Transcript NEUROMUSCULAR FATIGUE - The University of Texas at

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 exercisedependent and may be due to either
accumulation, depletion, or both.
Accumulation Hypothesis
 There is a buildup of metabolic by-products in
the muscle fiber
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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
++
Ca
1.
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
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2 aspects to phosphagen depletion:
1. Reduction in ATP
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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:
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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
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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.