scholarly journals Muscle Atrophy After ACL Injury: Implications for Clinical Practice

2020 ◽  
Vol 12 (6) ◽  
pp. 579-586
Author(s):  
Lindsey K. Lepley ◽  
Steven M. Davi ◽  
Julie P. Burland ◽  
Adam S. Lepley
Keyword(s):  
Clinical Review ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Cruciate Ligament ◽  
Muscle Loss ◽  
Disuse Atrophy ◽  
Tissue Quality ◽  
Level Of Evidence ◽  
Joint Injury ◽  
Inducing Factors

Context: Distinct from the muscle atrophy that develops from inactivity or disuse, atrophy that occurs after traumatic joint injury continues despite the patient being actively engaged in exercise. Recognizing the multitude of factors and cascade of events that are present and negatively influence the regulation of muscle mass after traumatic joint injury will likely enable clinicians to design more effective treatment strategies. To provide sports medicine practitioners with the best strategies to optimize muscle mass, the purpose of this clinical review is to discuss the predominant mechanisms that control muscle atrophy for disuse and posttraumatic scenarios, and to highlight how they differ. Evidence Acquisition: Articles that reported on disuse atrophy and muscle atrophy after traumatic joint injury were collected from peer-reviewed sources available on PubMed (2000 through December 2019). Search terms included the following: disuse muscle atrophy OR disuse muscle mass OR anterior cruciate ligament OR ACL AND mechanism OR muscle loss OR atrophy OR neurological disruption OR rehabilitation OR exercise. Study Design: Clinical review. Level of Evidence: Level 5. Results: We highlight that (1) muscle atrophy after traumatic joint injury is due to a broad range of atrophy-inducing factors that are resistant to standard resistance exercises and need to be effectively targeted with treatments and (2) neurological disruptions after traumatic joint injury uncouple the nervous system from muscle tissue, contributing to a more complex manifestation of muscle loss as well as degraded tissue quality. Conclusion: Atrophy occurring after traumatic joint injury is distinctly different from the muscle atrophy that develops from disuse and is likely due to the broad range of atrophy-inducing factors that are present after injury. Clinicians must challenge the standard prescriptive approach to combating muscle atrophy from simply prescribing physical activity to targeting the neurophysiological origins of muscle atrophy after traumatic joint injury.

scholarly journals Increasing autophagy does not affect neurogenic muscle atrophy

2018 ◽  
Vol 28 (3) ◽  
Author(s):  
Eva Pigna ◽  
Krizia Sanna ◽  
Dario Coletti ◽  
Zhenlin Li ◽  
Ara Parlakian ◽  
...  
Keyword(s):  
Muscle Mass ◽  
Muscle Atrophy ◽  
Ubiquitin Proteasome System ◽  
Autophagic Flux ◽  
Molecular Pathways ◽  
Muscle Loss ◽  
Relative Contribution ◽  
Ubiquitin Proteasome ◽  
Muscle Mass Loss ◽  
Kinetics Of

Physiological autophagy plays a crucial role in the regulation of muscle mass and metabolism, while the excessive induction or the inhibition of the autophagic flux contributes to the progression of several diseases. Autophagy can be activated by different stimuli, including cancer, exercise, caloric restriction and denervation. The latter leads to muscle atrophy through the activation of catabolic pathways, i.e. the ubiquitin-proteasome system and autophagy. However, the kinetics of autophagy activation and the upstream molecular pathways in denervated skeletal muscle have not been reported yet. In this study, we characterized the kinetics of autophagic induction, quickly triggered by denervation, and report the Akt/mTOR axis activation. Besides, with the aim to assess the relative contribution of autophagy in neurogenic muscle atrophy, we triggered autophagy with different stimuli along with denervation, and observed that four week-long autophagic induction, by either intermitted fasting or rapamycin treatment, did not significantly affect muscle mass loss. We conclude that: i) autophagy does not play a major role in inducing muscle loss following denervation; ii) nonetheless, autophagy may have a regulatory role in denervation induced muscle atrophy, since it is significantly upregulated as early as eight hours after denervation; iii) Akt/mTOR axis, AMPK and FoxO3a are activated consistently with the progression of muscle atrophy, further highlighting the complexity of the signaling response to the atrophying stimulus deriving from denervation.

Alterations of protein turnover underlying disuse atrophy in human skeletal muscle

2009 ◽  
Vol 107 (3) ◽  
pp. 645-654 ◽  
Author(s):  
S. M. Phillips ◽  
E. I. Glover ◽  
M. J. Rennie
Keyword(s):  
Protein Synthesis ◽  
Muscle Mass ◽  
Protein Turnover ◽  
Cultured Cells ◽  
Muscle Protein ◽  
Human Muscle ◽  
Muscle Loss ◽  
Disuse Atrophy ◽  
In Vivo Measurements

Unloading-induced atrophy is a relatively uncomplicated form of muscle loss, dependent almost solely on the loss of mechanical input, whereas in disease states associated with inflammation (cancer cachexia, AIDS, burns, sepsis, and uremia), there is a procatabolic hormonal and cytokine environment. It is therefore predictable that muscle loss mainly due to disuse alone would be governed by mechanisms somewhat differently from those in inflammatory states. We suggest that in vivo measurements made in human subjects using arterial-venous balance, tracer dilution, and tracer incorporation are dynamic and thus robust by comparison with static measurements of mRNA abundance and protein expression and/or phosphorylation in human muscle. In addition, measurements made with cultured cells or in animal models, all of which have often been used to infer alterations of protein turnover, appear to be different from results obtained in immobilized human muscle in vivo. In vivo measurements of human muscle protein turnover in disuse show that the primary variable that changes facilitating the loss of muscle mass is protein synthesis, which is reduced in both the postabsorptive and postprandial states; muscle proteolysis itself appears not to be elevated. The depressed postprandial protein synthetic response (a phenomenon we term “anabolic resistance”) may even be accompanied by a diminished suppression of proteolysis. We therefore propose that most of the loss of muscle mass during disuse atrophy can be accounted for by a depression in the rate of protein synthesis. Thus the normal diurnal fasted-to-fed cycle of protein balance is disrupted and, by default, proteolysis becomes dominant but is not enhanced.

scholarly journals Fueling for Performance

2017 ◽  
Vol 10 (1) ◽  
pp. 47-53 ◽  
Author(s):  
Jeffrey R. Bytomski
Keyword(s):  
Clinical Review ◽  
Muscle Mass ◽  
Study Design ◽  
Food Sources ◽  
Food Groups ◽  
Level Of Evidence ◽  
Lean Muscle Mass ◽  
Current Weight

Context: Proper nutrition is crucial for an athlete to optimize his or her performance for training and competition. Athletes should be able to meet their dietary needs through eating a wide variety of whole food sources. Evidence Acquisition: PubMed was searched for relevant articles published from 1980 to 2016. Study Design: Clinical review. Level of Evidence: Level 4. Results: An athlete should have both daily and activity-specific goals for obtaining the fuel necessary for successful training. Depending on the timing of their season, athletes may be either trying to gain lean muscle mass, lose fat, or maintain their current weight. Conclusion: An athlete will have different macronutrient goals depending on sport, timing of exercise, and season status. There are no specific athletic micronutrient guidelines, but testing should be considered for athletes with deficiency or injury. Also, some athletes who eliminate certain whole food groups (eg, vegetarian) may need to supplement their diet to avoid deficiencies.

scholarly journals Mitochondrial pathways in sarcopenia of aging and disuse muscle atrophy

2013 ◽  
Vol 394 (3) ◽  
pp. 393-414 ◽  
Author(s):  
Riccardo Calvani ◽  
Anna-Maria Joseph ◽  
Peter J. Adhihetty ◽  
Alfredo Miccheli ◽  
Maurizio Bossola ◽  
...  
Keyword(s):  
Quality Control ◽  
Muscle Atrophy ◽  
Current Knowledge ◽  
Control Mechanisms ◽  
Muscle Loss ◽  
Disuse Atrophy ◽  
Skeletal Myocytes ◽  
Disuse Muscle Atrophy ◽  
Myocyte Function ◽  
Cellular Pathways

Abstract Muscle loss during aging and disuse is a highly prevalent and disabling condition, but knowledge about cellular pathways mediating muscle atrophy is still limited. Given the postmitotic nature of skeletal myocytes, the maintenance of cellular homeostasis relies on the efficiency of cellular quality control mechanisms. In this scenario, alterations in mitochondrial function are considered a major factor underlying sarcopenia and muscle atrophy. Damaged mitochondria are not only less bioenergetically efficient, but also generate increased amounts of reactive oxygen species, interfere with cellular quality control mechanisms, and display a greater propensity to trigger apoptosis. Thus, mitochondria stand at the crossroad of signaling pathways that regulate skeletal myocyte function and viability. Studies on these pathways have sometimes provided unexpected and counterintuitive results, which suggests that they are organized into a complex, heterarchical network that is currently insufficiently understood. Untangling the complexity of such a network will likely provide clinicians with novel and highly effective therapeutics to counter the muscle loss associated with aging and disuse. In this review, we summarize the current knowledge on the mechanisms whereby mitochondrial dysfunction intervenes in the pathogenesis of sarcopenia and disuse atrophy, and highlight the prospect of targeting specific processes to treat these conditions.

Autophagy in health and disease. 3. Involvement of autophagy in muscle atrophy

2010 ◽  
Vol 298 (6) ◽  
pp. C1291-C1297 ◽  
Author(s):  
Marco Sandri
Keyword(s):  
Signaling Pathways ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Molecular Mechanisms ◽  
Muscle Wasting ◽  
Muscle Loss ◽  
Muscle Proteins ◽  
Therapeutic Approaches ◽  
New Therapeutic Approaches ◽  
Health And Disease

Loss of muscle mass aggravates a variety of diseases, and understanding the molecular mechanisms that control muscle wasting is critical for developing new therapeutic approaches. Weakness is caused by loss of muscle proteins, and recent studies have underlined a major role for the autophagy-lysosome system in regulating muscle mass. Some key components of the autophagy machinery are transcriptionally upregulated during muscle wasting, and their induction precedes muscle loss. However, it is unclear whether autophagy is detrimental, causing atrophy, or beneficial, promoting survival during catabolic conditions. This review discusses recent findings on signaling pathways regulating autophagy.

scholarly journals Interventional strategies to combat muscle disuse atrophy in humans: focus on neuromuscular electrical stimulation and dietary protein

2018 ◽  
Vol 125 (3) ◽  
pp. 850-861 ◽  
Author(s):  
Marlou L. Dirks ◽  
Benjamin T. Wall ◽  
Luc J. C. van Loon
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Dietary Protein ◽  
Nutritional Support ◽  
Muscle Protein ◽  
Muscle Protein Synthesis ◽  
Neuromuscular Electrical Stimulation ◽  
Muscle Loss ◽  
Disuse Atrophy ◽  
Muscle Disuse

Numerous situations, such as the recovery from illness or rehabilitation after injury, necessitate a period of muscle disuse in otherwise healthy individuals. Even a few days of immobilization or bed rest can lead to substantial loss of skeletal muscle tissue and compromise metabolic health. The decline in muscle mass is attributed largely to a decline in postabsorptive and postprandial muscle protein synthesis rates. Reintroduction of some level of muscle contraction by the application of neuromuscular electrical stimulation (NMES) can augment both postabsorptive and postprandial muscle protein synthesis rates and, as such, prevent or attenuate muscle loss during short-term disuse in various clinical populations. Whereas maintenance of habitual dietary protein consumption is a prerequisite for muscle mass maintenance, supplementing dietary protein above habitual intake levels does not prevent muscle loss during disuse in otherwise healthy humans. Combining the anabolic properties of physical activity (or surrogates) with appropriate nutritional support likely further increases the capacity to preserve skeletal muscle mass during a period of disuse. Therefore, effective interventional strategies to prevent or alleviate muscle disuse atrophy should include both exercise (mimetics) and appropriate nutritional support.

Attenuation of skeletal muscle atrophy via protease inhibition

2005 ◽  
Vol 99 (5) ◽  
pp. 1719-1727 ◽  
Author(s):  
Carl A. Morris ◽  
Linda D. Morris ◽  
Ann R. Kennedy ◽  
H. Lee Sweeney
Keyword(s):  
Skeletal Muscle ◽  
Serine Protease ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Hindlimb Unloading ◽  
Cathepsin G ◽  
Skeletal Muscle Atrophy ◽  
Variable Component ◽  
Disuse Atrophy ◽  
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.

scholarly journals Increased Total Cost and Lack of Diagnostic Utility for Emergency Department Visits After ACL Injury

2021 ◽  
Vol 9 (5) ◽  
pp. 232596712110067
Author(s):  
Lambert T. Li ◽  
Carlin Chuck ◽  
Steven L. Bokshan ◽  
Brett D. Owens
Keyword(s):  
Emergency Department ◽  
Socioeconomic Status ◽  
Low Socioeconomic Status ◽  
Cruciate Ligament ◽  
Acl Injury ◽  
Emergency Department Visits ◽  
Level Of Evidence ◽  
Total Cost ◽  
Acl Tear ◽  
Chi Square Analysis

Background: Patients are commonly evaluated at the emergency department (ED) with acute anterior cruciate ligament (ACL) tears, but providers without orthopaedics training may struggle to correctly diagnose these injuries. Hypothesis: It was hypothesized that few patients would be diagnosed with an ACL tear while in the ED and that these patients would be of lower socioeconomic status and more likely to have public insurance. Study Design: Cohort study; Level of evidence, 3. Methods: The 2017 State Ambulatory Surgery and Services Database (SASD) and State Emergency Department Database (SEDD) from the state of Florida were utilized in this study. Cases with Current Procedural Terminology code 29888 (arthroscopically aided ACL reconstruction [ACLR]) were selected from the SASD, and data from the SEDD were matched to patients who had an ED visit for a knee injury within 120 days before ACLR. Chi-square analysis was used to test for differences in patient and surgical variables between the ED visit and nonvisit patient groups. A generalized linear model was created to model the effect of ED visit on total cost for an ACL injury. Results: While controlling for differences in patient characteristics and concomitant procedure usage, a visit to the ED added $4587 in total cost ( P < .001). The ED visit cohort contained a greater proportion of patients with Medicaid (20.2% vs 9.1%), patients who were Black (18.4% vs 10.3%), and patients in the lowest income quartile (34.4% vs 25.0%) ( P < .001 for all). In the ED visit cohort, 14.4% of patients received an allograft versus 10.1% in the non-ED visit cohort ( P = .001) despite having a similar mean age. An ACL sprain was diagnosed in only 29 of the 645 (4.5%) patients who visited the ED. Conclusion: Utilizing the ED for care after an ACL injury was expensive, averaging a $4587 increase in total cost associated with ACLR. However, patients rarely left with a definitive diagnosis, with only 4.5% of patients who underwent ACLR being correctly diagnosed with an ACL tear in the ED. This additional cost was levied disproportionately on patients of low socioeconomic status and patients with Medicaid.

scholarly journals Injuries to the anterolateral ligament are observed more frequently compared to lesions to the deep iliotibial tract (Kaplan fibers) in anterior cruciate ligamant deficient knees using magnetic resonance imaging

2021 ◽  
Author(s):  
Armin Runer ◽  
Dietmar Dammerer ◽  
Christoph Kranewitter ◽  
Johannes M. Giesinger ◽  
Benjamin Henninger ◽  
...  
Keyword(s):  
Pediatric Patients ◽  
Cruciate Ligament ◽  
Injury Rate ◽  
Anterolateral Ligament ◽  
Anatomical Reconstruction ◽  
Level Of Evidence ◽  
Iliotibial Tract ◽  
Anterolateral Complex ◽  
Anterior Cruciate ◽  
Combined Injuries

Abstract Purpose To determine the accuracy of detection, injury rate and inter- and intrarater reproducibility in visualizing lesions to the anterolateral ligament (ALL) and the deep portion of the iliotibial tract (dITT) in anterior cruciate ligament (ACL) deficient knees. Methods Ninety-one consecutive patients, out of those 25 children (age 14.3 ± 3.5 years), with diagnosed ACL tears were included. Two musculoskeletal radiologists retrospectively reviewed MRI data focusing on accuracy of detection and potential injuries to the ALL or dITT. Lesion were diagnosed in case of discontinued fibers in combination with intra- or peri-ligamentous edema and graded as intact, partial or complete tears. Cohen’s Kappa and 95% confidence intervals (95% CI) were determined for inter- and intrarater reliability measures. Results The ALL and dITT were visible in 52 (78.8%) and 56 (84.8%) of adult-and 25 (100%) and 19 (76.0%) of pediatric patients, respectively. The ALL was injured in 45 (58.5%; partial: 36.4%, compleate: 22.1%) patients. Partial and comleate tears, where visualized in 21 (40.4%) and 16 (30.8%) adult- and seven (28.0%) and one (4%) peditric patients. A total of 16 (21.3%; partial: 13.3%, compleate: 8.0%) dITT injuries were identified. Partal and complete lesions were seen in seven (12.5%) and five (8.9%) adult- and three (15.8%) and one (5.3%) pediatric patients. Combined injuries were visualized in nine (12.7%) patients. Inter-observer (0.91–0.95) and intra-observer (0.93–0.95) reproducibility was high. Conclusion In ACL injured knees, tears of the ALL are observed more frequently compared to lesions to the deep iliotibial tract. Combined injuries of both structures are rare. Clinically, the preoperative visualization of potentially injured structures of the anterolateral knee is crucial and is important for a more personalized preoperative planning and tailored anatomical reconstruction. The clinical implication of injuries to the anterolateral complex of the knee needs further investigation. Level of evidence II.

scholarly journals Transcriptome analysis of gravitational effects on mouse skeletal muscles under microgravity and artificial 1 g onboard environment

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Risa Okada ◽  
Shin-ichiro Fujita ◽  
Riku Suzuki ◽  
Takuto Hayashi ◽  
Hirona Tsubouchi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Transcriptome Analysis ◽  
Fiber Type ◽  
Expression Profiles ◽  
Space Station ◽  
Gene Expression Profiles

AbstractSpaceflight causes a decrease in skeletal muscle mass and strength. We set two murine experimental groups in orbit for 35 days aboard the International Space Station, under artificial earth-gravity (artificial 1 g; AG) and microgravity (μg; MG), to investigate whether artificial 1 g exposure prevents muscle atrophy at the molecular level. Our main findings indicated that AG onboard environment prevented changes under microgravity in soleus muscle not only in muscle mass and fiber type composition but also in the alteration of gene expression profiles. In particular, transcriptome analysis suggested that AG condition could prevent the alterations of some atrophy-related genes. We further screened novel candidate genes to reveal the muscle atrophy mechanism from these gene expression profiles. We suggest the potential role of Cacng1 in the atrophy of myotubes using in vitro and in vivo gene transductions. This critical project may accelerate the elucidation of muscle atrophy mechanisms.

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