Chapter 6 Overuse Injury and Muscle Damage
Overuse use injuries result from repetitive subtraumatic forces. Breakdown of microscopic tissue occurs faster than the tissue can heal or repair itself. The results are inflammation, ligament failure, tendonitis, tendon ruptures, muscle fatigue, and muscle damage.1,2 In 2000 approximately 60 million children between the ages of 5 and 18 years old lived in the United States.3 Approximately 72% of middle and high school children sustained a physical activity–related injury that was treated by a physician or nurse.3,4 Muscle injuries are the most common injury in sports. Their incidence has been reported to be as high as 55% of all injuries sustained in sports events.
In 2001 an estimated 18 million children (30% of 60 million) were treated for a sports/physical activity–related injury. Approximately 50% of those injuries (9 million) were attributed to overuse mechanisms resulting in muscle damage.3,4
ETIOLOGY OF OVERUSE INJURY TO MUSCLE
Predisposing Factors of Muscle Damage
Muscle strains occur with the highest frequency in muscles that cross two joints and in those with the highest proportion of Type II fibers.5 In addition, eccentric exercise appears to predispose muscle to pain and damage. Eccentric exercises can cause damage to the muscle, which has been associated with delayed onset of muscle soreness (DOMS).5 Eccentric exercises can be therapeutic or potentially damaging to the muscle and its musculotendinous junction (MTJ).6
Muscle is the best force attenuator in the body. Eccentric or lengthening action of muscle dampens the forces of weight bearing. At heel strike, the lower limb is slowly lowered to the ground by the action of muscle-lengthening contractions.7 Flexion of the knee is controlled by the eccentric action of the quadriceps femoris muscle.
Muscle imbalances are commonly associated with overuse injuries. Muscle imbalances may be alterations in muscle function secondary to a dysfunction between the antagonist and agonist. The disparity may include muscle weakness, poor flexibility, and inadequate endurance for musculoskeletal performance during specific functional activities. Alterations in muscle function secondary to muscle imbalances may result in inadequate or abnormal movement patterns during activities such as running. For example, Elliot and Achland1 used high-speed cinematography to study the effect of fatigue on the mechanical characteristics in highly skilled long-distance runners. They found that, toward the end of a race, the runners exhibited less efficient positioning of the foot at foot strike, as well as decreased stride length and stride rate. Alteration in muscle function during running may cause bones, ligaments, and tendons to be overworked, producing tissue breakdown and pathology.8 Weakness of the hamstring muscle can cause increased strain to the anterior cruciate ligament (ACL). Hamstring muscle tightness in the presence of quadriceps femoris muscle weakness has been associated with anterior knee pain including chondromalacia patellae. In the presence of hamstring tightness, patellofemoral joint compressive forces increase during the swing-through phase of gait or recovery phase of running.8 Quadriceps femoris muscle weakness, especially in the vastus medialis muscle, can result in lateral patellar tracking during knee flexion and extension. Because the quadriceps femoris muscle controls knee flexion during the stance phase of walking or running, weakness can result in increased shock to the ankle and knee. Weakness of the quadriceps femoris muscle places increased stress on the lower leg, resulting, with repetitive exercise, in overuse.
Imbalance among gastrocnemius-soleus muscles and weak pretibial muscles, anterior tibialis, extensor hallucis longus, and extensor digitorium longus muscles has been associated with anterior shin splints, especially during repetitive hill running.9 During uphill running, pretibial muscles forcefully contract in the recovery phase of running to dorsiflex the ankle, allowing the foot to clear the surface of the ground. Additionally, during downhill running, at heel strike, the pretibial muscles contract eccentrically to control ankle plantar flexion and prevent foot-slap. Overactivation of these muscles can occur in the presence of tight antagonists (the gastrocnemius-soleus muscles). The result may be microtrauma and inflammation of the pretibial muscles, tendons, and bony attachments.9
In the shoulder rotator cuff, imbalance is often associated with overuse. The external rotators of the glenohumeral joint should be 70% of the strength of the internal rotators in overhead-throwing athletes.10 The eccentric overload of the external rotators in the overhead-throwing athlete weakens the glenohumeral external rotators. In some cases the external rotator strength decreased to 50% of the internal rotator strength. On the basis of clinical observation, the author considers the previous ratio to be pathological and may result in damage to the glenohumeral joint or the rotator cuff muscles.
Precipitating Factors of Muscle Damage
Prolonged or strenuous exercise can lead to muscle overuse injuries resulting in pain and dysfunction. Fatigue may be a major precipitating factor leading to muscle damage causing pain, aches, and cramps. The term fatigue is typically described as a general sensation of tiredness and accompanying decrements in muscular performance. The underlying causes of fatigue include accumulation of metabolic by-products, such as lactic acid, failure of the muscle fiber’s contractile mechanism, depletion of muscle glycogen, and failure of nerve impulse transmission.11 Further discussion of muscle fatigue is discussed in depth in Chapter 5.
If the athlete pushes beyond the point of fatigue and its warning signs, further damage to the muscle and the musculotendinous junction is possible. Muscle pain, aches, and cramps may lead to ruptures. Hematoma formation, necrosis of myofibers, and inflammatory cell reaction are all precursors to tendon or muscle ruptures, or both.12
Demanding physical activities, either at work or sport related, require concentric and eccentric muscle contraction. The most damaging types of exercise are those requiring excessive eccentric loading, such as heavy weight training and repetitive eccentric loading activities of an overhead-throwing athlete. Maximum power can be reduced by 50% or more after damaging exercise. Muscle strength reaches its lowest value immediately after eccentric exercise and recovers slowly over 10 days.13 In addition, the joint range of motion can be impaired immediately after exercise or as a result of muscle imbalances.14 The combination of decreased strength and flexibility may result in significant muscle damage, such as a rupture.
Perpetuating Factors of Muscle Damage
Muscle damage, especially in athletes, is often difficult to treat because the athlete usually resumes the same training or exercise regimens (precipitating factors). In addition, the same muscle deficits and imbalances continue and in many cases become worse. The perpetuating factors of muscle damage therefore are the combination of the predisposing and precipitating factors already discussed. To treat muscle damage successfully, the predisposing and precipitating factors must be eliminated or modified. For each patient the rehabilitation specialist must evaluate muscle flexibility and strength. In addition, the clinician must have a thorough understanding of the anatomical and physiological demands of the sport in which the athlete is participating. Furthermore, the clinician must determine the best type of exercise regimen to take the athlete from rehabilitation back to his or her sport.
MUSCLE DAMAGE: THE PHYSIOLOGY, EVALUATION, CLASSIFICATION AND MANAGEMENT
Muscle damage by unaccustomed or high-intensity exercise is common. Muscle strains appear to occur with the highest frequency in muscle that crosses two joints and in muscle with the highest proportion of Type II muscle fibers.10 As previously noted, unaccustomed eccentric exercise appears to be predisposed to pain and is more likely to cause muscle damage than other types of muscular activity. Gleeson 15 demonstrated that the severity of symptoms of exercise-induced muscle damage (EIMD) is reduced by a prior bout of eccentric exercise. Because of the specificity of muscle adaptation to training or the SAID (S pecific A daptations to I mposed D emands) principle, prior concentric training increases the susceptibility of muscle to EIMD following eccentric exercise.
Two hypotheses explain muscle damage: metabolic overload and mechanical factors. Metabolic overload means the demand for ATP exceeds it production.16–18 To support the metabolic overload theory, several observations have reported that exercise-induced muscle damage resembles ischemic muscle damage. Furthermore, creatine kinase (CK) activity in serum is frequently used as a marker for muscle damage. Although CK is used as a marker for muscle damage, its value as an adequate quantitative marker is poor. Recently, an additional metabolic marker indicating muscle damage was discovered. One study showed that downhill running induced eccentric injury as evidenced by plasma troponin-I levels.19 The presence of proteins, such as troponin-I, might be better markers of muscle damage because of their association with the contractile apparatus of generation and regulation of tension within muscle.
Lieber and Friden20 hypothesized that excessive strain to the sarcomeres permits extracellular or intracellular membrane disruption that may cause myofibrillar disruption. Inflammation that occurs after injury further degrades the tissue, but prevention of inflammation leads to a long-term loss in muscle function.
The second hypothesis is that mechanical factors are a cause of EIMD. Faulkner and Brooks21 demonstrated in laboratory mice local damage to muscle fiber through overuse. The extensor digitorum longus muscle of a mouse was activated by stimulation of the peroneal nerve. The muscle was either shortened or lengthened through 20% of the fiber length. Contractions were elicited every 4 to 5 seconds over periods of 5 minutes to 30 minutes or for 5 minutes with 5 minutes of rest, repeated three times. The local damage of the muscle fiber was determined by infiltration of phagocytes, reduced muscle spindles, and nerve and artery appearance. The ultrastructural damage of the muscle was not observable with light microscopy. Despite the relationship between the number of damaged fibers and the force deficit, the force deficit at day 3 is about 15% greater than the extent of the muscle damage observed in histological sections. The researchers concluded that the force deficit provides a better estimate of the totality of contraction-induced injury.21 Furthermore, a greater loss of force was created after a lengthening contraction (eccentric) than a shortening contraction (concentric), and the least for isometric contractions. Although shortening and isometric contractions produced significant fatigue immediately and for several hours after the exercise protocols, there was no evidence of injury at day 3. In comparison the lengthening contraction exercise protocols demonstrated morphological changes of muscle fiber throughout the first 5 days. The changes in muscle fiber included damage to the sarcoplasmic reticulum, actin and myosin filaments, and possibly capillaries. The magnitude of the injury is a function of the duration of the lengthening contraction. Friden and Lieber22 compared different types of muscle contractions in the limb of a rabbit. This study demonstrated similar findings to the previous study. The magnitude of force deficit was a function of the treatment method. Following 30 minutes of cyclic passive stretch the force deficit was 13%; following isometric contraction it decreased by 31%; and following eccentric contraction it decreased by 69%. Immediately after a protocol of 75 lengthening contractions the force deficit was measured at 3 and 24 hours. The initial force deficit was 35% immediately after the protocol of eccentric contractions and a maximum force deficit of 55% at day 3.
Morgan 23 demonstrated that the stretching of weak sarcomeres beyond the overlap of the myosin and actin filaments resulted in the initial injury to a protein called titin. The titin links the myosin filaments in series contributing to myofibular stability during muscle contraction.
Reduction of sarcomeres in series decreases the muscle compliance and changes the length-tension relation of muscle contraction. Concentric contractions have been recently suggested as contributing to a reduction of sarcomeres in series. Conversely, eccentric exercise contributed to an increase in sarcomeres in series, making the muscle more resistant to EIMD.24 The secondary injury to the muscle fiber resulted from the decreased capacity of the muscles’ ability to develop force.
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