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As our knowledge increases regarding the health benefits of exercise, more and more people attempt to stay healthy and physically fit with sports-related activities. As a result, sports injuries are no longer confined to a small group of competitive athletes but affect an ever-growing segment of the population. Improper training techniques, over-ambitious routines, and the use of faulty equipment have led to an increase in sports injuries (especially overuse injuries) and resultant pain syndromes. In the pediatric population, younger and younger children engage in highly competitive sports with training schedules that put them at increased risk for injury. Elite athletes, under the pressure of commercial interests and more widely disseminated knowledge about exercise physiology and training methods, are driven to greater extremes in order to gain small but significant advantages over the competition. This has led to overambitious workouts with inadequate rest periods. Many athletes suffer from chronic pain and injury as a result.

This chapter presents a brief review of the essential elements of bone, joint, tendon, ligament, and muscle physiology to lay the foundation for understanding both acute and repetitive stress injuries that are commonly seen in athletics. We then give an overview of treatment strategies for both acute and more chronic pain syndromes.


Bone is composed of organic proteins, matrix, and cells. The organic component of bone is 90% collagen type I and provides the tensile strength. The mineral phase of bone matrix accounts for 50% of the volume and 65% of the weight of bone and is composed of highly structured hydroxyapatite crystals and amorphous calcium phosphates. Bone cells account for only 3% of bone volume and include osteoblasts, osteoclasts, and osteocytes. Bone remodeling is ongoing throughout life and occurs predominantly at the trabecular part of the skeleton. Wolff’s law of adaptation states that mechanical remodeling of bone occurs in response to deforming strain. Both osteoblasts (responsible for erosion of existing bone) and osteoclasts (responsible for repair and remodeling of erosions) are involved. The exact mechanism of how mechanical strain activates osteocytes to initiate remodeling is still unknown, but both chemical messengers (dependent on the prostaglandins PGI2 and PGE2, IGF-1, and parathyroid hormone) and piezoelectric effects are believed to be involved.1

High levels of physical activity and stress loading in athletes increase bone density. The degree of increase in bone density is proportional to the level of stress loading accomplished in the athletic activity. For example, the bone mineral density (BMD) of the distal femur is found to be highest in world-class weightlifters followed by throwers, runners, soccer players, and then swimmers. This positive effect on BMD from mechanical loading is also observed in young women skaters and may counter the adverse estrogen-deficient effects on bone density seen in woman who are thin and amenorrheic.

Studies on both the elderly and young confirm that strength training at higher loads increases ...

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