Chapter 11
Physical Activity and Osteoporosis
“MY
S T R E N G T H FA I L E T H B E C A U S E O F M I N E I N I Q U I T Y A N D M Y B O N E S A R E C O N S U M E D .”
PSALMS 31:10
P-274
Osteoporosis or “porous bone” is a disease characterized by abnormally low bone mass and
microstructural deterioration of bone tissue that leads to brittle bones and increased risk of
fractures.
The WHO defined osteoporosis as a bone mineral density (BMD) measurement more than 2.5
standard deviations (SD) below the average in young white adults.
For each SD decrease in bone mass there is a 50%-100% increase in the risk of fracture.
Osteopenia: BMD between 1 and 2.5 SD below that of young adults 20-29—a direct risk factor
for osteoporosis.
The WHO: physical inactivity is also a risk factor for osteoporosis.
For each SD decline in bone mass in the hip, the risk of fracture increases 3 x. A woman’s
lifetime risk of hip fracture is equal to her combined risk of breast, uterine and ovarian cancer.
Like other diseases we have covered—osteoporosis has been around a long time. King David
(ruler of Israel from 990-970 BC) probably suffered from osteoporosis.
About 1 in 5 patients who fracture a hip (most after age 75) die in the years following the fracture
and 50% of the survivors become dependent on others for care.
Magnitude of the Problem: The annual prevalence of diagnosed osteoporosis in the USA is
about 10 mill people, 80% women. It is estimated that 44 mill people (USA) age 50+, 55% of
adults have either osteoporosis or osteopenia.
Fractures and Mortality: Osteoporosis and osteopenia are responsible for more than 2 mill
fractures in the US each year which includes hip, vertebral, wrist and others.
Etiology of Osteopenia and Osteoporosis
2 main categories of osteoporosis: (1) Primary includes age-related (type I or senile) bone loss
and postmenopausal (type II) bone loss. (2) Secondary is caused by another disease but may not
be independent of age or menopause.
Osteoporosis (the focus of this chapter) results mainly from loss of trabecular bone mass and
micro-damage within the bone.
Dietary calcium and vit D, as well as regular physical activity, contribute to peak bone mass,
particularly before age 20.
Bone loss among women is related to estrogen levels and to a lesser degree androgen levels and
bone loss accelerates after menopause.
Men lose bone at about half the rate of women.
Biologically available testosterone (the fracture not bound to globulin) declines about 60% in
men between ages 20-80. It appears that estrogen (converted from testosterone by the enzyme
aromatase) has a greater effect on bone than does testosterone in men.
Sex differences (P-277). At all ages men have more bone mass than women. It is thought that the
marked decline in the levels of estrogen account for the greater bone loss in women; 75% or more
of the bone loss in women occurs during the first 15 years after menopause and is attributable to
estrogen deficiency. Men lose bone mass faster after 60 but bone loss can be associated with a
decline in gonadal function in some men.
Without HRT women can lose up to 20% of their bone mass within 5-7 years after menopause.
Bone Renewal and Involution
P-278
Bone involution: bone loss
Endosteum: In anatomy the endosteum (plural endostea) is a thin layer of connective tissue that
lines the surface of the bony tissue that forms the medullary cavity of long bones.[1] This
endosteal surface is usually resorbed during long periods of malnutrition, resulting in less cortical
thickness. The outer surface of a bone is lined by a thin layer of connective tissue that is very
similar in morphology and function to endosteum. It is called the periosteum, or the periosteal
surface.
Cortical and Trabecular Bone
Bone in human and other mammal bodies is generally classified into two types 1: Cortical bone,
also known as compact bone and 2) Trabecular bone, also known as cancellous or spongy bone.
These two types are classified as on the basis of porosity and the unit microstructure. Cortical
bone is much denser with a porosity ranging between 5% and 10%. Cortical bone is found
primary is found in the shaft of long bones and forms the outer shell around cancellous bone at
the end of joints and the vertebrae. A schematic showing a cortical shell around a generic long
bone joint is shown below:
Osteoclasts & Osteoblasts
An osteoclast (from the Greek words for "bone" (Οστό) and "broken" (κλαστός)) is a type of
bone cell that removes bone tissue by removing its mineralized matrix and breaking up the
organic bone (organic dry weight is 90% collagen). This process is known as bone resorption.
Osteoclasts were discovered by Kolliker in 1873.[1] Osteoclasts and osteoblasts are instrumental
in controlling the amount of bone tissue: osteoblasts form bone, osteoclasts resorb bone.
osteoid A soft material, consisting mainly of collagen, that is secreted by osteoblasts and
constitutes the uncalcified matrix of bone. Osteoid is converted into hard bone matrix when it
combines with calcium phosphate (hydroxyapatite) deposited from the blood.
Increases (during growth)and decreases (with age) in BMD depend on the balance of activity of
osteoclasts and osteoblasts. During growth and maturation during youth osteoblastic activity
exceeds osteoclastic activity so bones grow and increase their BMD. After peak bone mass is
attained, osteoclastic activity gradually outpaces that of osteoblasts leading to cavities in the
bone’s osteoid matrix.
Hormonal influences: Parathyroid hormone contributes to bone remodeling by stimulating
resorption of calcium from the bone, while calcitonin inhibits resorption.
It is not really understood how reproductive hormones (estrogen & testosterone) help protect
against bone loss.
Risk factors & prevention: P-280. Risk factors are partly inherited—however, most of the genes
that regulate bone growth are undiscovered. Both genetic and family influences are modifiable by
age (increased risk of falling as one ages) and environmental (diet, exercise).
Diseases in life and drugs may also contribute to osteoporosis.
Early high BMD is key to prevention of osteoporosis later in life.
Dietary Calcium and Vitamin D
Vit D and Calcium are key in bone health and reducing osteoporosis.
Calcium is the main component of bone which stores 99.5% of the body’s calcium as well as
supplying the body’s calcium needs of nerve conduction and muscle contraction via the blood.
1000-1300 mg daily of calcium is advised.
Vit D is necessary for the body to absorb calcium from food—and it depends upon sun exposure.
About 10-15 min per day directly on face and extremities 2-3 days per week. 400-800 IU per day.
HRT (estrogen alone or estrogen and progestin): Pluses and minuses (P-281-282). Progestins are
hormones. They are used by both men and women for different purposes.
Progestins--To properly regulate the menstrual cycle and treat unusual stopping of the menstrual
periods (amenorrhea). Progestins work by causing changes in the uterus.
Bone Measurement Techniques
P-283
No symptoms accompany bone loss.
Measuring bone strength—MES (NSCA). Minimal Essential Strain—1/10 the force required to
break a bone and the minimum strain needed to make it stronger. Wolff’s Law---P-294
Physical Activity and Osteoporosis: The Evidence.
The bending strength of bone can be increased by exercise even when overall bone density is not
changed.
Even small improvements in BMD after mechanical loading (exercise) result in substantial
resistance to fracture.
Even in young men—bed rest (4 months) may cause 2-10% BMD loss due to reduced
gravitational load—as in space travel.
Rapidly applied forces may increase BMD best.
Endurance training (P-286).
Resistance training (P-287). [Skeletal Loading, Standing exercises, etc.].
Site-specific loading: eccentric contractions; mechanical loading.
P-289: Although estrogen-deficient women can benefit from weight-bearing exercises, exercise
alone cannot substitute for HRT during the early postmenopausal phase of rapid bone loss.
During the first 5years after menopause women who do not take estrogen can lose up to 35% of
their bone mass. The combination of HRT and exercise may yield the greatest effect on bone
because estrogen may enhance the osteogenic effect of mechanical loading.
Physical Activity and Risks of Falls or Fractures: A greater amount of physical activity (FITT) has an inverse
dose-response relationship with the risk of fractures and may help prevent falls as well.
Strength of the Evidence: Studies collectively suggest that resistance exercise: (1) an increase in peak bone mass
(2) slowing of osteopenia during middle age. In addition, resistance training may: (1) cause a reversal of bone mass
loss in old age (2) a reduction in risk factors for falls and the incidence of falls (3) a reduction in fractures resulting
from falls among the elderly
Biological Plausibility: During exercise the skeleton has 2 main intrinsic forces acting upon it: (1) gravity (2) the
pull of the muscle-tendon unit during muscular contraction, locomotion and maintenance of posture.
Wolff’s Law: Wolff's law is a theory developed by the German anatomist and surgeon Julius Wolff (1836–1902) in
the 19th century that states that bone in a healthy person or animal will adapt to the loads under which it is
placed.[1] If loading on a particular bone increases, the bone will remodel itself over time to become stronger to
resist that sort of loading.[2] The internal architecture of the trabeculae undergoes adaptive changes, followed by
secondary changes to the external cortical portion of the bone,[3] perhaps becoming thicker as a result. The inverse
is true as well: if the loading on a bone decreases, the bone will become weaker due to turnover, it is less
metabolically costly to maintain and there is no stimulus for continued remodeling that is required to maintain
bone mass.[
Bone formation may also be stimulated by increased blood flow to the bones as a response to the
metabolic demands of exercise which can increase the diffusion surface area of bone cells and
deliver more nutrients to osteocytes, perhaps increasing their production of bone growth factors.
Also, hormonal responses during exercise may stimulate the activity of osteoblasts.
The Error-Strain Distribution Theory of Bone Remodeling (P-295)
Bone Turnover After Exercise
The Error-Strain Distribution Theory of Bone Remodeling
•Bone cells sense mechanical strain from weight-bearing or resistance exercises.
•Load imbalances are communicated among cells locally, leading to an influx of calcium ions.
•The calcium ions are followed by prostaglandins, nitric oxide and growth hormones, leading to
bone remodeling.