Skeletal Myosteatosis is Associated with Systemic Inflammation and a Loss of Muscle Bioenergetics in Stable COPD

Persson, Hans Lennart; Sioutas, Apostolos; Kentson, Magnus; Jacobson, Petra; Lundberg, Peter; Leinhard, Olof Dahlqvist; Forsgren, Mikael

doi:10.2147/jir.s366204

Cited by 9 publications

(6 citation statements)

References 66 publications

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“…Capillarization has notably been found impaired specifically in type I muscle fibers, which has a deep impact on the muscle’s oxidative capacity [ 14 , 15 ]. Adipose tissue infiltration has also been reported in COPD muscle, in a similar way to senescent muscle in the aging population, particularly in the obese sarcopenic phenotype where adipose inflammation leads to the redistribution of fat to the intra-abdominal area and skeletal muscle tissue [ 16 , 17 ] ( Figure 1 ).…”

Section: Histopathological Alterations Of Copd Skeletal Muscle Tissuementioning

confidence: 82%

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

Henrot

Dupin

Schilfarth

et al. 2023

IJMS

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Chronic obstructive pulmonary disease (COPD) is a worldwide prevalent respiratory disease mainly caused by tobacco smoke exposure. COPD is now considered as a systemic disease with several comorbidities. Among them, skeletal muscle dysfunction affects around 20% of COPD patients and is associated with higher morbidity and mortality. Although the histological alterations are well characterized, including myofiber atrophy, a decreased proportion of slow-twitch myofibers, and a decreased capillarization and oxidative phosphorylation capacity, the molecular basis for muscle atrophy is complex and remains partly unknown. Major difficulties lie in patient heterogeneity, accessing patients’ samples, and complex multifactorial process including extrinsic mechanisms, such as tobacco smoke or disuse, and intrinsic mechanisms, such as oxidative stress, hypoxia, or systemic inflammation. Muscle wasting is also a highly dynamic process whose investigation is hampered by the differential protein regulation according to the stage of atrophy. In this review, we report and discuss recent data regarding the molecular alterations in COPD leading to impaired muscle mass, including inflammation, hypoxia and hypercapnia, mitochondrial dysfunction, diverse metabolic changes such as oxidative and nitrosative stress and genetic and epigenetic modifications, all leading to an impaired anabolic/catabolic balance in the myocyte. We recapitulate data concerning skeletal muscle dysfunction obtained in the different rodent models of COPD. Finally, we propose several pathways that should be investigated in COPD skeletal muscle dysfunction in the future.

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Section: Histopathological Alterations Of Copd Skeletal Muscle Tissuementioning

confidence: 82%

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

Henrot

Dupin

Schilfarth

et al. 2023

IJMS

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“…When muscle wasting occurs, the expression levels of pro-inflammatory cytokines and their receptors are upregulated, leading to metabolic disturbances in muscle tissue ( 25 ), ultimately resulting in sarcopenia ( 26 ). Besides muscle wasting, patients with more severe COPD often have deposits of ectopic fat, including visceral adipose tissue, and muscle fat infiltration; both of which are associated with elevated markers of systemic inflammation ( 12 ). Clinical studies have found increased levels of interleukin (IL)-6, IL-10, hypersensitive C-reactive protein (CRP), and tumor necrosis factor (TNF)-α in patients with coexisting COPD and sarcopenia ( 27 , 28 ).…”

Section: Pathogenesismentioning

confidence: 99%

Role of nutrition in patients with coexisting chronic obstructive pulmonary disease and sarcopenia

et al. 2023

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Chronic obstructive pulmonary disease (COPD) is one of the most common chronic diseases in the elderly population and is characterized by persistent respiratory symptoms and airflow obstruction. During COPD progression, a variety of pulmonary and extrapulmonary complications develop, with sarcopenia being one of the most common extrapulmonary complications. Factors that contribute to the pathogenesis of coexisting COPD and sarcopenia include systemic inflammation, hypoxia, hypercapnia, oxidative stress, protein metabolic imbalance, and myocyte mitochondrial dysfunction. These factors, individually or in concert, affect muscle function, resulting in decreased muscle mass and strength. The occurrence of sarcopenia severely affects the quality of life of patients with COPD, resulting in increased readmission rates, longer hospital admission, and higher mortality. In recent years, studies have found that oral supplementation with protein, micronutrients, fat, or a combination of nutritional supplements can improve the muscle strength and physical performance of these patients; some studies have also elucidated the possible underlying mechanisms. This review aimed to elucidate the role of nutrition among patients with coexisting COPD and sarcopenia.

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“… 5 Metabolic disturbances of cells’ handling of iron, relevant for the resistance against oxidative damage, 6 , 7 and muscle tissue bioenergetics, important for normal muscle function, are some mechanisms implicated in COPD pathogenesis. 8 …”

Section: Introductionmentioning

confidence: 99%

“…5 Metabolic disturbances of cells' handling of iron, relevant for the resistance against oxidative damage, 6,7 and muscle tissue bioenergetics, important for normal muscle function, are some mechanisms implicated in COPD pathogenesis. 8 Possibly, due to a progression from a local airway inflammation to a systemic one, COPD may involve muscle cells in skeletal muscles, causing myosteatosis, which in turn trigger BaPA by a reduced physical performance. 8,9 In addition to common risk factors, such as smoking and advanced age, a low-grade systemic inflammation is thought to be involved in the pathogenesis of chronic heart failure (CHF).…”

Section: Introductionmentioning

confidence: 99%

“…8 Possibly, due to a progression from a local airway inflammation to a systemic one, COPD may involve muscle cells in skeletal muscles, causing myosteatosis, which in turn trigger BaPA by a reduced physical performance. 8,9 In addition to common risk factors, such as smoking and advanced age, a low-grade systemic inflammation is thought to be involved in the pathogenesis of chronic heart failure (CHF). 10 CHF is a common comorbidity among patients with COPD with an estimated prevalence of 5-41%.…”

Section: Introductionmentioning

confidence: 99%

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Applying the Rome Proposal on Exacerbations of Chronic Obstructive Pulmonary Disease: Does Comorbid Chronic Heart Failure Matter?

Jacobson,

Lind,

Persson

2023

COPD

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Background Chronic heart failure (CHF) is a common comorbidity among patients with chronic obstructive pulmonary disease (COPD). Both exacerbations of COPD (ECOPDs) and exacerbations of CHF (ECHFs) display worsening of breathlessness at rest (BaR) and breathlessness at physical activity (BaPA). Comorbid CHF may have an impact on the vital signs assessed, when the Rome proposal (adopted by GOLD 2023) is applied on ECOPDs. Thus, the aim of the present study was to investigate the impact of comorbid CHF on ECOPDs severity, particularly focusing on the influence of comorbid CHF on BaR and BaPA. Methods We analysed data on COPD symptoms collected from the telehealth study The eHealth Diary. Patients with COPD (n = 43) and patients with CHF (n = 41) were asked to daily monitor BaR and BaPA, employing a digital pen and scales for BaR and BaPA (from 0 to 10). Twenty-eight patients of the COPD patients presented with comorbid CHF. Totally, 125 exacerbations were analysed. Results Exacerbations in the group with COPD patients and comorbid CHF were compared to the group with COPD patients without comorbid CHF and the group with CHF patients. Compared with GOLD 2022, the GOLD 2023 (the Rome proposal) significantly downgraded the ECOPD severity. Comorbid CHF did not interfere significantly on the observed difference. Comorbid CHF did not worsen BaR scores, assessed at inclusion and at the symptom peak of the exacerbations. Conclusion In the present study, we find no evidence that comorbid CHF would interfere significantly with the parameters included in the Rome proposal (GOLD 2023). We conclude that the Rome proposal can be safely applied even on COPD patients with very advanced comorbid CHF.

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Skeletal Myosteatosis is Associated with Systemic Inflammation and a Loss of Muscle Bioenergetics in Stable COPD

Cited by 9 publications

References 66 publications

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

Main Pathogenic Mechanisms and Recent Advances in COPD Peripheral Skeletal Muscle Wasting

Role of nutrition in patients with coexisting chronic obstructive pulmonary disease and sarcopenia

Applying the Rome Proposal on Exacerbations of Chronic Obstructive Pulmonary Disease: Does Comorbid Chronic Heart Failure Matter?

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