Physiology, Health and Exercise
Advanced Higher Biology
Diabetes Mellitus and Osteoporosis
Diabetes Mellitus is a disorder occurring in adults and children which results in a failure to
control blood glucose levels and impaired ability to store glucose in the form of liver and
muscle glycogen.
Glucose is an important source of energy for the body and blood glucose levels must be kept
between fairly narrow limits. If there is too much glucose in the blood it is converted to
glycogen in the liver until it is required (preventing hyperglycaemia). If glucose levels are too
low glycogen is converted back to glucose for use in the body (preventing hypoglycaemia).
Blood glucose levels are controlled by the opposing action of two hormones, insulin and
glucagon which are secreted by specialised cells in the Islets of Langerhans in the pancreas.
Insulin is secreted by β cells, glucagon by α cells.
Insulin is secreted when blood glucose levels are high. This hormone causes the
conversion of glucose to glycogen and therefore blood glucose levels fall. Glucagon is
secreted when blood glucose levels are low. This hormone causes the conversion of
glycogen to glucose in the liver therefore blood glucose levels rise. The control of blood
glucose levels is an example of homeostasis and negative feedback (see figure 31).
Insulin affects a number of different cell types, mainly skeletal muscle, liver and fat cells. It is
a hormone which binds to specific receptors in the cell membrane of target cells resulting in a
series of reactions which allow glucose to pass through the cell membrane (see figure 32).
Insulin is a protein and will be broken down by the digestive system. It must therefore be
administered by injection.
There are two types of diabetes mellitus: Type 1 – Insulin dependent diabetes mellitus
(IDDM) and Type 2 – Non-Insulin dependent diabetes mellitus (NIDDM).
Type 1 (IDDM): Accounts for 5-10% of cases, is rapid in onset/progress and is caused by the
destruction of insulin-producing β cells of the pancreas resulting in inadequate insulin
production.
Commonly occurs in childhood and treatment involves regular injections of
insulin.
Type 2 (NIDDM): Much more common (90-95% of cases), typically develops later in life,
mainly in overweight individuals. With this condition individuals produce insulin (often at
higher than normal levels) but the tissues become less sensitive – or resistant to insulin. The
targets cells often appear to have a deficiency of insulin receptors which reduces their ability
to take up glucose. Most individuals develop insulin resistance first, often as a consequence
of becoming obese. The pancreas tries to compensate by producing more insulin and
eventually the β cells wear out and insulin production decreases. There is a subsequent
increase in blood glucose and diabetes develops. Type 2 diabetes is becoming more
common in children and young people and obesity appears to be the greatest risk factor for
NIDDM although heredity also plays a part. Sufferers of Type 2 (NIDDM) can control their
blood sugar levels by regular exercise and a carefully controlled diet although insulin
injections may also be necessary.
Diagnosis: When a person has high blood glucose levels their kidneys are unable to reabsorb
all the glucose passing through them. Excess glucose appears in the urine and can be
detected by clinistix. The high glucose excreted in urine carries a large volume of water
leading to large volumes of urine and a subsequent thirst. Other symptoms include rapid
weight loss
Glucose Tolerance Test: test for diagnosis of diabetes is based on the fasting individuals
response to drinking a prescribed volume of glucose solution. Blood glucose levels are then
measured every 30 mins over a 2/3 hr period (see figure 33).
Effect of exercise in prevention and treatment of Type 2 (NIDDM)
The ability of cells to take up glucose from blood is greater in physically fit individuals.
Regular exercise increases the capillary network, blood flow and number of insulin receptors
Physiology, Health and Exercise
Advanced Higher Biology
in skeletal muscle. It also increases enzymes associated with glucose storage. This
improved sensitivity through exercise training decreases within 5-7 days from last bout of
exercise so exercise must be regular.
Osteoporosis (“porous bones”):
Bone is a living tissue made up of collagen and minerals eg. calcium salts. Bone is constantly
being broken down and reconstructed. When bone formation exceeds rate of breakdown
bone gets denser and stronger. This happens during childhood, adolescence and young
adulthood with peak bone density occurring between 25-35 yrs. As part of the aging process,
minerals become more quickly removed from bone then they are added leading to more
porous bones. Osteoporosis is a long-term condition which increases the risk of fractures.
The wrist, spine and hip are the commonest sites of such fractures and unfortunately the
bones tend to shatter into tiny pieces rather than a clean break. Other effects include loss of
height, curvature of the spine and chronic back pain (see figure 34). Osteoporosis can affect
men, women and children but is more common in menopausal women.
Risk factors for osteoporosis:
Age: peak bone density occurs between 25-35yrs, after which mineral loss from bones
increases.
Sex: Men tend to have denser, stronger bones than women and so have a higher peak bone
density. Therefore men take longer to reach a level of bone loss which make their bones
brittle and more susceptible to fracture. Men also lose bone at a slower rate than women
(0.4% per annum compared to 1-3%).
Menopause: High levels of oestrogen contribute to bone density by promoting absorption of
calcium from the digestive system and preventing its removal from bone. After the
menopause oestrogen levels drop causing calcium to be lost from the bone. Early
menopause is associated with increased risk of osteoporosis.
Diet: Insufficient calcium and vitamin D increases risk of osteoporosis. Vitamin D promotes
absorption of calcium from the digestive system.
Family History: risk of developing osteoporosis at a younger age runs in families.
Smoking and excessive alcohol consumption: increase rate of bone loss.
Exercise: Both insufficient exercise and excessive exercise increases the risk of osteoporosis.
Bone strength is increased by weight bearing exercises eg walking, jogging, dancing. Young
women exercise regularly to maximise their peak bone density before bone loss begins.
However, excessive exercise and a restricted diet can decrease bone density if body fat
decreases to such a level that they stop menstruating (oestrogen levels drop).
Bone, like muscle, becomes stronger as a result of mechanical stress eg. weight bearing
exercises and resistance training. Activities such as swimming are thought to have little effect
on bone density.
Exercise will also strengthen tendons, ligaments and their points of
attachment with bones. Regular exercise should therefore be regarded as essential for the
development and maintenance of healthy bones, particularly for young women who must
maximise bone density before age related losses being to occur.
There is no cure for osteoporosis although exercise and hormone replacement therapy can
halt or even reverse the progress of the disease. Measures to prevent osteoporosis are far
better than any treatment and should include regular weight bearing exercise, and a diet rich
in calcium and Vitamin D.
REFERENCE:
Andersen, F., 2000. Physiology, Health and Exercise. Student Monograph. Scottish CCC.
www.scholar.hw.ac.uk