Muscle Physiology and movement controling

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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.

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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

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

Located in large arteries, around hair and in the eye Responds to neural or hormonal stimulation

Single-unit smooth muscle exhibits rhythmic contraction 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 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 + ATPCreatine phosphate + ADP

Motor UnitAll 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

ImmobilizationLoss 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

Skeletal Muscle Cardiac Muscle

Refractory Periods

Isometric Contraction Produces no movement Used in

StandingSittingPosture

Isotonic Contraction Produces movement Used in

WalkingMoving any part of the body

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

Muscle Sensory Feedback

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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 (alpha-motoneurons) that innervate extrafusal fibers 8.24

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 motor cortex

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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 groupsLateral 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 Ventral corticospinal tract: muscles of upper leg/trunk

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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 alpha-motoneurons 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 apraxia is caused by right parietal lobe damage

Person has difficulty with drawing pictures or assembling objects

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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

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Anatomy of the Basal Ganglia

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Parkinson’s disease (PD) involves muscle rigidity, resting tremor, slow movements Parkinson’s 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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Parkinson’s Disease

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 Parkinson’s disease

Electrode implants

Huntington’s Disease

Huntington’s 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 lobe is located at the caudal aspect of the cerebellum

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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