Muscle

• •  

• Skeletal muscle anatomy ( Fig. 1.40)

  • Cellular anatomy

    • Sarcolemma: plasma membrane surrounding cell

      • Extends into cell surrounding myofibrils

         

         

         

        FIG. 1.39 Hemophilic arthropathy. (A) Recurrent knee effusions and synovitis. (B) Radiograph of end-stage

        arthropathy. (C) Synovial proliferation of hemophilic arthropathy demonstrates phagocytic (type A) synovial cells laden with iron pigment but no giant cells, polymorphonuclear leukocytes, and rare lymphocytes.

        (D) Bloody ankle effusion presentation of teen whose grandfather had a history of bleeding disorder. (E) End-stage hemophilic arthropathy of ankle demonstrates flattening of the talus (arrow).

        From Rodriguez-Merchan EC: Musculoskeletal complications of hemophilia, HSS J 6:37–42, 2010; Mainardi CL et al: Proliferative synovitis in hemophilia: biochemical and morphologic observations, Arthritis Rheum 21:137–144, 1978; photo courtesy Texas Orthopedics Sports Medicine and Rehabilitation; and Rodriguez-Merchan EC: Prevention of the musculoskeletal complications of hemophilia, Adv Prev Med 2012:201271, 2012.

         

      • 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.

      • 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

           

  • Gross anatomy

• 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)

    • Fascia (tough connective tissue) covers muscle and allows sliding.

    • Epimysium (more delicate) surrounds bundles of fascicles.

    • Perimysium surrounds individual muscle fascicles (hundred of muscle fibers).

    • Endomysium surrounds individual myofibers.

    • Stretch receptors

      • Muscle spindles: located within muscle, transmit muscle length to CNS, control muscle stiffness

      • Golgi tendon organ: located at musculotendinous junction, helps prevent excess tendon lengthening

    • Myotendinous junction

      • Often the site of tears with eccentric contraction (forced lengthening of the myotendinous junction during contraction), which places maximum stress across this area

      • Myofilament bundles are linked directly onto collagen fibrils, with sarcolemma filaments interdigitating with the basement membrane (type IV collagen) and tendon tissue (type I collagen).

 

 

FIG. 1.40 Skeletal muscle architecture.

From Brinker MR, Miller MD: Fundamentals of orthopaedics, Philadelphia, 1999, Saunders, p 10.

 

 

FIG. 1.41 Sarcoplasmic reticulum. Action potentials travel down the transverse tubules, causing release of calcium from the outer vesicles.

From DeLee JC et al, editors: DeLee and Drez’s orthopaedic sports medicine: principles and practice, ed 3, Philadelphia, 2009, Saunders.

 

 

 

Table 1.23

 

Sarcomere

 

 

Band Description
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

 

 

From Brinker MR, Miller MD: Fundamentals of orthopaedics, Philadelphia, 1999, Saunders, p 11.

 

 

FIG. 1.42 Structure of the adult motor end plate (neuromuscular junction). (A) Motor nerve.

(B) Nerve branches that innervate many individual muscle fibers. (C) Presynaptic boutons, which terminate on the muscle fiber. (D) Nerve terminal.

From Miller RD et al: Miller’s anesthesia, ed 7, Philadelphia, 2010, Churchill Livingstone.

 

• Muscle physiology

  • Motor unit

    • 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.

      • Agents affecting impulse transmission are listed in Table 1.24.

    • 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.

       

      Table 1.24

       

      Agents That Affect Neuromuscular Impulse Transmission

       

       

      Agents Site of Action Mechanism Effect
      Nondepolarizing drugs (curare, pancuronium, vecuronium)	Neuromuscular junction	Competitively bind to acetylcholine receptor to block impulse transmission	Paralytic agents (long term)
      Depolarizing drugs (succinylcholine)	Neuromuscular junction	Bind to acetylcholine receptor to cause temporary depolarization of muscle membrane	Paralytic agents (short term)
      Anticholinesterases (neostigmine, edrophonium)	Autonomic ganglia	Prevent breakdown of acetylcholine to enhance its effect	Reverse effects of nondepolarizing drugs; muscarinic effects (bronchospasm, bronchorrhea, bradycardia)

       

      Table 1.25

       

      Types of Muscle Contractions

       

       

      Type of Muscle Contraction	Definition	Example	Phases
      Isotonic	Muscle tension is constant throughout ROM. Muscle length changes throughout ROM. This is a measure of dynamic strength.	Biceps curls with free weights	Concentric contraction: Muscle shortens during contraction. Tension within muscle is proportional to externally applied load. Example of an isotonic concentric contraction is the curl (elbow moving toward increasing flexion) portion of a biceps curl. Eccentric contraction: Muscle lengthens during contraction (internal force < external force). Eccentric contractions are the most efficient way to strengthen muscle but have the greatest potential for high muscle tension and muscle injury. Example of an isotonic eccentric contraction is the negative (elbow moving toward increasing extension) portion of a biceps curl.
      Isometric	Muscle tension is generated, but muscle length remains unchanged. This is a measure of static strength.	Pushing against an immovable object (e.g., wall)
      Isokinetic	Muscle tension is generated as muscle maximally contracts at a constant velocity over a full ROM. Isokinetic exercises are best for maximizing strength and are a measure of dynamic strength.	Isokinetic exercises require special equipment (e.g., Cybex machine).	Concentric contraction Eccentric contraction

  • Types of muscle contractions are summarized in Table 1.25.

    • Muscle cross-sectional area is a reliable predictor of the potential for contractile force.

    • Muscle tension is determined by the contractile force generated.

    • Muscle contraction velocity is determined by fiber length.

      • A well-conditioned muscle may be able to fire more than 90% of its fibers simultaneously.

      • At any velocity, fast-twitch (type II) fibers produce more force.

    • Isokinetic exercises produce more strength gains than do isometric exercises (see Table 1.25).

    • Plyometric (“jumping”) exercises, the most efficient method of improving power, consist of a muscle stretch followed immediately by a rapid contraction.

    • Closed-chain exercise involves loading an extremity with the most distal segment stabilized or not moving, allowing for muscular cocontraction around a joint and minimizing joint shear (e.g., less stress on the ACL).

    • Open-chain exercise involves loading an extremity with the distal segment of the limb moving freely (e.g., biceps curls).

• Types of muscle fibers ( Table 1.26)

  • Subtypes are based on variability in myosin heavy chains

    • Type I

 

• Type II

• 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

   

• 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)

   

  Table 1.26

   

  Characteristics of Types of Human Skeletal Muscle Fibers

   

   

  Characteristic	Types
  	Type I Type IIA Type IIB
  	Red, slow- twitch Slow oxidative	White, fast-twitch Fast oxidative glycolytic	Fast glycolytic
  Speed of contraction	Slow	Fast	Fast
  Strength of contraction	Low	High	High
  Fatigability	Fatigue-resistant	Fatigable	Most fatigable
  Aerobic capacity	High	Medium	Low
  Anaerobic capacity	Low	Medium	High
  Motor unit size	Small	Larger	Largest
  Capillary density	High	High	Low

   

   

  From Simon SR, editor: Orthopaedic basic science, Rosemont, IL, 1994, American Academy of Orthopaedic Surgeons, p 100.

   

  • Rapid fatigue

  • Low intramuscular triglyceride stores

  • Two subtypes:

    • Type IIA is intermediate.

    • Type IIB is most fatigable and has highest anaerobic capacity.

• Energetics ( Fig. 1.43)

  • ATP–creatine phosphate (phosphagen) system

    • Converts stored carbohydrates to energy without the use of oxygen and without producing lactate.

    • Intense muscle activities lasting up to 20 seconds (sprinting)

    • 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.

  • Lactic anaerobic system (lactic acid metabolism)

    • Muscle glycogen and blood glucose anaerobically converted to ATP

    • Incomplete oxidation leads to excess pyruvate, which is

      converted to lactic acid (via lactate dehydrogenase)

    • Intense muscle activities lasting 20 to 120 seconds

  • Aerobic system

    • Aerobic oxidation of glycogen and fatty acids through Krebs cycle

    • Sustained exercise such as distance running

• Athletic training, injury, and adaptation

  • Training

    • 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

    • 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

    • 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)

         

         

         

        FIG. 1.43 Energy sources for muscle activity. CP,

        creatine phosphate.

        From Simon SR, editor: Orthopaedic basic science, Rosemont, IL, 1994, American Academy of Orthopaedic Surgeons, p 102.

         

      • Improves neural activation

    • Both endurance training and strength training delay the lactate response to exercise.

    • A significant decline in aerobic fitness (“detraining”) occurs

      after only 2 weeks of no training.

  • Denervation

    • Causes muscle atrophy and increased sensitivity to acetylcholine

    • Leads to spontaneous fibrillations at 2–4 weeks after injury

  • Immobilization

    • Accelerates granulation tissue response

    • Immobilization in lengthened positions decreases contractures and maintains strength.

    • Atrophy results from disuse or altered recruitment.

      • Muscles that cross a single joint atrophy faster (nonlinear fashion).

    • Sarcomeres at the myotendinous junction are especially affected

    • Electrical stimulation can help offset these effects.

  • Muscle strains

    • Most common sports injury

    • Most occur at the myotendinous junction.

    • Occur primarily in muscles crossing two joints (hamstring, gastrocnemius) that have increased type II fibers

    • Initially there is inflammation, and later, fibrosis mediated by TGF-β occurs.

    • Immobilization or rest for 3–5 days followed by progressive stretching and strengthening

  • Muscle tears

    • Most occur at the myotendinous junction (e.g., rectus femoris tear at anterior inferior iliac spine).

    • Often occur during a rapid (high-velocity) eccentric contraction

    • Satellite cells act as stem cells and are most responsible for muscle healing.

    • Alternatively, the defect can heal with bridging scar tissue. TGF-β stimulates proliferation of myofibroblasts and increases fibrosis.

    • Surgical repair of clean lacerations in the muscle midbelly usually results in minimal regeneration of muscle fibers distally, scar formation at the laceration, and recovery of about half the muscle strength.

    • Prevention of tears—muscle activation (through stretching) allows twice the energy absorption before failure.

  • DOMS

 

• This phenomenon occurs 24–72 hours after intense exercise.

• Associated with eccentric muscle contractions

• Most common in type IIB fibers

• Caused by edema and inflammation in the connective tissue, with a neutrophilic response present after acute muscle injury

• May be associated with changes in the I band of the sarcomere

• NSAIDs relieve DOMS in a dose-dependent manner.

• Other modalities (ice, stretching, ultrasonography, electrical stimulation) have not been shown to affect DOMS.