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Summary human physiology RUG

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  • Human physiology
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  • Rijksuniversiteit Groningen (RuG)
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  • Human Physiology

Samenvatting lectures RUG boek Human physiology: An integrated approach 8th edition human physiology Summary lectures RUG book Human physiology: an integrated approach 8th edition

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  • Aangegeven in samenvatting
  • May 20, 2020
  • 54
  • 2019/2020
  • Summary

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  • human physiology
  • 8th edition
  • an integrated approach
  • rug
  • human physiology an integrated approach

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Human physiology
Lecture 1: Skeletal muscles

Myostatin: regulator for the muscular system, inhibiting muscle functioning and growth.

Somatic motor pathway
Somatic alpha motor neurons are in our spine. They have long axons and the axon terminals
project Ach directly on the ion-gated nicotinic receptors of the skeletal muscular system.
One neuron is required in the efferent pathway. The effect on the skeletal muscles are only
excitatory, so contraction. The peripheral components found outside the CNS are the axons
only. Summary of function: posture and movement.

Parasympathetic pathway
The primary neuron is always acetyl cholinergic projecting on a nicotinic receptor. The
second neuron is also acetyl cholinergic projecting on a muscarinic receptor. Autonomic
targets are smooth and cardiac muscle cells, some endocrine and exocrine glands and some
adipose tissue. The neurons are released from varicosities and axon terminals.

Sympathetic pathway
the primary neuron is acetyl cholinergic projecting on a nicotinic receptor. The second
neuron is noradrenergic projecting on a adrenergic receptor. However, with sweat glands,
the second receptor is a muscarinic receptor. The neurons are released from varicosities
and axon terminals.

Adrenal sympathetic pathway
The adrenal medulla is a modified postganglionic sympathetic neuron turned into an
endocrine organ that releases the hormone adrenaline into the blood (circulation)

Summary of function autonomic pathway
Visceral function, including movement in internal organs and secretion; control of
metabolism.

Neuromuscular junction
The axons of α-motor neurons in the skeletal muscle are myelinated. This is a fat layer
around the axons, causing the signal to be transferred very
rapidly. One somatic α -motor neuron can innervate multiple
muscle fibres. A fibre is a fused cell with nuclei that are
brought to the outside of the fibre. A fibre gets only
information from one neuron. The synapse of a somatic
motor neuron is called the neuromuscular junctions. These
are formed by Schwann cell sheaths, axon terminals and
motor end plates.
- Motor end plates are invaginations of the muscular fibre
membrane that lies opposite to the axon terminal,
which contains high concentrations of ACh receptors.
They are functioning in the specialisation of muscle membrane.

, - Schwann cells in the junction are functioning in the development of the junction and
the velocity of an action potential.
- The axon terminals are filled with mitochondria and synaptic vesicles.
The synaptic cleft contains collagen fibres that hold the axon terminal and motor end plates
in the proper alignment and tight and Ach can easily pass. The cleft also contains
acetylcholinesterase.

Release ACh
As soon a depolarization at the terminal arrives, voltage-gated calcium channels open and
calcium enters the axon terminals. Calcium entry causes synaptic vesicles filled with ACh to
fuse with the presynaptic membrane and release their Ach into the synaptic cleft. Ach binds
to nicotinic receptors. Acetylcholine is broken down by AChE. Rapid, short and precise
signal.

Binding of Ach to nicotinic receptor
there are two binding sites. As soon as Ach binds to the receptor, the calcium gate opens,
and sodium is allowed to enter the cell. Potassium is allowed to exit, but there is more
sodium entering than potassium is leaving. So, the sodium-influx causes the membrane
depolarization, which causes a contraction of muscle fibre. α-bungarotoxin (competitive
antagonist) binds competitive to the nicotinic skeletal muscle receptor and inhibits the
muscle to contract, and breathing is inhibited. Patients with myasthenia gravis have a
deficiency of ACh receptors on their skeletal muscles
and have weak muscle function as a result.

Neuronal action at the motor end plate
- No antagonistic innervation of muscle fibers
causing muscle relaxation
- relaxation: inhibition at the level of somatic alpha
motor neurons in CNS

Excitation-contraction coupling
1) Acetylcholine (ACh) is released from the somatic
motor neuron.
2) ACh initiates an action potential in the muscle
fiber.
3) The action potential travels across the surface of the muscle fiber and into the t-
tubules by the sequential opening of voltage- gated Na+ channels.
4) The muscle action potential act on DHP receptors that changes from conformation.
5) Calcium release channels (RyR receptors) open and release the calcium from the
sarcoplasmic reticulum to the cytosol.
6) Calcium combines with troponin and tropononin moves to the “on” position, initiating
contraction.

Relaxation: transfer calcium from the cytosol into the sarcoplasmic reticulum with use of a
calcium ATPase. Removal of Ca2+ allows tropomyosin to slide back and block actin’s
myosin-binding site. As the crossbridges release, the muscle fiber relaxes with the help of
elastic fibers in the sarcomere and in the connective tissue of the muscle.

,Regeneration: Skeletal muscle fibers are the largest cells in the body, created by the fusion
of many individual embryonic muscle cells. Committed stem cells called satellite cells lie just
outside the muscle fiber membrane. Satellite cells become active and differentiate into
muscle when needed for muscle growth and repair.

Under some conditions, axons in the peripheral nervous system can regenerate and
reestablish their synaptic connections. Schwann cells secrete neurotrophic factors that keep
the cell body alive and stimulate regrowth of the axon. This process is less efficient in adults.
System factors increased with aging: TGFβ and Wnt and decreased: GDF11, Oxytocin.

Muscle
a) skeletal muscles
- skeletal muscles are connected to the bone.
- Voluntary
- Excitation
- Locomotor movement
- fibres are large, multinucleate cells that appear striped or
striated under the microscope.
b) smooth muscle
- gut, stomach, lungs, blood vessels
- small fibres, lack striation
c) cardiac muscles
- smaller branched striated fibres, uninucleate. Cells are
joined in series by intercalated discs.

smooth muscle and heart muscle:
• Movement of content
• Not connected to bone
• Involuntary
• Multiple control (excitation-inhibition: autonomic nervous, intrinsic, endocrine)

Movement via joints
Flexion: moves bones closer together. Example: Contraction biceps underarm pulled to
yourself. When doing an arm curl, the radius and ulna move towards the humerus.
Extension: moves bones away from each other. Example: Contraction triceps underarm
pulled away from yourself. when doing a push-up, the radius and ulna move away from the
humerus.
Contraction biceps, inhibition contraction triceps.

Muscle terminology
Cell membrane: Sarcolemma
Cytoplasm: sarcoplasm
Modified endoplasmic reticulum: sarcoplasmic reticulum

,Skeletal muscles are composed of muscle fascicles. Collagen, elastic fibres, nerves and
blood vessels are found between the fascicles. that are composed of individual muscle
fibres. These muscle fibres contain:
- sarcolemma
- T-tubules: functionally linked to terminal cisternae of the sarcoplasmic reticulum.
allow action potentials to move rapidly from the cell surface into the interior of the
fibre so that they reach the terminal cisternae.
- multiple nuclei
- sarcoplasm
 sarcoplasmic reticulum
▪ concentrates and transfers ca with help of a ca ATPase in the SR
membrane.
▪ wraps around the myofibrils.
 mitochondria: produce ATP for muscle contraction
 glycogen granules: contain glycogen, reserve source of energy.
 myofibrils: highly organized bundles of contractile and elastic proteins that
carry out the work for contraction
▪ thin filaments
▪ thick filaments

Triad: One t-tubule and its two flanking terminal cisternae.

Myofibril
Myofibril proteins include the motor protein my-
osin, which forms thick filaments; the
microfilament actin, which creates thin filaments;
the regulatory proteins tropomyosin and troponin;
and two giant accessory proteins, titin and
nebulin. Myosin creates movement. A myosin
molecule forms a stiff tail of intertwined protein
chains. The elastic myosin heads both have a
heavy chain which binds ATP and uses the energy
from ATP’s high-energy phosphate bond to create movement and a light chain which and
which binds actin. Actin makes up the thin filament. One G-actin is a globular protein. Each
G-actin molecule has a single myosin-binding site, Polymerized G-actin molecules form two
twisted F-actin polymers. Myosin heads of the thick filaments interact with the actin
filaments, which draw the whole actin filaments inside. Crossbridges form when the myosin
heads of thick filaments bind to actin in the thin filaments

,Titin and nebulin
Titin is running over the thick filaments, the largest protein of the body and has also some
elasticity. Titin has two functions: (1) it stabilizes the position of the contractile filaments
and (2) its elasticity returns stretched muscles to their resting length. Titin is helped by
nebulin, an inelastic giant protein that lies alongside thin filaments and attaches to the Z
disk. Nebulin helps align the actin filaments of the sarcomere.

Slighting filament mechanism
Contraction is not shortening of the thick and thin filaments but shortening of the
sarcomere. Thin filaments are pulled past the thick filaments towards the centre of the
sarcomere. The thin filaments are pulled by the myosin heads of the thick filaments, which
continuously forms and breaks cross bridges with the actin molecules of the thin filaments.

Ca2+: initiation contraction
When calcium levels in the cytosol increase, troponin is bound to calcium. Tropomyosin,
which is running around the actin filament and is hindering the binding site for the myosin
heads, is pulled away by the tropononin-calcium complex. Myosin heads are no longer
hindered and actin binds these heads. As a result, cross bridges are formed, The inorganic
phosphate is released and the region is changed in conformation. Actin filament is pulled
inside and a movement (powerstroke) occurs.

Molecular basis of contraction
1) ATP binds to myosin
2) Myosin hydrolyses ATP. Myosin head rotates and binds to actin
3) power stroke. Calcium signal.
4) Myosin releases ADP.

Muscle relaxation: when calcium levels in the cytosol drop below its threshold value for
binding to troponin. This low calcium level can be obtained by sarcoplasmic calcium
ATPases, which removes calcium from cytosol back to the SR. Tropomyosin shifts back to
cover the myosin binding sites on actin. As a result, no cross bridges are formed. The thin
filaments slight back to their resting position.

There is a tight binding in the rigor state when you are dead: no ATP delivery

Rigor mortis: lack of ATP.
- transient: muscle relaxation via enzymatic breakdown of protein.

,Timing of E-C coupling




The somatic motor neuron action potential is followed by the skeletal muscle action
potential, which in turn is followed by contraction.
Twitch (contraction-relaxation cycle): one powerstroke is one event. 1 action potential in
muscle fibre produces 1 twitch. Muscle contraction creates force: muscle tension. A
contraction requires ATP.
Notice that there is a short delay—the latent period—between the muscle action potential
and the beginning of muscle tension development. This delay represents the time required
for calcium release and binding to troponin.
Once contraction begins, muscle tension increases steadily to a maximum value as
crossbridge interaction increases. Tension then decreases in the relaxation phase of the
twitch. During re- laxation, elastic elements of the muscle return the sarcomeres to their
resting length.
Exam question 12-11: what happens with calcium in the different stages

Energy supply muscles
In muscle fibres are a lot of mitochondria, important for ATP supply.
Metabolic production ATP:
• glucose via glycolysis to pyruvate; pyruvate (O2) into citric acid cycle (30 ATP)
• anaerobic: glucose to lactate (2 ATP)
• FFA’s in citric acid cycle: beta-oxydation
- slow; modest exercise

Available ATP: ± 8 twitches

Phosphocreatine: is the back-up energy source. It is similar to ATP and upon contraction,
the p of phosphocreatine can easily be transferred to ADP. Creatine kinase/ creatine
phosphokinase is helping with this transfer.

, Central fatigue: arise in the CNS. Protective mechanism. Low pH from acid production
during ATP hydrolysis is often mentioned as a possible cause of fatigue
Peripheral fatigue: arise anywhere between the neuromuscular junction and the contractile
elements of the muscle. if ACh is not synthesized in the axon terminal fast enough to keep
up with neuron firing rate, neurotransmitter release at the synapse decreases.
Consequently, the muscle end-plate potential fails to reach the threshold value needed to
trigger a muscle fiber action potential, resulting in contraction failure. Also, too much
potassium is leaving, so, less calcium release, no cross-bridge forming, and no power stroke.

SLOW AND FAST TWITCH FIBRES
slow twitch oxidative fibres fast twitch oxidative fast twitch glycolytic fibres
(type 1): glycolytic fibres (type 2): (type 2):
Muscle type Red muscle Red muscle White muscle
Speed Slowest Intermediate Fastest
development
of max.
tension
Myosin Slow Fast Fast
ATPase
splitting ATP
Diameter Small Medium Large
Contraction Longest Short Short
duration
Endurance Fatigue resistant Fatigue resistant Easily fatigued
Use Posture, marathon runner Standing, walking Jumping, running
Metabolism Oxidative Glycolytic, but more Glycolytic
oxidative with endurance
training
Capillary High Medium Low
density
Mitochondria Numerous Moderate Few
Color Dark red Red Pale

SACROMERE
The optimal resting length of a sarcomere is when exactly all myosin heads can bind to
actin. In the relaxed state, the sarcomere has not much overlap, which results in less tension
and less power/force.

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