Musculoskeletal Flashcards
Major properties of muscle
contractility
excitability
extensibility
elasticity
contractility
Ability of a muscle to shorten, accompanied by mechanical force generation: role in movement
excitability
capacity of muscle to respond to a stimulus
extensibility
Muscle can be stretched to its normal resting
length and beyond to a limited degree
elasticity
Ability of muscle to recoil to original resting length after being stretched
qualities of skeletal muscle
Attached to bones
– Nuclei are multiple per cell and peripherally located
– Striated
– Under voluntary and involuntary (reflex) control
What bundles of muscle fibers called
fascicle
What are tendons
– Fibrous connective tissue that connects muscle fibers, containing the contractile apparatus, to bones
–Serve as elastic anchors
what is a synergist?
Separate muscles that work together to cause a movement around a joint
What is a agonist?
Muscle causing a particular action (e.g., flexion) when it contracts
What is a antagonist?
a muscle working in opposition to agonist; typically relaxes during contraction of agonist
passive tension is exerted by
tendons - elastic components lying in series and parallel to contractile elements (muscle fibers)
For shortening during contraction
non-contractile parts of a muscle (tendons and surrounding connective tissue) are taut, owing to their elasticity
The net force of contraction includes both the…..
the active (ATP-dependent) and passive (elastic) contributions to shortening
muscle types (fiber)
parallel and pennate
Parallel muscle types
fiber arrangement– parallel to the longitudinal axis of the muscle, e.g. biceps brachii, etc.
Pennate muscle type
fiber arrangement— fibers are at an angle to the longitudinal axis of the muscle, e.g. deltoid, etc
(generate greater force but less range of motion)
connective tissue ___ muscle fibers
surrounds
organize muscle fibers and provide a parallel components of elasticity
Know where these are
muscle fiber, artery, nerve, vein, capillary, synapase (neuromuscular junction), axon of motor neuron, sarcolemma
Morphology of a muscle cell
~0.1 mm in diameter and several cms in length (big!!)
• Cylindrical in shape with tapered ends
• Elongated nuclei
– Located at the periphery of cells
– Lie just underneath the sarcolemma (plasma membrane)
• Is described as a multinucleated syncytium due to
its developmental origin as a fused aggregate of progenitor cells
during developments myoblasts ….
fuse to become myotubes
myoblasts
1 nucleus
lacks myofibrils (contractile proteins)
myotubes
develop myofibrils and other organelles for contraction
skeletal muscle fiber is formed by the fusion of numerous mononucleated cells
Myofibrils
bundles of myofilaments packed within muscle fiber and are the contractile machinery
sarcomere
the fundamental contractile structure
understand this picture
mechanism of contraction
Thick and Thin filaments slide in opposite directions via repeated cycles of binding interactions, individually shortening the sarcomeres and thereby the entire fiber
describe Ca2+ induced cross-bridge formation using tropomyosin and troponin
In the absence of Ca2+, the thin filament protein tropomyosin (on the actin fiber) STOPS interaction between actin and myosin filaments
• Ca2+ binding to troponin (which is also on the actin fiber) promotes a change in the conformation of tropomyosin, allowing the myosin “head” access to its binding sites on actin
tropomyosin (and actin) is not about myosin until it gets a taste of ca2+ on its troponin site and then is obsessed
steps of muscle contraction in terms of cross-bridge and its relation to ATP
- cross-bridge not attached to actin (has hydrolyzed ADP)
- Ca2+ allows cross-bridge to bond with actin
- change of orientation and loss of ADP and P cause filaments to slide
- ATP binding to myosin (cross-bridge) and they release from actin
- ATP is hydrolyzed and waiting back to 1
Why does rigor mortis occur?
no ATP available for muscles to release and stop contracting
sarcomere shortening is accomplished by ….
sliding of interdigitated myofilaments during power strokes of myosin cross-bridges
this leads to overall shortening of the muscle
relative force is dependent upon the number of functional myosin heads attaching to actin filaments
during contraction… (filaments and sarcomeres)
a) Sarcomere length shortens
b) Thick filaments (A bands) remain the same length.
c) Distance between ends of thick filaments in adjacent sarcomeres(I bands) shorten.
d) Distance between ends of thin filaments within a sarcomere (H bands ) also shorten.
How does action potential work on muscle
Transmission of electrical signals along the length of motor neurons or muscle fibers is accomplished by the action potential, a rapid net re-distribution of ions across the plasma membrane,
driven by concentration gradients, which depolarizes the membrane along length of cell
resting membrane potential of motor neuron and muscle cell?
motor: -70mV
muscle: -90mV
Ion channels: 2 critical properties that dictate function
- gating (opening/closing in response to a signal)
- selective permeability (each ion channel is restrictive to a certain ion: Na+, K+ etc)
Phases of action potential (think of the neuro lecture) 4 steps
Resting potential – governed by Na+ and K+ gradients and relatively high resting permeability to K+; interior of cell relatively negative compared to outside
- depolarization – above a threshold value, Na+ channels open, allowing an influx (inward flow) of Na+; temporary overshoot into a reverse polarized state (interior positive)
- repolarization – voltage-gated K+ channels open, allowing an efflux of K+ (outward flow) and re-establishment of the resting potential
- hyperpolarization – overshoot of K+ efflux
Membrane excitability and propagation of action potential (5 steps)
Think of the pump train. moving a signal down a membrane when the one next to it opens - depolarize, repolarize, hyperpolarize, back to normal
- At rest, the sarcolemma (plasma membrane) is polarized, owing to the action of the Na+/K+ ATPase and other ion pumps that establish ion concentration gradients across the membrane.
- Activation of the ACh receptor (AChR), a ligand-gated Na+/K+ channel, allows net inward flow of Na+ and outflow of K+, causing a local depolarization of the plasma membrane.
- The local depolarization is sensed by adjacent voltage-gated Na+ channels, which open in response
to the change in membrane potential. The Na+ influx causes the depolarization to move laterally along the surface of the muscle fiber. - The spreading local depolarization is sensed by neighboring voltage-ga`ted Na+ channels, which open accordingly, propagating the signal along the length of the muscle fiber.
- Repolarization is accompanied by transient inactivation of the voltage-gated Na+ channels, rendering them temporarily refractory to opening thus ensuring unidirectional spread of the action potential.
Excitation-contraction coupling (ECC)
• Mechanism whereby an action potential causes
muscle fiber contraction
• Involves
–Sarcolemma (plasma membrane)
–“T tubules,” infoldings of the sarcolemma
–Sarcoplasmic reticulum, a Ca2+ reservoir within cells
–Ca2+, Troponin
Calcium channels involved in ECC
DHPR and RyR
DHPR- lives in sarcolemma/t tubule, opens due to depolarizAtion, activates ryr
RyR- lives in sarcoplasmic reticulum membrane, releases stored Ca2+
What is SERCA
the sarcoplasmic reticulumn Ca2+ ATPase
an ion pump protein that moves Ca2+ from the sarcoplasm into the SR and restores Ca2+ gradient to end contractile response
How can the magnitude of force produced in whole-muscle contraction be controlled? (3)
- Varying numbers of motor units recruited for a contraction.
- Controlling the rate of stimulation (‘summation of twitches’).
- Initial length of muscle fibers (‘length-tension relationship’)
force generated depends on number of fibers engaged in contraction
What is a motor unit?
a motor neuron plus all muscle fibers that it connects
What are graded contractions
produced by variations in the number of motor units activated (varying degrees of force)
What are innervation ratios?
(fibers per neuron) can vary based on functional requirements of muscle in question.
Effect of stimulation rate on force of contraction
Twitch’
–Stimulated by a single isolated electrical stimulus
–Generates a fractional force of contraction that decays as fiber relaxes
• Summation of twitches
–More frequent stimuli, each producing units of contractile force
–Next stimulus arrives before relaxation from previous stimulus is complete, allowing summation
• Tetanic contraction
–Frequency high enough to produce steady contraction (no opportunity for relaxation) and maximal force development
Length-tension relationship (in a isolated muscle fiber)
Force exerted depends on the number of myosin heads engaged in cross- bridge cycling with actin filaments
• The tension that a muscle generates varies with its length at the time a stimulus to contract is received
forms bell curve
(peak force occurs when there is maximum potential for overlap of thick and thin filaments…. greatest number of myosin head/actin interactions to occur)
why is muscle a major consumer of chemical energy and metabolites
• Cross-bridge recycling
• Pumping of Na+, K+, Ca2+ and other ions
• Synthesis of contractile proteins
Length- Tension relationship (in a muscle unit)
• Force generation capacity increases when the muscle is initially stretched
• The force generated by active sliding filaments is combined
with the shortening contributed by passive elastic components (tendons) that have been stretched
Stretch-Shortening Interactions
• When a muscle is stretched prior to contraction, the resulting contraction is more forceful than in the absence of a pre-stretch.
• Elastic recoil: the effect of the series elastic component of the actively stretched muscle
• Stretch reflex in muscle stretched to an extreme: via an autonomic nervous signal to contract and thus shorten, protecting the muscle tissue
3 types of skeletal fibers (most muscles have all 3)
Slow-oxidative fibers
Fast-oxidative fibers
Fast-glycolytic fibers
Fast fibers
high myosin ATPase activity, thus more rapid crossbridge cycling and high shortening velocity. Fatigue rapidly.
slow fibers
slow myosin ATPase activity and lower shortening velocity. Fatigue more slowly.
oxidative fibers
numerous mitochondria, high capacity of oxidative phosphorylation. ATP production dependent on blood borne oxygen and fuel; contain myoglobin, increases rate of oxygen capture in the fiber.
glycolytic fibers
have few mitochondria but a high concentration of glycolytic enzymes and glycogen (polymer of glucose stored as fuel reserve in skeletal muscle and liver). Larger and have more thick and thin filaments and therefore can develop more tension. Fatigue rapidly.
Effects of exercise on skeletal muscle
exercise increases:
– size (hypertrophy) of muscle fibers
– numbers of myofilaments
– capacity for ATP production
• Low intensity exercise affects oxidative fibers
- mitochondria and capillaries
• High intensity exercise affects glycolytic fibers
- diameter of actin and myosin and production of glycolytic enzymes
• Fiber types may be able to interconvert
• Fatigue is associated with energy (ATP) depletion, loss of efficiency in Ca2+ storage and release.
mechanisms of exercise-induced changes in skeletal muscle
loss of muscle fibers w/ age
muscles get bigger due to thickening of fibers and addition of myofibrils
mechanical stress on muscles activates genes to produce more myosin and actin and gain more nuclei
What is atrophy
muscle wasting or loss
due to inactivity, disease, aging
(depressed protein synthesis, enhanced proteolysis or both)
can be very detrimental
