Fisiologi Otot Dan Kontrol Gerak
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Transcript of Fisiologi Otot Dan Kontrol Gerak
Muscle Physiology and movement controling
m d
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
8.3
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
8.4
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
8.6
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
8.22
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
8.27
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
8.30
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
8.35
Anatomy of the Basal Ganglia
8.36
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)
8.37
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
8.39
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
8.40