Summary that contains all the information from the lectures and the book Human Physiology. Covers all the important headlines and has a detailed practice exam questions with clear explanation including pictures
Lecture 1:skeletal muscles
Myostatin inhibits our muscle growth
Somatic alpha motor neurons are present in central nervous system always Ach to
nicotinic receptor (opening channels sodium enters). Always contracting and
depolarization skeletal muscles.u
Smooth muscles: autonomic nerves system/ skeletal muscles: somatic nerves system.
Reflexes.
Parasympathetic: presynaptic ACh to nicotinic and postsynaptic ACh to muscarinic
receptors.
Sympathetic: only presynaptic ACh to nicotinic. Postsynaptic is NE to a and b1 receptor.
Adrenal sympathetic: in adrenal medulla ACh causing release of adrenalin.
Question exam:
What are the similarities and differences of the somatic pathway and the autonomic
pathway?
Similarly: primary neurotransmitter always release of Ach. Also both a nicotinic receptor
that binds Ach.
Difference: autonomic has Ach/muscarinic NE. Autonomic = inhibitory and excitatory,
pre/post axons and visceral function. Somatic motor= only excitatory, only axons and for
posture and movement.
Motor end plate: contains high concentration ACh receptors and nicotinic ACh receptors. It
is a specialization of the muscle membrane
Myelin is not only for the rapid signaling but it also contains a kind of growth factor which
makes it possible to make the neuromuscular junction (=consist of axon terminals, motor end
plates and schwann cells)
Synaptic cleft filled with collagen:
To prevent too much movement because ACh should directly go to receptors
Makes a very tight connection (strong/stable)
Release ACh:
1. Action potential at axon terminal
2. Depolarization
3. Ca2+ channels open
4. Ca2+ into the cell
5. Vesicles fuse with the presynaptic membrane
6. Release of ACh into synaptic cleft. (because calcium change conformation Snap-25)
7. Broken down by AChE (acetylcholinesterase)
Botox prevents the release of Ach no contraction Sodium concentration is low in the cell.
Snake: a-bungarotoxin, a competitive antagonist of ACh. Causing relaxation paralyzed.
1
,Question exam:
Traveling of sodium and potassium. What goes faster? What goes slower? And what leads to
contraction?
Na+ influx depolarizes membrane contraction. There is more sodium entering than
potassium leaving depolarization. Thus:
Fast: sodium
Slow: potassium
Contraction: depolarization is rapidly going over whole environment of the fiber.
Question exam:
Were are your somatic alpha motor neurons?
Spinal cord.
No antagonistic innervation of muscle fibers causing muscle relaxation.
Relaxation: inhibition at the level of somatic alpha neurons in the CNS (tricep/bicep)
Myofibril: thick (myosin) and thin (actin) filaments move to each other or in opposite
direction.
T-tubules brings action potentials into interieur of muscle fiber. Action potential causes
release calcium. Calcium is the trigger of muscle contraction. Calcium creates movement of
the filaments to each other.
Question exam:
What is a sarcomere, z-disk?
Sarcomere is the total and the system of the filaments in the myofibrils. There are no
sarcomeres in smooth muscle cells, only in skeletal. Sarcomere can get shorter if Z-disk are
pulled to each other because of contraction. A band keeps it length; H and I band get shorter.
The filaments don’t become shorter. Because of sarcomeres striated structure.
Titin: biggest protein, regulates skeletal muscles. Its running through thick filaments. Is
elastic.
Nebulin: regulates stability, helps actin
Myosin heads have 2-bindingsites:
1. ATP
2. G(lobular)-actin
Tropomysosin can block the movement of filaments when it is bonded to myosin heads and
this can only be pushed away when calcium binds to molecules troponin. Troponin sits on
the large tropomyosin molecule.
Contraction skeletal muscle:
- ATP binds to myosin myosin releases actin.
- Myosin hydrolyses ATP Myosin head rotates and binds to actin.
- Power stroke
- Myosin releases ADP
Contraction smooth muscle:
- Ca2+ binds to calmodulin (CaM)
- Ca2+-calmodulin activates myosin light chain kinase (MLCK)
- MLCK phosphorylates light chain in myosin heads and increases myosin ATPase activity
- active myosine slide along actin and create muscle tension
2
, Difference:
smooth muscle: calmodulin
skeletal: troponin
There is more actin in smooth muscle cells and no troponin. Smooth muscle cells doesn’t
have sarcomeres.
Rigor mortis: lack of ATP.
1 action potential 1 twitch
With 1 twitch you can not walk or something, need more twitches
THIS COMES IN EXAM!!!!
Energy supply in muscles:
Available ATP: around 8 twitches.
Phosphocreatine in muscle fiber is alternative ATP. It can give a phosphor group to
ADP and produce ATP.
Creatine kinase helps delivering this pho
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-oxidation running, movement.
Ca2+ release:
Glycogen depletion in muscle
High levels free inorganic phosphate
Extracellular potassium levels.
Lactate is lowering pH lowering release Ca2+ in cytosol.
Relaxation muscle fiber
› Ca2+-ATPase SR
› Ca2+ release from troponin
› Tropomyosin slips back to position where it blocks myosin head binding to globular actin
Slow fiber
- oxidative
- smaller diameter
- not easy fatigue
- darker color due myoglobin
- exercise for long time
3
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