Molecular mechanisms involved in the positive effects of physical activity on coping with COVID-19

Abstract

Purpose: Physical activity (PA) represents the first line of defence against diseases characterised by increased inflammation status, such as metabolic and infectious diseases. Conversely, a sedentary lifestyle-associated with obesity, type 2 diabetes and cardiovascular disorders-negatively impacts on general health status, including susceptibility to infections. At a time of a pandemic SARS-CoV2 infection, and in the context of the multiorgan crosstalk (widely accepted as a mechanism participating in the pathophysiology of all organs and systems), we examine the complex interplay mediated by skeletal muscle contraction involving the immune system and how this contributes to control health status and to counteract viral infections. In so doing, we review the molecular mechanisms and expression of molecules modulated by PA, able to provide the proper molecular equipment against viral infections such as the current SARS-CoV2.

Methods: A critical review of the literature was performed to elucidate the molecular mechanisms and mediators induced by PA that potentially impact on viral infections such as SARS-CoV2.

Results: We showed the effects mediated by regular moderate PA on viral adverse effects through the regulation of biological processes involving the crosstalk between skeletal muscle, the immune system and adipose tissue. Evidence was provided of the effects mediated by modulation of the expression of inflammation markers.

Conclusion: A tigth association between PA and reduction in inflammation status allows effective counteracting of SARS-CoV2 infection. It is therefore essential to persuade people to keep active.

Keywords: COVID-19; Cytokines; Healthy lifestyle; Immune system; Inflammation; Metabolic disorders; Physical activity.

Fig. 1

Physical activity and anti-inflammatory response in SARS-CoV2 infection. Regular physical activity may reduce the acute inflammatory response through at least five mechanisms: (1) by reducing the inflammatory signalling pathway mediated by TLRs; (2) by increasing anti-inflammatory cytokines such as IL-10 and IL-37 which could inhibit the TLR-inflammatory signalling cascade and mitigate the inflammatory action produced by the inflammasome; (3) by reducing lung inflammation through the activation of AMPK and promoting the conversion from Ang II to Ang 1–7; (4) presumably, by the activation of ACE2-Mas receptor vasodilator pathway, reducing lung inflammation and promoting some beneficial multi-organ effects; (5) most probably, by restoring nitric oxide (NO) levels, in order to counteract the endothelial dysfunction, thus contributing to pulmonary vasodilation and antithrombotic activity

Fig. 2

Physical activity and anti-inflammatory response in muscle and adipose tissue. Physical activity induces an anti-inflammatory response in muscle and adipose tissue through the involvement of cells (e.g., macrophages), cytokines [e.g., interleukins (ILs)] and adipokines (e.g., adiponectin)

Fig. 3

Impact of physical activity on the response of adipose tissue to viral infections. Obese adipose tissue, contrary to lean adipose tissue, is characterised by several alterations that impair the anti-viral response (i.e., increased immune cells, increased pro-inflammatory cytokines, ACE2 overexpression). Regular physical activity improves most of these mechanisms (i.e., reduction in fat mass, improvement in immune function, amelioration of lipid metabolism), helping virus clearance