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Muscle Physiology and movement controling

Skeletal Muscle

Movements of our body are accomplished by contraction of the skeletal muscles


Flexion:

contraction of a flexor muscle draws in a limb Extension: contraction of extensor muscle


Skeletal muscle fibers have a striated appearance Skeletal muscle is composed of two fiber types:

Extrafusal: innervated by alpha-motoneurons from the spinal cord: exert force Intrafusal: sensory fibers that detect stretch of the muscle

Afferent fibers: report length of intrafusal: when stretched, the fibers stimulate the alpha-neuron that innervates the muscle fiber: maintains muscle tone Efferent fibers: contraction adjusts sensitivity of afferent fibers. 8.2

Skeletal Muscle Anatomy

Each muscle fiber consists of a bundle of myofibrils


Each

myofibril is made up of overlapping strands of actin and myosin During a muscle twitch, the myosin filaments move relative to the actin filaments, thereby shortening the muscle fiber

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Neuromuscular Junction

The neuromuscular junction is the synapse formed between an alpha motor neuron axon and a muscle fiber
Each

axon can form synapses with several muscle fibers (forming a motor unit) The precision of muscle control is related to motor unit size

Small: precise movements of the hand Large: movements of the leg

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ACh is the neuromuscular junction neurotransmitter


Release

of ACh produces a large endplate potential

Always cause muscle fiber to fire Voltage changes open CA++ channels

CA++

entry triggers myosin-actin interaction (rowing action)


CA++ as a cofactor that permits the myofibrils to extract energy from ATP

Movement

of myosin bridges shortens muscle fiber

Smooth and Cardiac Muscle

Smooth muscle is controlled by the autonomic nervous system


Multiunit

smooth muscle is normally inactive smooth muscle exhibits rhythmic contraction

Located in large arteries, around hair and in the eye Responds to neural or hormonal stimulation Muscle fibers produce spontaneous pacemaker potentials that elicit action potentials in adjacent smooth muscle fibers Single-unit muscle is found in gastrointestinal tract, uterus, small blood vessels

Single-unit

Cardiac muscle fibers resemble striated muscle in appearance, but exhibit rhythmic contractions like that of single-unit smooth muscle
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Creatine Phosphate

Molecule with stored ATP energy Creatine + ATP

Creatine phosphate + ADP

Motor Unit
All the muscle cells controlled by one nerve cell

Motor Unit Ratios

Back muscles
1:100

Finger muscles
1:10

Eye muscles
1:1

Muscle Fatique
Lack of oxygen causes ATP deficit Lactic acid builds up from anaerobic respiration

Muscle Atrophy
Weakening and shrinking of a muscle May be caused

Immobilization Loss

of neural stimulation

Muscle Hypertrophy

Enlargement of a muscle More capillaries More mitochondria Caused by


Strenuous

exercise Steroid hormones

Steroid Hormones

Stimulate muscle growth and hypertrophy

Muscle Tonus
Tightness of a muscle Some fibers always contracted

Tetany
Sustained contraction of a muscle Result of a rapid succession of nerve impulses

Tetanus

Refractory Period

Brief period of time in which muscle cells will not respond to a stimulus

Refractory

Refractory Periods

Skeletal Muscle

Cardiac Muscle

Isometric Contraction
Produces no movement Used in

Standing Sitting Posture

Isotonic Contraction
Produces movement Used in

Walking Moving

any part of the body

Muscle Sensory Feedback

Striated muscle contraction is governed by sensory feedback


Intrafusal

fibers are in parallel with extrafusal fibers Intrafusal receptors fire when the extrafusal muscle fibers lengthen (load on muscle)

Actually detect the length of muscle Intrafusal fibers activate agonist muscle fibers and inhibit antagonist muscle fibers Extrafusal contraction eliminates intrafusal firing

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Golgi

tendon organ (GTO) receptors are located within tendons


Sense degree of stretch on muscle GTO activation inhibits the agonist muscle (via release of glycine onto alpha-motoneuron GTO receptors function to prevent over-contraction of striated muscle

Spinal Cord Anatomy

Spinal cord is organized into dorsal and ventral aspects


Dorsal

horn receives incoming sensory information Ventral horn issues efferent fibers (alphamotoneurons) that innervate extrafusal fibers

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Spinal Cord Reflexes

Monosynaptic reflexes involve a single synapse between a sensory fiber from a muscle and an alpha-motor neuron
Sensory

fiber activation quickly activates the alpha motor neuron which contracts muscle fibers
Patellar reflex Monosynaptic stretch reflex in posture control

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Polysynaptic reflexes involve multiple synapses between sensory axons, interneurons, and motor neurons

Axons from the afferent muscle spindles can synapse onto


Alpha motoneuron connected to the agonist muscle An inhibitory interneuron connected to the antagonist muscle Signals from the muscle spindle activate the agonist and inhibit the antagonist muscle

Polysynaptic Reflex

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Motor Cortex

Multiple motor systems control body movements


Walking,

talking, postural, arm and finger movements

Primary motor cortex is located on the precentral gyrus


Motor

cortex is somatotopically organized (motor homunculus) Motor cortex receives input from

Premotor cortex Supplemental motor area Frontal association cortex Primary somatosensory cortex

Planning of movements involves the premotor cortex and the supplemental motor area which influence the primary 8.28 motor cortex

Motor Homunculus

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Cortical Control of Movement

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Descending Motor Pathways

Axons from primary motor cortex descend to the spinal cord via two groups
Lateral

group: controls independent limb movements


Corticospinal tract: hand/finger movements Corticobulbar tract: movements of face, neck, tongue, eye Rubrospinal tract: fore- and hind-limb muscles

Ventromedial

group control gross limb movements

Vestibulospinal tract: control of posture Tectospinal tract: coordinate eye and head/trunk movements Reticulospinal tract: walking, sneezing, muscle tone 8.31 Ventral corticospinal tract: muscles of upper leg/trunk

Corticospinal Tract

Neurons of the corticospinal tract terminate on motor neurons within the gray matter of the spinal cord

Corticospinal tract starts in layer 5 of primary motor cortex Passes through the cerebral peduncles of the midbrain Corticospinal neurons decussate (crossover ) in the medulla

80% become the lat. corticospinal tract 20% become the ventral corticospinal tract

Terminate onto internuncial neurons or alphamotoneurons of ventral horn


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Corticospinal tracts control fine movements


Destruction: loss of muscle strength, reduced dexterity of hands and fingers No effect of corticospinal lesions on posture or use of limbs for reaching

The Apraxias

Apraxia refers to an inability to properly execute a learned skilled movement following brain damage
Limb

apraxia involves movement of the wrong portion of a limb, incorrect movement of the correct limb part, or an incorrect sequence of movements

Callosal apraxia: person cannot perform movement of left hand to a verbal request (anterior callosum interruption prevents information from reaching right hemisphere) Sympathetic apraxia: damage to anterior left hemisphere causes apraxia of the left arm (as well as paralysis of right arm and hand) Left parietal apraxia: difficulty in initiating movements to verbal request

Constructional

damage

apraxia is caused by right parietal lobe

Person has difficulty with drawing pictures or assembling objects 8.34

The Basal Ganglia

Basal ganglia consist of the caudate nucleus, the putamen and the globus pallidus
Input

to the basal ganglia is from the primary motor cortex and the substantia nigra Output of the basal ganglia is to

Primary motor cortex, supplemental motor area, premotor cortex Brainstem motor nuclei (ventromedial pathways)

Cortical-basal

ganglia loop

Frontal, parietal, temporal cortex send axons to caudate/putamen Caudate/putamen projects to the globus pallidus Globus pallidus projects back to motor cortex via thalamic nuclei 8.35

Anatomy of the Basal Ganglia

8.36

Parkinsons Disease

Parkinsons disease (PD) involves muscle rigidity, resting tremor, slow movements

Parkinsons results from damage to dopamine neurons within the nigrostriatal bundle (projects to caudate and putamen) Slow movements and postural problems result from

Loss of excitatory input to the direct circuit (caudate-Gpi-VA/VL thalamus-motor cortex) Loss of output from the indirect circuit (which is overall an excitatory circuit for motor behavior)

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Neurological treatments for PD:


Transplants of dopamine-secreting neurons (fetal subtantia nigra cells or cells from the carotid body) Stereotaxic lesions of the globus pallidus (internal division) alleviates some symptoms of Parkinsons disease Electrode implants

Huntingtons Disease

Huntingtons disease (HD) involves uncontrollable, jerky movements of the limbs


HD

is caused by degeneration of the caudate nucleus and putamen Cell loss involves GABA-secreting axons that innervate the external division of the globus pallidus (GPe) The GPe cells increase their activity, which inhibits the activity of the subthalamic nucleus, which reduces the activity level of the GPi, resulting in excessive movements

HD is a hereditary disorder caused by a dominant gene on chromosome 4

This gene produces a faulty version of the protein huntingtin


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The Cerebellum

Cerebellum consists of two hemispheres with associated deep nuclei


Flocculonodular

cerebellum

lobe is located at the caudal aspect of the

This lobe has inputs and outputs to the vestibular system Involved in control of posture

Vermis

is located on the midline of the cerebellum

Receives auditory and visual information from the tectum and cutaneous information from the spinal cord Vermis projects to the fastigial nucleus which in turn projects to the vestibular nucleus and to brainstem motor nuclei

Damage to the cerebellum generally results in jerky, erratic and uncoordinated movements
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