Hypertrophy

It is an increase in the size of an organ or

tissue due to enlargement of individual cells
without increase in the
number of cells.
Hypertrophy is an increase in cell size by gain
of cellular substance.
With the involvement of a sufficient number of
cells, an entire organ can become
hypertrophic.
Hypertrophy is caused either by increased
functional demand or by specific endocrine
stimulations.
Not only the size, but also the phenotype of
individual cells can be altered in hypertrophy.
With increasing demand, hypertrophy can
reach a limit beyond which degenerative
changes and organ failure can occur.

It usually occurs in organs in whichproliferation and mitosis are

.restricted
.e.g. skeletal muscle and heart muscles

It may be physiological or.pathological

Physiological hypertrophy

e.g. pregnant uterus, and muscles of

athletes

Pathological hypertrophy
(adaptive hypertrophy )
e.g. a- hypertrophy of the stomach in pyloric
stenosis
b- cardiac muscle hypertrophy in
.chronically hypertensive patients

: a- Skeletal Muscle Hypertrophy

Skeletal muscle hypertrophy is an increase in a
muscles cross-sectional area.

 Skeletal muscle hypertrophy is governed by a host of

hormones and growth.
factors, including satellite cells, testosterone, IGF-I, IL-1
& IL-6, to name just a few. An increase in muscle CSA is

accomplished by:
a- Increase in the size of myofibrils :
o Incorporation of new contractile proteins into the Actin and
Myosin filaments.
o Incorporation of new proteins to the structural filaments.
b- Increase in Sarcoplasm :
c- Increase in the connective tissues surrounding the muscle,
myofibrils, and muscle fibers.
d- An increase in CSA can be accomplished by two forms of
hypertrophy: sarcomere and sarcoplasmic.
Sarcomere HypertrophyIncorporate of New Proteins in
Actin and Myosin

1-Sarcomere hypertrophy
Sarcomere hypertrophy is an enlargement of a muscle fiber
as a result of an increase in sarcomere number and size.
Sarcomeres, which contain the contractile proteins actin
and myosin are the functional units of myofibrils.
The incorporation of new contractile proteins into Actin
and Myosin filaments increases a muscle fibers size and
ability to produce force, commonly referred to as strength.
These new proteins must be created through the process of
protein synthesis.
2-Sarcoplasmic Hypertrophy
Sarcoplasmic HypertrophyIncrease in Sarcoplasm and
Connective Tissue

 Sarcoplasmic hypertrophy is an increase of the sarcoplasm

(muscle fiber semifluid cytoplasm) and noncontractile
proteins.
The fibers ability to produce force does not increase from
sarcoplasmic hypertrophy.
The emerging theory behind skeletal muscle hypertrophy
is that a bout of exercise causes protein degradation or
damage (myotrauma), which leads to a period of enhanced
protein synthesis or supercompensation when the bout
ceases (Zatsiorsky, 1995).
This increase in protein synthesis not only repairs the
damage from the bout of exercise, but also makes the
muscle stronger and therefore more resistant to future
damage.

Mechanical Stimuli Cell Damage Cell Clean Up' Cell Repair Cell Growth

b-Cardiac Hypertrophy :
Cardiac hypertrophy has been considered as
an important risk factor for cardiac morbidity
and mortality whose prevalence
has increased during the last few decades.

Cardiac hypertrophy, a disease associated

with the myocardium, is characterized by
thickening of ventricle wall of heart and
consequent reduction in the contracting ability
of heart to pump the blood.
Cardiac hypertrophy has been divided into two
types, i.e. physiological and pathological
hypertrophy.
The exercise-induced increase in the ability of
pumping blood leads to thickening of ventricle
wall, referred to as physiological hypertrophy.
On the other hand, reduced ability of pumping
blood as a result of hypertension and volume
overload on heart denotes pathological
hypertrophy.
Numerous mediators have been found to be
involved in the pathogenesis of cardiac
hypertrophy that include mitogen-activated
protein kinase (MAPK), protein kinase C (PKC)

insulin-like growth factor-I (IGFphosphatidylinositol 3-kinase (PI3K)-AKT/PKB,

calcinurin-nuclear factor of activated T cells
(NFAT) and mammalian target of rapamycin
(mTOR).
The prevention strategy for cardiac
hypertrophy involve thiazide diuretics,
angiotensinconverting enzyme (ACE)
inhibitors, angiotensin (Ang) II receptor
blockers, beta blockers and calcium channel
blockers.
The present review article highlights the
signaling mechanisms involved and the
approaches required in the treatment of
cardiac hypertrophy.