Each bout of exercise, particularly whole-body dynamic cardiorespiratory exercise, instantaneously mobilizes literally billions of immune cells, especially those cell types that are capable of carrying out effector functions such as the recognition and killing of virus-infected cells. The mobilized cells firstly enter the blood compartment from marginated vascular pools, the spleen and the bone marrow before trafficking to secondary lymphoid organs and tissues, particular to the lungs and the gut where increased immune defense may be required. The immune cells that are mobilized with exercise are primed and ‘looking for a fight.’ Their frequent recirculation between the blood and tissues functions to increase host immune surveillance, which, in theory, makes us more resistant to infection and better equipped to deal with any infectious agent that has gained a foothold. Exercise also releases various proteins that can help maintain immunity, particularly muscle-derived cytokines such as IL-6, IL-7 and IL-15. The cytokine IL-6 has been shown to ‘direct’ immune cell trafficking toward areas of infection, while IL-7 can promote the production of new T-cells from the thymus and IL-15 helps to maintain the peripheral T-cell and NK-cell compartments, all of which work in concert to increase our resistance to infection. Exercise is especially beneficial for older adults who are more susceptible to infection in general and have also been identified as a particularly vulnerable population during this COVID-19 outbreak.
In this regard, it is vitally important that we try to maintain our activity levels within recommended guidelines. Not only can exercise have a positive direct effect on the cells and molecules of the immune system, but it is also known to counter the negative effects of isolation and confinement stress on various aspects of immunity. Although no scientific data currently exists regarding the effects of exercise on coronaviruses, there is evidence that exercise can protect the host from many other viral infections including influenza, rhinovirus (another cause of the common cold) and herpesviruses such as Epstein-Barr (EBV), varicella-zoster (VZV) and herpes-simplex-virus-1 (HSV-1). Work from Jeff Woods’ lab at the University of Illinois showed that moderate-intensity exercise training during an active influenza infection protected mice from death. It also promoted a favorable immune cell composition and cytokine shift in the lungs that was associated with prolonged survival. A major focus of our research is to understand how exercise can mitigate the negative effects of stress to maintain immune function, particularly during prolonged periods of isolation and confinement such as space travel. We showed recently that astronauts who had higher pre-flight cardiorespiratory fitness and skeletal muscle endurance before a six-month mission to the International Space Station were less likely to reactivate EBV and VZV during the mission. Copies of EBV viral DNA were also lower in the fitter astronauts, indicating that their ability to infect others is also reduced. Moreover, those astronauts who had lower pre-flight fitness levels and returned to Earth with the greatest levels of cardiorespiratory deconditioning were more likely to have reactivated a virus during the mission. Viral reactivation is a global indicator that our immune system has been weakened, which, in this context, we believe to be largely due to the stressors associated with isolation and confinement. This research indicates that exercise, in addition to the aforementioned direct effects it can have on cells and molecules of the immune system, may be an effective stress-induced countermeasure to help maintain immune function and lower infection risk.