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This chapter presents an overview of osteoporosis and discuss special considerations related to exercise testing, prescription, and progression for individuals diagnosed with osteoporosis. The case study presented focuses on a woman diagnosed with osteoporosis who would like to begin an exercise program at her local fitness facility. This case study provides guidance for the design of a program that includes progressive resistance training, aerobic conditioning, and balance training, with the primary goal of preventing falls and fracture in an individual with diagnosed osteoporosis, or low bone mineral density (BMD).
Mrs. Case Study-BH
Mrs. Case Study-BH is a 65-year-old woman weighing 61.2 kg (134.6 lb) and with a height of 167.6 cm (66 in); her body mass index (BMI) is 21.8 kg ∙ m−2. She was diagnosed with osteoporosis, or low BMD, at her most recent physical examination. Her vertebral T-score was −2.7, and her hip T-score was −2.0. (The World Health Organization defines osteoporosis as a T-score less than 2.5.) After ruling out secondary causes of osteoporosis (e.g., malabsorptive disorders, hyperparathyroidism), her physician prescribed a bisphosphonate (anti-bone resorption drug) to improve her bone density, and she has been taking this medication for the past 2 months. She reports no previous falls or nontraumatic fractures, but her mother suffered an osteoporotic thoracic spine vertebral fracture in her mid-70s that left her with a kyphotic posture (rounding or curvature of the thoracic and cervical spine). Mrs. Case Study-BH is a semiretired elementary school counselor who currently works part-time where she spends the majority of her time sitting at her desk. When she is not working, she enjoys walking and gardening. She reports walking in her neighborhood and on the school’s outdoor track on average 3 days per week for approximately 30 minutes. She has no history of resistance training.
Mrs. Case Study-BH began menopause at age 48 years and is not taking a hormone replacement therapy. She reports having periodically taken a multivitamin supplement in the past but does not take any other dietary supplements. She has been a nonsmoker for approximately 20 years after beginning smoking at 17 years of age and consumes alcohol 2–3 days per week and wears corrective lenses. She is an otherwise healthy individual. In addition to the bisphosphonate prescription, Mrs. Case Study-BH’s physician recommended that she visit her local fitness facility and begin participating in an exercise program.
Mrs. Case Study-BH’s goal in pursuing an exercise program is to prevent a future fracture and maintain her current mobility and quality of life. She expressed concern over her osteoporosis diagnosis and fears that she will suffer a vertebral fracture and acquire a hunched posture like her mother or will fall and fracture a hip.
Based on Mrs. Case Study-BH’s Physical Activity Readiness Questionnaire for Everyone (PAR-Q+) responses, she currently engages in light-to-moderate levels of regular physical activity (walking 30 min on 3 d ∙ wk−1 for the past 5 yr) and does not have cardiovascular, metabolic, or renal disease and has no signs or symptoms suggestive of these diseases (ACSM’s Guidelines for Exercise Testing and Prescription, 10th edition [GETP10]). As part of her goal to prevent further bone loss and osteoporotic fracture, Mrs. Case Study-BH would like to continue her current activity level and also aims to incorporate physical activities that promote bone health. Mrs. Case Study-BH’s PAR-Q+ outcomes indicated that she is not required to seek medical clearance before initiating her exercise program. However, the exercise professional still may choose to request medical clearance from the physician of an individual with osteoporosis. Mrs. Case Study-BH’s exercise professional requested medical clearance, and her physician recommended avoiding any exercise that includes spinal flexion (e.g., toe touches). Her physician also recommended resistance training activities that load the spine and hip regions but to begin with light resistance at first and to progress only when Mrs. Case Study-BH can perform the exercises correctly with good form.
Given Mrs. Case Study-BH’s concern for osteoporotic fracture and kyphosis, her exercise program should aim to minimize bone loss, reduce fall risk, and improve her current physical fitness. Her exercise professional devised a 24-week program including progressive aerobic, resistance, and balance training progressions across three 8-week cycles.
Mrs. Case Study-BH has engaged in a regular, 3-day-per-week walking program of approximately 30 minutes per day for the past several years. Therefore, the initial goal of her 24-week aerobic training program was to progressively increase activity from light-to-moderate intensity over the first 8 weeks of her exercise program through moderate-intensity walking intervals of increasing duration.
During the second 8-week cycle, Mrs. Case Study-BH progressively increased her exercise frequency by 1 day per week with a dance class that met osteogenic (bone forming) requirements of generating unaccustomed loading patterns by performing multiaxial dance steps. Over the final 8-week cycle, Mrs. Case Study-BH gradually increased her time spent in each exercise bout from 30 to 45 minutes per day. The additional osteogenic component was met with short bouts of stair climbing in her home three times per day. Over the 24-week aerobic exercise program, Mrs. Case Study-BH progressively increased both frequency and time spent in aerobic endurance activities to achieve American College of Sports Medicine (2) guidelines for older adults by engaging in 30–45 minutes per day of moderate-intensity aerobic activity (accumulating 120–180 min ∙ wk−1).
Because Mrs. Case Study-BH reported no previous experience with resistance training, her resistance and balance program began with body weight exercises with a primary focus on proper form and spinal alignment. Across three 8-week cycles, Mrs. Case Study-BH’s exercises were aimed at improving strength and balance and progressed from body weight exercises toward incorporating resistance with bands, free weights, and resistance machines. The exercises addressed all the major muscle groups, and emphasis was placed on progressive overload through increasing numbers of sets, resistance, and exercise difficulty. Exercise difficulty included progressions from partial to full range of motion (avoid full spinal flexion), supported to unsupported movements, and body weight to loaded resistance. Endurance training for postural muscles began with isometric exercises performed in the supine position and progressed to daily spinal extensor training with progressions to prone and seated positions with resistance bands. Mrs. Case Study-BH began each 8-week cycle with one set of each exercise and gradually increased one set every 2–3 weeks. During the first 8-week cycle, Mrs. Case Study-BH’s balance training began with static positions (e.g., supported semitandem stance) with challenging progressions that reduced contact with support and shifted weight as she was able to demonstrate stance holding for each position (e.g., 30 s). During the subsequent cycles, she performed progressively challenging dynamic activities (e.g., semitandem walk and obstacle courses with cones). Once she demonstrated stability during the movement, increasingly challenging dual tasks were introduced (e.g., turning head toward a visual target during walking). Following Mrs. Case Study-BH’s 24-week exercise program, she reported feeling stronger; having increased endurance; and feeling less worried about falling, suffering, and fracture, which might leave her kyphotic like her mother.
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Osteoporosis is a skeletal disorder characterized by compromised bone strength that results in an increased susceptibility to fracture (11,28). It is estimated that approximately 200 million women worldwide currently have osteoporosis (34), and the prevalence among all adults is expected to rise with the increase in life expectancy and aging population (16). Osteoporosis and related fractures are more common in women than men, with 1 in 2 women suffering a fracture over the age of 50 years (11,35,45). The greater prevalence of fractures in women is the basis for the false belief that osteoporosis is a health concern only for women. Men are also at risk for fracture, with approximately 25% of all men over the age of 50 years suffering an osteoporotic fracture in their lifetime (33).
This increase in risk of fracture with low bone mass is the clinical relevance of osteoporosis. More than 1.5 million fractures are associated with osteoporosis each year. Osteoporotic fractures are low-trauma fractures that occur with forces generated by a fall from a standing height or lower and are most common at the spine, hip, and wrist. Regardless of the initial fracture site, adults who fracture have a much greater risk of fracturing again at any location (19). After the age of 50 years, it is estimated that approximately 1 in 2 women and 1 in 5 men will suffer from an osteoporosis-related fracture in their lifetime (11,35,45).
Hip fractures are considered to be the most devastating consequences of osteoporosis because they are associated with severe disability and increased mortality (6). Osteoporosis is a silent disease (i.e., often not accompanied by symptoms) and is commonly first detected by clinical screening or by experiencing an osteoporotic fracture. As a result, much of the attention in osteoporosis is focused on early prevention, detection, and treatment.
Fractures occur when the magnitude of a load on a bone is greater than the strength of a bone (14). Therefore, although osteoporosis denotes skeletal fragility, osteoporotic fractures are the result of both skeletal fragility and the load that occurs from a fall. Because most hip and wrist fractures occur as a consequence of falling, factors influencing both bone fragility and risk of falling should be considered when discussing the pathophysiology of osteoporotic fractures.
The characteristics of bone that determine its strength include the quantity of bone material present, the quality of the material, and the distribution of the material in space (i.e., the structure of the bone). These factors are determined by the dynamic cellular activities known as bone modeling and remodeling, which are regulated by bone’s hormonal and mechanical environments. Modeling is the independent action of osteoclasts (bone-resorbing cells) and osteoblasts (bone-forming cells) on the surfaces of bone, whereby new bone is added along some surfaces and removed from others. Modeling affects the size and shape of bones and is especially important for reshaping long bones as they grow in length during adolescence. Remodeling is a localized process that involves the coupled action of osteoclasts and osteoblasts, in which osteoclasts first resorb a pit of older bone, and osteoblasts are subsequently recruited to the site to form and mineralize new bone. This process happens throughout the lifespan and occurs diffusely throughout the skeleton. An important role of remodeling is to replace damaged bone with new, healthy bone. Like any material subjected to repetitive loading, bone experiences fatigue damage in the form of very small cracks. However, unlike inert materials, bones are able to replace damaged bone with new bone tissue through the process of targeted bone remodeling (52).
Characteristics of Bone Strength
As mentioned earlier, many skeletal characteristics contribute to bone strength and, consequently, bone fragility, including the quantity of bone material present, the quality of the material, and the structure of the material. It is important to understand how each of these features of bone strength change with age in order to understand why our bones become weaker and are more susceptible to fracture in later life.
Bone quantity refers to the amount of bone material present. The average pattern of change in bone mass across the lifespan is displayed graphically in Figure 21.1, although the actual pattern of bone mass change is more dynamic than shown both during growth and in later life. For example, approximately 26% of total adult bone mass is accrued in a 2-year period during adolescence (5). This is approximately equivalent to the entire amount of bone lost in later life (21). Overall, global bone formation continues at a faster pace than bone resorption until peak bone mineral accretion is attained sometime in the second or third decade of life (depending on site, region, and sex). In later life, the amount of bone formation within each remodeling site no longer equals the amount of bone that was resorbed, and thus, a small amount of bone is lost with each new remodeling cycle. This is referred to as a negative bone balance.
FIGURE 21.1. Bone is a dynamic tissue that is vascularized and innervated. Cortical bone is dense and stiff and makes up the shaft of long bones. Cortical bone also provides a shell of protection around trabecular bone, which is more porous and flexible and is found at the ends of long bones and in vertebrae. (Reprinted from American College of Sports Medicine. ACSM’s Resource Manual for Exercise Testing and Prescription. 7th ed. Philadelphia [PA]: Lippincott Williams & Wilkins; 2014. 896 p. Figure 42.1.)
FIGURE 21.2. Normal pattern of bone mineral accretion and loss throughout the lifespan in men and women. (Reprinted from American College of Sports Medicine. ACSM’s Resource Manual for Exercise Testing and Prescription. 7th ed. Philadelphia [PA]: Lippincott Williams & Wilkins; 2014. 896 p. Figure 42.3).
In later life, gonadal hormones (e.g., testosterone and estrogen) decrease in both men and women. Estrogen, in particular, suppresses activation of new remodeling cycles, and thus, low estrogen levels partially contribute to an increased rate of remodeling (67). As resorption precedes formation in the process of remodeling, and formation and subsequent mineralization are time-intensive processes, an increase in the rate of remodeling results in temporary decreases in bone mass. Although temporary losses in bone mass lead to a transient increase in bone fragility, increased rates of remodeling with a negative bone balance lead to sustained bone loss of approximately 9%–13% during the first 5 years after menopause (53). Bone turnover eventually slows to a rate similar to premenopausal years. Men also experience age-related bone loss but usually not until later in life than women (17).
Although the amount of bone in the human skeleton decreases with menopause and advancing age, there is evidence that properties of the remaining bone material may change with age in a way that increases susceptibility to fracture. Bone material from older individuals is less able to absorb energy before failure likely because of an increase in the proportion of mineral within bone tissue compared to collagen as well as changes in collagen properties that are associated with advancing age (18). Also, with advancing age comes susceptibility to fatigue damage. Microcracks have been shown to increase in number and length with age (69). This microdamage accumulation is associated with reduced bone strength (48).
Another important component of bone strength is the structure of bone, that is, how the material is distributed in space. Subtle changes in cross-sectional geometry can markedly increase or decrease bone strength with little or no changes in bone mass or density. Structural differences in cortical bone geometry may partially explain some of the differences in fracture rates between men and women. During growth, the long bones of boys have greater gains in periosteal (outer) diameter of the diaphyses, resulting in a greater overall bone size in boys that remains throughout life, whereas girls have a narrowing of the endocortical (inner) surface of the bone (62). In later life, bone is lost primarily from the endosteal surfaces (inner surface of long bones and intracortical surfaces within the cortex). Thus, the cortex becomes more porous, and the cortices become thinner and more fragile. To offset these losses, bone may be added to the periosteum (outside surface of bone), thereby increasing the diameter of bone and maintaining the strength of the structure in bending (9,62,63). However, as more bone is resorbed from the endocortical surface than is formed on the periosteal surface, the cortices continue to thin, becoming fragile, and are more likely to fracture.
Microarchitecture of trabecular bone is also an important contributor to skeletal fragility (15). For example, if the resorption phase of remodeling is aggressive, as is seen at menopause and thereafter, trabeculae may be penetrated, and the trabecular element may be lost (Fig. 21.3). In these cases, the loss in structural strength disproportionately exceeds the amount of bone lost (54). Furthermore, trabeculae that remain intact may be thinned by excessive remodeling, creating a declining ability to bear loads.
FIGURE 21.3. Normal pattern of bone mineral accretion and loss throughout the lifespan in men and women. (Reprinted from American College of Sports Medicine. ACSM’s Resource Manual for Exercise Testing and Prescription. 7th ed. Philadelphia [PA]: Lippincott Williams & Wilkins; 2014. 896 p. Figure 42.3).
Risks for and Prevention of Fracture
Although skeletal fragility increases susceptibility to fracture, it would be of little concern if damaging loads, such as those generated in a fall, were prevented. Most hip fractures occur after a sideways fall and landing upon the hip (49,68). The incidence of falls increases with age because several sensory systems that control posture (vestibular, visual, and somatosensory) become compromised with advancing age. Furthermore, muscle mass and strength, which prevent instability, decline 30%–50% between the ages of 30 and 80 years (39).
Although bones become more susceptible to fracture, and people become more susceptible to falls with advancing age, fortunately, there are several management tools for prevention and treatment of the condition. Management strategies involve both pharmacological therapy and lifestyle modifications. In this chapter, the focus on lifestyle management, with a particular emphasis on exercise.
Many lifestyle behaviors can be modified to offset risk of osteoporosis and related fractures. For example, all postmenopausal women and older men, regardless of fracture risk, should be encouraged to engage in behaviors that may reduce their risk for skeletal fragility and falls, including adequate calcium (1,000–1,500 mg ∙ d−1) and vitamin D (600–800 IU ∙ d−1) intake, regular exercise, smoking cessation, avoidance of excessive alcohol intake, and visual correction to decrease risk of falling. Of these lifestyle behaviors, exercise is the only one that can simultaneously ameliorate low BMD, augment muscle mass, promote strength gain, and improve dynamic balance — all of which are independent risk factors for fracture (36). Although there is currently no direct evidence that exercise reduces the risk of osteoporotic fracture, clinicians and exercise professionals are encouraged to embrace the theoretical basis behind exercise prescription for osteoporosis prevention and treatment (39).
Bone is a dynamic tissue that is capable of continually adapting to its changing mechanical environment. When a bone is loaded in compression, tension, or torsion, bone tissue is deformed. Deformation of bone tissue, or the relative change in bone length, is referred to as strain. Bone tissue strain can result in movement of fluid within the bone which may perturbs bone’s resident cells — osteocytes. These bone cells are embedded throughout bone tissue and are connected with one another, to other bone cells, and with the bone marrow through slender dendritic processes. The current prevailing theory is that this fluid flow along the osteocyte and its cell processes causes a release of molecular signals that lead to osteoclast and osteoblast recruitment (13,61). This process of turning a mechanical signal into a biochemical signal is called mechanotransduction. Mechanotransduction stimulates the physiological processes of modeling and remodeling that creates anatomical changes in bone, resulting in a bone that is better suited to its new mechanical environment.
It has been suggested that the response of bone to its mechanical environment is controlled by a “mechanostat” that aims to keep bone tissue strain at an optimal level by homeostatically altering bone structure (26). Indeed, when bone is subjected to lower than customary loads (as in space flight and immobilization), bone can adapt by ridding itself of excess mass. Alternately, when bone is subjected to greater loads such as uncustomary exercise, bone can become stronger by altering its structure and forming new bone on existing surfaces. Although mechanotransduction is an acute response to exercise, the adaptation of bone structure through modeling and remodeling takes several months to complete. In the case of bone modeling, bone does not respond to exercise by solely adding mass randomly to the skeleton. Rather, animal studies suggest that bone is added where strains are the highest — typically on the periosteal surface in long bones (56). This has the effect of increasing the diameter of long bones, making them more resistant to deformation with loading.
The prevalence of remodeling in bone is also increased with exercise. With the increase in bone tissue strain that occurs with exercise, there is an increase in the number of microcracks in bone. This damage is thought to be targeted for removal by osteoclasts, and new bone is formed in its place (10,53). Thus, one of the proposed chronic effects of exercise on the skeleton involves the maintenance of bone tissue quality through targeted remodeling.
Although osteoporosis is a disease associated with advancing age, there is almost universal consensus that healthy behaviors in youth are important for reducing the risk of osteoporosis in later life (21). The observation that more than 25% of adult bone mineral is laid down during the 2 years surrounding the age of peak linear growth emphasizes the importance of the adolescent years in optimizing bone mineral accrual (5). It is estimated that as much bone mineral is laid down during this period as an adult will lose from 50 to 80 years of age (3). Thus, optimizing bone mineral accrual during the growing years is an essential ingredient for the prevention of osteoporosis later in life.
Several reviews have concluded that appropriate physical activity augments bone development (4,7,41). Retrospective human studies clearly indicate that bone responds more favorably to physical activity that were undertaken during childhood and adolescence than during adulthood (23,50). Numerous randomized controlled intervention studies have also been conducted to investigate the change in bone mass and bone strength in children secondary to an exercise intervention. In general, the magnitude of the augmented response over 7–10 months of exercise intervention varied from 1% at the trochanteric region of the proximal femur (44) to ~3% at the femoral neck for a high-impact jumping intervention (27,47). When moderate activity was increased through daily physical education, a positive effect on bone accretion in prepubertal girls was noted (66). In a school-based intervention with a 10-minute, moderate-impact circuit training three times per week, the benefit doubled if the intervention continued for a second school year (41,42). In these studies, bone mass benefits increased from 2% to approximately 4% at the femoral neck and lumbar spine in both boys and girls. These and other studies suggest that the bone response to loading is optimized in prepuberty and early puberty (12,32,37).
