Abstract
The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has unmasked mankind’s vulnerability to biological threats. Although higher age is a major risk factor for disease severity in COVID-19, several predisposing risk factors for mortality are related to low cardiorespiratory and metabolic fitness, including obesity, cardiovascular disease, diabetes, and hypertension. Reaching physical activity (PA) guideline goals contribute to protect against numerous immune and inflammatory disorders, in addition to multi-morbidities and mortality. Elevated levels of cardiorespiratory fitness, being non-obese, and regular PA improves immunological function, mitigating sustained low-grade systemic inflammation and age-related deterioration of the immune system, or immunosenescence. Regular PA and being non-obese also improve the antibody response to vaccination. In this review, we highlight potential physiological, cellular, and molecular mechanisms that are affected by regular PA, increase the host antiviral defense, and may determine the course and outcome of COVID-19. Not only are the immune system and regular PA in relation to COVID-19 discussed, but also the cardiovascular, respiratory, renal, and hormonal systems, as well as skeletal muscle, epigenetics, and mitochondrial function.
Highlights
Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), rapidly increased to pandemic magnitude during the first quarter of 2020 [1]
Research has highlighted several predisposing risk factors for mortality in COVID-19, many of which are related to low cardiorespiratory and metabolic fitness, including obesity, cardiovascular disease (CVD), diabetes [2,4,8,9,10], and metabolic syndrome (MetS) [11]
Protective measures aiming to slow the spread of COVID-19 have affected the possibilities for physical activity (PA) and exercise according to data retrieved from activity trackers and mobile phones from all over the world [32,33]
Summary
Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), rapidly increased to pandemic magnitude during the first quarter of 2020 [1]. It is reasonable to assume that a physically active lifestyle results in physiological and molecular stress-induced adaptations in all tissues affected by exercise, which may be protective following SARS-CoV-2 infection, in contrast to the sedentary lifestyle associated with obesity [12]. The objective of this narrative review is to highlight potential physiological, cellular, and molecular mechanisms affected by regular physical activity (PA) and exercise that may regulate antiviral defenses and determine the course and outcome of COVID-19. In addition to the immune system, the cardiovascular, respiratory, renal, and hormonal systems, as well as skeletal muscle, epigenetics, and mitochondrial function in relation to regular PA and antiviral defense is discussed in novel aspects
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