NEUROMUSCULAR FATIGUE by benbenzhou

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									NEUROMUSCULAR
FATIGUE
 In Exercise Physiology, neuromuscular fatigue
  can be defined as a transient decrease in
  muscular performance usually seen as a failure
  to maintain or develop a certain expected force
  or power.
Importance of
Neuromuscular Fatigue
  Does O2 delivery alone limit exercise
   performance?
    Is it just O2 transport and O2 fuel utilization?
    Have we adequately explored other areas
     relating to muscle contractile function?
  TD Noakes – South Africa
    Only 50% of VO2 max trials result in a
     plateau – is there really a plateau?
    Is fatigue biochemical or CNS controlled
     anticipatory response?
Loss of Strength with
Fatigue
  Any volitional
   loss of strength
   during a
   sustained
   exercise is the
   basis of fatigue.
Effect of Fatigue on
Reflexes and Coordination
  A reflex arc is fatigable.
    If a reflex arc is stimulated repeatedly – it will
     eventually fail to elicit any type of expected
     reflex response.
       The more interneurons and synapses involved,
        the more quickly it may become fatigued.
  Coordination can be viewed the same
   way
    Irradiation of motor impulses to neighboring
     motor nerve centers – coordination is lost.
Effect of Fatigue on
Industrial Workers
  How much work can
   be done in an 8-hour
   time period without
   fatigue?
    Static work is more
     fatiguing than
     dynamic work
       Blood flow
       Rest periods
Basic Nature of Fatigue

  Relationship between intensity of work
   and endurance appears to be a
   fundamental characteristic of
   performance…
    Is there some equation that can be
     universally applied to calculate the highest
     sustainable workload?
       Physical Working Capacity at Fatigue Threshold
       PWCFT
Central versus Peripheral

  Where does fatigue occur?
   Central fatigue
     Proximal to the motor unit
   Peripheral fatigue
     Residing within the motor unit
Central Fatigue

  Brain and spinal cord; CNS fatigue
    Studies that used voluntary exhaustion and
     then additional electrical stimulation
       After voluntary exhaustion, electrical stimulation
        evoked sizable force production
       Central location of fatigue
Peripheral Fatigue

  Fatigue occurring within the local motor
   unit; local fatigue
    Studies that fatigued a muscle with electrical
     stimulation to the point of no muscle twitch
       Muscle action potentials were relatively
        unaffected
       Peripheral location of fatigue (but not at the NMJ)
So, where does fatigue
occur?
  In both central and peripheral locations.
     The location of fatigue is intensity-dependent
         Lower-intensity, longer duration fatigue will primarily occur
          centrally
         Higher-intensity, short duration fatigue will primarily occur
          peripherally
  Example  Why does pedaling rate decrease during
   the Wingate test?
  Example  Why can’t we do another repetition after a
   5RM lift?
  Example  Why do we slow down during the course of
   a 1600 m race? Do we slow down?
What Causes Fatigue?

  There are two hypotheses:
    The Accumulation hypothesis
    The Depletion hypothesis
  The origin of fatigue is exercise-
   dependent and may be due to either
   accumulation, depletion, or both.
Accumulation Hypothesis
 There is a buildup of metabolic by-products in
  the muscle fiber
     Lactic acid (lactate)
     Hydrogen ions (H+)
     Ammonia
     Inorganic phosphate
 Lactate is the primary marker associated with
  the accumulation hypothesis
 If you exercise at a high enough intensity, H+
  accumulation interferes with force production
   Applies to maximal exercise for 20 sec  3 minutes
Four Factors Associated with the
Decrease in Force Production Due
to H+ Accumulation


 1. H+ interferes with Ca++ release from the
    sarcoplasmic reticulum.
 2. H+ interferes with actin-myosin binding
    affinity
 3. H+ interferes with ATP hydrolysis
 4. H+ interferes with ATP production
1. Ca++release from the
sarcoplasmic reticulum
  Lactic acid (H+) accumulation disrupts the
   release of Ca++ from the sarcoplasmic
   reticulum, in part, by changing the
   membrane potential (ICF vs. ECF)
  When Ca++ is not released as effectively,
   less is available to bind with troponin-C.
2. Actin-myosin binding
affinity
  Actin and myosin do not bind as readily
   or as “tightly” in an increased acidic
   cellular environment (i.e.,
   microenvironment).
3. ATP hydrolysis

  H+ accumulation decreases the
   effectiveness of mATPase.
  Why?
4. ATP production

  H+ accumulation interferes with enzymes
   that catalyze reactions that produce ATP.
    What is the rate limiting step in glycolysis?
    Allosteric inhibition:
Acid Removal

  What are the two primary ways to clear
   H+ accumulation?
    Increased blood flow
    Buffering
      What is the body’s primary blood buffer?
Depletion Hypothesis

  2 aspects to the depletion hypothesis:
    Neural depletion
       Depletion of acetylcholine
    Depletion of energy substrates
       Phosphagen depletion
       Glycogen depletion
Neural Depletion
 Neural fatigue that is caused by a
  depletion of the stimulatory
  neurotransmitter ACh.
   You can induce neural depletion in an excised
    muscle, but can this happen in vivo?
   Two possible instances where it might have
    occurred:
      East German woman completing the final lap of a
       marathon
      Ironman Triathalon competition in Hawaii (same
       occurance)
Depletion of Energy
Substrates
  2 aspect of substrate depletion:
    Phosphagen depletion
    Glycogen depletion
Phosphagen Depletion
   2 aspects to phosphagen depletion:
    1. Reduction in ATP
         Small ATP stores in skeletal muscle
         Enough to provide 2 – 3 seconds of maximal
          muscular contraction
             Used quickly
    2. Depletion of phosphocreatine (PC)
         Enough PC stored to provide up to 20 – 30
          seconds of maximal muscular contraction
             Nearly completely depleted during maximal exercise
Glycogen Depletion
 Glycogen is a polymer of glucose that is created
  with glycogen synthase
   Glycogen is stored in relatively large amounts in
    skeletal muscle.
      About 2,000 kcals of energy stored in the form of glycogen
       (skeletal muscle)
          Where are the two primary locations for glycogen storage in the
           body?
      It takes approximately 100 kcals to run a mile, so we have
       enough glycogen stored for about 20 miles of running.
   Glycogen depletion occurs during long-term activities
    that are done at a medium to moderate intensity
      When this occurs, the body is forced to use alternative
       energy sources (that are not as powerful as glucose
       metabolism)
      Example: “Hitting the runner’s wall”
      What about glycogen supercompensation??
Muscle Temperature
Effect on Fatigue
  Optimal deep muscle temperature
   between 80 - 86 F
    At 103, the endurance time decreased 65%
      Due to metabolite accumulation or temperature
       effects of protein/enzyme function (titration).
    At 68, the endurance time decreased 80%
      Due to interference with neuromuscular
       transmission
Electromyographic
Observations of Fatigue
  EMG Amplitude (submaximal workloads)
    Increases linearly with exhaustion
    PWCFT
  EMG Amplitude (maximal workload)
    Remains constant or decreases with exhaustion
       “Muscle Wisdom” hypothesis
  EMG Frequency (max and submax)
    Decreases…
    Why?
Assignment for next week

  Read handout
    deVries & Housh
  Read Enoka, 2003 pgs. 374-389.
  Prepare for questions next week over this
   lecture.
Course Projects

  Pick one of the five neuromuscular
   disorders:
      Parkinsonism
      Muscular/Myotonic Dystrophy
      Cerebral Palsy
      Low Back Pain
      Peripheral neuropathy (generic)
Course Projects

  Give a 50-min lecture on the neuromuscular
   disorder that you chose
      Etiology
      Pathology
      Common signs / symptoms
      How does it affect motor unit function?
      Describe how we could investigate this disorder with
       surface EMG and MMG:
         Collect pilot data and report your results on 4 or 5 healthy
          subjects
         Extrapolate your findings to the diseased subjects
Course Projects

  Lectures given on:
    April 18
    April 25
    May 2
  Choice must be made by next week.

								
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