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Long article full of references supporting high intensity short duration exercise

Exercise is medicine: the anti-inflammatory effects of high intensity exercise

Exercise is a readily accessible, safe, and inexpensive anti-inflammatory medicine. Inflammation is the body's natural means of stimulating healing, but when continuous and chronic, it becomes damaging and detrimental to health. Properly performed exercise releases signaling molecules that stimulate a unique healing response that couples both inflammatory and anti-inflammatory mechanisms to repair, regenerate, and grow stronger tissue. Understanding the history and mechanism behind these effects creates new prescriptive opportunities for exercise. Unlike drugs, which have single targets and ignore the web-like interactions in the body, exercise works with the body's innate intelligence to produce broadly beneficial effects that improve whole-body function. High-intensity, short-duration movement that is tailored to the individual, uses short rest periods, and engages the whole body may be the chief means of attaining anti-inflammatory effects from exercise.

The human body was designed for activity and evolved with movement. The vast majority of human existence was steeped in the harsh realities of the natural world. Our ancestors did low-intensity activity all day, every day, and were forced to engage in vigorous movement to avoid danger and procure food. This extreme physical reality made injury and infection commonplace. Inflammation produced in response to physical insults was the body's natural protective mechanism for healing.

While inflammation is often thought of as destructive, it is actually a closely orchestrated event that first produces pain, redness, swelling, heat, and tissue destruction, but then is followed by repair. Over the millennia, the human body evolved and used acute inflammation to heal, repair, and regenerate itself. Movement was an essential part of this healing and regenerative process. The unique anti-inflammatory effects of movement have been circumvented in the modern era. With the arrival of the industrial and technological revolutions, human movement came to a crawl. This left inflammation unchecked by the anti-inflammatory and growth-stimulating effects of exercise.

In modern day, the human body is confronted with persistent stress. Along with this stressful lifestyle, humans are no longer dependent on movement and its growth-stimulating and healing effects. As a result, acute and controlled inflammation has given way to chronic, low-level inflammation. This type of inflammation is less detectable by objective or subjective measures, making it more insidious in nature. The lifestyle of prehistoric humans had substantial risks, yet their movement patterns kept chronic inflammation at bay. Their exercise patterns worked with inflammation to repair, replace, and regenerate damaged tissue. Without the balancing effects of exercise, inflammation is allowed to smolder at a low level, damaging tissue and destroying the quality and quantity of life.

Myokines: Muscle-Body Messengers

Every time the body moves, muscles release signaling molecules that communicate to the rest of the body. The endocrine properties of muscle, like fat, have been confirmed. (3,4,6) In the case of muscle, compounds called myokines are released in response to voluntary contraction. Myokinesarecytokines, yet are derived specifically from muscle. These myokines give instructions to the body about how to function, and they hold the key to controlling chronic inflammation. The most important myokine related to muscle and inflammation is Interleukin-6 (IL-6). When muscle contracts, IL-6 is released.

IL-6 is a well-known cytokine and has long been thought to be inflammatory in nature as part of what is known as the inflammatory triad: TNF-alpha, IL-1, and IL-6. However, like people, IL-6 seems to behave differently depending on its origin, amount, and other cytokines around with it. When released from muscle, and in high concentrations without TNF-alpha and IL-1, IL-6 is anti-inflammatory. (10,12) In fact, IL-6 acts to reduce the amount of TNF-alpha and IL-1 in circulation by increasing the cytokine inhibitors IL-1 receptor antagonist (IL-lra) and soluble TNF receptors (sTNFR). (5,7,8) IL-lra antagonizes the IL-1 receptor, decreasing IL-1 effects, while sTNFR binds up TNF-alpha before it can react at its target cells. At the same time, IL-6 triggers the release of the major anti-inflammatory cytokine IL-10. (7,8)

It appears exercise-induced IL-6 has unique action as opposed to TNF-alpha-mediated release of IL-6. (10) Exercise causes a huge rise in IL-6, far and above TNF-alpha levels. This is in sharp contrast to infection or sepsis, which shows an exponential rise in both. The ratio of IL-6 to TNF-alpha may be the real concern in regards to chronic inflammation. Epidemiological studies on TNF alpha and IL-6 genetic polymorphisms support this, showing those with the highest TNF alpha and lowest IL-6 levels have the greatest risk of diabetes. (37) Other researchers support TNF alpha as the real inflammatory culprit. (10) They speculate IL-6 levels may be a marker of whole body TNF-alpha levels and could be acting in direct opposition to the more inflammatory cytokines. The IL-6 effect implicates exercise as a first-line defense against inflammation and may explain the "counterintuitive" findings on the benefit of resistance training in highly inflammatory diseases like rheumatoid arthritis. (26)