Download Muscle

Muscle
3 types of muscle:
-Skeletal muscle is used for posture and locomotion. This is the muscle that enables our arms and legs to contract, under our conscious control.
-Cardiac muscle is responsible for the rhythmic contractions of the heart.
-Smooth muscle causes involuntary contraction in blood vessels, gut, bronchi and the uterus.
-Thin cells constituting muscles are called muscle fibers (can be 1 ft long)
-Muscle is attached at each end to tendons, which in turn attach to bone on both sides of a joint.
Contraction of skeletal muscle pulls on the tendons resulting in flexion of the joints.
-Muscle fibers are generated during development by the fusion
of a large number of small precursor cells called myoblasts.
Each myobast has a single nucleus, whereas the fiber is a
multinucleated cell.
-The striations within each myofibril are caused by alternating light I-bands
and dark A-bands. In the center of each light band is a dark line called the Zline. These structures delineate the sarcomere, the contractile unit of skeletal
muscle.
-Each sarcomere consists of two sets of parallel and partially overlapping
protein filaments: thick filaments extending from one end of the A band to
the other, and thin filaments, attached to the Z lines and extending across
the I band and part way into the A band.
-Thin filaments are physically attached to Z lines.
-Thin filaments consist of actin. Each actin filament is formed from two
chains of globular actin subunits, twisted into a helix.
The myofibril is a lattice of thick and thin filaments.
-Muscle contraction occurs when the thin filaments slide over the thick filaments.
Neither the thick or thin filaments change in length.
-The thin filaments are pulled over the thick filaments by the myosin
headgroups, which repeatedly grab, pull and release the thin filaments.
The reaction is driven by ATP hydrolysis.
-Headgroups: Reach out – Grab - Pull – Release
-The sarcomere contracts when thin filaments slide over thick filaments.
-Contraction of the sarcomeres shortens the entire myofibril.
-Actin molecules have binding sites for myosin
headgroup
-When binded, change of conformation occurs and
leads to release of ADP+Pi.
-Power stroke is caused by the release of ADP+Pi
-When headgroup binds ATP, it is able to let go.
-Motor unit=motor neuron+all the muscle fibers it
innervates.
-Size varies: number of fibers innervated by a single
motor neuron may range from 10 (ex. extraocular
muscles) to 100 (muscles of the hand) to several
thousand (large flexor&extensor muscles of leg).
-Motor neurons are found in spinal cord (arms,
legs…) and the brain stem (face…).
-End plate potential is like an enormous EPSP (only one is required
to get to the threshold)
-Sarcoplasmic reticulum is intracellular compartment surrounded
by plasma membrane
-T tubules are holes in plasma membrane going deep down into muscle fiber
Troponin: small globular protein, dotting the filament and
binding calcium (then changes shape and physically
pushes on tropomyosin)
Tropomyosin: thin protein that wraps around the
filament and covers up actin’s binding sites to myosin
headgroup
Types of skeletal muscle fibers:
-Slow oxidative fibers:
Myosin with low ATPase activity.
Myoglobin to facilitate oxygen transport from blood (“red muscle”).
For generation of low levels of force over long periods of time.
(long distance runnes’ muscles: more efficient but not bigger)
-Fast glycolytic fibers:
Myosin with high ATPase activity.
no myoglobin (“white muscle”)
For generation of large force over short periods of time.
(weightlifters’ muscles: more and more myofibrils)
-Fast oxidative fibers:
Intermediate properties
-Contraction of muscle fiber in response to a single action potential is called a twitch. The twitch lags behind the muscle action potential, because of
delays associated w/ excitation-contraction coupling. The duration of contraction reflects, primarily, the time it takes for the calcium concentration in
muscle cell to return to baseline.
-Force exerted by a muscle is controlled by recruitment (increase in the number of active fibers) and by summation (the additive effects of several
closely spaced twitches).
-Summation applies to individual muscle fibers. Single action potentials in
the motor neuron, spaced more than a few hundred milliseconds apart,
cause a transient twitch of the muscle fiber. If the action potentials are
applied more rapidly, the twitches begin to add together. A rapid burst of
action potentials in the motor neuron enables maximal, sustained
contraction of the muscle fiber, called tetanus.
-Recruitment of additional motor unit is a more important mechanism in
increasing muscle tension.
-Slow oxidative fibers are recruited first and fast glycolytic fibers last.
Muscle fatigue:
For short duration, high intensity activity, this fatigue is thought to reflect at least three factors:
-Failure of the muscle action potential, caused by buildup of potassium in the t-tubules (depolarized membrane, muscle paralysed, when you “can’t
hold it anymore”)
-Lactic acid buildup, which reduces muscle pH, altering protein structure and function
-Inhibition of cross-bridge cycling, due to buildup of ADP and Pi within the muscle fiber (safety mechanism: muscle fatigues long before ATP level gets
too low)
For low-intensity, long-duration exercise, depletion of fuel substrates is likely to be the major cause of fatigue
Diseases of the motor unit
-Neurogenic disorders due to changes in motor neuron cell bodies or axons (clinical features include muscle atrophy, fasciculations, decreased muscle
tone)
-Myopathic disorders due to degeneration of muscle, with little or no change in motor neurons (characterized by muscle weakness, myotonia,
myoglobinurea (heme-containing proteins in urine), and increase in sarcoplasmic enzymes in plasma)
-Upper motor neuron (neuron in brain, w/ synapses w/ motor neuron in spinal cord),diseases cause overactive reflexes, spasticity.
Ex of motor neuron disease :
Amyotropic lateral sclerosis (such as Stephen Hawking’s or Lou Gehrig’s disease): degeneration of both upper and lower motor neurons. Symptoms
include muscle atrophy, weakness and fasciculations (characteristic of lower motor neuron disease) as well as hyperreflexia (characteristic of upper
motor neuron disease). Disorder is progressive and invariably fatal with no effective treatment
Ex of myopathy :
Duchene muscular dystrophy: inherited, X-linked disorder, affects males only, starts in legs, progresses rapidly, caused by mutation in gene encoding
dystrophin. 430 kDa protein, critical component of muscle cytoskeleton (muscle just falls apart, degenerates without that protein)
Smooth muscle (uterus, intestine, blood vessels…):
-cells (smaller and more elongated) are called this way because they have no stripes.
-smooth muscle can take its time about contracting and doesn’t have to generate as much force as skeletal muscle.
-activated by various way (different in uterus and in intestine or blood vessels) but still metabotropic receptors
-signal to contract is an increase in calcium concentration
Autonomic Nervous System
-sensory and motor system, innervating visceral tissues and organs, intimately connected to the idea of homeostasis, the ability of the organism to
maintain a relatively stable internal environment in the face of changing external conditions, nervous system controlling the inside of the body.
(body temperature, blood pressure, contraction of digestive track, distribution of oxygen, osmolarity…)
-3 branches: sympathetic (emergency fight-or-flight reactions w/ irrigation to muscles, acceleration of heart rate and palm sweating), parasympathetic
(rest-and-digest processes, constriction of intestine, deep breathing) & enteric system (separated system, responsible for various secretions in GI track)
Ganglion=collection of cell bodies & synapses outside the central nervous system
-The anatomical organization of the autonomic motor pathways differs from that of the somatic motor pathways. The autonomic motor neurons (also
referred to as postganglionic neurons) are located outside the spinal cord in cell groups called the autonomic ganglia. They are activated by
preganglionic neurons, whose cell bodies are located in the spinal cord or brainstem.
-Sympathetic preganglionic neurons (short axons) release acetylcholine,
which activates postganglionic neurons through nicotinic acetylcholine
receptors. The postganglionic neurons release norepinephrine, which
modulates target tissues through interaction with α adrenergic and β
adrenergic receptors (metabotropic receptors).
-Parasympathetic preganglionic neurons (long axons) also release
acetylcholine, activating postganglionic neurons through nicotinic
acetylcholine receptors. Parasympathetic postganglionic fibers release
acetylcholine; however, ACh modulates the target tissue through
activation of muscarinic acetylcholine receptors (metabotropic)
-The sympathetic and parasympathetic systems tend to have opposing effects on target tissues. (Ex Cardiovascular reflexes: sympathetic stimulation
increases heart rate and strength of heart contraction while parasympathetic stimulation decreases heart rate and contraction)
-The autonomic nervous system responds to a variety of sensory inputs: most sensory information from visceral organs reaches the brain by way of the
vagus nerve. Visceral sensory information from head and neck enter the brain through the glossopharyngeal and facial nerves. These inputs synapse in
the brainstem in the nucleus of the solitary tract. This brain region mediates direct autonomic reflexes and projects to higher brain areas (ex. the
hypothalamus and cerebral cortex), which regulate more complex autonomic responses.
-Nucleus=collection of neurons and synapses in the brain or central nervous system
Brainstem = region w/ all the automatic functions.
-Homeostasis is maintained through negative feedback, such as the baroreceptor reflex: sympathetic activation results in an increase in cardiac output
and an increase in blood pressure. This results in activation of pressure-sensitive baroreceptor neurons in the aortic arch and the carotid sinus,
signaling the increased blood pressure to the nucleus of the solitary tract. This results in parasympathetic activation and a resulting fall in blood
pressure and heart rate. (fainting, or drop of pressure, for instance when giving blood)
-Enteric nervous system (controlling the gastrointestinal tract, the pancreas and the gallbladder) can operate completely independently but autonomic
nervous system can also modulate its activity. It contains about 100 millions of neurons (as many as the spinal cord). The enteric system consists of two
plexuses of neuronal cell bodies and fibers along the entire length of the gastrointestinal tract. The myenteric plexus principally controls gut motility,
whereas the submucosal plexus controls secretory functions of the gut.
-Hypothalamus controls the pituitary gland (master of glands) and regulates 5 basic physiological needs:
Blood pressure and electrolyte balance.
Body temperature.
Energy metabolism
Reproduction
Emergency responses to stress
The hypothalamus regulates these processes by three mechanisms:
•It receives sensory information from the entire body and contains internal sensory neurons that respond to changes in local temperature, osmolality,
glucose, etc
•It compares sensory information with biological set points (ex. the normal set point for temperature is from 36,5 to 37,5°c)
•When the hypothalamus detects a deviation from a set point, it adjusts various autonomic, endocrine and behavioral responses to restore
homeostasis
-Hypothalamus is related to motivation & pleasure.
-The autonomic nervous system interacts with a set of brain structures called the limbic system, which includes the amygdala, the hippocampus and
cingulate cortex. The limbic system plays a central role in emotions, in relating visceral responses to emotional states, and in tagging the emotional
significance of memories.
-The amygdala links autonomic responses and to emotions&feelings. The amygdala is required for our ability to remember emotionally charged events
more than emotionally neutral events. It is the bridge between autonomic nervous system and prefrontal cortex region.
-Phineas Gage got his left frontal lobe destroyed during railroad construction and lost his social intelligence and decision making skills but kept all other
cognitive abilities.