Physiology Muscles
Terms
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- Long cells attached to bone (usually at both ends [the tongue is an exception]). The cells of a given muscle require activation by the nervous system and total force reflects the sum of the forces developed by activated cells.
- Skeletal muscle
-
walls of hollow organs: regulation of the internal environment.
regulated by the autonomic nervous system and many hormones,
directly communicate with one another and are capable of contracting without direct neural innervation. - Smooth muscle
- muscle type bridges the characteristics of skeletal and smooth muscles—it forms a hollow organ that contracts as a unit with autonomic and hormonal control, yet the cells have the microscopic characteristics of skeletal muscle.
- Cardiac muscle
-
connective tissue sheath: epimysium, fascicles each surrounded by perimysium
Muscle fibers are composed of myofibrils - Skeletal muscle
- Myofibrils are made up of _______.
- myofilaments
-
myofilaments organized into
________. - sarcomeres
- myofilaments are divided into ______.
-
Thick filament: myosin
Thin filament: actin - the basic unit of contraction in the skeletal muscle
- sarcomere:
- Sarcomere boundary:
- Z line
- Center of the sarcomere:
- M line at center of the H zone of the A band (made up of thick filaments)
- Edge of sarcomere:
- I band (made up of thin filaments
- Thick filament: consist of?
-
300-400 myosin molecules
1. Rod shaped portion (tail)
2. Double globular head portion - Thin filament: consist of
-
2 chains of actin molecules
1. Tropomyosin
2. Troponin (3 subunits) - Crossbridge formation:
- myosin heads interact with actin forming a link that allows contraction of the sarcomere according to the sliding filament hypothesis.
- internal membranes of a muscle fiber
-
Sarcolemma
Triad: t-tubules - Structure of cardiac muscle
-
Striated
Intercalated disc: specialized connection between cells: functional synctium - acts as 1 cell because of gap junctions and desmosomes - Structure of smooth muscle
-
1. Typically form layers around hollow organs, contraction causes reduction in diameter of organ (e.g., arteriole).
2. Not striated. No z-disks, thin filaments attached to dense bodies in the myoplasm.
3. Cell-to-cell contacts: functional and mechanical linkage via gap junctions, low resistance pathways for spread of action potentials and low-molecular weight substances.
4. No t-tubule system. Cells are small, Ca++ diffuses from extracellular fluid via channels in the sarcoplasmic reticulum. -
sliding filament hypothesis
o Length of A bands stays constant but length of I bands (thin filament areas)_____ as the muscle contracts - shortens
-
sliding filament hypothesis o Length of thick and thin filaments remains constant during contraction
o Therefore, changes in overlap between the two fiber types must occur: the _____filaments slide toward the M line - thin
-
sliding filament hypothesis
o Small amount of _______in each sarcomere adds up to large contraction of muscle fiber - shortening
- sliding filament theory: shows that some overlap of thick and thin filaments is needed for crossbridges to form and force to be generated
- Isometric length-tension curve supports
-
Steps in contraction of skeletal muscle
Discharge of a motor neuron - Step 1
-
Steps in contraction of skeletal muscle
Release of transmitter (_____ at the motor end-plate (neuromuscular junction or myoneural junction) - acetylcholine
-
Steps in contraction of skeletal muscle
Binding of acetylcholine to ___________receptors - nicotinic acetylcholine
-
Steps in contraction of skeletal muscle
Increased __ and __conductances in end-plate membrane - Na+& K+
-
Steps in contraction of skeletal muscle
Generation of ______potential - end-plate
-
Steps in contraction of skeletal muscle
generation of_____ in muscle fibers - action potential
- Steps in contraction of skeletal muscle Inward spread of _____along t-tubules
- depolarization
- Release of___ from the terminal cisterns of sarcoplasmic reticulum and diffusion to thick and thin filaments
- Ca++
- Steps in contraction of skeletal muscle Binding of_____ to __, uncovering myosin binding sites on actin
-
Ca++
troponin C - Steps in muscle contraction Initiation of crossbridge cycles (as long as ATP and Ca++ are present), resulting in the pulling of______ further into the myosin filament array, resulting in contraction of the fiber
- actin filaments
-
Steps in relaxation
____ pumped back into sarcoplasmic reticulum - Ca++
-
Steps in relaxation
Release of Ca++ from ______ - troponin
-
Steps in relaxation
cessation of interaction between ________. - actin and myosin
- ____ is depleted, crossbridges cannot detach and muscle cannot relax
- ATP
- - increase in force with no change in length
- Isometric
- change in length with no change in tension
- Isotonic -
- increase force sufficient to start lift, shortening occurs isotonicall
- . Mixed -
- - single response to stimulus
- Twitch
- - increase in force generated due to summation of contractions
- Tetanus
- Red: color due to content_______; tends to use oxidative metabolism for production of ATP
- myoglobin
- Type I:_____ contraction velocity, high myoglobin content, small fiber diameter, small motor unit size, early recruitment during movement; found in greatest numbers in postural muscles
- slow
- Type IIA:____ contraction velocity, high myoglobin capacity, intermediate glycolytic capacity, intermediate fiber diameter, motor unit size and recruitment order; medium endurance, found in mixed fiber muscles; relatively infrequent in humans
- fast
- White: color due to lack of _____ , used glycolysis for ATP production (anaerobic)
- myoglobin
- Type IIB: ____ contraction velocity, high glycolytic capacity, large fiber diameter, large motor unit size and late recruitment order; found in muscles used for rapid, powerful movements (eye, hand); fatigue quickly
- fast
- Number and type of muscle fibers begins to be established_______.
- before birth and becomes set in childhood
- Endurance training: primarily affectss _________ - increase myoglobin
- slow fiber
- high intensity training (weight lifting): primarily affects __________ fibers -
- glycolytic
- ANS innervation via varicosities and sensitive to hormones
- Smooth muscle
- Phasic: contract rhythmically or intermittantly (e.g., in the walls of the gastrointestinal or urinary systems).
- Smooth muscle
- Typically contract in response to action potentials that pass from cell to cell.
- Smooth muscle
- continuously active (e.g. smooth muscles in sphincters and in the walls of blood vessels). Tone is not usually associated with action potentials but is related to membrane potential.
- Tonic:
- affected by ANS and hormones Pacemaker activity in absence of innervation
- Cardiac muscle:
- autoimmune disease affecting ACH receptors
- Myasthenia gravis:
- number of diseases, usually Duchenne muscular dystrophy; genetic defect causing gradual degeneration of muscle fibers and early death
- Muscular dystrophy:
- Genetic disorder in which individuals have a mutant form of the Ca++ release channel on the sarcoplasmic reticulum.
- Malignant hyperthermia:
- muscle fibers which are surrounded by _________.
- endomysium
- muscle fiber contains bundles of filaments called
- myofibrils
- Muscle fibers are grouped together into fascicles and are then surrounded by a connective tissue called
- perimysium
- Has thick and thin filaments that are not arranged in sarcomeres and they appear homogenous and not striated
- Smooth muscle:
- forms layers around hollow organs and can be circumferential and longitudinal
- Smooth muscle
- __________muscle fibers have branching interconnections and the myocardial fibers are separated by sarcolemmas with intercalated disks, thus causing an all or nothing response to stimulus.
- Cardiac
- _________system to exchange substances between capillary blood and myocardial cells
- transverse (T)-tubular
- How does Ca++ get to the interior of muscle fibers?
- SR & T-tubules
- How does Ca++ regulate crossbridge formation between actin and myosin?
- The amount of Calcium that gets released from the SR which binds with Troponin-C
- What differences exist in the handling of Ca++ between skeletal and smooth muscle?
- Smooth Lack a T-tubule system for delivery of Ca+. the intracellular calcium concentration , and hence contract smooth muscle, without changing the membrane potential.
- what symptoms of myasthenia gravis?
-
Aggravating factors:
⬢ Systemic disease: Infections; Thyroid
⬢ Emotional stress
⬢ Person often has a recent history of recurring upper respiratory tract infections
⬢ Clinical manifestations may first appear during pregnancy, during the postpartum period, or in conjunction with the administration of certain anesthetic agents
⬢ Medications - Current Therapies to tx myasthenia gravis?
- ⬢Anticholinesterase drugs, steroids,immunosuppressants ⬢Plasmapheresis, thymectomy
- Diagnosis of myasthenia gravis is made on basis of a response to this medication?
- edrophonium chloride (Tensilon
- 13. What are the causes of muscular dystrophy
- a group of genetically determined degenerated disorders
- What is most common form of muscular dystrophy
- Duchenne muscle dystrophy is the most common. The most prevalent of the muscle diseases in childhood
- What are the Symptoms of muscular dystrophy?
-
Symptoms:
Progressive, symmetric weakness and wasting of skeletal muscle.
Muscle cells show necrosis and phagocytosis, and fibers are eventually replaced with fat and connective tissues -
Pseudohypertrophic (Duchenne)
Characteristics -
⬢ X-linked recessive
⬢ Elevated serum enzymes (CPK, LDH, AST)
⬢ Rapid progression
⬢ Frequent mental retardation - Characteristics Facioscapulohumeral MD.
-
⬢ Autosomal dominant
⬢ Several distinct muscle pathologies
⬢ Moderate rate of progression
⬢ Occasional mental retardation - Characteristics Limb Girdle MD.
-
⬢ Poorly defined or recessive
⬢ Collection of several disease
⬢ Variable rate of progression
⬢ Variable mental retardation - Are Therapies for MD Effective?
- No effective treatment for Duchenne muscular dystrophy
- . What are the causes of malignant hyperthermia?
- mutant form of the Ca++ release channel on the sarcoplasmic reticulum)
- What are current malignant hyperthermia therapies and are they effective?
-
⬢Dantrolene: 2mg/kg IV q 5 minutes to a total of 10mg/kg
⬢Hyperventilation: Sodium bicarbonate; Cooling
⬢Discontinue anesthesia
⬢Maintain urine output: 2ml/kg/hr
⬢Avoid calcium, Calcium antagonists, beta blockers - What are the symptoms of malignant hyperthermia?
- Symptoms resemble those of coma- unconsciousness, absent reflexes, fixed pupils, apnea and a flat electroencephalogram (sometimes). Oliguria and anuria are common
- How does ALS (amyotrophic lateral sclerosis) cause paralysis of skeletal muscles?
- Causes paralysis when there is an interruption of the normal innervation of muscle, scarring of the corticospinal tract in the lateral column of the spinal cord, refers to the upper motor neuron and eventually neuron dies.
- How does polio cause paralysis of skeletal muscles?
- virus being neurotrophic infiltrates the motor neurons of the anterior horn of the spinal cord, though it can also attack the spinal ganglia, cranial nerves, and motor nuclei, and this causes the paralysis
- What do t-tubules do in relation to the muscle cell action potential?
- t-tubules then, draw or transmit the electrical activity into the depths of the muscle fiber.
- What do t-tubules do in relation to Ca++ and excitation-contraction coupling?
- action potential is transmitted along the sarcolemma of the muscle fiber and down the t-tubules, Ca++ is released from the cisternae SR into the myoplasm. This release of Ca++ from the SR raises the intracellular Ca++ concentration, which in turn promotes actin-myosin interaction and contraction.
- You should understand the molecular basis for the sliding filament hypothesis. How is force created?
- the number of myosin on the thick filament interact with actin on the thin filament.
- How does shortening occur? (sliding filament hypothesis)
- Shortening occurs as the thin filament gets pulled toward the middle of the sarcome.
- . What is the significance of the amount of overlap of thick and thin filaments? (sliding filament hypothesis
- The overlap of the two filaments allows for the myosin and actin to interact. With the more overlapping you have a better chance of more myosin interacting and causing a greater force of contraction.