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Progress in Cardiovascular Diseases 2022Exercise limitation is a cardinal manifestation of many cardiovascular diseases (CVD) and is associated with poor prognosis. It is increasingly well understood that... (Review)
Review
Exercise limitation is a cardinal manifestation of many cardiovascular diseases (CVD) and is associated with poor prognosis. It is increasingly well understood that exercise-based cardiac rehabilitation (CR) is an intervention that portends favorable clinical outcomes, including improvements in exercise capacity. The etiology of exercise limitation in CVD is multifactorial but is typically governed by terminal sensations of pain, fatigue, and/or breathlessness. A known but perhaps underestimated complication of CVD that contributes to breathlessness and exercise intolerance in such patients is inspiratory muscle dysfunction. For example, inspiratory muscle dysfunction, which encompasses a loss in muscle mass and/or pressure generating capacity, occurs in up to ~40% of patients with chronic heart failure and is associated with breathlessness, exertional intolerance, and worse survival in this patient population. In this review, we define inspiratory muscle weakness, detail its prevalence in a range of CVDs, and discuss how inspiratory weakness impacts physiological function and clinical outcomes in patients with CVD often referred to CR. We also evaluate the available evidence addressing the effects of exercise-based CR with and without concurrent specific inspiratory muscle training (IMT) on inspiratory muscle function, general physiological function, and clinical outcomes in patients with CVD. Finally, we consider whether the assessment of global respiratory muscle function should become standard as part of the patient intake assessment for phase II CR programs, giving practical guidance on the implementation of such measures as well as IMT as part of phase II CR.
Topics: Cardiac Rehabilitation; Cardiovascular Diseases; Dyspnea; Exercise Tolerance; Humans; Muscle Strength; Muscle Weakness; Respiratory Muscles
PubMed: 34688670
DOI: 10.1016/j.pcad.2021.10.002 -
Acta Bio-medica : Atenei Parmensis Nov 2020Several inherited disorders involve chronic fatigue, muscle weakness and pain. These conditions can depend on muscle, nerve, brain, metabolic and mitochondrial defects.... (Review)
Review
Several inherited disorders involve chronic fatigue, muscle weakness and pain. These conditions can depend on muscle, nerve, brain, metabolic and mitochondrial defects. A major trigger of muscle weakness and fatigue is exercise. The amount of exercise that triggers symptoms and the frequency of symptoms are highly variable. In this review, the genetic causes and molecular pathways involved in these disorders are discussed along with the diagnostic and treatment options available, with the aim of fostering understanding of the disease and exploring therapeutic options.
Topics: Exercise; Genetic Testing; Humans; Muscle Weakness; Syndrome
PubMed: 33170160
DOI: 10.23750/abm.v91i13-S.10642 -
Clinical Science (London, England :... Nov 2020Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovitis and the presence of serum autoantibodies. In addition, skeletal muscle weakness is... (Review)
Review
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovitis and the presence of serum autoantibodies. In addition, skeletal muscle weakness is a common comorbidity that contributes to inability to work and reduced quality of life. Loss in muscle mass cannot alone account for the muscle weakness induced by RA, but instead intramuscular dysfunction appears as a critical factor underlying the decreased force generating capacity for patients afflicted by arthritis. Oxidative stress and associated oxidative post-translational modifications have been shown to contribute to RA-induced muscle weakness in animal models of arthritis and patients with RA. However, it is still unclear how and which sources of reactive oxygen and nitrogen species (ROS/RNS) that are involved in the oxidative stress that drives the progression toward decreased muscle function in RA. Nevertheless, mitochondria, NADPH oxidases (NOX), nitric oxide synthases (NOS) and phospholipases (PLA) have all been associated with increased ROS/RNS production in RA-induced muscle weakness. In this review, we aim to cover potential ROS sources and underlying mechanisms of oxidative stress and loss of force production in RA. We also addressed the use of antioxidants and exercise as potential tools to counteract oxidative stress and skeletal muscle weakness.
Topics: Animals; Arthritis, Rheumatoid; Humans; Muscle Weakness; Muscle, Skeletal; Oxidation-Reduction; Oxidative Stress; Signal Transduction
PubMed: 33146370
DOI: 10.1042/CS20190728 -
Practical Neurology Oct 2020Skeletal muscle biopsy remains an important investigative tool in the diagnosis of a variety of muscle disorders. Traditionally, someone with a limb-girdle muscle...
Skeletal muscle biopsy remains an important investigative tool in the diagnosis of a variety of muscle disorders. Traditionally, someone with a limb-girdle muscle weakness, myopathic changes on electrophysiology and raised serum creatine kinase (CK) would have a muscle biopsy. However, we are living through a genetics revolution, and so do all such patients still need a biopsy? When should we undertake a muscle biopsy in patients with a distal, scapuloperoneal or other patterns of muscle weakness? When should patients with myositis, rhabdomyolysis, myalgia, hyperCKaemia or a drug-related myopathy have a muscle biopsy? What does normal muscle histology look like and what changes occur in neurogenic and myopathic disorders? As with Kipling's six honest serving men, we hope that by addressing these issues we can all become more confident about when to request a muscle biopsy and develop clearer insights into muscle pathology.
Topics: Adult; Biopsy; Creatine Kinase; Female; Humans; Male; Muscle Weakness; Muscle, Skeletal; Muscular Diseases; Myositis; Rhabdomyolysis; Young Adult
PubMed: 32503899
DOI: 10.1136/practneurol-2019-002465 -
Respiratory Care Sep 2006Neuromuscular abnormalities culminating in skeletal-muscle weakness occur very commonly in critically ill patients. Intensive-care-unit (ICU) acquired neuromuscular... (Review)
Review
Neuromuscular abnormalities culminating in skeletal-muscle weakness occur very commonly in critically ill patients. Intensive-care-unit (ICU) acquired neuromuscular abnormalities are typically divided into 2 discrete classes: polyneuropathy and myopathy. However, it is likely that these 2 entities commonly coexist, with myopathy being the most common cause of weakness. Major risk factors for ICU-acquired neuromuscular abnormalities include sepsis, corticosteroid administration, and hyperglycemia, with other associated factors including neuromuscular blockade and increasing severity of illness. The pathogenesis of these disorders is not well defined, but probably involves inflammatory injury of nerve and/or muscle that is potentiated by functional denervation and corticosteroids. ICU-acquired neuromuscular abnormalities are associated with multiple adverse outcomes, including higher mortality, prolonged duration of mechanical ventilation, and increased length of stay. The only intervention proven to reduce the incidence of ICU-acquired neuromuscular abnormalities is intensive insulin therapy. Additional research is necessary to better delineate the causes and pathogenesis of these disorders and to identify potential preventive and therapeutic strategies. In addition, consensus guidelines for its classification and diagnosis are needed.
Topics: Humans; Incidence; Intensive Care Units; Muscle Weakness; Paresis; Risk Factors
PubMed: 16934167
DOI: No ID Found -
Anesthesiology Jan 2016Muscle weakness is common in the surgical intensive care unit (ICU). Low muscle mass at ICU admission is a significant predictor of adverse outcomes. The consequences of... (Review)
Review
Muscle weakness is common in the surgical intensive care unit (ICU). Low muscle mass at ICU admission is a significant predictor of adverse outcomes. The consequences of ICU-acquired muscle weakness depend on the underlying mechanism. Temporary drug-induced weakness when properly managed may not affect outcome. Severe perioperative acquired weakness that is associated with adverse outcomes (prolonged mechanical ventilation, increases in ICU length of stay, and mortality) occurs with persistent (time frame: days) activation of protein degradation pathways, decreases in the drive to the skeletal muscle, and impaired muscular homeostasis. ICU-acquired muscle weakness can be prevented by early treatment of the underlying disease, goal-directed therapy, restrictive use of immobilizing medications, optimal nutrition, activating ventilatory modes, early rehabilitation, and preventive drug therapy. In this article, the authors review the nosology, epidemiology, diagnosis, and prevention of ICU-acquired weakness in surgical ICU patients.
Topics: Critical Care; Critical Illness; Humans; Iatrogenic Disease; Intensive Care Units; Length of Stay; Muscle Weakness; Respiration, Artificial
PubMed: 26445385
DOI: 10.1097/ALN.0000000000000874 -
Cancer May 2015Young adult childhood cancer survivors are at an increased risk of frailty, a physiologic phenotype typically found among older adults. This phenotype is associated with... (Review)
Review
Young adult childhood cancer survivors are at an increased risk of frailty, a physiologic phenotype typically found among older adults. This phenotype is associated with new-onset chronic health conditions and mortality among both older adults and childhood cancer survivors. Mounting evidence suggests that poor fitness, muscular weakness, and cognitive decline are common among adults treated for childhood malignancies, and that risk factors for these outcomes are not limited to those treated with cranial radiation. Although the pathobiology of this phenotype is not known, early cellular senescence, sterile inflammation, and mitochondrial dysfunction in response to initial cancer or treatment-related insults are hypothesized to play a role. To the authors' knowledge, interventions to prevent or remediate frailty among childhood cancer survivors have not been tested to date. Pharmaceutical, nutraceutical, and lifestyle interventions have demonstrated some promise.
Topics: Adult; Cellular Senescence; Child; Chronic Disease; Cognitive Dysfunction; Cranial Irradiation; Dietary Supplements; Exercise Tolerance; Hand Strength; Humans; Incidence; Inflammation; Mitochondria; Muscle Weakness; Neoplasms; Risk Factors; Risk Reduction Behavior; Survivors
PubMed: 25529481
DOI: 10.1002/cncr.29211 -
International Journal of Environmental... Jul 2022Background: This study aimed to analyze the prevalence of sarcopenia in elderly people from Northern Brazil according to muscle weakness or walking slowness. Methods:...
Background: This study aimed to analyze the prevalence of sarcopenia in elderly people from Northern Brazil according to muscle weakness or walking slowness. Methods: The sample consisted of 312 elderly people (72.6 ± 7.8 years). For walking slowness, a gait speed ≤ 0.8 m/s was used as a cut-off value, and for muscle weakness the following handgrip strength criteria were used for men and women, respectively: CI: <27.0/16.0 kg; CII: <35.5/20.0 kg; CIII: grip strength corrected for body mass index (BMI) < 1.05/0.79; CIV: grip strength corrected for total fat mass: <1.66/0.65; CV: grip strength corrected for body mass: <0.45/0.34. Results: Walking speed was reduced in 27.0% of women and 15.2% of men (p < 0.05). According to grip strength criteria, 28.5% of women and 30.4% of men (CI), 58.0% of women and 75.0% of men (CII), 66.0% of women and 39.3% of men (CIII), 28.8% of women and 19.6% of men (CIV), and 56.5% of women and 50.0% of men (CV) were identified as having sarcopenia. Conclusions: Walking slowness is more prevalent in women and muscle weakness is more prevalent in men in Northern Brazil. Walking slowness proved to be more concordant with muscle weakness in both sexes when the CI for handgrip strength was adopted.
Topics: Aged; Brazil; Cross-Sectional Studies; Female; Hand Strength; Humans; Male; Muscle Strength; Muscle Weakness; Paresis; Sarcopenia; Walking; Walking Speed
PubMed: 35954652
DOI: 10.3390/ijerph19159297 -
The Clinical Respiratory Journal Feb 2022Although COPD patients commonly present respiratory complaints despite pharmacological treatment, dyspnea does not correlate directly and linearly with spirometric data,...
INTRODUCTION
Although COPD patients commonly present respiratory complaints despite pharmacological treatment, dyspnea does not correlate directly and linearly with spirometric data, a fact that makes it difficult to select patients for pulmonary rehabilitation. Thus, seems logical that the measurement of respiratory muscle strength could help in this initial assessment if it presents a good correlation with exercise capacity. The aim of this study is to assess whether patients with muscle weakness, characterized as a reduction in maximal inspiratory pressure (PImax) below 70% of predicted value, have a good relationship between the assessed respiratory muscle strength and the exercise capacity measured by the 6-min walk test (6MWT) in patients with COPD.
METHODS
Patients diagnosed with COPD according to the 2019 Global Initiative for Chronic Obstructive Lung Disease (GOLD) on regular use of their medications, without exacerbations for 3 months or more and with respiratory muscle weakness (PImax < 70% of predicted) performed 6MWT in a 30-m-long flat corridor.
RESULTS
Data from 81 patients were analyzed. There was a strong correlation between the distance of the 6MWD with the PImax (r = 0.764, p < 0.0001). When separating the sample by the 350-m cut in the 6MWD, we found that the patients with the worst performance in the test are those who present the greatest respiratory muscle weakness.
CONCLUSION
PImax correlates well with exercise capacity, and patients with respiratory muscle weakness could be referred to a pulmonary rehabilitation protocol tied to inspiratory muscle training.
Topics: Breathing Exercises; Exercise Test; Exercise Tolerance; Humans; Muscle Weakness; Pulmonary Disease, Chronic Obstructive; Respiratory Muscles
PubMed: 34551459
DOI: 10.1111/crj.13449 -
Current Opinion in Clinical Nutrition... Jan 2013Age-related muscle weakness causes a staggering economic, public, and personal burden. Most research has focused on internal muscular mechanisms as the root cause to... (Review)
Review
PURPOSE OF REVIEW
Age-related muscle weakness causes a staggering economic, public, and personal burden. Most research has focused on internal muscular mechanisms as the root cause to strength loss. Here, we briefly discuss age-related impairments in the brain and peripheral nerve structures that may theoretically lead to muscle weakness in old age.
RECENT FINDINGS
Neuronal atrophy in the brain is accompanied by electrical noise tied to declines in dopaminergic neurotransmission that degrades communication between neurons. Additionally, sensorimotor feedback loops that help regulate corticospinal excitability are impaired. In the periphery, there is evidence for motor unit loss, axonal atrophy, demyelination caused by oxidative damage to proteins and lipids, and modified transmission of the electrical signal through the neuromuscular junction.
SUMMARY
Recent evidence clearly indicates that muscle weakness associated with aging is not entirely explained by classically postulated atrophy of muscle. In this issue, which focuses on 'Ageing: Biology and Nutrition' we will highlight new findings on how nervous system changes contribute to the aging muscle phenotype. These findings indicate that the ability to communicate neural activity to skeletal muscle is impaired with advancing age, which raises the question of whether many of these age-related neurological changes are mechanistically linked to impaired performance of human skeletal muscle. Collectively, this work suggests that future research should explore the direct link of these 'upstream' neurological adaptions and onset of muscle weakness in elders. In the long term, this new focus might lead to novel strategies to attenuate the age-related loss of muscle strength.
Topics: Aged; Aging; Humans; Muscle Contraction; Muscle Strength; Muscle Weakness; Muscle, Skeletal; Neuromuscular Junction; Neurons
PubMed: 23222705
DOI: 10.1097/MCO.0b013e32835b5880