1.

When anabolic steroids are used to build muscle mass, what are possible:
a. negative physical effects on both men and women? b. negative psychological
effects on both men and women?
A.
Anabolic steroid abuse has been associated with a wide range of adverse side
effects.
Men abusing steroids more or less develop physically unattractive over time,
such as acne and breast development and can possibly lead to life threatening
risks, such as heart attacks and liver cancer
In women taking steroids leads to a deeper, scratchier voice due to
testosterone's effects on the vocal cords. The testosterone causes the vocal cords to
grow longer and thicker. Once the vocal cords are longer and thicker, they can never
return to their previous state.
Most effects of steroids are reversible if the abuser stops taking the drugs,
but some are permanent, such as voice deepening in females.
B.
In terms of negative effects on the psychology of its abusers, it is said that it
is as harmful as the physical toll it causes the body. Steroid abusers often
experience roid rage or the state of uncontrollable bursts of anger or extreme
irritability. That can sometimes lead to aggression and violence. Recent studies also
point the correlation of depression and tendency of suicide to users and abusers of
steroids. Needless to say, abusing steroids opens someone to several mental and
health risks.

2. What is happening at the cellular muscular level with this disease?

People suffering from muscle dystrophy lack the presence of a chemical
(protein) called dystrophin, which is necessary for muscles to function properly. The
lack of dystrophin leads to muscle fibre damage and a gradual weakening of the
muscles. The shortage of dystrophin is caused by a faulty gene.
Microscopic examination of affected muscle would show the following changes:
A. degenerating skeletal muscle fibers (i.e. "cells").
B. proliferation of endomysial connective tissue around the degenerating muscle
cells.
C. numerous macrophages (i.e. scavenger white blood cells) in the area, whose job
it is to clear the cellular debris in the damaged muscle tissue.
D. while some of the muscle fibers are breaking down (as seen in a cross section),
other fibers appear to be more dense (or dark in color). These latter cells are
presumably in a state of excessive contraction (i.e. more overlap between actin and
myosin), probably because other segments of these cells (not in the microscopic
viewing field) are experiencing breakdown of the cell membrane. Destruction of the
cell membrane would, of course, allow calcium ions to flow into the cell from the
extracellular fluid (down their electrochemical gradient). As calcium floods the
interior of these cells, it binds to troponin and causes a shift in tropomyosin, thus
exposing the globular head binding sites on actin. Cross-bridges form and, in the
muscle cell's "last breath," it contracts.

3. At the time of this diagnosis, James had an elevated serum creatine kinase (i.e.
creatine phosphokinase) level. What is creatine kinase, and why was this level
elevated in James's blood?
Creatine kinase ("CK"), also known as creatine phosphokinase ("CPK"), is an
enzyme in skeletal muscle cells that transfers phosphate groups between creatine
phosphate and ADP. Creatine phosphate acts as a large storage area for high-energy
phosphate bonds. When muscle cells are at rest and there is an abundance of ATP in
the cell, the high-energy phosphate bonds of the ATP are transformed by the CK
enzyme into high-energy phosphate bonds of creatine phosphate. Later, when that
muscle cell is called upon to contract, CK removes phosphate groups from creatine
phosphate and transfers them to ADP to create ATP. The ATP is then used as a quick
energy source to drive the contraction.

Creatine kinase is located inside skeletal muscle cells. It should not be

present in very large quantities outside of cells (e.g. in the bloodstream). In fact,
when levels of CK in the bloodstream are elevated, this usually means that there
has been large-scale destruction of muscle cells. Duchenne muscular dystrophy
causes muscle cell membranes to break down, allowing creatine kinase to spill out
into the bloodstream. Interestingly, the best way to diagnose a myocardial infarction
(i.e. a heart attack) is to measure blood-CK levels, which are elevated due to
destruction of heart muscle cells.

4. Why is James susceptible to repeated lower respiratory tract infections?

James has gradual weakening of his respiratory muscles, and therefore has a
difficult time completely expanding his lungs. Lungs that are less-well-aerated are
more prone to infection (i.e. pneumonia). Furthermore, weakness of his diaphragm
and abdominal wall muscles makes his cough very weak. He thus has a difficult time
clearing his bronchi of secretions. Weakness of his pharyngeal wall muscles may
alter his swallowing mechanism and cause him to aspirate -- i.e. inhale food or liquid
into the respiratory tract. This too increases his chance of developing a pulmonary
infection. Finally, his scoliotic deformity may limit rib cage expansion.
5. Skeletal muscle is metabolically higher active. It contains three unique structures
or strategies that allow it to obtain additional oxygen, glucose and ATP to supply
energy. Discuss these three structures or strategies.
Exercise demands energy (ATP) at rates up to 1,000 times higher than rest.
There are three major biochemical pathways that are responsible for generating
ATP: 1) the phosphagen system, 2) the glycolytic system, and 3) mitochondrial
respiration.
The phosphagen system is composed of three reactions. The main reaction
relies on phosphocreatine (CrP) to transfer a phosphate group to ADP to regenerate
ATP. The kinetics of this system are still being worked out, but it has been shown
that the CrP system is the primary ATP generation system within the initial 10-15
sec of intense exercise. Replenishment also occurs rapidly. Within about 1.5 min
about 65% of CrP is restored and nearly 95% after 13.6 min.
Exogenous glucose or the breakdown of glycogen feeds glycolysis.

This

pathway is activated when exercise continues for more than a few seconds. In
anaerobic exercise (for example a 30 sec sprint), it is approximated that about 49%
of ATP is generated via glycolysis; the phosphagen system accounts for about 23%
and mitochondrial respiration accounts for about 28%. Because glycolysis generates

pyruvate faster than mitochondrial respiration can process it, some pyruvate is
converted into lactate. This reaction also generates NAD+ which is used by
glycolysis to generate more ATP. Although many believe that lactate is the primary
cause of acidosis in the blood, this theory is undergoing critical review by many
experts.
Mitochondrial respiration accounts for an increasing proportion of ATP
until about 50-60 min of exercise, when it becomes the primary source. During
mitochondrial respiration, products of glycolysis are shuttled into the TCA
cycle. Products from the TCA cycle are then used in the electron transport chain in
conjunction with molecular oxygen to produce ATP. Alternatively, fatty acids can be
activated (so they can cross the mitochondrial membrane), and subsequently
oxidized to produce ATP via the electron transport system.