Contusion And Injury In College Athletes

Introduction
Alcohol is commonly used by Americans across the United States. (Maurel, Boisseau, Benhamou, Jaffré, 2012). Some of the highest rates of alcohol consumption occur in the college student population, with studies showing that college athletes having a higher drinking rate than there non-athlete peers. Not only do they have a higher frequency of alcohol consumption, but they also have a higher tendency to participate in binge drinking, which is defined as drinking five or more drinks in a row for men and four drinks in a row for women (Wechsler, Davenport, Dowdall, Grossman, Zanakos, 1997).
Athletes also have a high rate of injury. This is especially true in regard to college football (Steiner, Berkstresser, Richardson, Elia, Wang,

Contusion, also known as muscle bruising, occurs as a result of direct impact that causes intramuscular hemorrhage. Strains are injuries that occur in musculotendinous units when muscle fibers (myofibers) as well as connective tissues tear and partially necrotize. They are a result of overstretching an inactive muscle and my overloading a muscle during either concentric or eccentric phases. Strains are categorized as Mild (grade I), Moderate (grade II) and Severe (grade III). Mild refers to tearing only a few muscle fibers with slight swelling, some discomfort and minimal loss of function. Moderate often occur at or near the musculotendinous junction and refers to a greater number of myofiber tears with higher amounts of swelling, pain and a clear decrease in function. Severe refers to complete or nearly complete tearing of the entire cross-sectional area of the muscle. This is accompanied by severe pain, hemorrhaging, swelling and nearly complete I not total loss in function (Järvinen, 2014) (Whiting, 2015). There is no significant difference in the regenerative responsive of muscle to strain or contusion therefore skeletal muscle heals with consistent patterns regardless of injury type. (Järvinen,

(Järvinen, Järvinen, Kääriäinen, Kalimo, Järvinen, 2005) (Järvinen, 2014). The destruction phase begins with torn or ruptured myofibers that have become necrotized of only a few hours. The necrosis of the entire myofiber is prevented by a “Fire door” or contraction banded that forms around the rupture and is sealed by new sarcolemma. The torn myofibers contract leaving a gap between the torn ends of the myofiber. This gap is filled with blood, giving inflammatory cells that have been activated by the injury, direct access to the ruptured myofibers. Chemotactic signals including growth factors and cytokines are released by macrophages and fibroblast and are activated in the extracellular matrix for the circulating inflammatory cells (Järvinen, 2014) (Järvinen, 2005).The repair phases begins as macrophage cells continue a process call phagocytosis to remove the necrotized tissues while committed satellite cells begin to differentiate into myoblast. Undifferentiated satellite cells begin to proliferate within 24 hours and contribute to the production of myoblasts. These myoblasts form together to create myotubes which regenerate myofibers. Within 5 to 6 days the necrotized myofiber will be replaced with the regenerating myofiber, which connects with the connective scar tissue between the two ruptured ends of the myofiber. The remodeling phases begins as new