Evaluating and prescribing exercise for elderly patients

Research has demonstrated that exercise training benefits the elderly, just as it does younger age groups. Among benefits reported are improved cardiovascular and respiratory function, reduced coronary artery disease risk, decreased body fat and increased lean body mass, increased bone mass, increased work capacity, greater flexibility, reduced susceptibility to depression, improved self-esteem, and more independence. Before starting a vigorous training program, however, the elderly should undergo a thorough physical examination, including medical history, and an exercise stress test to evaluate cardiovascular status. These test results should be used to indicate intensity, duration, and frequency of exercise, as well as reassure patients of its safety. With this approach, full benefits of regular endurance exercise can be realized.     

Bone disease in patients with haemophilia A and B – where are we now?

It is evident that haemophilia A and B are associated with decreased bone mass in both adults and children. Decreased physical activity and vitamin D deficiency are some of the major factors leading to bone loss. Hepatitis C virus (HCV) infection may also contribute to low bone mineral density (BMD). However, definite conclusions regarding the exact prevalence and pathogenesis of osteoporosis cannot be conducted yet, due to the small sample size and significant heterogeneity among studies. Discordant findings with regard to the skeletal site of low BMD have also been reported. Furthermore, data on fracture risk are sparse. The use of the Fracture Risk Assessment Tool (FRAX) for assessing fracture risk, regular BMD assessment at the age of 25 and thereafter, careful evaluation of risk factors associated with bone loss and optimal calcium and vitamin D intake are recommended. Long‐term prophylactic factor replacement therapy, resistance exercise and bisphosphonates, in severe cases of increased fracture risk, can prevent bone loss.     

Effects of short-term aerobic exercise with and without external loading on bone metabolism and balance in postmenopausal women with osteoporosis

The aim of this study is to evaluate the effect of submaximal aerobic exercise with and without external loading on bone metabolism and balance in postmenopausal women with osteoporosis (OP). Thirty-six volunteer, sedentary postmenopausal women with OP were randomly divided into three groups: aerobic, weighted vest, and control. Exercise for the aerobic group consisted of 18 sessions of submaximal treadmill walking, 30 min daily, 3 times a week. The exercise program for the weighted-vest group was identical to that of the aerobic group except that the subjects wore a weighted vest (4–8 % of body weight). Body composition, bone biomarkers, bone-specific alkaline phosphatase (BALP) and N-terminal telopeptide of type 1 collagen (NTX), and balance (near tandem stand, NTS, and star-excursion, SE) were measured before and after the 6-week exercise program. Fat decreased (p = 0.01) and fat-free mass increased (p = 0.005) significantly in the weighted-vest group. BALP increased and NTX decreased significantly in both exercise groups (p ≤ 0.05). After 6 weeks of exercise, NTS score increased in the exercise groups and decreased in the control group (aerobic: +49.68 %, weighted vest: +104.66 %, and control: ?28.96 %). SE values for all directions increased significantly in the weighted-vest group. Results showed that the two exercise programs stimulate bone synthesis and decrease bone resorption in postmenopausal women with OP, but that exercise while wearing a weighted vest is better for improving balance.     

Effects of physical activity on bone remodeling

Physical exercise is recommended to improve bone mass in growing children and decrease bone loss in elderly men and women. However, the specific mechanisms by which exercise influences bone metabolism are still not thoroughly understood. The effect of physical activity on the skeleton is generally evaluated by dual-energy x-ray absorptiometry, which measures bone mineral density. However, a relatively long period is needed to detect even a minor variation in bone mineral density with this technique, limiting its usefulness. Bone biochemical markers that reflect the cellular activities of bone formation and resorption are thus also useful tools, both to monitor the acute effects of exercise on bone remodeling and to investigate the mechanisms of exercise-induced changes in bone mass. This article describes the effects of physical activity on bone remodeling in various types of population. The comparison of sedentary individuals and athletes with many years of high-volume sports practice, for example, has clarified some of the long-term effects of exercise. Moreover, the acute variation in bone cell activities after brief exercise or a training program is here examined. The interpretation of results is difficult, however, because of the many parameters, such as age, that are involved. The various populations are therefore categorized to reflect the biological factors implicated in the modulation of bone marker response during exercise.     

Weight training decreases vertebral bone density in premenopausal women: a prospective study

The effect of exercise on bone mass is unclear. To determine the skeletal effect of weight-bearing exercise in premenopausal women, we prospectively evaluated the effects of a weight-training program on lumbar spine bone mass in 10 women (mean +/- SEM, 36.2 +/- 1.3 yr) and compared the results with those in 7 sedentary women (40.4 +/- 1.6 yr). None of the women had previously participated in a weight-training program, and all ingested a 500-mg calcium supplement each day throughout the study. Axial loading and balance of large muscle groups were emphasized. Individual strength increased by 57 +/- 8% over 9 months. Despite the increase in muscle strength, lumbar spine bone density in the exercising women decreased by 2.90% at 4.5 months and 3.96% at 9 months (P = 0.01). In contrast, there was no change in lumbar density in the controls over the 9-month period. We conclude that short term weight training at this frequency and intensity decreases vertebral bone mass in premenopausal women.     

Exercise and other lifestyle factors for prevention of osteoporosis during growth and young adulthood

Increased mechanical loading of the skeleton results in bone gain, whereas unloading the skeleton leads to bone loss. Regular exercise, especially resistance and high-impact activities, contributes to development of high peak bone mass and the greatest effects on bone mass appear to occur in early adolescence. Therefore, it seems reasonable to turn our attention to intervening in the younger population to establish lifelong exercise habit that maximize peak bone mass. Adequate calcium intake together with exercise is crucial to develop optimal peak bone mass and to preserve bone mass throughout life. This lifelong exercise may prevent osteoporosis and reduce fracture risk by attenuating age-related bone loss and lowering the incidence of falls. Moreover such lifestyle as sitting on Tatami mat could also stimulate bone accumulation in early adolescent girls. Sports participation may offset the negative effect of smoking on bone mass.     

Prevention of involutional bone loss by exercise

To ascertain whether exercise could prevent involutional bone loss, we studied 18 postmenopausal women, half of whom exercised for 1 h three times a week. Total and regional bone mass were measured before and after 1 year of exercise by the techniques of total-body neutron activation analysis (total body calcium) and photon absorptiometry (bone mineral content) of the distal radius. Total body potassium was measured by whole body counting. Bone mineral content and total body potassium did not change significantly in either group. Total body calcium increased in the exercise group from 781 +/- 95 g of 801 +/- 118 g (SD). In contrast, total body calcium decreased in each subject in the sedentary group. The daily calcium balance derived from the difference in total body calcium measurements was significantly different in the two groups of women (P less than 0.001). These data support the hypothesis that exercise can modify involutional bone loss.     

Anorexia nervosa and osteoporosis

Anorexia nervosa (AN), a condition of severe undernutrition, is associated with low bone mineral density (BMD) in adults and adolescents. Whereas adult women with AN have an uncoupling of bone turnover markers with increased bone resorption and decreased bone formation markers, adolescents with AN have decreased bone turnover overall. Possible contributors to low BMD in AN include hypoestrogenism and hypoandrogenism, undernutrition with decreased lean body mass, and hypercortisolemia. IGF-I, a known bone trophic factor, is reduced despite elevated growth hormone (GH) levels, leading to an acquired GH resistant state. Elevated ghrelin and peptide YY levels may also contribute to impaired bone metabolism. Weight recovery is associated with recovery of BMD but this is often partial, and long-term and sustained weight recovery may be necessary before significant improvements are observed. Anti-resorptive therapies have been studied in AN with conflicting results. Oral estrogen does not increase BMD or prevent bone loss in AN. The combination of bone anabolic and anti-resorptive therapy (rhIGF-I with oral estrogen), however, did result in a significant increase in BMD in a study of adult women with AN. A better understanding of the pathophysiology of low BMD in AN, and development of effective therapeutic strategies is critical. This is particularly so for adolescents, who are in the process of accruing peak bone mass, and in whom a failure to attain peak bone mass may occur in AN in addition to loss of established bone.     

Adverse Effects of Drugs on Bone and Calcium Metabolism/Physiology

Drugs may affect bone turnover and density in many ways. However, the disease for which the drugs are administered may also contribute to bone loss. Infection with human immunodeficiency virus leads to a loss of bone mineral, while treatment with highly active antiretroviral therapy does not seem to contribute to further bone loss. Type 1 diabetes is associated with a decrease in bone mineral, while type 2 diabetes is associated with an increase. The new class of thiazolidinediones (glitazones) has been associated with an increased loss of bone mineral. In breast cancer treatment, tamoxifen is associated with an increased bone mineral, while the newer class of aromatase inhibitors through a decrease in serum oestradiol are associated with an increased loss of bone mineral. Strong analgesics (opioids) may decrease bone mineral density through inhibition of gonadotrophins while weak analgesics such as the non-steroidal anti-inflammatory drugs may increase bone mineral through an effect on the prostaglandin system. However, possibly through an increased risk of falls, the weak analgesics are associated with an increased risk of fractures. Proton pump inhibitors may lead to a decreased calcium absorption and thus a decreased bone mineral and an increased risk of fractures.     

Eating disorders as risk factors for osteoporosis

Eating disorders (TCA per its abbreviation in Spanish) are common in young women, with an estimated prevalence of 4-5%. One of the physical complications of eating disorders, especially anorexia nervosa (AN) and eating disorder not otherwise specified (TANE) is bone mass loss, which affects both cortical and trabecular bone. The synergistic effect of malnutrition and estrogen deficiency produces significant bone mass loss, resulting from the uncoupling of bone turnover characterized by a decrease in osteoblastic bone formation and an increase in osteclastic bone resorption. The mechanisms implied in the pathogenesis of bone loss are the hypoestrogenism, hypercortisolism, serum leptin levels and insulin-like growth factor decrease. Severity of bone loss in anorexia nervosa varies depending on duration of illness, the minimal weight ever and sedentarism or strenuous exercise. Long term consequences occur, such as a fracture risk increase in patients who have suffered anorexia nervosa, compared with the general population. The first treatment line to recover bone mass is nutritional rehabilitation together with weight gain. Hormonal replacement therapy may be effective if combined with an anabolic method. Osteopenia and osteoporosis are terms adopted to define the deficiency of bone mass in adults. Authors have used these terms to define densitometric data in young subjects who have not reached their peak bone mass. We suggest the term "hypo-osteogenesia" to define the deficiency in the development of bone mass in adolescents or children.     

Muscle training for bone strength

The main function of bone is to provide the mechanical integrity for locomotion and protection; accordingly, bone mass and architecture are adjusted to control the strains produced by mechanical load and muscular activity. Age-related patterns involve peak bone mass during growth, a plateau in adulthood, and bone loss during aging. The decline in bone mass and structural integrity results in increased risk of fractures, particularly in post-menopausal women. Athletes competing in strength and power events, such as weight-lifting and jumping, have superior bone mass and structure compared with their untrained counterparts in all age groups. Exercise seems to be most effective during rapid growth, the average gain in bone mineral content (BMC) and density (BMD) in controlled trials being of the order of 2-5% per year. The net gain of BMD after exercise interventions among older people is modest, at a level of 1-3% per year, but it is not clear whether positive effects can be maintained over a longer time. Although aerobic exercise is important in maintaining overall health, the resistance type of muscle training may be more applicable to the basic rules of bone adaptation and site-specific effects of exercise, have more favorable effects in maintaining or improving bone mass and architecture, and be safe and feasible for older people. It has been suggested that there is an opportunity for resistance training, for improved effects on BMD in postmenopausal women in bones which have less daily loading. In addition to BMC and BMD, bone geometry and mass distribution may also change as a result of training and other treatment, such as hormonal replacement therapy, thereby further improving bone strength and reducing fracture risk. Appropriate training regimens may reduce the risk of falls and the severity of fall-related injuries, and also constitute potential therapy to improve functional ability and the quality of life in osteoporotic patients. However, further research is needed on dose-response relationships between exercise and bone strength, the feasibility of high-load, high-speed and impact-type of physical training, and the risks and benefits of intensive exercisein elderly individuals.     

Knee strength maintained despite loss of lean body mass during weight loss in older obese adults with knee osteoarthritis

BACKGROUND: The effects of weight loss on muscle function in older adults have not been well studied. This study determined the effects of a 6-month weight-loss intervention on muscle strength and quality in older obese adults with knee osteoarthritis. METHODS: Participants were randomized to a weight loss (WL) (n = 44, 70 +/- 6 years) or weight stable (WS) (n = 43, 69 +/- 6 years) group. The WL intervention consisted of weekly educational meetings, a meal replacement diet, and a three-session-per-week structured exercise program to achieve 10%-12% weight loss. The WS intervention included bimonthly group meetings and newsletters. Body composition and knee extensor strength were measured at baseline and after intervention. RESULTS: The WL group decreased body weight, lean body mass, fat mass, and percent body fat (p <.001 for all). Concentric extension strength increased 25% in WL (p >.05), whereas eccentric extension decreased 6% in WS (p =.028). Concentric muscle quality (strength per kg body weight or lean body mass) increased in WL (p <.05), whereas eccentric muscle quality decreased in WS (p <.05). Changes in lean body mass and fat mass were inversely associated with changes in most muscle strength and quality measures (p <.05). Men and women did not differ in response to the intervention in knee strength outcomes. CONCLUSIONS: Hypocaloric dieting in combination with exercise training had beneficial effects on muscle strength/quality, despite loss of lean body mass in this sample of older men and women. Greater fat loss was associated with greater gains in muscle strength and quality. More studies are needed regarding the mechanisms by which loss of fat mass increases muscle strength and quality.     

Bone loss in Crohn's disease: exercise as a potential countermeasure

Crohn's disease (CD) is associated with a number of secondary conditions including osteoporosis, which increases the risk of bone fracture. The cause of metabolic bone disease in this population is believed to be multifactorial and may include the disease itself and associated inflammation, high-dose corticosteroid use, weight loss and malabsorption, a lack of exercise and physical activity, and an underlying genetic predisposition to bone loss. Reduced bone mineral density has been reported in between 5% to 80% of CD sufferers, although it is generally believed that approximately 40% of patients suffer from osteopenia and 15% from osteoporosis. Recent studies suggest a small but significantly increased risk of fracture compared with healthy controls and, perhaps, sufferers of other gastrointestinal disorders such as ulcerative colitis. The role of physical activity and exercise in the prevention and treatment of CD-related bone loss has received little attention, despite the benefits of specific exercises being well documented in healthy populations. This article reviews the prevalence of and risk factors for low bone mass in CD patients and examines various treatments for osteoporosis in these patients, with a particular focus on physical activity.     

A soluble bone morphogenetic protein type IA receptor increases bone mass and bone strength

Diseases such as osteoporosis are associated with reduced bone mass. Therapies to prevent bone loss exist, but there are few that stimulate bone formation and restore bone mass. Bone morphogenetic proteins (BMPs) are members of the TGFβ superfamily, which act as pleiotropic regulators of skeletal organogenesis and bone homeostasis. Ablation of the BMPR1A receptor in osteoblasts increases bone mass, suggesting that inhibition of BMPR1A signaling may have therapeutic benefit. The aim of this study was to determine the skeletal effects of systemic administration of a soluble BMPR1A fusion protein (mBMPR1A-mFc) in vivo. mBMPR1A-mFc was shown to bind BMP2/4 specifically and with high affinity and prevent downstream signaling. mBMPR1A-mFc treatment of immature and mature mice increased bone mineral density, cortical thickness, trabecular bone volume, thickness and number, and decreased trabecular separation. The increase in bone mass was due to an early increase in osteoblast number and bone formation rate, mediated by a suppression of Dickkopf-1 expression. This was followed by a decrease in osteoclast number and eroded surface, which was associated with a decrease in receptor activator of NF-κB ligand (RANKL) production, an increase in osteoprotegerin expression, and a decrease in serum tartrate-resistant acid phosphatase (TRAP5b) concentration. mBMPR1A treatment also increased bone mass and strength in mice with bone loss due to estrogen deficiency. In conclusion, mBMPR1A-mFc stimulates osteoblastic bone formation and decreases bone resorption, which leads to an increase in bone mass, and offers a promising unique alternative for the treatment of bone-related disorders.     

Vertebral deformities and inflammatory bowel disease

Loss of bone mass and an increased risk of fractures is an issue of major concern for physicians treating inflammatory bowel disease patients. Multiple causes for decreased bone mass have been identified in the past, but the role of inflammation may be of pivotal importance. We here discuss the latest insights into the pathogenesis of inflammatory bowel disease-related bone loss and the implications for treatment.     

Nonpharmacological approaches to improve bone health and reduce osteoporosis

PURPOSE OF REVIEW: With an aging population, osteoporosis has become a public health concern and an area of increased awareness among both patients and medical practitioners. Timely screening and pharmacologic treatment of low bone mass effectively reduces fracture risk. Nonpharmacologic interventions, however, deserve equal emphasis both in the prevention and treatment of osteoporosis. RECENT FINDINGS: Recent advances in bone biology have established that exercise in the form of short, repetitive mechanical loading leads to the greatest gains in bone strength. As demonstrated by both observational and randomized exercise intervention trials, these gains are best achieved in childhood but can be maintained in adulthood with continued regular weight-bearing exercise. In the later years, evidence supports the implementation of balance training to decrease fall risk, especially in elderly patients with low bone mass. Following an osteoporotic fracture, a multidisciplinary rehabilitation program with an emphasis on early mobilization, fall prevention, use of orthoses, and noninvasive surgical procedures is emerging as a promising approach. SUMMARY: Clinically, these findings should imply greater emphasis on high impact exercise during skeletal growth and on maintenance of weight bearing and balance training in the later years. Future research should examine the effect of these interventions on fracture prevention.     

Osteoporosis: diagnostic screening and its place in current care

Osteoporosis, or decreased total bone mass, results from a number of factors: accelerated trabecular bone loss in postmenopausal women; age-related loss of trabecular and cortical bone; and multiple chronic diseases and medications. Routine laboratory and radiographic tests are not helpful in assessing bone turnover. However, a ratio of urinary calcium to creatinine exceeding 0.16 on a spot urine sample obtained in the fasted state suggests high bone turnover. Both single and dual photon absorptiometry are useful research tools but are unproved screening tests, especially in light of the more frequent use of preventive measures, such as postmenopausal hormone replacement therapy, calcium supplementation, and weight-bearing exercise.     

Effects of moderate physical training on prednisone-induced protein wasting: a study of whole-body and bone protein metabolism

This study investigated the possibility of preventing prednisone-induced protein wasting by regular physical activity. Eight healthy untrained volunteers took prednisone (30 mg/d for nine days), once after a 4-week exercise program that consisted of jogging 2.5 miles four times a week, and once without exercise. Whole body protein turnover was measured from the 15N enrichment plateau of urinary ammonia during ingestion of 15N glycine at hourly intervals. Whole-body protein synthesis and breakdown were derived from nitrogen flux, nitrogen intake, and urinary nitrogen elimination. Muscle myofibrillar protein breakdown was explored by measuring urinary 3-methylhistidine excretion. Bone protein metabolism was studied by measuring serum bone GLA protein (BGP), a specific marker of bone protein synthesis, and urinary elimination of hydroxyproline, an index of bone resorption. Whole-body protein turnover was significantly increased by exercise and prednisone (+19% and +17%, respectively); this effect was related to increased protein synthesis during exercise training (+27%, P less than .01) and to increased protein breakdown during prednisone administration without exercise (+21%, P less than .05). In contrast, values of protein turnover, synthesis, and breakdown were not different from control when the subjects took prednisone after training. Urinary excretion of 3-methylhistidine was decreased (-15%, P less than .05) at the end of the prednisone administration period but was identical to the control value when the subjects took prednisone in association with exercise. In contrast, serum BGP was significantly decreased by prednisone, with or without exercise (-35%, P less than .001). These data suggest that moderate exercise training can prevent, at least in part, the protein loss induced by prednisone.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of thyroid status on bone metabolism: a primary role for thyroid stimulating hormone or thyroid hormone?

Thyroid hormones are essential for normal skeletal growth and the maintenance of bone mass in adulthood, although their mechanism of action in bone is poorly understood. Hypothyroidism causes impaired bone formation and growth retardation whereas thyrotoxicosis results in accelerated growth, advanced bone age and decreased bone mass. Adults with thyrotoxicosis or a suppressed thyroid stimulating hormone (TSH) from any cause have an increased risk of osteoporotic fracture. Conventionally, bone loss in thyrotoxicosis has been regarded as a direct consequence of thyroid hormone excess acting locally on bone. Recently, however, it has been proposed that TSH may be a direct negative regulator of bone turnover acting via the TSH receptor on both osteoblasts and osteoclasts. Thus, TSH deficiency could be partly responsible for the skeletal loss seen in thyrotoxicosis. Here we provide an overview of the molecular actions of thyroid hormone in bone and discuss in detail the current evidence relating to a possible role for TSH in bone metabolism.