Athletes and coaches have long known that strenuous exercise causes inflammation. Many products are currently on the market that claim to limit inflammation including cryotherapy methods, NSAIDS, nutritional supplements, and compression gear. However, there is compelling evidence that exercise induced muscle inflammation can lead to performance adaptation. Recent research is leading many to question if and when it is appropriate to use products that are aimed at reducing inflammation. In response to this, First Endurance will be releasing a series of 3 blog posts. This post will cover the basics of exercise induced inflammation. The second will cover how to systematically manage inflammation to maximize training. The final article will be a practical approach to managing inflammation in order to maximize race day performance.
Inflammation is defined literally as “to set on fire.” The accepted definition of inflammation in a sports research setting is a “normal part of the biological response to harmful stimuli.” Inflammation is a normal response to any assault to the body from varying sources such as bacterial infection or exercise. The end goal of the inflammatory process is to restore homeostasis.
Prior to going further with this discussion, an important clarification needs to be made. The inflammatory response can refer to any response to viral or bacterial invasion, arthritis, sports injury, or trauma from training. The purpose of the series of three blog posts is to address only inflammation which results from activity related trauma. Exercise induced muscle damage is an “injury from a mechanical force applied externally, causing structural stress or strain that results in a cellular or tissue response.” This is typically seen in endurance sports as result of the cyclic loading and overuse on specific tissues. As load stress and strains increase, a cellular and matrix response is promoted leading to inflammation. Inflammation may lead to injury; however it most often leads to performance adaptation. Thus, it can be found extremely valuable to have an understanding of how to manage inflammation both for injury prevention and performance gains.
Strenuous physical activity invokes a variety of different stress responses in the body. One of these is the inflammatory response. This typically occurs whenever forces or loads applied to the connective tissues exceed biomechanical or metabolic limits. While historically, inflammation has been an unwanted process in sport, it plays a vital role in the necessary healing and repair process. In short, if no inflammation is initiated, many performance related adaptations would be impossible.
Sports induced inflammation has been shown to be caused by the disruption of the sarcomeres (the contractile unit in a muscle fiber), the break up of cytoskeletal elements involved in force transmission, damage to the membrane of the muscle cells, and loss of a number of electrolytes and minerals involved in a muscle contraction. This type of inflammation typically results in soreness, stiffness, decreased range of motion, reduction of force production, and often swelling in the affected muscles. While eccentric contractions have been shown to cause greater damage to the sarcomere, repeated concentric contractions as well as continued overextension of the sarcomeres can also lead to damage causing inflammation.
Delayed Onset Muscle Soreness (DOMS) is a common side effect of exercise-induced muscle damage. Typically, DOMS manifests 24-48 hours post exercise and is limited to the affected muscle. While different theories exist, the most accepted thought is that the soreness is due to the irritation of mechanical nociceptors (pain receptors) due to the chemical changes associated with exercise induced inflammation. Type II muscle fibers (glycolytic) are most susceptible to DOMS due to the increased structural support of the Type I muscle fibers. Furthermore, Type I muscle fibers have more heat shock proteins and other mechanical proteins that help protect the muscle from mechanical stress. DOMS is also typically more severe in unconditioned subjects or when an athlete increases intensity or duration. It is also well accepted that the inflammatory response is directly related to exercise type, intensity and duration, and the mass of the muscles recruited. Diet macronutrient composition can also affect exercise induced muscle damage.
Once the inflammatory process has been initiated within the skeletal muscle, fluid, plasma proteins, and inflammatory cell populations infiltrate the affected tissues. This process normally begins as quickly as 45 minutes after exercise and peaks around 24 hours after exercise. It’s been observed 2-3 days post activity and may be present for up to 10 days after exercise. Neutrophils are the first to accumulate in the affected tissues and responsible for destroying damaged tissues through phagocytosis while working with the macrophages which are already located in the muscle. Additional macrophages as well as T-lymphocytes begin to accumulate and are responsible for removing cellular debris and muscle repair.
Endurance related trauma that leads to inflammation can lead to adaptation. Exercise induced muscle damage leading to the inflammatory process results in an increase in satellite cell behavior in skeletal muscles. Skeletal muscles are permanent cells which typically do not replicate. However, they are endowed with a stem cell called a satellite cell. These cells play an important role in muscle growth and repair. Satellite cells are attached to the outside of the muscle cell. When the muscle cell is damaged or has grown, the satellite cell divides and donates the additional nucleus to the muscle fiber. This enhances the muscle’s ability to synthesize new proteins thus supporting muscle growth and repair. In short, muscle damage leads to inflammation which increases satellite cell behavior leading to performance related adaptation. Exercise induced muscle damage has been shown to alter gene expression resulting in strengthening of the muscle tissues and prevention of further damage. This is known as the SAID principle (specific adaptations to implied demands).
We discussed in our Vitamin C review that thwarting inflammation is not always the best approach. We also know that more inflammation is not good either. Research has suggested that a threshold exists beyond which additional damage will not yield adaptation. Furthermore, excessive exercise induced muscle damage can certainly lead to many overuse injuries. Thus, coaches and athletes alike would likely benefit greatly from increasing their knowledge of as well as when and how best to manage inflammation. Understanding the mechanisms of inflammation will certainly help with the development of better strategies for reducing muscle injury, promoting healing, and understanding how to maximize adaptation. These topics will be covered in subsequent posts.
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