Chronic Inflammation - Exercise and Inflammation - Exercise-induced Acute Inflammation

Exercise-induced Acute Inflammation

Acute inflammation of the muscle cells, as understood in exercise physiology, can result after induced eccentric and concentric muscle training. Participation in eccentric training and conditioning, including resistance training and activities that emphasize eccentric lengthening of the muscle including downhill running on a moderate to high incline can result in considerable soreness within 24 to 48 hours, even though blood lactate levels, previously thought to cause muscle soreness, were much higher with level running. This delayed onset muscle soreness (DOMS) results from structural damage to the contractile filaments and z-disks, which has been noted especially in marathon runners whose muscle fibers revealed remarkable damage to the muscle fibers after both training and marathon competition. The onset and timing of this gradient damage to the muscle parallels the degree of muscle soreness experienced by the runners.

Z-disks are the point of contact for the contractile proteins. They provide structural support for the transmission of force when the muscle fibers are activated to shorten. However, in marathon runners and those who subscribe to the overload principle to enhance their muscles, show moderate Z-disk streaming and major disruption of the thick and thin filaments in parallel groups of sarcomeres as a result of the force of eccentric actions or stretching of the tightened muscle fibers.

This disruption of the muscle fibers triggers white blood cells to increase following the induced muscle soreness, leading to the inflammatory response observation from the induced muscle soreness. Elevations in plasma enzymes, myoglobinemia, and abnormal muscle histology and ultrastructure are concluded to be associated with the inflammatory response. High tension in the contractile-elastic system of muscle results in structural damage to the muscle fiber and plasmalemma and its epimysium, perimysium, and/or endomysium. The mysium damage disrupts calcium homeostasis in the injured fiber and fiber bundles, resulting in necrosis that peaks about 48 hours after exercise. The products of the macrophage activity and intracellular contents (such as histamines, kinins, and K+) accumulate outside the cells. These substances then stimulate the free nerve endings in the muscle; a process that appears accentuated by eccentric exercise, in which large forces are distributed over a relatively small cross-sectional area of the muscle.