-local vasoconstriction: lasting from a few seconds to as long as 10 minutes, larger blood vessels constrict in response to signals from neurotransmitters, capillaries and set arterioles and venules constrict due to the influence of serotonin and catecholamines released from the platelets and serum during injury, the resulting reduction in the volume of blood flow in the region promoted increased blood viscosity or resistance to the blow which further reduced blood loss at the injury site
-platelet reaction: provokes clotting as individual cells irreversibly combine with each other with fibrin to form a mechanical plug that occluded the end of a ruptured blood vessel, produces an array of chemical mediators that play significant roles in the inflammatory and proliferation phases of healing, mediators include: serotonin, adrenaline, nonradrenaline, histamine;, also found in platelets is the enzymes adenosine triphosphate (atpase): central in supplying the energy needed for healing
-activation of the coagulation cascade: a cascade is heightened physiologic response consisting of several different interrelated processes, fibrinogen molecules are converted into fibrin for clot formation through two different pathways, extrinsic pathway is activated by thromboplastin which is released from damaged tissue, intrinsic pathway inside the blood vessels is enabled by the interaction between platelets and the hageman factor, both paths result in the formation of the prothrombin activator that converts prothrombin into thrombin
Muscle fibers (form adhesions) are permanent cells that do not reproduce or proliferate in response to either injury or training; there are reserve cells in the basement membrane of each muscle fiber that are able to regenerate muscle fiber following injury.
Severe muscle injury can result in scarring or the formation of adhesions within the muscle, which inhibits the potential for fiber regeneration from the reserve cells; consequence: muscle may regain only about 50% of its preinjury strength.
Because tendons and ligaments (slower heal) have few reparative cells, healing of these structures is a slow process that can take more than a year; regeneration is enhanced by proximity to other soft tissues that can assist with supply of the chemical mediators and building blocks required; isolated ligaments (e.g., anterior cruciate) have poor chances for healing;
If tendons and ligaments undergo abnormally high tensile stress before scar formation is complete, the newly forming tissues can be elongated; if this occurs in ligaments, joint instability may result.
Because tendons, ligaments, and muscles hypertrophy (increase in size) and atrophy (decrease in size) in response to levels of mechanical stress, complete immobilization of the injury leads to atrophy, loss of strength, and decreased rate of healing in these tissues; the amount of atrophy is generally proportional to the time of immobilization; immobilization may be necessary to protect the injured tissues during the early stages of recovery, but strengthening exercises should be implemented as soon as appropriate during rehabilitation of the injury.