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Flashcards in Miller-Tendon/muscle Deck (34)
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1

Review skeletal muscle architecture

2

Review the sarcomere

A band: Contains actin and myosin

I band: Contains actin only

H band: Contains myosin only

M line: Interconnecting site of the thick filaments

Z line: Anchors the thin filaments

3

Review muscle anatomy

Sarcolemma: plasma membrane surrounding cell

Extends into cell surrounding myofibrils

Forms the transverse tubules (Fig. 1.41).

Multiple nuclei: typically located adjacent to sarcolemma

Sarcoplasmic reticulum (SR)

Smooth endoplasmic reticulum that surrounds the individual myofibrils

Stores calcium in intracellular membrane–bound channels.

Ryanodine receptors (e.g., RYR-1) regulate the release of calcium from the SR and serve as a connection between the SR and sarcolemma-derived transverse tubule.

Abnormality of ryanodine receptors is implicated in persons susceptible to malignant hyperthermia.

Dantrolene decreases loss of calcium from the SR.

Contractile elements

Sarcomere: basic functional unit of muscle contraction

Myofibrils

Set of sarcomeres parallel to axis of cell

(1–3 μm in diameter and 1μ2 cm long)

Sarcomere organization causes the banding pattern (striations) seen in skeletal muscle (Table 1.23; see Fig. 1.40).

Costamere connects the sarcomere to the sarcolemma at the Z disc.

4

What is the sarcoplasmic reticulum?

Sarcoplasmic reticulum. Action potentials travel down the transverse tubules, causing release of calcium from the outer vesicles.

5

review muscle contracture

Contractile elements

Sarcomere: basic functional unit of muscle contraction

Myofibrils

Set of sarcomeres parallel to axis of cell

(1–3 μm in diameter and 1μ2 cm long)

Sarcomere organization causes the banding pattern (striations) seen in skeletal muscle (Table 1.23; see Fig. 1.40).

Costamere connects the sarcomere to the sarcolemma at the Z disc.

Z disc (or line) represents terminus of sarcomere

Contains desmin, α-actinin, and filamin

A-band (or dark band) represents thick filaments.

Thick filaments composed of myosin

Also contains myosin [H-band], M protein, C protein, titin, and creatine kinase

I-band represents thin filaments.

Primarily composed of actin

Also contains

Troponin: has binding site for Ca

Tropomyosin: prevents myosin-actin interaction

Attach to Z disc

Involved in delayed-onset muscle soreness (DOMS)

6

review the gross anatomy of muscle:

Contractile elements

Sarcomere: basic functional unit of muscle contraction

Myofibrils

Set of sarcomeres parallel to axis of cell

(1–3 μm in diameter and 1μ2 cm long)

Sarcomere organization causes the banding pattern (striations) seen in skeletal muscle (Table 1.23; see Fig. 1.40).

Costamere connects the sarcomere to the sarcolemma at the Z disc.

Z disc (or line) represents terminus of sarcomere

Contains desmin, α-actinin, and filamin

A-band (or dark band) represents thick filaments.

Thick filaments composed of myosin

Also contains myosin [H-band], M protein, C protein, titin, and creatine kinase

I-band represents thin filaments.

Primarily composed of actin

Also contains

Troponin: has binding site for Ca

Tropomyosin: prevents myosin-actin interaction

Attach to Z disc

Involved in delayed-onset muscle soreness (DOMS)

7

review the motor endplate

The α-motoneuron and the myofibers it innervates

Each myofiber is innervated by a single axon but an axon can innervate multiple myofibers

Smaller and more delicate muscles have fewer myofibers per motor unit (<5 fibers per unit in extraocular muscles but as many as 1800 fibers per unit in gastrocnemius muscle)

Contraction

Response to mechanical or electrochemical stimuli generated at the motor end plate (neuromuscular junction) where the axon contacts an individual myofiber (Fig. 1.42).

Depolarization reaches motor neuron axon terminal, and acetylcholine (ACh) is released from presynaptic vesicles.

ACh diffuses across the synaptic cleft (50 nm) and binds to postsynaptic receptors on sarcolemma, which begin depolarization.

Myasthenia gravis is due to IgG antibodies to the Ach receptor. Manifests initially as ptosis and diplopia. Weakness worse with muscle use.

Botulinum A injections reduce spasticity by blocking presynaptic acetylcholine release. Commonly used for spastic muscles in cerebral palsy.

Sarcoplasmic reticulum releases calcium.

Ca binds to troponin and causes conformational change, which stops tropomyosin inhibition of myosin-actin cross-bridges.

Myosin binds to actin, hydrolyzes ATP, and “pushes” actin on thin filament, leading to muscle contraction

8

isometric

muscle length remains unchanged

 

planks

9

isokinetic

Muscle tension is generated as muscle maximally contracts at a constant velocity over a full ROM.

 

best for maximizing strength

10

isotonic 

Muscle tension is constant

 

i.e biceps curls

11

what is the cause of myathenia gravis?

Myasthenia gravis is due to IgG antibodies to the Ach receptor. Manifests initially as ptosis and diplopia. Weakness worse with muscle use.

12

Type 1 muscle fibers

Type I

Slow-twitch, oxidative, “red” fibers (mnemonic: “slow red ox”)

Aerobic

Have more mitochondria, enzymes, and triglycerides (energy source) than type II fibers

Low concentrations of glycogen and glycolytic enzymes (ATPase)

Enable performing endurance activities, posture, balance

Are the first lost without rehabilitation

13

type II muscle fibers

Fast-twitch, glycolytic, “white” fibers

Anaerobic

Contract more quickly and have larger, stronger motor units (increased ATPase) than type I fibers

Less efficient than type I but with large amount of force per cross-sectional area, high contraction speeds, and quick relaxation times

Well suited for high-intensity, short-duration activities (e.g., sprinting)

Rapid fatigue

Low intramuscular triglyceride stores

Two subtypes:

Type IIA is intermediate.

Type IIB is most fatigable and has highest anaerobic capacity.

14

review the energy source for muscle

15

review strength training

Strength training—increased tension and decreased repetitions

Induces hypertrophy (increased cross-sectional area) of fast-twitch (type II) fibers

Induces myofibrillar muscle protein synthesis (MPS)

Improves neural activation

16

review endurance training

decreased tension and increased repetitions

Induces hypertrophy of slow-twitch fibers

Increases capillary density, mitochondria, and oxidative capacity

Increases resistance to fatigue and cardiac output

Improves blood lipid profiles

17

which athletes have which kind of muscles?

Specific training can selectively alter fiber composition.

Endurance athletes—higher percentage of slow-twitch fibers

Sprinters and athletes in “strength” sports—higher percentage of fast-twitch fibers

18

review creatine

Creatine supplementation can increase work produced in the first few maximum-effort anaerobic trials but does not increase peak force production.

Creatine shifts fluid intracellularly; the shift may present a risk for dehydration, although cramps are the more common side effect.

19

what is decorin?

Decorin—most predominant proteoglycan in tendons. Regulates tendon diameter and provides cross-links between collagen fibers. Also shown to have antifibrotic properties via inhibition of TGF-β1.

20

tgf-b and muscle injury

TGF-β stimulates proliferation of myofibroblasts and increases fibrosis

21

review the stages of tendon healing

Three stages of tendon healing

Inflammation

Hematoma formation following by resorption

Type III collagen is produced at the injury site by tenocytes.

Weakest stage of repair

Proliferation: maximal type III collagen production

Remodeling:

Begins at 6 weeks

Decreases cellularity

Type I collagen predominates

Two mechanisms:

Intrinsic: recruitment of local stem/progenitor cells from endotenon and epitenon

Extrinsic: cells from surrounding tissue invade damaged area.

Faster but primary source of adhesions

Achilles, patellar, and supraspinatus tendons are prone to rupture at hypovascular areas.

Achilles tendon is hypovascular 4–6 cm proximal to calcaneal insertion.

Responsive to different cytokines and growth factors

PDGF genes transfected into tenocytes show collagen formation.

VEGF genes transfected into tenocytes show TGF-βupregulation and adhesion formation.

When exposed to PMNs (as with inflammation), tenocytes upregulate genes for inflammatory cytokines, TGF-β, and MMPs while suppressing type I collagen expression.

Surgical tendon repairs: weakest at 7–10 days

Maximum strength achieved at 6 months, reaching two-thirds of original strength.

No evidence in favor of a trough (exposing tendon to cancellous bone) over direct repair to cortical bone.

Motion and mechanical loading have beneficial effects on tenocyte function.

Immobilization decreases strength at tendon-bone interface.

22

review the mechanical properties of tendons

Anisotropic: properties vary depending on direction of applied force

Viscoelastic: properties vary depending on rate of force application

Creep: increasing deformation under constant load

Stress relaxation: decreasing stress with constant deformation (elongation)

Hysteresis: during loading and unloading, the unloading curve is different from the loading curve. The difference between the two represents the amount of energy that is lost during loading.

Stress-strain curve

Rest: collagen fibers are “crimped.”

Toe region: flattening of crimp; nonlinear; tendon stretched easily

Linear region: intermediate loads

Failure

23

surgical tendon repair pearls

Surgical tendon repairs: weakest at 7–10 days

Maximum strength achieved at 6 months, reaching two-thirds of original strength.

No evidence in favor of a trough (exposing tendon to cancellous bone) over direct repair to cortical bone.

Motion and mechanical loading have beneficial effects on tenocyte function.

Immobilization decreases strength at tendon-bone interface.

24

ligament overview

Characteristics

Originates and inserts on bone

Stabilizes joints and prevents displacement of bones

Contains mechanoreceptors and nerve endings that facilitate joint proprioception

Like tendon, displays viscoelastic behavior

Structure and composition

Composition

Similar to that of tendon

Water: 60%–70% of total weight

Collagen: 80% of dry weight

90% type I collagen; also types III, V, VI, XI, and XIV collagen

More collagen type I is seen at the origin and insertion, with collagen III seen midsubstance.

Elastin (1% dry weight)

Proteoglycans (1% dry weight)—function in water retention and contribute to viscoelastic behavior

Fibroblast

Primary cell, oriented longitudinally

Functions to synthesize ECM, collagen, and proteoglycans

Epiligament

Similar to that in epitenon; carries the neurovascular and lymphatic supply of tendons

Compared with tendon

Less total collagen but more type III collagen

More proteoglycans and therefore more water

Less organized collagen fibers that are more highly cross-linked and intertwined

“Uniform microvascularity”—receives supply at insertion site by the epiligamentous plexus

Insertion

Similar to that of tendon

Direct (fibrocartilaginous) insertion

Four layers: tendon, fibrocartilage, mineralized fibrocartilage, and bone

More common

Deep fibers attach at 90-degree angles

Indirect

Superficial fibers insert into the periosteum and deep fibers insert into bone via Sharpey fibers (perforating calcified collagen fibers).

25

ligament injury

Knee and ankle ligaments are most commonly injured

Ligaments do not plastically deform.

They “break, not bend.”

Midsubstance ligament tears are common in adults.

Avulsion injuries are more common in children.

Typically occurs between unmineralized and mineralized fibrocartilage layers

Healing

Increased number of collagen fibers but

Fewer mature cross-links (45% of normal at 1 year)

Decrease in mass and diameter

Three phases, as in bone

Inflammatory—early acute mediators (PMNs and then macrophages), with production of type III collagen and growth factors

Proliferative—around 1–3 weeks, with replacement of type III collagen by type I collagen (Think of macrophages as weakening the structure—weakest point.)

Remodeling and maturation

Factors that impair ligament healing

Intraarticular ligamentous injury

Old age, smoking, NSAID use

Diabetes mellitus

Alcohol use

Local injection of corticosteroids

Factors that improve ligament healing experimentally

Extraarticular ligamentous injury

Compromised immunity

IL-10 (antiinflammatory)

IL-1 receptor antagonists

Mesenchymal stem cells

Scaffolds (such as collagen–platelet-rich plasma hydrogels)

Neuropeptides

Calcitonin gene–related peptide

Immobilization

Adversely affects ligament strength: elastic modulus decreases

In rabbits, breaking strength reduced dramatically (66%) after 9 weeks of immobilization.

Effects reverse slowly upon remobilization.

Prolonged immobilization disrupts collagen structure, which may not return to normal within insertion sites.

Exercise

Improves mechanical and structural properties

Increases strength, stiffness, and failure load

26

Review intervertebral disks

Allow spinal motion and stability

Also function as cushioning for axial loads on the spine

Two components

Central nucleus pulposus

Derived from notochord

Hydrated gel with compressibility

Low collagen (type II)/high proteoglycan (and glycosaminoglycan) content

Proteoglycans make up higher percentage of dry weight.

With time, the nucleus pulposus undergoes loss of proteoglycans and water (desiccation).

Surrounding annulus fibrosis

Derived from mesoderm

Extensibility and increased tensile strength

High collagen (type I)/low proteoglycan content

Proteoglycans make up lower percentage of dry weight.

Superficial layer contains nerve fibers.

Composition:

Water (85%)

Proteoglycans

Type II collagen (20% of dry weight) in the nucleus pulposus

Type I collagen (60% of dry weight) in the annulus fibrosis

Neurovascularity

Dorsal root ganglion gives rise to the sinuvertebral nerve, which then innervates the superficial fibers of the annulus.

Avascular—nutrients and fluid diffuse from the vertebral end plates. This diffusion is impaired by calcification with aging.

Aging disc

Early degenerative disc disease is an irreversible process, with IL-1β stimulating the release of MMPs, nitric oxide, IL-6, and prostaglandin E2 (PGE2).

Decreased water content and conversion to fibrocartilage

A result of decreased hydrostatic pressure due to fewer large proteoglycans (aggrecan)

Fibronectin cleavage or fragmentation is also associated with degeneration.

Increase in keratan sulfate concentration and decrease in chondroitin sulfate

Increase in relative collagen concentration, with no change in absolute quantity

27

review the aging intervertebral disk

Early degenerative disc disease is an irreversible process, with IL-1β stimulating the release of MMPs, nitric oxide, IL-6, and prostaglandin E2 (PGE2).

Decreased water content and conversion to fibrocartilage

A result of decreased hydrostatic pressure due to fewer large proteoglycans (aggrecan)

Fibronectin cleavage or fragmentation is also associated with degeneration.

Increase in keratan sulfate concentration and decrease in chondroitin sulfate

Increase in relative collagen concentration, with no change in absolute quantity

Avascular—nutrients and fluid diffuse from the vertebral end plates. This diffusion is impaired by calcification with aging.

28

where is the annulus fibrosis derived from?

mesoderm

29

where is the central nucleus derived from?

Central nucleus pulposus

30

review nerve architecture