Associations of Dynapenic Obesity and Sarcopenic Obesity with the Risk of Complications in COVID-19

Abstract

Ageing is associated with changes in body composition, such as low muscle mass (sarcopenia), decreased grip strength or physical function (dynapenia), and accumulation of fat mass. When the accumulation of fat mass synergistically accompanies low muscle mass or reduced grip strength, it results in sarcopenic obesity and dynapenic obesity, respectively. These types of obesity contribute to the increased risk of cardiovascular disease and mortality in the elderly, which could increase the damage caused by COVID-19. In this review, we associated factors that could generate a higher risk of COVID-19 complications in dynapenic obesity and sarcopenic obesity. For example, skeletal muscle regulates the expression of inflammatory cytokines and supports metabolic stress in pulmonary disease; hence, the presence of dynapenic obesity or sarcopenic obesity could be related to a poor prognosis in COVID-19 patients.

Keywords: COVID-19; ageing; complications; dynapenic obesity; sarcopenic obesity.

Figure 1

Phenotypes of obesity. In older people, sarcopenic obesity and dynapenic obesity are related to worsening disability. Appendicular skeletal muscle mass divided by height squared (ASMM/h²); fat mass (FM); muscle strength (MS).

Figure 2

Mechanisms and factors related to the pathogenesis of sarcopenic obesity and dynapenic obesity. In sarcopenic obesity and dynapenic obesity, the muscle mass and strength loss with increased adipose tissue induces an inflammatory cascade and accumulation of immune cells, as well as leukocyte activation, adipogenesis, and adipocyte death. Added to physical inactivity, carbohydrate overload and lower protein intake cause a vicious circle of insulin resistance, where there is an increase in free fatty acids and M1 macrophages with alterations in mitochondrial metabolism by inactivation of regulators of energy homeostasis and inducers of regulated fatty acid oxidation, vitamin D deficiency, and D receptor gene polymorphism. G6PC, glucose-6-phosphatase; PKC1, phosphoenolpyruvate carboxykinase 1; AMPK, AMP-activated protein kinase; ACC1, acetyl-CoA carboxylase 1; NEFAs, nonesterified fatty acids; PLIN 5, perilipin 5; PPARꙋ, peroxisome proliferator-activated receptor gamma; GLUT4, glucose transporter type 4.

Figure 3

Complications in COVID-19 due to sarcopenic obesity and dynapenic obesity. Alterations in the metabolism, respiratory system, cardiovascular system, and immune system of the SO and/or DO patient with a propensity for complications during COVID-19. SO, sarcopenic obesity; DO, dynapenic obesity; ROS, reactive oxygen species; hs-CRP, high-sensitivity C-reactive protein; ACE2, angiotensin-converting enzyme 2; NETs, neutrophil extracellular traps; GM-CSF, granulocyte macrophage colony-stimulating factor; IFN-γ, gamma interferon; HIF-1a, hypoxia-inducible factor-1α; IRF5, interferon regulatory factor 5; VLDL, very low-density lipoprotein; ADEM, acute disseminated encephalomyelitis; GBS, Guillain–Barré syndrome; RAAS, renin–angiotensin–aldosterone system; DIC, disseminated intravascular coagulation; MINOCA, myocardial infarction with nonobstructive coronaries.