COVID-19 caused by infection with the SARS-CoV-2 virus particularly affects people who have certain risk factors (advanced age, male) or a comorbidity such as chronic respiratory disease, obesity, cardiovascular disease, diabetes, hypertension and cancer (see this article). A healthy lifestyle, including eating well, not smoking, consuming alcohol in moderation, and exercising regularly, is the best way to prevent many diseases such as diabetes, cancer and cardiovascular disease. Also, certain conditions are associated with a decrease in immune activity, for example, stress, diabetes and the deficiency of certain dietary compounds like vitamin D and zinc. By its action on these conditions, exercise is likely to influence our resistance to infections.
Can exercise prevent acute respiratory infections, including COVID-19? Researchers at the Cochrane Library recently updated a systematic review of the effect of exercise on the occurrence, severity and duration of acute respiratory infections. The systematic review included 14 studies of 1377 healthy individuals aged 18 to 85 who were followed for a median period of 12 weeks. The participants were randomly separated into two groups: one who did not exercise and one who exercised regularly. In most cases, the exercise was supervised and was performed at least three times per week. The exercise sessions lasted 30 to 45 minutes and consisted of moderate intensity exercise such as walking, cycling, treadmill or a combination of these exercises. Exercise did not have a significant effect on biochemical parameters, quality of life or number of injuries.
Exercise did not decrease the number of acute respiratory infections (ARI) episodes, nor the proportion of participants who had at least one episode of ARI during the study, or the number of days with symptoms during each of these episodes. On the other hand, exercise was associated with a decrease in symptom severity in two studies and in the number of days with symptoms during the total study duration (4 studies). The study authors indicate that certainty about the data is low and that data from ongoing or future studies may impact their conclusions.
Exercise and the immune system
The immune system is very responsive to exercise, depending on both the duration and the intensity of effort (see this review article). Exercise causes multiple micro-injuries to the muscles, triggering a local and systemic inflammation reaction. During a moderate to high intensity exercise session lasting less than 60 minutes, the number of leukocytes (white blood cells) and several cytokines (proteins produced by the immune system to stimulate the proliferation of defence cells) increases rapidly in the bloodstream. The increase in the number of neutrophils (a type of white blood cell) often lasts for up to 6 hours after the end of the exercise session. This physiological response to stress caused by exercise is followed, during the recovery period, by a drop in the number of leukocytes in the bloodstream to a level below that measured at the start of the exercise session.
Although exercise transiently increases markers of inflammation, including several cytokines (interleukins, chemokines, interferons, and others), at rest, people who exercise regularly have lower blood levels of these pro-inflammatory proteins than people who exercise little or not at all or who are obese. Regular exercise therefore appears to moderate the inflammatory response and promote an anti-inflammatory environment in the body. The persistent increase in markers of inflammation (chronic inflammation) is linked to several conditions and diseases, including obesity, osteoarthritis, atherosclerosis and cardiovascular disease, chronic kidney disease, liver disease, metabolic syndrome, insulin resistance, type 2 diabetes, chronic obstructive pulmonary disease, dementia, depression, and various types of cancers. In short, exercise reduces the negative effects on the immune system of a recognized factor that is diabetes and the associated insulin resistance.
It is known that in severe forms of COVID-19 an exaggerated inflammatory reaction called “cytokine storm” destroys the cells of the pulmonary endothelium that allow oxygenation of the blood and body. Could regular exercise that provides a less inflammatory environment protect us in the event of a SARS-CoV-2 virus infection? This has not been demonstrated, but it is certainly a hypothesis that will need to be examined. Moreover, it seems that in the elderly, immune aging (also called “immunosenescence”) is associated with a decline in the cells that regulate the immune response. It is because of this decline that we observe an increase in immune disorders such as autoimmune diseases and an increase in cancers. However, the cytokine storm would be secondary to the lack of control by these cells. A healthy immune system would be less likely to lack these “regulatory” cells.
Suppression of immunity in athletes: Myth or reality?
In recent decades, an idea has taken root in the scientific literature according to which aerobic exercise, particularly if it is vigorous and of long duration, can interfere with immunocompetence, i.e. the body’s ability to produce a normal immune response in response to exposure to an antigen. This idea is now increasingly questioned and has even been called a myth by some researchers. This hypothesis dates from the early 20th century, when fatigue was believed to contribute to infections that caused pneumonia, but it was not until the 1980s–1990s that studies verified this assertion with professional and amateur athletes. In general, it is increasingly certain that it is “psychological” stress rather than physical stress that is immunosuppressive. For example, a study in the 1980s among medical students showed that immune capacity collapsed within 24 to 48 hours of exams. The “mental” stress on the eve of competitions could be the comparison. Exercise is a great stress reliever for most people.
One of the studies indicated that one third of the 150 runners participating in the 1982 Two Oceans ultramarathon (56 km) in South Africa reported symptoms of upper respiratory tract infection (runny nose, sore throat, sneezing) within two weeks of the race. The control group reported half as many symptoms of upper respiratory tract infection than runners. Similar results were obtained from athletes who participated in the Los Angeles Marathon (42 km) in 1987. Among the 2311 participants who completed the race and who had not reported symptoms of infection in the week before the race, 12.9% reported symptoms of infection in the week following the race. Only 2.2% of participants who dropped out of the race (for reasons other than health reasons) reported symptoms of infection in the week after the race. Another study conducted at the same time did not find an association between aerobic exercise and the risk of upper respiratory tract infection for runs over shorter distances, namely 5 km, 10 km, and 21 km (half marathon). This suggested that the risk of infections increases only after exercising for a very long period of time.
The major problem with these studies is that they are questionnaire-based and none of the infections reported by athletes were confirmed in the laboratory. In a 2007 study, researchers took swabs and tested athletes who reported symptoms of upper respiratory tract infection over a period of 5 months. Only 30% of the cases reported by the participants were associated with the presence of viruses, bacteria, or mycoplasmas. These results suggest that the symptoms experienced by athletes in previous studies may not have been caused by infection, but rather by other causes, including allergies, asthma, inflammation of the mucous membranes, or trauma to the epithelial cells of the airways caused by increased breathing or exposure to cold air.
The decrease in leukocytes in the bloodstream that is observed after exercise has led to the so-called “open window” hypothesis that intense exercise causes transient immunosuppression during the recovery period. During this “open window”, athletes would be more susceptible to viral and bacterial infections. Another hypothesis would be that of the recruitment of white blood cells to repair small damage to the muscles. Indeed, tissue damage, whether mechanical or infectious, causes the release of cytokines, which “call” the defences to “see what happens.” Yet, contrary to the studies cited above, recent studies indicate that exercise is rather associated with a reduction in the incidence of infections. There are as many epidemiological studies that show that regular exercise is associated with a reduction in infections as there are that show that regular exercise is associated with an increase in infections, but the former are less taken into account than the latter in the literature on exercise immunology.
For example, a Swedish study of 1509 men and women aged 20 to 60 found that high levels of physical activity are associated with a reduced incidence of upper respiratory tract infections. Studies of ultramarathon runners, one of the most taxing sports, have shown that these people report fewer days of absence from school or work due to illness compared to the general population. For example, the average number of sick days reported annually was 1.5 days in a study of 1212 ultramarathon runners and 2.8 days in another study of 489 161-km ultramarathon runners, while that year the number of sick days reported in the American population was 4.4 days. An often overlooked aspect of outdoor exercise is its vitamin D intake with exposure to the sun. The longer the routes, the greater the exposure and endogenous skin production of vitamin D. Vitamin D intake would be beneficial for the regulatory cells of the immune system.
In summary, contrary to the immunosuppression (“open window”) hypothesis, regular exercise can be beneficial for the immune system, or at least not harmful. Exercise does not increase the risk of diagnosed opportunistic infections. Exercise can improve the immune response to viruses, bacteria, and other antigens. Regular physical activity and frequent exercise may reduce or delay the aging of the immune system.