BIOL 253L

• Electromyography (EMG)


  a technique that measures the electrical activity of skeletal muscles at rest and during contraction. The data recorded is an electromyogram.
• Intramuscular EMG


  Needle electrodes are inserted through the skin into the muscle. Don't worry, we're not going to do this to you.
• Surface EMG


  Electrodes are placed on the skin's surface. This is what we'll be doing in the lab.
• What does an EMG record?

  EMG provides a depiction of the pattern of muscle activity during complex movements over time.

  
  

  The raw surface EMG signal reflects the electrical activity of the muscle fibers active at that time.

  
  

  -At any time, this may represent the combined electrical activity of perhaps thousands of individual muscle fibers.

  -As the number of electrically active muscle fibers increases, and the frequency of of those muscle fibers' action potentials increases, the strength of the resulting EMG signal also increases.

  -Although contraction strength is normally correlated with the electrical activity, EMG does not record contractile strength. Only electrical activity
• motor unit


  A neuron and the muscle fibers it controls. All muscles within a motor unit act synchronously. Motor unit recruitment is one way to increase contractile strength of a whole muscle. As more strength is required by the central nervous system, more and more motor units are stimulated.

  
  

  There may be times, with exceedingly weak contractions, when only a single motor unit is firing at any one time. So it is possible that the activity of a single motor unit can be seen in an EMG.
• muscle coactivation


  a phenomenon in which contraction of an agonist muscle leads to minor activity in the antagonist muscle.

  
  

  Coordination between agonist and antagonist muscles are essential for a range of movement

  
  

  The physiological significance of this is not entirely clear, but it has been suggested that it helps to stabilize the joint.
• Evoked EMG


  signals are produced by the electrical stimulation of a motor nerve supplying a muscle

  
  

  electrical stimulation with muscle recording
• Agonist

  muscles are sometimes called "prime movers" as they are the primary muscle responsible for generating movement through their contraction.

  
  

  part of antagonistic pair
• Antagonist


  muscles control (or oppose) specific movement, and return the muscle to its initial position. Depending on the movement, agonist and antagonist muscles may change roles.

  
  

  part of antagonistic pair
• Muscle Fatigue


  a state of physiological inability to contract effectively. It is associated with a variety of psychological and physiological factors, including:

  1. loss of central drive

  2. reduction in blood flow

  3. changes in sense of effort

  4. build up of lactic acid.
• Adenosine triphosphate (ATP) can be remade from adenosine diphosphate (ADP) by the addition of a phosphate group - this can occur by three pathways:


  1. When enough O2 is present, pyruvate (from the breakdown of fats, glycogen or glucose) can enter the citric acid cycle and is broken down to CO2 and H2O. This is known as aerobic glycolysis and it generates large amounts of ATP through oxidative phosphorylation (the electron transport chain).

  
  

  2. If O2 supplies are insufficient, pyruvate cannot enter the citric acid cycle and instead gets converted to lactic acid in a process called anaerobic glycolysis. This makes a small amount of ATP but does not require O2.

  
  

  3. In resting muscle, some ATP transfers a phosphate to creatine obtained through the circulation from the liver, creating a store of phosphocreatine. During intense exercise, phosphocreatine can be used to resynthesize ATP, allowing contraction to continue.
• Physiologial causes of fatigue

  When ATP production fails to keep pace with ATP usage, muscles contract less and less effectively. Ultimately, muscle fatigue sets in and muscle activity ceases, even though the muscle may still be receiving stimuli.

  
  

  Excessive accumulation of lactic acid and associated H+, together with ionic imbalances also contribute to muscle fatigue. The pH drop, associated with the lactic acid production may cause fatigue and limits the usefulness of the anaerobic mechanism for ATP production.

  
  

  Some specialized muscle fibers (slow twitch) are more resistant to fatigue than others (fast twitch). Several factors may contribute to this. For example, muscles may have more mitochondria and hence a greater capacity for oxidative metabolism, or they may have greater stores of phosphocreatine.
• Factors proposed to explain muscle fatique

  - Changes in one's motivation or sense of effort.

  - Decline in central nervous system command of motor units (central drive).

  - Failure of neuromuscular propagation. Neurons may temporarily run low on neurotransmitter.

  - Reduction in Ca2+ release in excitation-contraction coupling.

  - Metabolic changes in the muscle cell (such as build-up of lactic acid which can make the skeletal muscle acidic inhibiting any further anaerobic glycolysis).

  - Reduction in muscle blood flow owing to compression of blood vessels.
• In skeletal muscle, ATP is not generated through

  lactic acid metabolism

  
  

  It is through:

  - aerobic metabolism

  - anaerobic metabolism

  - breakdown of phosphocreatine
• How could you relieve fatigued muscles?

  Rest the muscles to allow blood flow to re-establish pH and replenish nutrients needed for ATP production.
• Factors in muscle fatigue

  - build up of lactate and associated H+ ions (lactic acid) in muscles

  - Failure of neuromuscular propagation

  - Loss of "central drive" - Reduction in Ca2+ release in excitation-contraction coupling
• Not factors in muscle fatique

  - increased blood flow

  - prolonged muscle cell depolarization
• Neurological disorders


  disorders of the nerves
• Peripheral neuropathy


  associated with various combinations of motor, sensory, and autonomic dysfunction
• Motor Neuron Disease


  - a condition affecting only the motor neurons

  - characterized by a progressive loss of lower motor neurons

  - no sensory of autonomic symptoms - only motor abilities are affected
• peripheral neuropathy

  the damage or disease of the lower motor neurons of their myelin sheaths. Nerve conduction studies are used to help distinguish between the causes of neuropathies

  
  

  Peripheral neuropathy is associated with various combinations of motor, sensory, and autonomic dysfunction:

  Motor problems:

  - symptoms and signs include weakness, cramps, spasms, muscle wasting, and fasciculations

  Sensory symptoms:

  - Loss of sensation and disordered sensation with parathesia (tingling), numbness and a heightened sense of pain

  - Balance may be impaired

  Autonomic symptoms:

  - Can result in abnormal control of blood pressure and heart rate, decreased ability to sweat, constipation or diarrhea, incontinence, and sexual dysfunction
• Motor Endplate Conditions

  1) signal from motor neuron arrives at the nerve terminal

  2) Calcium moves into nerve terminal (motor endplate)

  3) ACh is released into the NMJ and binds to ACh receptors

  4) Influx of Na+ initiates an action potential in the muscle fiber
• cessation of signal across the neuromuscular jxn occurs b/c

  1) neurotransmitter may diffuse away from the nicotinic ACh receptors on the motor end plate

  2) AChE breaks down ACh in the synapse, preventing its activation of the ACh receptors. The breakdown products are taken back into the axon terminal in a process of reuptake
• Myasthenia gravis


  an auto-immune disease resulting most commonly from antibodies to ACh receptors

  
  

  symptoms:

  - fatigue quickly during activity, with improvements after periods of rest

  - usually affects muscles in the eyes, face, and neck first

  - muscles controlling eye and eyelid movement, facial expression, chewing, talking, and swallowing are especially susceptible

  - the majority of patients also have thymus abnormalities
• Lambert-Eaton Myasthenic Syndrome (LEMS)


  Auto-Immune; antibodies formed against voltage gated Ca2+ channels at NMJ; prevents fusion

  
  

  Sx: skeletal muscle weakness in limbs
• Botulism


  paralytic illness caused by the botulism toxin, a neurotoxic protein, produced by Clostirdium botulinum

  
  

  produces muscle paralysis by inhibiting the release of ACh from muscle endplates

  
  

  descending paralysis (first muscles to be affected are those controlling eye and eyelid movement, facial expression, chewing, talking, and swallowing
• motor endplate disease


  there are no sensory changes

  includes botulism and myasthenia gravis

  aka NMJ disease
• Mypathy


  disease affect of the muscle

  includes Duchenne muscular dystrophy
• Duchenne's muscle dystrophy


  - recessive x-linked condition that usually develops in young boys before the age of 5

  - effects skeletal muscle and cardiac muscle

  - mutation in dystophin gene, a protein that connects the cell cytoskeleton to the extracellular matrix

  - excess Ca2+ ions enter muscle cells leading to damage of mitchondria, leading to cell death

  - patients commonly end up wheelchair bound
• Becker's Muscular Dystrophy


  milder version

  arises from deletions in the dystrophin gene that permits synthesis of a shorter but semifunctional protein
• Neurolopathy

  - includes amyotrophic lateral sclerosis (ALS)

  - can result from damage to the myelin sheath

  - can result from physical damage to motor neurons
• Why is it important to lightly abrade the skin, and clean the area with alcohol swabs prior to attaching EMG electrodes?

  this reduces the electrical resistance of the skin
• Unlike the discrete wavefrom from an ECG, the EMG waveform is irregular. Why?


  EMG is irregular b/c is records data from multiple different muscle fibers
• How many muscle fibers may a single motor neuron innervate?

  several muscle fibers
• How is ACh removed from the synaptic cleft?

  the enzyme AChE hydrolyzes the ACh within the synaptic cleft
• What does EMG record?

  Electrical activity of the innervated muscle fibers
• Which describes the phenomenon of "coactivation"

  It is the weaker contraction of the antagonist muscle during the contraction of the agonist muscle
• 1. What are the main causes of fatigue addressed for each of the three variables tested? (brief periods of rest, encouragement and visual feedback)

  - Brief periods of rest = decline of central/motor drive on contraction

  - Encouragement = decrease in motivation on contraction

  - Visual Feedback: sense of effort the person was exerting on contraction
• 2. The muscle cell does not store large quantities of ATP. How does the muscle ensure enough ATP is available for intense exercise?

  Muscles stores phosphocreatine and during intense exercise, it is taken and used by the cell to resynthesize ATP, allowing contraction to continue
• 3. During repeated skeletal muscle contraction, what happens to calcium within a single motor unit that may lead to fatigue? What is its overall effect?

  During repeated skeletal muscle contraction, the release of intracellular calcium decreases, which ultimately leads to a decrease in force of contraction within that motor unit. This is because calcium binds to troponin, which then moves tropomyosin out of the way in order to allow for contraction, so a lack of calcium would inhibit this process.