guyton and hall lectures medical physiology

1. Topic: Types of Muscle Tissue: The Function of Skeletal, Cardiac, and Smooth Muscle
About half of your body’s weight is muscle. In the muscular system, muscle tissue is categorized
into three distinct types: skeletal, cardiac, and smooth. Each type of muscle tissue in the human
body has a unique structure and a specific role. Skeletal muscle moves bones and other
structures. Cardiac muscle contracts the heart to pump blood. The smooth muscle tissue that
forms organs like the stomach and bladder changes shape to facilitate bodily functions. Here are
more details about the structure and function of each type of muscle tissue in the human
muscular system.
1. The Human Body Has Over 600 Skeletal Muscles That Move Bones and Other
Structures

2. sSkeletal muscles attach to and move bones by contracting and relaxing in response to voluntary
messages from the nervous system. Skeletal muscle tissue is composed of long cells called
muscle fibers that have a striated appearance. Muscle fibers are organized into bundles supplied
by blood vessels and innervated by motor neurons.
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2. The Walls of Many Human Organs Contract and Relax Automatically
Smooth muscle is found in the walls of hollow organs throughout the body. Smooth muscle
contractions are involuntary movements triggered by impulses that travel through the autonomic
nervous system to the smooth muscle tissue. The arrangement of cells within smooth muscle
tissue allows for contraction and relaxation with great elasticity. The smooth muscle in the walls
of organs like the urinary bladder and the uterus allow those organs to expand and relax as
needed. The smooth muscle of the alimentary canal (the digestive tract) facilitates the peristaltic
waves that move swallowed food and nutrients. In the eye smooth muscle changes the shape of
the lens to bring objects into focus. Artery walls include smooth muscle that relaxes and
contracts to move blood through the body

3. 3. Cardiac Muscle Contracts in Response to Signals from the Cardiac Conduction System
The heart wall is composed of three layers. The middle layer, the myocardium, is responsible for
the heart’s pumping action. Cardiac muscle, found only in the myocardium, contracts in response
to signals from the cardiac conduction system to make the heart beat. Cardiac muscle is made
from cells called cardiocytes. Like skeletal muscle cells cardiocytes have a striated appearance,
but their overall structure is shorter and thicker. Cardiocytes are branched, allowing them to
connect with several other cardiocytes, forming a network that facilitates coordinated
contraction.

4. Skeletal muscle cells
Characteristics
Skeletal muscle cells are long, cylindrical, and striated. They are multi-nucleated meaning that
they have more than one nucleus. This is because they are formed from the fusion of embryonic
myoblasts. Each nucleus regulates the metabolic requirements of the sarcoplasm around it.
Skeletal muscle cells have high energy requirements, so they contain many mitochondria in order
to generate sufficient ATP.
Cardiac muscle cells
Characteristics
Cardiomyocytes are short and narrow, and fairly rectangular in shape. They are around 0.02 mm
wide and 0.1 mm (millimeters) long. Cardiomyocytes contain many sarcosomes, which provide
the required energy for contraction. Unlike skeletal muscle cells, cardiomyocytes normally
contain a single nucleus. Cardiomyocytes generally contain the same cell organelles as skeletal
muscle cells, although they contain more sarcosomes.
Cardiomyocytes are large and muscular, and are structurally connected by intercalated
discs which have gap junctions for diffusion and communication. The discs appear as dark bands
between cells and are a unique aspect of cardiomyocytes. They result from membranes of
adjacent myocytes being very close together, and form a kind of glue between cells. This allows
the transmission of contractile force between cells as electrical depolarization propagates from

5. cell to cell. The key role of cardiomyocytes is to generate enough contractile force for the heart
to beat effectively. They contract together in unison, causing enough pressure to
force blood around the body.
Smooth muscle cells
Characteristics
Smooth muscle cells are spindle-shaped and contain a single central nucleus. They range from 10
to 600 μm (micrometers) in length, and are the smallest type of muscle cell. They are elastic and
therefore important in the expansion of organs such as the kidneys, lungs, and vagina. The
myofibrils of smooth muscle cells are not aligned like in cardiac and skeletal muscle meaning
that they are not striated, hence, the name smooth.
Smooth muscle cells are arranged together in sheets and this organisation means that they can
contract simultaneously. They have poorly developed sarcoplasmic reticulums and do not
contain T-tubules, due to the restricted size of the cells. However, they do contain other normal
cell organelles such as sarcosomes but in lower numbers.

6. Topic: Atrphy and hypertrophy
Atrophy and hypertrophy are two opposite conditions that can be found in pathological
or diseased muscles.
Atrophy is characterized by a wasting or loss of the muscle mass (A1) and usually
involves a decrease in the size or cross-sectional area (CSA) (A2) of an individual myofibre or a
number of myofibres. In contrast, hypertrophy is an increase in muscle mass and CSA,
specifically due to an increase in the CSA of individual muscle fibres. As a result, the muscle
strength (A3) and the bone mass are significantly affected.
To maintain homeostasis, the biological response of the human body generates a dynamic
balance between synthetic and degradative processes for both atrophic and hypertrophic muscles.
This dynamic balance occurs in response to any stimuli, due to processes that promote muscle
growth via increased protein content.
Moreover, it can result either from increased protein production, decreased protein breakdown,
or a combination of both of these aspects of protein turnover. The processes that govern the
extent of muscle atrophy are based on the magnitude of the regulated decline in rate of protein
synthesis, increased level of oxidative damage (A4), and subsequent unregulated protein
degradation. For example, inhibitors of the proteosome block increases in protein breakdown
normally seen in atrophy, the level of ubiquitinated conjugates increase during atrophy and genes
that encode various components of the ubiquitin pathway increase during atrophy. An increase in
muscle activity stimulates the expression of a protein growth factor known as insulin-like growth
factor I (IGF-I). IGF-I has been shown to be sufficient to induce hypertrophy through either
autocrine or paracrine mechanisms. IGF-I expression is increased during compensatory
hypertrophy caused experimentally by removing several muscles to force those remaining to take
up the resultant increase in load.
Muscle atrophy
The causes of muscle atrophy are from several sources, such as neuromuscular diseases,
immobilization and denervated conditions. In addition, the muscle atrophy may also take place,
secondary to some devastating injuries or common health problems, such as spinal cord injury
(SCI), ageing and various systemic diseases (A5), respectively. Moreover, the condition may be
exacerbated by starvation, micro-gravity (A6), detraining (A7), reduction in neuromuscular
activity (Fitts et al. 2000), decreased levels of hormones (A8), increases in protein degradation
(A9), decreases in protein synthesis (A10), decreases in protein content, and various forms of
reduced use (A11). Among acute and critically ill patients, the onset of muscle atrophy is rapid
and severe, beginning within 4 h of hospitalization. In the first few weeks during hospitalization,
the antigravity or the extensor group muscles will show greater atrophy than non-antigravity or
flexor group muscles. During extended periods of hospitalization, a prolonged unused limb leads
not only to an impairment of the muscle function (A12), but also to a deleterious alteration in the

7. muscle morphology (Bloomfield 1997), manifested in symptoms such as a decrease in muscle
mass (A13), a reduction of the muscle fibre diameter, and a reduction in the overall number of
muscle fibres. Moreover, this condition may also have a negative affect on bone health by
decreasing bone mineral density at the lumbar spine, femoral neck and calcaneus. Interestingly,
the duration of immobility has been shown to be positively correlated with the degree of muscle
atrophy (A14). The early signs of muscle atrophy found in these patients are accompanied by
general weakness (A15) and fatigue (A16), especially in the lower limb (A17). In fact, these
clinical signs may be caused either by the medication or pathological condition per se. Therefore,
it is inappropriate to conclude the patient’s condition based only on muscle testing alone. Some
other clinical assessments such as electrodiagnosis, computerized muscle strength analysis and
biochemical analyses are essential for providing verification and further confirmation of the
status of the muscles in question. The clinical assessments for disuse muscle atrophy can be
performed at the bedside, accompanied with the strength assessment by observing muscle
movement, muscle tone, muscle size and muscle strength.
Muscle hypertrophy
Hypertrophy of a muscle is a multidimensional process involving several factors such as
growth factors (GFs), IGFs (A29), clenbuterol, anabolic steroids, hormones (A30), the immune
system, and satellite cells (A31). For example, in a study investigating IGF-I peptide levels in
human muscle following 10 weeks of strength training in old men and women (aged 72–98
years), it was shown that there was a c. 500% increase in the levels of IGF-I within the muscle
fibres of these subjects after the training period, as determined using immunohistochemistry.
This demonstrates that the peptide levels in older muscles may adapt over the longer-term to
exercise training. Indeed, the results of longitudinal strength training studies have confirmed that
the muscles of even very elderly people are able to exhibit a hypertrophy response to resistance
exercise (A32).
IGF-I is also thought to be involved in the activation of satellite cells, satellite cells are
small mononucleate muscle stem cells located between the sarcolemma and basal lamina of
muscle fibres. Recently, the link between satellite cell number and myofibre size has been
demonstrated in both untrained and hypertrophied human muscle fibres. These cells, when
activated, are believed to proliferate and differentiate into myoblasts, which then fuse with
existing fibres, thus providing new nuclei to maintain the ratio of DNA to protein for fibres
undergoing hypertrophy. The link between IGF-I, satellite cells, and hypertrophy has been
shown in studies where localised infusion of IGF-I into the tibialis anterior muscle of adult rats
resulted in an increased total muscle protein and DNA content. More recently, Bamman et al.
(2001) reported a 62% increase in IGF-I mRNA concentration in human muscle 48 h after a
single bout of eccentric resistance type exercise.