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• Biomechanics


  Plays an important role in understanding the functional importance of macro and microstructural factors of the muscle-tendon unit
• Most general concepts about human movement, such as muscle strength or range of motion, depend on many biomechanical factors that interact to determine how movement is affected
• Muscle forces


  The basic internal motors and brakes for human movement
• Sliding Filament Theory


  1. No interaction between myosin and actin at rest

  2. Calcium into the cell when the muscle is stimulated input increases

  3. Combining calcium with troponin C opens hotspots on actin that are blocked by the troponin tropomyosin complex

  4. Myosin heads bind to actin, actin- myosin cross bridges are built

  5. ATPase enzyme at the myosin head breaks down ATP

  6. The energy released causes the myosin heads to bend (power stroke)

  7. Thin filaments are pulled to the middle

  8. ATP is resynthesized and the myosin head binds to a new hotspot and coils

  9. During the relaxation process, calcium within the cell is pumped back into the sarcoplasmic reticulum by active transport

  10. From the SR, Ca diffuses into the terminal cisterns and is stored there until the next action potential

  11. The hotspots close, the cruciate clavicles dissolve, and the muscle relaxes

  12. The length of the muscle is shortened by 1% during each attachment and detachment event

  13. Each thick filament contains approximately 500 myosin heads

  14. In a rapid contraction, the myosin heads repeat the same process about five times per second

  
• Motor unit


  It includes a motor neuron and all the muscle fibers it innervates
• Each muscle fiber must be connected to a motor nerve ending
• One motor nerve fiber can simultaneously stimulate many muscle fibers
• A human motor unit may consist of 6-30 muscle fibers (eye muscles), or may consist of more than 1000 muscle fibers (strong leg muscles)
• Resting membrane potential of skeletal muscle

  • 90 mV
• Action potential duration


  1. 4 ms
• Action potential propagation speed

  5 m/s
• Depolarization phase


  Entry of Na into the cell
• Repolarization phase


  Outflow of K from the cell
• Neuromuscular connection


  1. Voltage-gated calcium channels in the membrane at the end of the nerve open and calcium enters the muscle cell

  2. The incoming calcium activates the secretory vesicles containing acetylcholine and causes them to discharge their contents (approximately 125 acetylcholine vesicles) from the terminal (terminal nerve branches) to the synaptic space (the thin space between the nerve and muscle)

  3. The released acetylcholine clings to the acetylcholine receptors on the membrane of the opposite muscle cell, and opens these receptors, which are also a cation channel

  4. While Na enters the cell, some K goes out of the cell, causing the muscle cell to depolarize

  5. Depolarization propagates across the membrane, causing voltage-gated fast sodium channels in adjacent regions to open, generating an action potential of the muscle cell

  6. The resulting action potential travels across the membrane to induce contraction

  7. When the action potential spreads to the muscle fiber membrane, it diffuses deep into the muscle fiber along the T-tubules, and the resulting action potential spreads through the sarcolemma via the T-tubules, causing Ca release from the sarcoplasmic reticulum
• Skeletal muscle fibers


  Innervated by large myelinated fibers originating from large motor neurons of the anterior horn of the spinal cord
• Muscle Contraction


  1. Axons of myelinated motor neurons divide into terminal branches as they approach the muscle

  2. These branches lose the myelin sheath at their end regions and each comes in contact with a muscle fiber (postsynaptic region) and motor endplate (nerve-muscle junction)

  3. Ca binds to troponin changes position of tropomyosin complex

  4. With this change, the troponin-tropomyosin complex slides over actin, exposing the myosin binding sites

  5. Ca also increases the ATPase activity of the myosin head, and ATP is hydrolyzed

  6. Energy is released

  7. The released energy is "stored" in the myosin head, which is used to form a cross-bridge by extending the myosin head towards the actin myofilament

  8. Myosin heads pull actin myofilaments in a way called force pulsation so that the myofilaments are intertwined

  9. Thus, the sarcomere becomes shorter and shorter (contraction occurs), the Z discs approach each other, the sarcomere shortens (contraction), the muscle fiber shortens, the whole muscle shortens

  10. Muscle contraction is achieved

  11. When contraction occurs, it is seen that there is no change in the length of the A band, and the I band shifts inward (ie, thin bridges slide between thicker bridges with this energy)

  12. Contraction in the form of no change in the length of the A band, shortening of the I band, slipping of thin filaments between thick filaments, is called contraction according to the SLIDING FLAMENTS THEORY

  13. After contraction, ATP in the sarcoplasm binds to the myosin head with the activation of Ca, allowing the head to separate from actin

  14. The cycle repeats as the muscle continues to shorten in length
• End of Contraction


  1. Neurostimulation terminates and calcium is released from Troponin, pumped back to SR

  2. The myosin binding portion of actin is reclosed and the cross bridges are separated

  3. When Calcium is removed from the environment, AtPase enzyme activity also decreases and this causes the termination of the contraction

  
• Pathomechanics of the Muscle Function

  Muscle function can be impaired in two directions: 1) Innervational Disorder (Hyperinnervation caused by an excessive stimulus reaching the muscle, Hypoinnervation caused by Motor Neuron or Lower Motor Neuron disease), 2) Disturbance in Muscle Metabolism (flaccid muscles appear to occur, myopathies)
• Old Classification of Muscle Fibers

  • Red fibers / Slow twitch (ST)
  • White fibers/ Fast twitch (FT)
• New Classification of Muscle Fibers

  • Type I
  • Type IIa
  • Type IIb
• Type I Muscle Fibers

  • Contraction speed: Slow
  • Contraction strength: Low
  • Fatigue speed: Gets tired late
  • Aerobic capacity: High
  • Anaerobic capacity: Low
  • Magnitude of fibers: Small
  • Capillary density: High
• Type IIa Muscle Fibers

  • Contraction speed: Fast
  • Contraction strength: High
  • Fatigue speed: Gets tired fast
  • Aerobic capacity: Medium
  • Anaerobic capacity: Medium
  • Magnitude of fibers: Medium
  • Capillary density: High
• Type IIb Muscle Fibers

  • Contraction speed: Fast
  • Contraction strength: High
  • Fatigue speed: Gets tired very fast
  • Aerobic capacity: Low
  • Anaerobic capacity: High
  • Magnitude of fibers: Big
  • Capillary density: Low
• Type II Fiber Ratios in the Quadriceps Muscles

  • Marathoners: 18%
  • Swimmers: 26%
  • An Average Individual: 55%
  • Weightlifters: 55%
  • Sprinters: 63%
  • Jumpers: 63%
• Types of Muscle Contraction

  • Isotonic, dynamic or concentric: Muscle length shortens, muscle tension remains the same
  • Isometric or static: There is no change in muscle length, muscle tension increases
  • Eccentric contraction: As muscle tension increases, muscle length increases
  • Isokinetic: The muscle shortens in length, the rate of contraction is constant, but the resistance is variable
• Eccentric contractions


  Common in all muscles and in nearly every human movement, high-intensity, repetitive, or eccentric movements during fatigue are associated with muscle injury, a muscle injury can occur when eccentrically active muscles are rapidly pressed by external forces
• When people do physical activity beyond general levels, especially eccentric muscle movements, the result is often delayed muscle soreness
• It is important in conditioning to include both the eccentric and concentric phases of the exercises
• Some athletic activities will benefit from eccentric training, for example, long jumpers and javelin throwers need strong eccentric force when jumping
• Agonist muscles


  The muscles that are responsible for the actual movement, the most effective of these is the prime mover
• Antagonist muscles


  Agonist muscle or muscle groups that act against the muscles or prevent their movements, controls or brakes the movement of the joint in the opposite direction
• Fixator (stabilizer) muscles


  They fix the body against any force, the force can be a contraction of another muscle or a weight being lifted, muscles that immobilize the start of agonist muscles during movement
• Synergist muscles


  The muscles that help make the same movement
• Neutralizing muscles


  Preventing unwanted action of agonists while movement occurs
• Active Tension


  The forces created between actin and myosin fibers in the sarcomeres of activated engine units, the force generated by the contractile proteins (actin and myosin) using the chemical energy stored in ATP
• Passive Tension


  The force from the extension of the connective tissue components of the muscle-tendon unit, the internal resistance of the muscle-tendon unit to the extension of the tension
• Passive tension in stretching exercises can be quite large and may be responsible for muscle weakness after stretching
• Passive inability of poor hamstring flexibility can lead to poor performance or risk of injury in activities that require combined hip flexion and knee extension, such as karate front kick
• Factors Effecting the Tension in the Muscle Tissue


  • Frequency of the stimulus
  • Effective number of engine units
  • Muscle length (length-tension relationship)
  • Contraction speed
• Motor Unit


  A single motor nerve and all the muscle fibers it stimulates, motor units contract according to the "all or nothing" rule, the number of motor units varies according to the functions of the muscles