletal muscle hypertrophy and atrophy in vivo. The Akt/mTOR pathway was upregulated during hypertrophy and downregulated during muscle atrophy. Furthermore, rapamycin, a selective blocker of mTOR, blocked hypertrophy in all models tested, without causing atrophy in control muscles. In contrast, the calcineurin pathway was not activated during hypertrophy in vivo, and inhibitors of calcineurin, cyclosporin A and FK506 did not blunt hypertrophy. Finally, genetic activation of the Akt/mTOR pathway was sufficient to cause hypertrophy and prevent atrophy in vivo, whereas genetic blockade of this pathway blocked hypertrophy in vivo. We conclude that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of the Akt/mTOR pathway can oppose muscle atrophy induced by disuse.

Animals↗

PubMedDate not supplied

Glucocorticoid-induced muscle atrophy: mechanisms and therapeutic strategies.

OBJECTIVE: To analyze the mechanisms of action of glucocorticoids in causing muscle atrophy and to examine the therapeutic effect of testosterone as well as other treatment modalities in counteracting this adverse effect. METHODS: We reviewed selected publications to analyze the mechanisms of glucocorticoid-induced muscle atrophy in animal models and in humans. The pathophysiologic features of glucocorticoid-induced hypogonadism and the possible relationship to the muscle atrophy in patients receiving glucocorticoids were assessed. The beneficial effects of testosterone on the muscles of hypogonadal and eugonadal men were also reviewed. Other measures such as exercise and glutamine and their possible therapeutic and preventive effects were examined in the context of hypercortisolemia. RESULTS: Glucocorticoids induce rapid muscle breakdown and proximal muscle atrophy. The mechanism of glucocorticoid-induced muscle atrophy relies on the degradation of the myosin heavy chain (catabolic effect), the most important contractile protein in muscle, associated with a decrease of its synthesis (antianabolic effect). One of the contributing factors in the development of muscle atrophy is hypogonadism that is induced by long-term glucocorticoid use. Androgen possesses anabolic and anticatabolic effects in vitro and in animal models. Androgens can be used safely to counteract the catabolic effects of cortisol. Other measures such as exercise, glutamine, and alanyl-glutamine are promising in animal models of glucocorticoid-induced muscle atrophy. CONCLUSION: This study suggests the possible efficacy of testosterone and glutamine on glucocorticoid-induced muscle atrophy. Testosterone and glutamine are natural biologic products with safe pharmacologic profiles, and their bioefficacy merits active research in humans.

Journal Article↗

PubMed2005

MRI of rotator cuff muscle atrophy in relation to glenohumeral joint incongruence in brachial plexus birth injury.

PURPOSE: To evaluate rotator cuff muscles and the glenohumeral (GH) joint in brachial plexus birth injury (BPBI) using MRI and to determine whether any correlation exists between muscular abnormality and the development of glenoid dysplasia and GH joint incongruity. MATERIALS AND METHODS: Thirty-nine consecutive BPBI patients with internal rotation contracture or absent active external rotation of the shoulder joint were examined clinically and imaged with MRI. In the physical examination, passive external rotation was measured to evaluate internal rotation contracture. Both shoulders were imaged and the glenoscapular angle, percentage of humeral head anterior to the middle of the glenoid fossa (PHHA) and the greatest thickness of the subscapular, infraspinous and supraspinous muscles were measured. The muscle ratio between the affected side and the normal side was calculated to exclude age variation in the assessment of muscle atrophy. RESULTS: All muscles of the rotator cuff were atrophic, with the subscapular and infraspinous muscles being most severely affected. A correlation was found between the percentage of humeral head anterior to the middle of the glenoid fossa (PHHA) and the extent of subscapular muscle atrophy (r(s)=0.45, P=0.01), as well as between its ratio (r(s)=0.5, P P=0.01). Severity of rotator cuff muscle atrophy correlated with increased glenoid retroversion and the degree of internal rotation contracture. CONCLUSIONS: Glenoid retroversion and subluxation of the humeral head are common in patients with BPBI. All rotator cuff muscles are atrophic, especially the subscapular muscle. Muscle atrophy due to neurogenic damage apparently results in an imbalance of the shoulder muscles and progressive retroversion and subluxation of the GH joint, which in turn lead to internal rotation contracture and deformation of the joint.

Adolescent↗

PubMed2006

Merg1a K+ channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway.

Skeletal muscle atrophy results from an imbalance in protein degradation and protein synthesis and occurs in response to injury, various disease states, disuse, and normal aging. Current treatments for this debilitating condition are inadequate. More information about mechanisms involved in the onset and progression of muscle atrophy is necessary for development of more effective therapies. Here we show that expression of the mouse ether-a-go-go related gene (Merg1a) K+ channel is up-regulated in skeletal muscle of mice experiencing atrophy as a result of both malignant tumor expression and disuse. Further, ectopic expression of Merg1a in vivo induces atrophy in healthy wt-bearing mice, while expression of a dysfunctional Merg1a mutant suppresses atrophy in hindlimb-suspended mice. Treatment of hindlimb-suspended mice with astemizole, a known Merg1a channel blocker, inhibits atrophy in these animals. Importantly, in vivo expression of Merg1a in mouse skeletal muscle activates the ubiquitin proteasome pathway that is responsible for the majority of protein degradation that causes muscle atrophy, yet expression of a dysfunctional Merg1a mutant decreases levels of ubiquitin-proteasome proteolysis. Thus, expression of Merg1a likely initiates atrophy by activating ubiquitin-proteasome proteolysis. This gene and its product are potential targets for prevention and treatment of muscle atrophy.

Animals↗

PubMed1996

Biochemical and clinical study of muscle atrophy at thenar and hypothenar eminences in patients with cirrhosis.

The results of various biochemical examinations in 14 patients with cirrhosis (6 males and 8 females) with muscle atrophy at the thenar and hypothenar eminence (muscle atrophy group; mAG) were compared with those in 13 patients (8 males and 5 females) with cirrhosis without muscle atrophy at these sites (non-muscle atrophy group; NmAG). All patients were elderly men and women (mAG and NmAG, mean age, 69 +/- 3 years and 60 +/- 7, respectively). In most mAG patients, muscle atrophy was accompanied by palmar erythema. Muscle atrophy was histologically demonstrated by biopsy. Furthermore, electromyography and magnetic resonance study of the cervical spinal cord revealed that the atrophy was of myogenic rather than neurogenic origin. The Child-Pugh score, body mass index and sex hormone level in urine (total 24 h) in the two groups were compared along with the biochemical results. There were no significant differences between the two groups in urine estrogen and testosterone levels. The urinary creatinine excretion was significantly reduced in mAG. The creatine phosphokinese, lactate dehydrogenase isoenzyme and aldolase levels in serum did not differ significantly in the two groups, whereas the serum albumin level was significantly increased in NmAG. Significant differences were observed only for the serum albumin level, age and body mass index. Thus, we consider that palmar muscle atrophy in patients with cirrhosis is not due to hormonal excess in serum, but may be attributable to advanced age and diminished physical strength.

Aged↗

PubMed2005

Transgenic overexpression of locally acting insulin-like growth factor-1 inhibits ubiquitin-mediated muscle atrophy in chronic left-ventricular dysfunction.

Metabolic abnormalities develop in various chronic diseases and lead to progressive catabolism with decrements in the skeletal musculature that result in muscle atrophy. We investigated pathways of skeletal muscle proteolysis using an experimental model of chronic left-ventricular dysfunction. Skeletal muscle atrophy developed in wild-type mice 12 weeks following myocardial infarction accompanied by an increase in total protein ubiquitination and enhanced proteasome activity, activation of Foxo transcription factors, and robust induction of the ubiquitin-protein ligase atrogin-1/MAFbx. Further studies identified skeletal muscle myosin as a specific target of ubiquitin-mediated degradation in muscle atrophy. In contrast, transgenic overexpression of a local isoform of insulin-like growth factor-1 prevented muscle atrophy and increased proteasome activity, inhibited skeletal muscle activation primarily of Foxo4, and blocked the expression of atrogin-1/MAFbx. These results suggest that skeletal muscle atrophy occurs through increased activity of the ubiquitin-proteasome pathway. The inhibition of muscle atrophy by local insulin-like growth factor-1 provides a promising therapeutic avenue for the prevention of skeletal muscle wasting in chronic heart failure and potentially other chronic diseases associated with skeletal muscle atrophy.

Animals↗

PubMed2006

Insights into muscle atrophy and recovery pathway based on genetic models.

PURPOSE OF REVIEW: Muscle atrophy is a pervasive problem that occurs with disuse, aging, and a myriad of disease conditions. The purposes of this review are to describe recent advances in studying muscle atrophy that have elucidated pathways involved at the molecular level; to compare different types of atrophy--primary (e.g. bed rest, immobilization) and secondary (when the atrophy is related to pathology as well as disuse, e.g. injury, sepsis etc.) and their multiple common features; to review progress in studying the recovery process and clinical status. RECENT FINDINGS: Major advances have been made at the molecular level. There are two phenotypes for muscle atrophy--primary, which is mainly related to disuse (e.g. bed), and secondary, when the atrophy is related to pathology as well as disuse. It appears that the two forms have multiple elements in common. Studies on the recovery process reveal a very complex sequence of events that are not the simple reverse of the muscle loss process. In contrast to the progress at the molecular level, progress in treating muscle atrophy or accelerating recovery has been disappointing. SUMMARY: Although nutritional supplementation and pharmacological agents continue to have the potential to minimize muscle atrophy, given its minimal risks, exercise sets a very high standard for treatment options when medically appropriate. Identification of pathways and control points offers the potential for new approaches.

Bed Rest↗

PubMed2004

Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression.

Skeletal muscle atrophy is a debilitating response to starvation and many systemic diseases including diabetes, cancer, and renal failure. We had proposed that a common set of transcriptional adaptations underlie the loss of muscle mass in these different states. To test this hypothesis, we used cDNA microarrays to compare the changes in content of specific mRNAs in muscles atrophying from different causes. We compared muscles from fasted mice, from rats with cancer cachexia, streptozotocin-induced diabetes mellitus, uremia induced by subtotal nephrectomy, and from pair-fed control rats. Although the content of >90% of mRNAs did not change, including those for the myofibrillar apparatus, we found a common set of genes (termed atrogins) that were induced or suppressed in muscles in these four catabolic states. Among the strongly induced genes were many involved in protein degradation, including polyubiquitins, Ub fusion proteins, the Ub ligases atrogin-1/MAFbx and MuRF-1, multiple but not all subunits of the 20S proteasome and its 19S regulator, and cathepsin L. Many genes required for ATP production and late steps in glycolysis were down-regulated, as were many transcripts for extracellular matrix proteins. Some genes not previously implicated in muscle atrophy were dramatically up-regulated (lipin, metallothionein, AMP deaminase, RNA helicase-related protein, TG interacting factor) and several growth-related mRNAs were down-regulated (P311, JUN, IGF-1-BP5). Thus, different types of muscle atrophy share a common transcriptional program that is activated in many systemic diseases.

Adenosine Triphosphate↗

PubMed1987

Quadriceps muscle atrophy and long-term recovery after knee ligamentous injury.

The aim of the study was to clarify if atrophy of the quadriceps muscle was in itself related to clinical and radiological long-term outcome of primary knee ligament surgery. At Tampere University Central Hospital clinical and radiological reexamination was performed in 61 patients on an average 40 months after primary operation of acute knee ligament injury. The study group consisted of 26 patients having clear quadriceps muscle atrophy in the injured knee at the follow-up. Thirty four patients, having equal circumference of the thighs, served as controls. One patient was excluded. The groups did not differ significantly from each other in respect to age, sex, physical activity, type of ligament injury, meniscectomy, and follow-up time. In clinical reexamination the patients with quadriceps atrophy were placed significantly more often in groups of fair or poor healing than the patients with normal quadriceps muscle, and they had also more posttraumatic osteoarthritic changes in the injured knee. According to this study it seems that quadriceps muscle atrophy plays an important role as a poor prognostic factor of knee ligament injuries being thus a good target for efforts to stop the continuous deterioration of the injured knee.

Adult↗