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