By Dov Michaeli
It is not very common that you reason how Mother Nature should work, and she obliges. More commonly, she confounds us with something totally unexpected. So when I read the article in the November issue of British Journal of Sports Medicine, my reaction was YES!
Innate immunity –the “dumb” part of the immune response
The immune response is in a sense a misnomer: we have several immune responses, all working in concert.
Our first line of defense is called the innate immune response. This is how we fight bacteria and viruses immediately upon the onset of the invasion. This line of defense is very ancient; we know it because it is found at various level of complexity in all multi cellular (non-bacterial) organisms. There are 3 cell types that play a central role in innate immunity.
- Neutrophils. These are the most common type of white blood cells in the bloodstream, and are among the first immune cells to defend against infection. They ingest bacteria and other foreign cells. Neutrophils contain granules that release enzymes to help kill and digest the invading bacteria. Neutrophils circulate in the bloodstream and must be signaled to leave the bloodstream and enter tissues. The signal comes mostly from the invading bacteria themselves. Think of these cells as trackers on a safari who recognize the foot prints and other signs (like the shape of the poop) left behind by the animal.
- Macrophages. Unlike the neutrophils that rush to the site of the invasion and start acting within minutes, macrophages take hours to become fully functional at the invasion site. But they are the heavy artillery. While neutrophils’ life span can be measured in hours, macrophages can linger at the site for many days. They kill the invading bacteria in 2 ways: they either engulf them and kill them once they are inside the macrophage, or they secrete enzymes that punch a hole in the bacteria’s cell membrane –which is its death sentence.
- Killer T cells. This name conjures up an image of deadly gangsters –and they are. Viruses are not recognized by the neutrophils and the macrophages –they are simply too small, and don’t leave any telltale signals behind them. So they invade cells with impunity; except that there is no perfect crime. Once they successfully invade the cell they move to the nucleus to take over its DNA machinery. In the process they take off their protein coat. And that’s their downfall. Fragments of the protein coat migrate to the cell membrane, and are displayed there for all to see. The T killers recognize these proteins and move in for the kill. They punch holes in the membrane of the virus-infected cell, and kill it. The virus, caught naked without its coat, is released into the circulation together with the innards of the dying cell –and get digested by enzymes present in the circulation.
Sounds pretty sophisticated, so why did we consider it dumb? Because you must have noticed, these cells recognize molecular patterns of cells and bacteria, but don’t have the specific recognition that antibodies possess; these proteins can recognize and bind to a species of bacteria -and only to that species; once they encounter it and bind to it our immune response will form immune memory that can last for years (this is the basis of vaccination).
Stress and immunity
There is another problem with the innate immune response. When there are no signals of danger it is basically on standby; some of the cells patrol the circulation, but a major portion of the cells are inactive, adhering to the blood vessel walls. What will make them jump into action are stress hormones, like cortisol and adrenaline. So when we experience acute physical stress, like exercise, the innate immune response is mobilized, and should, in theory at least, give us excellent protection against viruses and bacteria.
Exercise and colds
Now we have the experiment to prove it.
A group of 1002 adults (ages 18–85 years, 60% female, 40% male) were followed for 12 weeks during the winter and fall seasons while monitoring upper respiratory tract infection symptoms and severity. Subjects reported frequency of aerobic activity, and rated their physical fitness level using a 10-point scale.
The number of days with upper respiratory infections during the 12-week period was significantly reduced, 43% in subjects reporting ≥5 days/week aerobic exercise compared to those who were largely sedentary (≤1 day/week) and 46% when comparing subjects in the high versus low fitness. Severity and symptomatology were also reduced 32% to 41% between the high and low aerobic activity and physical fitness groups.
Attention: danger! -fever
Atención: peligro! -fiebre
Achten: gefahr! -fieber
Attention: danger! -fievre
Attendite: periculo! -febris
שים לב :סכנה ! חום
The eternal question: can I exercise when I have a cold? My answer: a definite maybe!
If you just have the sniffles, no muscle aches, no big deal –go ahead and exercise to heart’s content.
If you have a fever >100°F, don’t exercise. There are 2 main reasons for avoiding exercise. First, with running a fever you may increase your body temperature (especially with a vigorous exercise), which can lead to dehydration and hyperthermia. Second, in rare cases the virus can invade your heart muscle and pericardium (the membrane enveloping the heart), causing myocarditis (inflammation of the heart muscle) and pericarditis (inflammation of the pericardium) –both risks definitely not worth taking.
What about muscle aches and no fever? I would err on the side of caution and not exercise.
With these caveats in mind –just do it!