Premorbid obesity, but not nutrition, prevents critical illness‐induced muscle wasting and weakness

Goossens, Chloë; Marques, Mirna Bastos; Derde, Sarah; Perre, Sarah Vander; Dufour, Thomas; Thiessen, Steven; Güiza, Fabián; Janssens, Thomas; Hermans, Greet; Vanhorebeek, Ilse; Bock, Katrien De; Berghe, Greet Van den; Langouche, Lies

doi:10.1002/jcsm.12131

Cited by 62 publications

(73 citation statements)

References 51 publications

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“…53,54 Skeletal muscle density has been suggested to be an independent marker of clinical outcome. 66 Low levels of testosterone or vitamin D were not prognostic for muscle mass and function in middle-aged and elderly men, while low insulin-like growth factor 1 (IGF-1) levels were found to predict alterations in gait speed in men aged ≥70 years. 34 Another contributing factor to sarcopenia is a variable degree of malnutrition 56 that may be caused by inflammatory cytokines, 57-59 which have been known to contribute to anorexia in chronic disease.…”

Section: Chronic Heart Failure and Muscle Maintenancementioning

confidence: 97%

“…65 Interestingly, premorbid obesity, but not exogenous macronutrients, attenuated muscle wasting in critical illness. 66 Low levels of testosterone or vitamin D were not prognostic for muscle mass and function in middle-aged and elderly men, while low insulin-like growth factor 1 (IGF-1) levels were found to predict alterations in gait speed in men aged ≥70 years. 67 A recent study has identified low testosterone in men as an independent risk factor in CHF.…”

Section: Chronic Heart Failure and Muscle Maintenancementioning

confidence: 97%

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Skeletal muscle wasting in chronic heart failure

2018

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Patients suffering from chronic heart failure (CHF) show an increased prevalence (~20% in elderly CHF patients) of loss of muscle mass and muscle function (i.e. sarcopenia) compared with healthy elderly people. Sarcopenia, which can also occur in obese patients, is considered a strong predictor of frailty, disability, and mortality in older persons and is present in 5–13% of elderly persons aged 60–70 years and up to 50% of all octogenarians. In a CHF study, sarcopenia was associated with lower strength, reduced peak oxygen consumption (peak VO2, 1173 ± 433 vs. 1622 ± 456 mL/min), and lower exercise time (7.7 ± 3.8 vs. 10.22 ± 3.0 min, both P < 0.001). Unfortunately, there are only very limited therapy options. Currently, the main intervention remains resistance exercise. Specialized nutritional support may aid the effects of resistance training. Testosterone has significant positive effects on muscle mass and function, and low endogenous testosterone has been described as an independent risk factor in CHF in a study with 618 men (hazard ratio 0.929, P = 0.042). However, the use of testosterone is controversial because of possible side effects. Selective androgen receptor modulators have been developed to overcome these side effects but are not yet available on the market. Further investigational drugs include growth hormone, insulin‐like growth factor 1, and several compounds that target the myostatin pathway. The continuing development of new treatment strategies and compounds for sarcopenia, muscle wasting regardless of CHF, and cardiac cachexia makes this a stimulating research area.

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Section: Chronic Heart Failure and Muscle Maintenancementioning

confidence: 97%

Section: Chronic Heart Failure and Muscle Maintenancementioning

confidence: 97%

Skeletal muscle wasting in chronic heart failure

2018

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“…Recently, premorbid overweight/obesity has been shown to protect against muscle wasting and weakness in both critically ill patients and in septic mice [15]. In these septic mice, the overweight/obese preserved their muscle mass while losing fat mass.…”

Section: Introductionmentioning

confidence: 99%

Adipose tissue protects against sepsis-induced muscle weakness in mice: from lipolysis to ketones

et al. 2019

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Background: ICU-acquired weakness is a debilitating consequence of prolonged critical illness that is associated with poor outcome. Recently, premorbid obesity has been shown to protect against such illness-induced muscle wasting and weakness. Here, we hypothesized that this protection was due to increased lipid and ketone availability. Methods: In a centrally catheterized, fluid-resuscitated, antibiotic-treated mouse model of prolonged sepsis, we compared markers of lipolysis and fatty acid oxidation in lean and obese septic mice (n = 117). Next, we compared markers of muscle wasting and weakness in septic obese wild-type and adipose tissue-specific ATGL knockout (AAKO) mice (n = 73), in lean septic mice receiving either intravenous infusion of lipids or standard parenteral nutrition (PN) (n = 70), and in lean septic mice receiving standard PN supplemented with either the ketone body 3hydroxybutyrate or isocaloric glucose (n = 49). Results: Obese septic mice had more pronounced lipolysis (p ≤ 0.05), peripheral fatty acid oxidation (p ≤ 0.05), and ketogenesis (p ≤ 0.05) than lean mice. Blocking lipolysis in obese septic mice caused severely reduced muscle mass (32% loss vs. 15% in wild-type, p < 0.001) and specific maximal muscle force (59% loss vs. 0% in wild-type; p < 0.001). In contrast, intravenous infusion of lipids in lean septic mice maintained specific maximal muscle force up to healthy control levels (p = 0.6), whereas this was reduced with 28% in septic mice receiving standard PN (p = 0.006). Muscle mass was evenly reduced with 29% in both lean septic groups (p < 0.001). Lipid administration enhanced fatty acid oxidation (p ≤ 0.05) and ketogenesis (p < 0.001), but caused unfavorable liver steatosis (p = 0.01) and a deranged lipid profile (p ≤ 0.01). Supplementation of standard PN with 3-hydroxybutyrate also attenuated specific maximal muscle force up to healthy control levels (p = 0.1), but loss of muscle mass could not be prevented (25% loss in both septic groups; p < 0.001). Importantly, this intervention improved muscle regeneration markers (p ≤ 0.05) without the unfavorable side effects seen with lipid infusion. Conclusions: Obesity-induced muscle protection during sepsis is partly mediated by elevated mobilization and metabolism of endogenous fatty acids. Furthermore, increased availability of ketone bodies, either through ketogenesis or through parenteral infusion, appears to protect against sepsis-induced muscle weakness also in the lean.

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“…Hierbei legen Studiendaten zu verschiedenen Erkrankungen nahe, dass ein höherer BMI mit einer geringeren Mortalität assoziiert ist, z. B. beim Myokardinfarkt und bei der Sepsis [7,8]. Allerdings werden diese Studien methodisch angegriffen, insbesondere da es sich in der Regel um reine Beobachtungsstudien handelt, Confounder wie Tabakkonsum nicht ausreichend berücksichtigt werden oder eine unbewiesene Kausalität postuliert wird [9,10].…”

Section: Das Adipositas-paradoxonunclassified

Der Einfluss des Body Mass Index auf die Mobilisation von Patienten in der Frührehabilitation

Liebl

Schwedtke

Schröder

et al. 2018

Phys Med Rehab Kuror

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Zusammenfassung Hintergrund Die Mobilisierung stellt in der Frührehabilitation adipöser Patienten eine zentrale Aufgabe und gleichzeitig eine besondere Herausforderung dar. Insbesondere bei höhergradiger Adipositas ist ein erhöhter Personal- und Materialaufwand notwendig. In der vorliegenden Arbeit soll der Zusammenhang zwischen Body Mass Index und der Entwicklung der mobilitätsbezogenen Funktionsfähigkeit untersucht werden. Material und Methoden Diese retrospektive Kohortenstudie wurde an einer Stichprobe von n=129 initial immobilen Patienten in der fachübergreifenden Frührehabilitation (FR) an einer Universitätsklinik durchgeführt. Hauptzielkriterium war der Mobilisierungsfortschritt der Patienten. Die Mobilität wurde mittels Charité Mobilitäts-Index erfasst (CHARMI®, eine Mobilitäts-Rangskala von 0 bis 10 Punkten). Die Mobilisierungsfortschritte (CHARMI®-Werte pro Behandlungstag) wurden nach BMI-Gruppen verglichen. Ergebnisse Die Gruppen der Normalgewichtigen (0,13 CHARMI-Punkte/Tag) und der Untergewichtigen (0,13) zeigten eine schnellere Mobilisierung als die Gruppen der Übergewichtigen (0,11) und der Adipösen (0,09). Adipöse Patienten erreichen am Ende der Frührehabilitation zwar annähernd das gleiche Mobilisationsniveau wie Patienten ohne Übergewicht, benötigen hierfür jedoch im Median 9 Tage länger (29 statt 20) als Normalgewichtige. Diskussion Die Verteilung der Werte zeigt eine lineare Assoziation zwischen einem erhöhten BMI und geringeren Mobilisierungsfortschritten. Diese beschriebene Assoziation besteht trotz maximaler Therapiedichte und Mehraufwand für stark adipöse Patienten in der durchgeführten Frührehabilitation. Klinisch lässt sich daraus folgern, dass durch eine Maximalversorgung auch bei schwer adipösen Patienten eine Mobilisierung erzielt werden kann, die annähernd der von normalgewichtigen Patienten entspricht. Dieser Zustand kann jedoch nur mit einem deutlichen Mehraufwand an Personal, Material und Zeit erreicht werden.

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Premorbid obesity, but not nutrition, prevents critical illness‐induced muscle wasting and weakness

Cited by 62 publications

References 51 publications

Skeletal muscle wasting in chronic heart failure

Skeletal muscle wasting in chronic heart failure

Adipose tissue protects against sepsis-induced muscle weakness in mice: from lipolysis to ketones

Der Einfluss des Body Mass Index auf die Mobilisation von Patienten in der Frührehabilitation

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