Resistance training is essential to stop the progression of, or reverse, osteoporosis!
Topic for Summary and Critique - by Derek Chan
Contents
Statement of the Topic
Resistance training is essential to stop the progression of, or reverse, osteoporosis!
Introduction
Osteoporosis is an important health problem affecting the elderly in the Western world (Sinaki, 1989). It is characterized by reduced bone density with micro-architectural deterioration, which increases the risk of fractures after minimal trauma (Riggs and Melton, 1986). It is a major cause of fractures in postmenopausal women, with common fracture sites being the wrist, spine and hip. However, hip fractures increase significantly in the later part of life (Riggs and Melton, 1986). Every year, the medical costs to manage the osteoporosis-related fracture are huge (Riggs and Melton, 1986, Sinaki, 1989). Prevention or treatment to reduce the incidence of osteoporosis related fractures is therefore important to reduce the tremendous medical expenses. In this paper, one of the strategies, resistance exercise, will be discussed in relation to the prevention, or reversal of osteoporosis.
Literature Review
Age-related Bone Loss
Peak bone mass in the human skeleton is achieved in the third decade of life (Sinaki, 1989) and thereafter decreases with age in both men and women. The rate of loss was found to be 0.3% per year in both men and women in the early phase of bone loss. The rate of bone loss was found to increase to 2% to 3% per year from the early menopausal period and to continue for 5 to 8 years after menopause (Sinaki, 1989). A cohort study regarding Australian born women found that the bone loss accelerated in both the femoral neck and the lumbar spine during the transition from the premenopausal to postmenopausal period (Guthrie et al., 1998). Over their lifetimes, women lose about 35 percent of their cortical bone and 50 percent of their trabecular bone (Riggs and Melton, 1986). Cortical bone predominates in the shafts of long bone. Trabecular bone, which is concentrated in the vertebrate, pelvis, other flat bones, and in the ends of long bone, is metabolically much more active, and more responsive to changes in mineral homeostasis (Riggs and Melton, 1986).
Mechanism of Age-related Bone Loss
Bone formation and bone resorption do not occur randomly throughout the skeleton. The adult skeleton undergoes a continuous process of remodelling in which the bone resorption is coupled with the bone formation. At the remodeling cycle, osteoclasts appear on a previously inactive surface and over a period of about two weeks, construct a tunnel in cortical bone or a lacuna on the surface of trabecular bone. The osteoclasts are replaced by osteoblasts, which fill in the resorption cavity over a period of three to four months to create a new structural unit of bone (Riggs and Melton, 1986, Sinaki, 1989).
The accelerated phase of bone loss which occurs in women soon after menopause is associated with a high rate of bone turnover: there are more osteoclasts and each creates a deeper resorption cavity (Riggs and Melton, 1986). Also an increased secretion of parathyroid hormone with aging would increase bone turnover by increasing the number of bone-remodeling units and when resoprtion and formation are uncoupled, would lead to increase bone loss (Riggs and Melton, 1986).
Management of Osteoporosis
There are a number of factors known to increase the risk of developing osteoporosis. These include improper nutrition, lack of exercise, genetic factors, certain medications and perhaps habits such as excessive smoking. Certain medical conditions also cause bone loss. These include deficiencies in sex hormones, excesses in hormones such as thyroid hormone, parathyroid hormone or cortisol, abnormalities in kidney or liver function and several types of malignant cancers. Physicians take these and many other factors into account when considering if tests need to be performed to assess whether an individual has osteoporosis and then determine its cause. Prevention is the only cost-effective approach for osteoporosis. Commonly proposed ways of preventing osteoporosis include estrogen replacement therapy, calcium supplement and Vitamin D supplement in the dietary intake, exercises and elimination of cigarettes and alcohol (Riggs and Melton, 1986).
Hormone replacement therapy is the primary treatment option for postmenopausal women or for men with low hormone levels. Estrogen therapy in women, in addition to improving the bones, also reduces the risk of heart disease, urinary tract infections, cancer of the ovaries and perhaps stroke. However, the potential side effects of estrogen replacement such as breast carcinoma, menstrual bleeding, headache, weight gain, depression, gallbladder or liver disease have created controversy in regard to the acceptance of estrogen replacement (Sinaki, 1989). Therefore, alternatives such as exercise deserve further investigation.
Physical Activity
Evidence in the past 20 years has shown that bone loss is found in inactive healthy patients placed on bed rest (Sinaki, 1989; Bloomfield et al., 1993; Chilibeck et al., 1995). Other studies have demonstrated that decreased bone density can occur in the astronauts as a result of lengthy stay in space (Sinaki, 1989; Bloomfield et al., 1993). These imply the importance of activity and the weight bearing to the bone growth.
Cross-sectional studies mentioned in Chilibeck et al. (1995) and Cohen et al. (1995) have shown that athletes have a higher bone mineral density (BMD) than the normal population. Tennis players have been shown to exhibit cortical bone hypertrophy and increased BMD in their playing arms (Chilibeck et al., 1995). Others studies have shown increased BMD in the os calcis of runners and the lumbar spines of weightlifters (Chilibeck et al., 1995). However, the body composition and genetic make up of athletes differ from those of an age-matched control group. For this reason, it is too early to draw conclusions indicating possible benefits of exercise to osteoporosis sufferers.
Intervention studies may be a better indicator in showing the relationship between exercise and change of bone mineral density. Cohen et al. (1995) did a study in 17 young male rowers. They trained for seven months using rowing, weight training and running each week, compared with eight age-matched control subjects. Results showed that there was significant increase in BMD and bone mineral content (BMC) in the lumbar spine, but not, however, in the greater trochanter, Ward�s angle and femoral neck. This indicates exercise can have some effect in increasing BMD over a period of physical training.
In the osteoporotic population, Hartard et al. (1996) did a controlled trial in postmenopausal women. They measured the BMD of the lumbar vertebrae and the femoral neck before and after six months of strength training with 70% of 1 RM resistance. The result showed that there was no significant difference in the pre-training and post-training but there was significant bone loss in the control group. Therefore, they concluded that the continuous, adaptive strength training was an effective and safe method of bone loss prevention. This is also supported by the randomised study by Nelson et al. (1994). They demonstrated that there was significant increase in the BMD in both lumbar vertebrae and femoral neck after 12 months of 80% of 1 RM resistance training.
In a study by Ayalon et al. (1987), the bone density of the radius in a group of postmenopausal women was found to be increased by 3.8% after a series of weight bearing, tensile loading and twisting exercises of the forearm, while that of the control group continued to decline. This may indicate site specific training is important. In contrast, however, Smidt et al. (1991) showed that there was no significant difference between the exercise group and the control group at the lumbar vertebrae and femoral neck, after sit ups, trunk extension and abdominal exercises only. They tried to demonstrate the effect of direct muscle pulling on bone formation. The intensity, lack of supervision and the lack of the weight bearing effect in those exercises could be a factor in explaining the result. It seems weight bearing activity may play quite a major role in the prevention of osteoporosis. However, the study done by Bloomfield et al. (1993) shown that the exercise training on the ergonmeter, which minimizes the gravitational effect on body parts, significantly increased BMD in the lumbar spine. One point which needs to be argued, though, is that the lumbar spine is subjected to compressive loading in the upright posture on the ergometer.
| Researcher | Subjects | Training regimen | Measurement | Effect |
|---|---|---|---|---|
| Cohen | 17 rowers 8 control |
8 hr rowing 1 hr running 1 hr wt training |
DXA | Increase in Lx |
| Nelson | 20 exercise 27 control |
80% 1RM to hip, trunk, and lat dorsi. pull down |
DPA | Increase in Lx and FN |
| Hartard | 16 exercise 15 control |
70% 1RM to hip, trunk, leg press | DXA | No diff in ex, but decline in control |
| Avalon | 14 exercise 26 control |
Wt bearing, traction, twisting ex to arm | Crompton scattering | 3.8% increase in radius |
| Simdt | 22 exercise 19 control |
Sit up, abdominal ex, trunk extension ex. | DPA | No difference |
| Bloomfield | 7 exercise 7 control |
Cycling exercise | DPA | Increase in Lx |
Clinical Implications
From these studies, we can see resistance training is effective in increasing bone mineral density, and the prevention of bone loss during the training period. The resistance exercise should be site specific. The whole period of training has to be longer than six months as this duration of training parallels the process of bone remodelling. Longer periods of training may be needed to create a beneficial effect on cortical bone, as the turnover rate is slower than the trabecular bone. Weight bearing can be one of the components of training. However, optimum intensity and frequency of training may vary and cannot yet be determined due to different methods of training and the measurement instruments. As the change of BMD is so small, precision of measurement is essential in order to develop significant and reliable results.
Conclusion
In conclusion, resistance exercise was shown to be effective in the prevention or reversal of osteoporosis. Further research is still needed to determine the optimum level and form of the most appropriate exercise regimen.
References
- Ayalon E, Simkin A, Leichter I and Raifmann S (1987)
- Dynamic bone loading exercises for postmenopausal women: Effect on the density of distal radius. Archives of Physical Medicine and Rehabilitation 68:280-283.
- Bloomfield S, Williams N, Lamb D and Jackson R (1993)
- Non-weight bearing exercise may increase lumbar spine bone mineral density in healthy postmenopausal women. American Journal of Physical Medicine and Rehabilitation 70:204-209.
- Chilibeck P, Sale D and Webber C (1995)
- Exercise and bone mineral density. Sports Medicine 19:103-122.
- Cohen B, Mist B, Millett P, Laskey M and Rushton N (1995)
- Effect of exercise training programme on bone mineral density in novice college rowers. British Journal of Sports Medicine 29:85-88.
- Guthrie J, Ebeling P, Hopper J, Barrett-Connor E, Dennerstein L et al (1998)
- A prospective study of bone loss in menopausal Australian-born women. Osteoporosis 8:282-290.
- Hartard M, Haber P, Ilieva D, Preisinger E, Seidl G and Huber J (1996)
- Systematic strength training as a model of therapeutic intervention: A controlled trial in postmenopausal women with osteopenia. American Journal of Physical Medicine and Rehabilitation 75:21-28
- Nelson M, Fiatarone M, Morganti C, Trice I, Greenberg R and Evans W (1994)
- Effects of high intensity strength training on multiple risk factors for osteoporotic fractures. Journal of the American Medical Association 272:1909-1921.
- Riggs B and Melton L (1986)
- Involutional osteoporosis. New England Journal of Medicine 314:1676-1686.
- Sinaki M (1989)
- Exercise an osteoporosis. Archives of Physical Medicine and Rehabilitation 70:220-229.
- Smidt G, Lin S, O'Dwyer K and Blanpied P (1991)
- The effect of high intensity trunk exercise on bone mineral density of postmenopausal women. Spine 17:280-285