Diet and exercise in frailty and sarcopenia. Molecular aspects.

Function declines throughout life although phenotypical manifestations in terms of frailty or disability are only seen in the later periods of our life. The causes underlying lifelong function decline are the aging process "per se", chronic diseases, and lifestyle factors. These three etiological causes result in the deterioration of several organs and systems which act synergistically to finally produce frailty and disability.

Molecular mechanisms of cancer cachexia. Role of exercise training.

Cancer-associated cachexia represents a multifactorial syndrome mainly characterized by muscle mass loss, which causes both a decrease in quality of life and anti-cancer therapy failure, among other consequences. The definition and diagnostic criteria of cachexia have changed and improved over time, including three different stages (pre-cachexia, cachexia, and refractory cachexia) and objective diagnostic markers. This metabolic wasting syndrome is characterized by a negative protein balance, and anti-cancer drugs like chemotherapy or immunotherapy exacerbate it through relatively unknown mechanisms.

Real-Life Outcomes of a Multicomponent Exercise Intervention in Community-Dwelling Frail Older Adults and Its Association with Nutritional-Related Factors.

Most of the studies on physical exercise in older adults have been conducted through randomized clinical trials performed under tight experimental conditions. Data regarding Real-Life physical exercise intervention programs in older adults with different conditions and in different settings, are lacking. This is an interventional, prospective and pragmatic Real-Life study in which fifty sedentary and frail individuals were enrolled.

The radiographic assessment of lung edema score of lung edema severity correlates with inflammatory parameters in patients with coronavirus disease 2019-Potential new admission biomarkers to predict coronavirus disease 2019 worsening.

Background: Coronavirus disease 2019 (COVID-19) has placed enormous pressure on intensive care units (ICUs) and on healthcare systems in general. A deeper understanding of the pathophysiology of the most severe forms of COVID-19 would help guide the development of more effective interventions. Herein, we characterized the inflammatory state of patients with COVID-19 of varying degrees of severity to identify admission biomarkers for predicting COVID-19 worsening.

Role of Redox Signaling and Inflammation in Skeletal Muscle Adaptations to Training.

The inflammatory response to exercise-induced muscle damage has been extensively described. Exercise has important modulatory effects on immune function. These effects are mediated by diverse factors including pro-inflammatory cytokines, classical stress hormones, and hemodynamic effects leading to cell redistribution.

Interplay of oxidants and antioxidants during exercise: implications for muscle health.

Muscle contraction results in generation of reactive oxygen and nitrogen species (RONS) at a rate determined by the intensity, frequency, and duration of the exercise protocols. Strenuous exercise causes oxidation of protein, lipid, and DNA, release of cytosolic enzymes, and other signs of cell damage; however, only exhaustive exercise is detrimental. Indeed, the regulation of vascular tone, the excitation-contraction coupling, growth, and differentiation in skeletal muscle, are governed in part by RONS.

Role of free radicals and antioxidant signaling in skeletal muscle health and pathology.

Skeletal muscle contraction, growth, differentiation and adaptation are governed by complicated biological mechanisms still being studied intensively. Generation of reactive oxygen and nitrogen species (RS) is one of the most prominent events during contractile activity that could influence muscle function and health. While RS generation is known to cause oxidative stress, activate certain pathogenic pathways and aging, they also serve as useful signaling molecules to regulate gene expression of proteins and enzymes that play a vital role in the normal muscle function and defense against detrimental effects of RS.

Role of nuclear factor kappaB and mitogen-activated protein kinase signaling in exercise-induced antioxidant enzyme adaptation.

Activation of nuclear factor (NF) kappaB and mitogen-activated protein kinase (MAPK) pathways in skeletal muscle has been shown to enhance the gene expression of several enzymes that play an important role in maintaining oxidant-antioxidant homeostasis, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). While an acute bout of exercise activates NF kappaB and MAPK signaling and upregulates MnSOD and iNOS, administration of chemical agents that suppress reactive oxygen species (ROS) production can cause attenuation of exercise-induced MnSOD and iNOS expression. Thus, ROS generation during exercise may have duel effects: the infliction of oxidative stress and damage, and the stimulation of adaptive responses favoring long-term protection.

Exercise and hormesis: activation of cellular antioxidant signaling pathway.

Contraction-induced production of reactive oxygen species (ROS) has been shown to cause oxidative stress to skeletal muscle. As an adaptive response, muscle antioxidant defense systems are upregulated after heavy exercise. Nuclear factor (NF) kappaB and mitogen-activated protein kinases (MAPKs) are the major oxidative stress-sensitive signal transduction pathways in mammalian tissues.