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Summary Human physiology lectures
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- Human Physiology
- Instelling
- Rijksuniversiteit Groningen (RuG)
Summary of all human physiology lectures
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Elaborations on lectures Human PhysiologyLecture 1 Buwalda: Skeletal muscles
The somatic motor control of muscles goes via the CNS (Central Nervous System) that contains a
soma (cell body) which leads to the target skeletal muscle via an axon. The skeletal muscle is
activated by Acetyl Choline which will bind to a nicotinic
receptor. The motor unit consists of a somatic motor
neuron plus all the muscle fibers that it stimulates. Next
to the somatic nervous system there is the autonomic
nervous system. This goes via the parasympathetic
pathway, sympathetic pathway or the adrenal
sympathetic pathway. The difference between the two
nervous systems is the neurotransmitters
and the effects of the target tissue. The
neuromuscular junction consists of axon
terminals, motor end plates on the muscle
membrane and Schwann cell sheaths. The
motor end plate is a region of muscle
membrane that contains high
concentrations of nicotinic receptors. The axons of the somatic motor neuron branch at the end and
make contact with the skeletal muscle fibre, the synaptic vesicles containing Acetyl Choline will fuse
with the presynaptic membrane and will release the Acetyl Choline into the synaptic cleft, the Acetyl
Choline will the bind to the Nicotinic Acetyl Choline receptors. The synaptic cleft is filled with
collagen. The action potential running through the nerve will arrive at the axon terminal, when doing
so the voltage-gated Ca channels will open causing Ca to go into the cell. The Ca in the cell will cause
excretion of the synaptic vesicles, they will fuse with the presynaptic membrane and thus release
Acetyl Choline into the synaptic cleft. When Acetyl Choline binds to the nicotinic receptors the
channel will open and Na will flow into the cell and K out of the cell. This will cause the cell to
depolarise and the muscle fiber to contract. When the muscle fibers are not innervated they will
relax. Stem cells are able to regenerate when still young but when aged the regeneration is deficient.
There are three types of muscles, skeletal muscle, cardiac muscle and smooth muscle. Skeletal
muscle have large fibers and contain multinucleate cells (more than 1 nucleus per cell) that appear
striped or striated under the microscope. Cardiac muscle fibers are also striated but they are smaller,
branched and uninucleate. Cells are joined in series by junctions called intercalated discs. Smooth
muscle fibers are small and lack striations. Skeletal muscles are used when performing locomotor
movement (from one location to another), the muscles are connected to the bone, they move
voluntary and are under the control of the somatic motor neuron, the muscles can only be excited.
Smooth muscle and heart muscle are used for the movement of content, they are not connected to
the bone and move involuntary. These muscles have multiple control systems and can either be
excited or inhibited. Antagonistic muscle groups move bones in the opposite directions (bicep and
tricep). Muscle contraction can pull on a bone but can never
push a bone away. The flexion movement occurs when the
bones move closer together. Extensions cause the bones to
,move away from each other. Different terms are used when
talking about muscles in comparison to the general terms. The
anatomy of the skeletal muscle is important to know by heart.
The sarcoplasmatic reticulum of the muscle fiber consists of a
thin filament and
a thick filament.
Myofibrils are
part of the
cytoskeleton of
the muscle, they
are built from
long protein
chains. The
contractile proteins are actin and
myosin, the regulatory proteins are
tropomyosin and troponin. The M line
has the thick filaments attached to itself,
the Z disk is attached to the thin
filaments. The length of the sarcomere
will decrease when the muscle contracts,
then the myosin will walk towards the
actin and will pull it in. In this way the
muscle is contracted and the I band will
decrease as well as the H zone. The
filaments do not shorten when
contracting or relaxing after the
contraction, the A band will keep its
length whilst the H and I band shorten.
The filaments ‘slide’. The thin filaments
attached to the Z disk are strings of actin,
the M line has thick filaments of myosin
attached to it. To these myosin titin is
attached through the myosin and to the M line and the Z
disk. The titin provides elasticity and stabilizes myosin.
When a Ca initiation contraction happens the Ca levels
increase in the cytosol due to an action potential. The Ca
will then bind to troponin to form a complex. Troponin-Ca
complex pulls tropomyosin away from actin’s myosin-
binding site. Myosin binds to actin and completes power
stroke which will cause actin filaments to move. In order
to perform all the activity, enough energy should be
present. When in a relaxted state there is sufficient ATP
available for the muscle to contract. When suffering from
Rigor mortis there is a lack of ATP. Due to this there will be muscle relaxation via enzymatic
breakdown of proteins.
Excitation-Contraction coupling
Acetyl Choline is released in neuromuscular junction, this will cause in a rise of the Na influx into
, muscle fiber. This influx will cause a depolarization in the cell and release an end plate potential. This
potential will alter the conformation of the DHP receptor. The DHP receptor will then open RyR Ca
release channels in the sacroplasmic reticulum and Ca will enter the cytoplasm. The Ca released will
bind to troponin, allowing actin-myosing binding. Myosin heads execute power stroke which will
cause actin filaments to slide towards the center of the sacromere. This ofcourse, leading to a
contraction. In the relaxation phase the sacroplasmic Ca-ATPase pumps Ca back into the
sarcoplasmic reticulum and the concentration of Ca in the cell will decrease which cause the Ca to
unbind from troponin. Tropomyosin re-covers the binding site, causing the myosin heads to release
and thin filaments to be moved back to their relaxed
position, this is done by elastic elements, tintin. A twitch is
the period that the muscle needs to contract and relax
again. One action potential will lead to one twitch. About 8
twitches are available in muscles, muscle fiber contains
phosphocreatine which contain high-energy phosphate
bonds. There is never a lack of ATP in muscles. The energy
that is being produced is consumed according to the
following table. Your muscles can fatigue due to the
following causes; low pH, neural, glycogen depletion in
muscle fiber, high levels of free inorganic phosphate or
extracellular potassium levels. This will
cause a Ca release. Slow-twitch oxidative
muscle fibers will not fatigue, they have a
smaller diameter and a darker colour due
to myoglobin. The fast-twithc glycolytic
muscle fibers have a larger diameter, pale
color and can easily fatigue. The length of
the sacromere tells you what the tension in
the muscle fiber is. One motor unit contains
fibers that all have a similar type. There are
differences when comparing different
motor units, edurance versus power for example. Forces increase with recruitment motor units,
different excitation thresholds for motor neurons are created. Low-threshold: fatigue resistant slow-
twitch. Intermediate threshold: fatigue resistant fast-twitch oxidative glcolytic. High-threshold: easily
fatigued glycolytic fast-twitch. With an isotonic contraction the muscle will contract, shorten and
create enough force to move the load. With an isometric contraction the muscle contracts but does
not shorten so the load is not moved by the force. When a muscle is at rest the first contraction will
most likely be an isometric contraction, the muscle has not yet shortened. The sacromeres shorten
generating a force but the elastic elements stretch allowing muscle length to remain the same.
Hereafter a isotonic contraction will follow; sarcomeres shorten more but, because elastic elements
are already stretched, the entire muscle must shorten. Muscle
dysfunction has various reasons. Cramp is sustained contraction
by hyperexcitability of the somatic motor neuron. The muscle can
be overused or could have prolonged inactivity. Also, toxins can
cause muscle dysfunction, think of botulism and tetanus.
Sarcopenia is the loss of skeletal muscle and the poor quality of
muscles. This has several consequences, frailty, metabolism,
fatigue and cognitive skills will all be limited due to this. Skeletal
muscles have voluntary but subconscious reflexes. The speed at
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