The new century, characterized by increasing individual participation in high-speed travel, complex industry, and competitive and recreational sports, also is marked by significant increases in primary musculoskeletal system injury and conditions that have enormous impact on society.
The fact that the skeletal system with its associated soft tissues provides a protective covering for important structures such as the brain and heart and essentially makes up the limbs puts this system at risk for traumatic and repetitive insults and injuries (Box 22-1).
More than ever, the gap between science and clinical applications of therapeutic exercise has been narrowed. New diagnostic technology, the genome project, and a new branch of study called genomics are providing an increasing understanding of the molecular basis for disease and injury. This new knowledge is changing the approach for health care intervention in many areas, including the musculoskeletal system.
The ability to document the influence and effects of exercise at the molecular and cellular levels has resulted in early functional rehabilitation, preventive exercise programs, and the use of exercise as first-line intervention for many conditions. Maintaining good musculoskeletal health and recovering quickly from musculoskeletal injury or disease contribute to an individual’s overall health, welfare, and quality of life.
Better technology has made it possible to measure what happens to muscle with age without painful and invasive muscle biopsies. For example, newer imaging methods are measuring fatty infiltration of skeletal muscle, a contributor to metabolic problems and muscle dysfunction with aging. Magnetic spectroscopy (MRS) and computerized tomography (CT) are being used to characterize this fatty infiltration. Scientists are looking for ways to reduce the risk of falls, fractures, and disability from changes in the supportive and protective skeletal muscle. Intervention strategies including various kinds of exercise are under investigation.
Preclinical disability is a new concept observed in aging adults (65 years of age or older). It is defined as progressive and detectable but unrecognized decline in physical function.45 Early signs of decline in physical function are observed in the ability to perform mobility tasks and activities of daily living needed to maintain an independent living status.18
Preclinical disability may be seen as an increased time to complete a task, modification of a task, or decrease in the frequency with which a task is performed. Individuals with preclinical disability are at increased risk for progression to more severe disability; early identification of decline in physical function is important if intervention to stop the decline is possible.44,45
More than 50% of injuries in the United States are to the musculoskeletal system; 28.6 million Americans incur musculoskeletal injuries each year. Fractures, sprains and strains, and dislocations account for nearly half of all musculoskeletal injuries.
Annually, an estimated 7 million Americans receive medical attention for sports-related injuries.28 Children younger than 15 years old account for more than 3.8 million sports-related injuries in the United States each year. Violence-related sports and recreational injuries (e.g., being pushed, hit) are increasing among children and adolescents.27 See the section on Occupational Injuries and Diseases in Chapter 4.8,22
Severe cerebral palsy and other developmental disorders (see Chapters 23 and 35) are more common than ever before, because many infants with these complications at birth now survive and live into adulthood. The age span of humans has become progressively longer, with a variety of accompanying age-related conditions such as osteoporosis and degenerative joint or disc disease. Arthritis is the leading chronic condition reported by Americans age 65 years and older.78
In addition, the musculoskeletal system often is confronted with immobilization secondary to major illness or injury, bed rest, or casting or splinting of a specific body region. The musculoskeletal system reacts quickly to the lack of mechanical stress and normal loading (immobilization) in ways that may adversely affect recovery and rehabilitation.
The physical and physiologic responses of the musculoskeletal tissues and resultant deterioration occur within days but take many months to reverse. In fact, 3 weeks of bed rest has a more profound impact on physical work capacity than three decades of aging.37,46 See the section on Tissue Response to Immobilization in Chapter 6; see Table 6-7.
Like all other body systems, the musculoskeletal system does not function in isolation. Therefore, primary disease of the musculoskeletal system can significantly affect other body systems and vice versa. In addition, certain diseases are systemic, meaning that all body systems, including the musculoskeletal system, can be involved to some degree. The challenge to develop an effective rehabilitation program is heightened when one is faced with complex, multisystem disorders (see Chapter 5).
Many musculoskeletal disorders are drug induced or are side effects of treatment for conditions such as cancer. Drug-induced musculoskeletal disorders represent a broad clinical spectrum, from asymptomatic biologic abnormalities to severe and even life-threatening diseases. Myopathies, arthralgias, arthropathies, connective tissue diseases, and periarticular disorders (e.g., tendinopathy, enthesopathy, adhesive capsulitis) have been linked with medications. An increasing number of drugs have been implicated in inducing rheumatic symptoms and/or syndromes. All drug classes can induce musculoskeletal disorders, but the majority are caused by corticosteroids, vaccines, antibacterials, and lipid-lowering agents.12
The purpose of this section is to provide an overview of the musculoskeletal system, including the biologic response to trauma and examples of how primary diseases in other organs affect the musculoskeletal system, and vice versa, and to begin to examine the local (musculoskeletal) and systemic (e.g., immune system, endocrine system, gastrointestinal system) effects of exercise. An approach that assesses all the systems and considers underlying pathology is essential when identifying the source of dysfunction.
Over the past 10 years, advances in molecular biology techniques have extended the potential for understanding musculoskeletal disorders from the microscopic (histologic) level down to the molecular level of gene expression within individual cells. These advances are initiating new avenues of research and, ultimately, novel clinical interventions.6
Orthopedic surgery has been revolutionized by tissue engineering, including biologic manipulation for spinal fusion36; synthetic skeletal substitute materials12; preservation and restoration, transplantation, or fabrication of avascular tissue (e.g., meniscus, articular cartilage)71,80; and joint restoration instead of joint replacement.55
Other technologic advances are under scientific investigation, such as bone implants to stimulate bone development and prevent limb loss associated with cancer16,89; injectable bone substitute that eliminates the need for bone grafts, strengthens osteoporotic vertebral bodies, or heals compression and nonunion fractures33,36; synthetic muscle regeneration; and new materials and plastics making it possible to replace spinal discs or extend joint replacements by an additional 10 years or more.
Recently the influence of biopsychosocial-spiritual stress on the physical body has come to the forefront of research in a field of study referred to as psychoneuroimmunology. Approximately 40% to 80% of adults in primary care report only their physical symptoms (including musculoskeletal manifestations), leaving a large portion of clients with significant psychologic distress undiagnosed.57 Physical therapists often see clients demonstrating various somatoform disorders (see Chapter 3); recognizing this underlying component is important in understanding the biology (and pathology) of the musculoskeletal system and therefore planning appropriate intervention.
Gender discrepancies in rates of injuries and muscle mass response to strength training or deconditioning are also under investigation.11,30 Differences in ligamentous laxity, muscle strength, endurance, muscle reaction time, and muscle recruitment time in males versus females and athletes versus nonathletes may provide additional important information for prevention and rehabilitation of musculoskeletal injuries.61
Women double their rate of injury during ovulation, when levels of estrogen are the highest. Training and conditioning differently during different times of the month may help protect women from injury.24,31,53 The effectiveness of neuromuscular and proprioceptive training in preventing anterior cruciate ligament injuries in female athletes has been demonstrated.63
Men increase their muscle volume about twice as much in response to strength training compared with women; men also experience larger losses in response to detraining than women.56,64
The military has recognized that females undertaking strenuous exercise alongside males are at increased risk of injury. Equal opportunities legislation has been interpreted to require identical training for males and females, but some segregation of training may be necessary to reduce the excess risk of injury to females, provided the outcome of training is no less favorable to either gender.15
See also Specific Tissue or Organ Repair in Chapter 6.
The immediate biologic response to trauma is a generalized inflammatory reaction regardless of what tissue is damaged or the nature of the injury. The response is marked by vascular, chemical, and cellular events, with the ultimate purpose being to prepare the area for repair. The primary objective of the vascular response to injury is to mobilize and transport the body’s defenses (white blood cells).
Vasoconstriction occurs initially along with reduced fluid flow through the injured area, resulting from development of fibrinogen clots in the tissue spaces and lymphatic channels (which prevents the spread of bacteria and toxins). Vasoconstriction allows for the white blood cells to migrate to the periphery of the vessel in a process called margination (see Chapter 6). These white blood cells eventually adhere to the walls of the damaged capillary, a process called pavementing.
Shortly after the injury and vasoconstriction, vasodilation of the local blood vessels occurs. The increased blood flow is accompanied by increased permeability of the small blood vessels. The permeability changes occur secondary to direct trauma to the vessels and to the presence of chemical mediators such as histamines, serotonin, and bradykinins.
The increased permeability allows for the white blood cells to squeeze through the blood vessel wall. This process is called diapedesis (see Fig. 6-12). The increased blood volume and vessel permeability also result in a significant transfer of fluid into the injured area. The fluid shift occurs because of the heightened intravascular hydrostatic pressure and the altered osmotic pressure gradient (as larger molecules escape into the tissues).
Once beyond the blood vessel walls the white blood cells are guided to the site of injury by a process called chemotaxis (see Fig. 6-12). Numerous elements of the damaged tissue (i.e., bacterial toxins and tissue polysaccharides) draw the white blood cells to the area of highest concentration of these elements.
Upon arriving at the site of damage, the white blood cells begin to clean up the area by the process of phagocytosis. The neutrophils, monocytes, and macrophages recognize, engulf, and digest debris, necrotic tissue, red blood cells, and proteins to prepare the area for repair and growth of new tissue.
The cardinal signs of acute inflammation are listed in Table 6-3. Accompanying clinical findings include increased muscle tone or spasm and loss of function. Movements of the involved area are generally slow and guarded. Cyriax describes two components of passive movement testing that also suggest acute inflammation: a spasm end feel and pain reported before resistance is noted by the practitioner as the limb is moved passively.29
If surgery is not indicated, the most effective interventions for acute inflammation are pharmacotherapy and physical therapy. Salicylates (except aspirin) and nonsteroidal antiinflammatory drugs (NSAIDs; see Chapter 5; see also Tables 5-1 and 5-2) are the most commonly administered medications for pain and inflammation.
The antiinflammatory effect is attained chiefly by inhibition of the biosynthesis of prostaglandins. Other antiinflammatory mechanisms include decreasing the release of chemical mediators from granulocytes, basophils, and mast cells; decreasing the sensitivity of vessels to bradykinin and histamine; and reversing or controlling the degree of vasodilation.
Much has been written about the effects of aging on the musculoskeletal system, especially in light of exercise as an effective intervention for so many diseases and conditions. Participation in a regular exercise program is an effective intervention to reduce or prevent a number of functional declines associated with aging.
Endurance training can help maintain and improve various aspects of cardiovascular function (as measured by maximal VO2, cardiac output, and arteriovenous oxygen difference) and enhance submaximal performance. Importantly, reductions in risk factors associated with disease states (e.g., heart disease, diabetes) improve health status and contribute to an increase in life expectancy.9,10
Strength training helps offset the loss in muscle mass and strength typically associated with normal aging. Additional benefits from regular exercise include improved bone health and therefore reduction in risk for osteoporosis; improved postural stability, thereby reducing the risk of falling and associated injuries and fractures; and increased flexibility and range of motion.
Although not as abundant, evidence also suggests that involvement in regular exercise also can provide a number of psychologic benefits related to preserved cognitive function, alleviation of depressive symptoms and behavior, and an improved concept of personal control and self-determination.9,10
Sports-related injuries among people born between 1946 and 1964, now referred to as “boomeritis,”7 are on the increase as older adults continue to participate actively in sports of all kinds. Physical therapists can provide valuable preventive education regarding the aging process as it relates to the musculoskeletal system and exercise. This presentation is a brief summary of the findings to date; more in-depth discussion is available.34,50,70,91
Overview and Definition.: Age-related loss in muscle mass, strength, and endurance accompanied by changes in the metabolic quality of skeletal muscle is termed sarcopenia. Sarcopenia involves both the reduction of muscle mass and/or function as well as the impairment of the muscle’s capacity to regenerate.35
Muscle mass is lost at a rate of 4% to 6% per decade starting at age 40 in women and age 60 in men.54 The greatest decline in both men and women occurs with inactivity, acute illness, and after age 70, at which time the mean loss of muscle mass has been measured as 1% per year.94 At all ages, females appear to be more vulnerable to loss of lean tissue than males; however, in men and women, muscle strength can be maintained through exercise well into the eighth decade.43,58
Etiology.: The etiology is multifactorial, involving changes in muscle metabolism, endocrine changes (e.g., low testosterone levels), nutritional factors, and mitochondrial and genetic factors.69,73 It remains uncertain how much age-related loss of muscle function is an inevitable consequence of aging, nutritional status, or dysregulation of neurologic, hormonal, and/or immunologic homeostasis.
Likewise, it remains unknown how much sarcopenia reflects a decline in physical activity and exercise capacity, and as part of a broad cycle, whether this decline is a function of age, lack of motivation, decline in neuromuscular function from disuse or loss of motoneurons, age-associated decreases in metabolism, or other factors such as anemia or high levels of inflammatory markers.23,95
Pathogenesis.: The identification of the molecular chain able to reverse sarcopenia is a major goal of studies on human aging. Animal studies suggest that myofiber regeneration in sarcopenic muscle is halted at the point where reinnervation is critical for the final differentiation into mature myofibers.
Combined evidence points to a decreased capacity among motoneurons to innervate regenerating fibers. There are also changes observed in the expression of several cytokines known to play important roles in establishing and maintaining neuromuscular connectivity during development and adulthood.38
The decline in muscle mass previously thought to be the result of proteins’ breaking down faster than they were being created and restored may be linked instead to other potential reasons such as diet and nutrition, the body’s ability to use protein from food, and hormonal changes.93 For example, inadequate dietary intake of protein also results in loss of skeletal muscle mass; the current recommended daily allowance (RDA) may not be adequate to completely meet the metabolic and physiologic needs of virtually all older people.21
Loss of muscle function appears to be due to decreased total fibers, decreased muscle fiber size, impaired excitation-contraction coupling mechanism, or decreased high-threshold motor units. For example, at midthigh, muscle accounts for 90% of the cross-sectional area in young, active adults. However, this same measurement taken in older adults is only 30%.46
Additionally, selective loss of motor unit number or atrophy (particularly after 70 years) of fast twitch (type IIa) muscle fibers98 occurs. Some researchers suggest that no preferential loss of type I or type II muscle fibers occurs with age, but rather, both types are equally affected and type II fiber cross-sectional area is reduced, which accounts for the significant decrease in muscle strength.1
Other studies have shown that type II fibers are preferentially affected by aging and that fiber II atrophy is associated with a decline in satellite cells (essential for skeletal muscle growth and repair).93
Other researchers hypothesize an extrinsic apoptotic pathway to explain how type II fiber–containing skeletal muscles may be more susceptible to muscle mass losses.74 Several signaling pathways of skeletal muscle apoptosis are currently under intense investigation, with particular focus on the role played by mitochondria.65 However it occurs, the clinical significance of this loss is that it leads to diminished strength and exercise capacity.90
Effects of Sarcopenia.: From a clinical perspective, loss in muscle mass accounts for the age-associated decreases in basal metabolic rate contributing to metabolic disorders such as type 2 diabetes mellitus and osteoporosis and decreases in muscle strength and activity levels, which, in turn, are the cause of the decreased energy requirements of the aging adult.41
Loss of muscle mass (i.e., atrophy) and definition and loss of muscle function resulting in subsequent muscle weakness are implicated in difficulty accomplishing activities of daily living (e.g., rising from a chair, climbing stairs, carrying groceries), slow gait speed, impaired balance reactions, and increased risk of vertebral compression (and other) fractures. There does not appear to be a relationship between age-related sarcopenia and the bone mass loss also prevalent in the same age group.25
Aging workers notice increasing difficulty continuing a job they have previously performed without trouble. Slowing down of reflexes and coordination combined with loss of muscle mass and strength can make it difficult to remain in the same job or train for a new job.
By age 65, changes in the muscle mass, muscle weakness, and decreased levels of physical activity are evident in the increased numbers of falls and injuries. Injuries in an aging musculoskeletal system take longer to recover, contributing to further physical deconditioning, potentially creating additional comorbidities.
Exercise and Sarcopenia.: (See also the Musculoskeletal System and Exercise in this chapter). Appropriate exercise can alter, slow, or even partially reverse some of the age-related physiologic changes that occur in skeletal muscle, including sarcopenia. Skeletal muscle adaptations in response to strength training in older adults occur with progressive resistance training (PRT) or high-intensity training (e.g., two to six sets of eight repetitions at approximately 80% of the person’s one-repetition maximum).97
Understanding muscle fiber types and the impact of physical therapy interventions on muscle fiber type conversions is becoming increasingly important in today’s evidence-based practice. An excellent review of these concepts is available.79 We know, for example, that age-related changes can be counteracted and physical function improved by increased physical activity of a resistive nature.87 Mechanical load on muscle can increase the cross-sectional area of the remaining fibers but does not restore fiber numbers characteristic of young muscle.1
Strength training has been shown to improve insulin-stimulated glucose uptake both in healthy older adults and in individuals with diabetes. Strength training also improves muscle strength in healthy adults and in those who have chronic diseases. Increased strength leads to improved function and a decreased risk for falls, injuries, and fractures.32 These results also promote increased independence and improved quality of life.101
Aging muscle may be resistant to insulin-like growth factor I (IGF-I); IGF-I promotes myoblast proliferation, differentiation, and protein assimilation in muscle through multiple signaling mechanisms. Exercise may be able to help aging muscle that is resistant to IGF-I by reversing this effect.1
High-resistance training exercise has been of significant benefit to sarcopenia.69 In fact, after 6 months of exercise training, resistance exercise has been shown to reverse mitochondrial dysfunction for genes that are affected by both age and exercise.68 Combinations of resistance exercise, aerobic exercise, and stretching have shown beneficial effects on sarcopenia, but the optimum regime for older adults remains unclear.49,60
Many older adults would like to be more physically active but do not have the experience or knowledge to develop and build up an exercise regimen without appropriate supervision such as the physical therapist can offer. Others have participated in athletics throughout adulthood and continue to train and remain in good health. The therapist can help educate older adults about the importance of maintaining strength training and endurance with the emphasis on strength, which decreases more rapidly than endurance.47
At the same time as changes in bone and muscle are taking place, a progressive loss of flexibility and changes in connective tissue starts contributing to an increased incidence of joint problems beginning in middle age and progressing through old age. Loss of flexibility also contributes to increased risk of falls and other injuries. Connective or periarticular tissue, including fascia, articular cartilage, ligaments, and tendons, becomes less extensible with resultant decreased active and passive range of motion.
It is not clear whether this decreased flexibility occurs as a consequence of biologic aging, inactivity, degenerative disease, adhesion molecules, or a combination of all these factors.98 One possible cause is related to fibrinogen, produced in the liver and converted to fibrin, which constantly circulates throughout the body to serve as a clotting mechanism (with superglue-like effects) should an injury occur.
Fibrinogen normally leaks out of the vasculature in small amounts into the intracellular space and then adheres to cellular structures, causing microfibrinous adhesions among the cells. Activity and movement normally break down these adhesions along with macrophagic activity to dissolve unused fibrinogen and fibrin.
In the aging process, less fibrinogen and fewer (less efficient) macrophages are available. These factors, along with less physical activity and movement, allow these microadhesions to accumulate in muscle and fascia, resulting in an increased sense of overall stiffness.
Others have shown that aging collagen has increased cross-links between molecules, increasing the mechanical stability of collagen but also contributing to increased tissue stiffness.76 Increased collagen content in the endomysium of animal intramuscular connective tissue has been shown to correlate with increased stiffness of the whole muscle.4
Regardless of the exact physiologic mechanism for the gradual increase in stiffness associated with aging, physical activity has an important influence in alleviating stiffness. Further research is needed to understand how and what kind of physical activity influences or possibly prevents stiffness.70,99
Articular cartilage, which cushions the subchondral bone and provides a low-friction surface necessary for free movement, contains few cells, is aneural and avascular, and often starts to break down with increasing age.34 The main proteoglycan in articular cartilage (aggrecan) binds with hyaluronan to form massive aggregates that expand the collagen matrix of the tissue to provide it with its compressive and tensile strength.
With age, proteoglycan aggregation is reduced and smaller proteoglycans are synthesized with an increase in keratin sulfate and reduced chondroitin sulfate content. The hydrophilic proteoglycans have been shown to become shorter in aged tissue and therefore lose their ability to hold water in the matrix.20 Dehydrated articular cartilage may have a reduced ability to dissipate forces across the joint.70
Degeneration and thinning or damage of articular cartilage with loss of water content contribute to a significant increase in incidence of osteoarthritis with aging. By age 60, as much as 80% of the population shows evidence of such, although only about 15% present with symptoms.98
Knowledge of these changes has resulted in new interventions such as glucosamine-chondroitin supplementation and joint viscosupplementation for osteoarthritis (see Chapter 27). With or without a symptomatic presentation, educating adults about the importance of joint protection is an important role of the physical therapist.
Tendons exhibit a lower metabolic activity associated with aging that has implications for injury and healing in the aging population.2,3 Also an age-related decrease occurs in the tensile strength of some tendons and ligament-bone interfaces, and loss of integrity of some joint capsules occurs. For example, rotator cuff impairment with loss of joint function is common in older people. A gradual loss of connective tissue resistance to calcium crystal formation occurs in the older adult, leading to an increase in the incidence of crystal-related arthropathies34 (e.g., gout, pseudogout; see Chapter 27).
Joint proprioception, described as sensations generated to increase awareness of joint orientation at rest and in motion, declines with age, especially in the knee and ankle.72 Joint proprioception provides both a sense of joint position and sense of joint movement. Mechanoreceptors located in the joint capsules, ligaments, muscles, tendons, and skin provide the sensory information needed for a sense of joint position.
The presence of osteoarthritis seems to make joint proprioception even worse, though it is unclear whether impaired joint sense promotes arthritic change or whether arthritic change causes the sensory loss. There is some evidence that proprioception may be reduced before the development of joint degenerative change.59
The skeletal system serves numerous functions in the human body throughout the lifespan. Bone is the primary storage depot for calcium, phosphate, sodium, and magnesium. Bones are the hosts for the hemopoietic bone marrow (growth and development of elements of blood). Bones also serve important mechanical functions, such as protection of components of the nervous system and visceral organs; provision of rigid internal support for the trunk and extremities; and provision of attachment sites for numerous soft tissue structures.
Bone is remodeling constantly throughout life. While osteoclasts resorb the existing bone, new bone is being formed by osteoblasts. Three primary influences affect this remodeling process: (1) mechanical stresses; (2) calcium and phosphate levels in the extracellular fluid; and (3) hormonal levels of parathyroid hormone, calcitonin, vitamin D, cortisol, growth hormone, thyroid hormone, and sex hormones.
Aging adversely affects the “quality” of human bone material, both the stiffness and strength of bone and its “toughness.” These effects are caused by factors such as architectural changes, compositional changes, physiochemical changes, changes at the micromechanical level, and the degree of prior in vivo microdamage.102
The bone density of the skeleton reaches its peak during an adult’s twenties and remains stable for about two decades. Around the time of menopause for women, resorption, the process by which bone is broken down and calcium is released from the bone for use by the body, increases, while formation, the bone-rebuilding process, fails to keep pace. This imbalance, which is triggered by declining estrogen levels, leads to rapid bone loss during the first decade after menopause, with moderate bone loss thereafter. In women with low peak bone mass, it can result in osteoporosis with the increased potential for vertebral, hip, or other fracture.51
The same progressive decrease of calcium can occur in men, only at a reduced and slowed rate. In women, loss occurs at a rate of approximately 1% per year after age 35 with acceleration especially during the first 5 years after menopause. Men lose 10% to 15% by age 70 years and 20% by age 80.
In women the loss is greater, amounting to about 20% by age 65 and 30% by age 80.5,84 In both genders, by age 65, bone loss generally has progressed to a point where the older adult is predisposed to fractures, especially when other comorbidities exist (e.g., diabetes, balance or vestibular impairment, renal impairment, immobilization).98
By the year 2030, 70 million people in the United States will be 65 years or older; people 85 years and older will be the fastest growing segment of the population. As more individuals live longer, the importance of exercise and physical activity to improve health, functional capacity, quality of life, and independence will increase in this country.9,10
Strength training is considered a promising intervention for reversing the loss of muscle function and the deterioration of muscle structure that is associated with advanced age. The capacity of older men and women to adapt to increased levels of physical activity is preserved, even in the most aged adult.19,92
For example, the relationship of exercise to insulin action is important because increased body fat (especially abdominal obesity) and decreased exercise is linked to the increased incidence of diabetes in the aging population.
Regularly performed exercise can affect nutritional needs and functional capacity in the older adult, contributing a preventive effect.38 Combining knowledge of exercise principles with nutrition is important for all people but especially in the older adult population, disabled individuals, athletes, adolescents, and anyone with a medical condition, disease, or illness.100
Human muscles contain two different types of muscle fibers based on speeds of shortening and morphologic differences. Type I muscle fibers, known also as slow oxidative slow twitch fibers, are the fatigue-resistant red fibers. The red color is the result of high amounts of myoglobin and a high capillary content. Greater myoglobin and capillary content contributes to the increased oxidative capacity of red muscles compared to white muscles (type II).79
Type II fibers, or fast twitch fibers, have two different characteristics. Type IIa, which are bigger and faster than type I, are also fatigue resistant and are referred to as fast oxidative fibers. Type IIb fibers are the classic white fibers, which lack aerobic enzymes and therefore fatigue rapidly. Each muscle contains type I and type II fibers in various proportions.
The basic distribution of fiber types is thought to be an inherited characteristic. Although distribution varies among individuals, the average ratio of fast to slow twitch fibers is 50: 50. Individuals trained in endurance activities usually have a higher proportion of slow twitch fibers, and those trained for high-intensity, high-speed activities have more high twitch fibers. The oxidative capacity of both fibers can be increased greatly by endurance training, but the glycolic capacity and contractile properties are not modified.81
Muscle function can be described in terms of strength and endurance, which is also how we focus training of muscle. Strength can be defined in several ways depending on the specific method of measurement but is usually related to the diameter of the muscle fiber, which has been consistently shown to increase with strength training.
Endurance can be measured as the ability to work over time; local muscle endurance is distinguished from general body endurance as the ability of an isolated muscle group to continue a prescribed task rather than the ability to continue an activity such as running, swimming, or jogging for an extended period of time.81
As a result of specificity of training and the need for maintaining muscular strength and endurance, and flexibility of the major muscle groups, a well-rounded training program including aerobic and resistance (strength and endurance) training and flexibility exercises is recommended.
Strength training refers to exercise directed at improving the maximum force-generating capacity of muscle. There is evidence that strength training has a positive effect on aging skeletal muscle.97
Collectively, studies indicate that strength training in the older adult (1) produces substantial increases in the strength, mass, power, and quality of skeletal muscle; (2) can increase endurance performance; (3) normalizes blood pressure in those with high-normal values; (4) reduces insulin resistance; (5) decreases both total and intraabdominal fat; (6) increases resting metabolic rate in older men; (7) prevents the loss of bone mineral density with age; (8) reduces risk factors for falls; and (9) may reduce pain and improve function in those with osteoarthritis in the knee.
Significant strength gains are possible in all populations, including older adults, when exposed to an adequate strength training program. Strength gains occur from enhanced neuromuscular activation over the initial 8 weeks and from increased fiber density and hypertrophy during subsequent weeks.62
Considerable evidence exists that sarcopenia can be prevented, reduced, and reversed with prescriptive strength training programs that emphasize gradual, progressive, high-intensity resistance exercises (e.g., high load/low repetition) for the upper and lower extremities.13,77,79
Resistance training significantly increases muscle size and increases energy requirements and insulin action in adults over age 65 years. A program of once-or twice-weekly resistance exercise (carried out at a level described as “reasonably difficult” or “difficult”) achieves muscle strength gains similar to 3 days/wk training in older adults and is associated with improved neuromuscular performance.88 The goal is to design a program for each individual to provide the proper amount of physical activity and exercise to attain maximal benefit at the lowest risk.9,10
Strength training does not increase maximal oxygen uptake beyond normal (i.e., individuals attain the same maximal VO2 before and after training).66,67 In postmenopausal women, muscle performance, muscle mass, and muscle composition are improved by hormone replacement therapy (HRT). The beneficial effects of HRT combined with high-impact physical training appear to exceed those of HRT alone.82,83,86 Long-term results remain under investigation.
Endurance training refers to exercise directed at improving stamina (the duration that a person can maintain strenuous activity) and aerobic capacity (VO2max). Endurance training places a high metabolic demand on the muscle and will increase the oxidative capacity of all muscle fiber types.79
Endurance exercise can reverse the decline in physical conditioning associated with aging. An endurance training program using relatively modest intensity of training can reverse 100% of the loss of cardiovascular capacity, returning some healthy older adults to levels of aerobic power present in young adulthood. Even an older person who has failed to maintain fitness over time can benefit from an exercise program.66,67
In middle-aged adults, the mechanism responsible for decline in cardiovascular capacity appears to be a reduced plasticity of heart muscle; improved aerobic power after training appears to be directly related to peripheral oxygen extraction (i.e., the muscles’ ability to take up and use oxygen).
Aerobic exercise results in improvements in functional capacity and reduced risk of developing type 2 diabetes mellitus in the older adult. Aerobic endurance training for fewer than 2 days/wk at less than 40% to 50% VO2 and for less than 10 minutes is generally not a sufficient stimulus for developing and maintaining cardiovascular fitness in healthy adults.
As discussed earlier, tendons, ligaments, and muscles around the joints have less water content, resulting in increased stiffness, with increasing age. Articular cartilage has less tensile strength and biochemical composition changes, often leading to osteoarthritis.75
Joint changes with deterioration of subchondral bone and atrophy of the synovium also can occur. Well-regulated exercise does not produce or exacerbate joint symptoms and actually may improve symptoms.26 This concept is discussed in greater detail in the section on osteoarthritis (see Chapter 27).
The relationship between bone mass and activity is well established. Complete immobilization and weightlessness result in rapid onset of accelerated bone resorption; bone mass recovers when activity resumes, but whether bone loss is completely reversible is unknown. Immobilization also leads to changes in collagen, ligaments, and the musculotendinous junction at the joint, causing reduced range of motion.
Osteopenia, osteomalacia, and osteoporosis affect the mineralization of bone matrix and can impact the bone health of the aging adult. Older adults are at greater risk for osteoporosis-related fractures, both age related for all adults and postmenopause related for women. Fractures are discussed in more detail in Chapter 27.
Resistance training is an integral component in the comprehensive health program promoted by major health organizations such as the American Heart Association, American College of Sports Medicine, Surgeon General’s office, and others. Population-specific guidelines have been published, and the current research indicates that for healthy people of all ages and many people with chronic diseases, single-set programs of up to 15 repetitions performed a minimum of twice per week are recommended.
Each workout session should consist of 8 to 10 different exercises that train the major muscle groups. Single-set programs are less time consuming and generally result in greater compliance. The goal of this type of program is to develop and maintain a significant amount of muscle mass, endurance, and strength to contribute to overall fitness and health.
Although age in itself is not a limiting factor to exercise training, a more gradual approach in applying prescriptive exercise at older ages may be necessary because exercise programs also can cause injury, especially in the presence of comorbidities such as arthritis, obesity, neurologic disease, postural instability, cardiovascular impairment, previous joint injuries, joint deformity, or other musculoskeletal complications, such as tendonitis or shoulder impingement syndrome. High-intensity resistance training (above 60% of the onerepetition maximum) has been demonstrated to cause large increases in strength in the older adult (older than 65 years).17,40
People with chronic diseases may have to limit range of motion for some exercises and use lighter weights with more repetitions.42,52 Otherwise, older adults do not have to “take it easy” when performing exercise. The presence of heart disease, diabetes, cancer, or other comorbidities may require some initial progression in the prescribed program.97
Overall, therapists should pay careful attention to finding exercise intensities that are optimally suited to induce the desired training effects. The skeletal muscle of older people is more easily damaged with the loading that occurs during training compared with the skeletal muscle of younger adults. Care should be taken to monitor soreness and prevent muscle injuries after exercise.97
Recommendations for the quantity and quality of exercise for developing and maintaining cardiorespiratory and muscular fitness and flexibility in healthy adults also have been published. A certain combination of frequency (3 to 5 days/wk), intensity (55% or 65% to 90% of maximum heart rate or 40% or 50% to 85% of VO2max), and duration (20 to 60 minutes continuously or 10-minute bouts intermittently throughout the day) of exercise performed consistently over time has been found effective for producing a training effect.9,10
Fatigue, the inability to continue to maintain a given activity, may develop as a result of depletion of muscle and liver glycogen, decreases in blood glucose, dehydration, and increases in body temperature. In a strength training program for adults over 65 years, repeated maximum voluntary contractions resulting in fatigue may differ from those for younger populations. This may be relevant for designing optimal strength training programs for older adults specifically requiring closer supervision to ensure that each repetition is completed without substitution or incomplete range of motion and to adjust rest times between contractions. Alternatively, electrical stimulation may provide more consistent muscle activation during strength training in this age group.85
Exercise guidelines for the very old (older than 85 years) also have been published by the American College of Sports Medicine as follows: frequency of at least 2 days/wk, preferably 3 days; intensity of 40% to 60% of heart rate reserve; duration of at least 20 minutes. Walking, leg/arm ergometry, seated stepping machines, and water exercises are recommended.
Additional recommendations for resistance training include two to three sets of 8 to 12 repetitions performed with good form and through the entire range of motion for each exercise performed on each training day (one set may be sufficient); some standing postures with free weights and balance training should be included.9,10 When 12 repetitions can be completed without difficulty (observe for increased respiration, extremity tremors, facial grimacing), the weight can be increased by 5% with a lower number of repetitions to begin a new training cycle.
Although not nearly as common as traumatic and repetitive or overuse injuries, musculoskeletal system diseases are significant from the standpoint of disability, mortality, and cost in terms of health care dollars. The most serious of these diseases are cancer and infection. The pathogenesis of these two types of diseases illustrates the intricate interrelationships between the musculoskeletal system and other body systems.
The primary highways or communication networks connecting the musculoskeletal and other body systems are the circulatory and lymphatic systems. These pathways are the routes utilized by disease to travel from one system to another. In addition, these highways deliver the nutrients and other supplies needed by the musculoskeletal system.
Although primary malignant bone and soft tissue tumors are rare, metastatic disease of the musculoskeletal system is relatively common. Bone is one of the three most favored sites of solid tumor metastasis, indicating that the bone microenvironment provides fertile ground for the growth of many tumors. Although lung, breast, and prostate are the three primary sites responsible for most metastatic bone disease, tumors of the thyroid and kidney, lymphoma, and melanoma also can metastasize to the skeletal system.
Cancer cells typically invade the thin-walled lymphatic channels, capillaries, and venules as opposed to the thicker-walled arterioles and arteries. Once the cancer cells enter the bloodstream, they must lodge in the vascular network of the host tissue before the secondary cancer can develop.
Organs with extensive circulatory or lymphatic systems, like the lungs and liver, are the most common sites of metastasis. Of the other potential sites of metastasis, the axial skeleton is among the most common. The blood supply to the axial skeleton is extensive compared with that to the distal components of the extremities, and the spinal blood flow through the thin-walled, valveless veins is slow and sluggish. This gives the circulating cancer cells ample opportunity to attach to the vessels’ endothelia. The bony thorax, lumbar spine, and pelvis are the most common components of the axial skeleton for seeding of cancer to occur, and the vertebral bodies, because of the extensive venous plexus, appear to be the initial site for development of disease.
As with primary bone tumors, the major manifestation of metastatic bone cancer is pain, especially on weight bearing and at night. The pain can be caused by stretching of the periosteum or irritation of a nerve root or spinal cord, or can be secondary to bone collapse (pathologic fracture).
Once the cancer begins to spread, clients report fatigue, malaise, fever, nausea, and other symptoms. Therapists working with clients diagnosed with cancer must be vigilant for symptoms or signs suggestive of systemic compromise and be aware of common sites of metastasis for the particular primary tumor.
An awareness of signs and symptoms associated with the potential target organs is important, and any suspicious findings should be reported to the physician. Unfortunately, often the initial presenting symptom associated with the disease is pain from the bone metastasis (back pain), which can result in a delay in the diagnosis. See Chapters 9 and 26 for extensive information related to cancer.
As with cancer, infection can originate in the musculoskeletal system or it can spread to the musculoskeletal system from elsewhere in the body. The most common cause of osteomyelitis is direct extension of bacterial organisms by penetrating wounds, fractures, or surgical intervention. Staphylococci and streptococci are the most common infecting agents (see Chapter 8).
The other common mechanism by which bacterial organisms reach the musculoskeletal system is via the hematogenous route. The original infection could be of the urinary tract (adults) or skin or teeth (children). In adults, the most common site of osteomyelitis is the vertebral body or intervertebral disc. The sluggish blood flow through the valveless veins facilitates bacterial seeding. Cases have been described illustrating the lengthy delay in diagnosis of vertebral osteomyelitis when back pain is the primary presentation (see the section on Osteomyelitis in Chapter 25).
Back pain can occur as a symptom of many diseases. Anyone with back pain of nontraumatic or unknown origin must be screened for medical disease, especially possible gastrointestinal or abdominal involvement related to infections (e.g., diverticulitis, appendicitis, pelvic inflammatory disease, Crohn’s disease).
If infection occurs and penetrates the pelvic floor or retroperitoneal tissues (i.e., those organs outside the peritoneum such as the kidneys, colon, and bladder), abscesses may result in isolated referred hip or thigh pain and antalgic gait.
A variety of objective test procedures may be employed by the therapist to assess for iliopsoas abscess formation, including the pinch-an-inch test (see Fig. 16-24), the iliopsoas muscle test, the obturator test, and palpation of the iliopsoas muscle (see Figs. 16-14 and 16-15).
Approximately 25% of all clients with inflammatory bowel disease (IBD; e.g., Crohn’s disease, ulcerative colitis, diverticulitis) may present with migratory arthralgias, monarthritis, polyarthritis, or sacroiliitis. The joint problems and gastrointestinal disorders may appear simultaneously, the joint problems may manifest first (sometimes even years before bowel symptoms), or intestinal symptoms may present along with articular symptoms but be disregarded as part of the whole picture by the client.
Any time a client presents with low back, hip, or sacroiliac pain of unknown origin, the therapist must screen for medical disease by asking a few simple questions about the presence of accompanying intestinal symptoms, known personal or family history for IBD, and possible relief of symptoms after passing stool or gas.48
Joint problems usually respond to treatment of the underlying bowel disease but in some cases require separate management. Interventions for the musculoskeletal involvement follows the usual protocols for each area affected.
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