Download Fatigue During Muscular Exercise

Fatigue
Brooks Ch 33
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Outline
• Definitions
– Central Fatigue
– Peripheral Fatigue
• Exhaustion (depletion) Hypothesis
– Phosphagens
– Glycogen / glucose
• Accumulation Hypothesis
–
–
–
–
–
pH
Phosphate
Calcium
Potassium (Foss p 65)
Oxygen
• Future of Fatigue
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Fatigue During Exercise
• Fatigue - inability to maintain a given exercise intensity
or power output
– Reversible with rest (recovery)
– rarely completely fatigued - can maintain lower intensity
output
– Studied with EMG and observation of contractile function
with electrical (nerve) or magnetic stimulation (cortex)
– Observe reduction in force and velocity and a prolonged
relaxation time after fatigue
• The effect of exercise at an absolute or relative
exercise intensity will be more severe on an untrained
individual
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Advanced Neuromuscular Exercise Physiology - Human Kinetics 2011
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Fatigue During Exercise
• Causes of muscle fatigue have been classified into central
and peripheral
• Central - includes CNS, motivation and psychological factors
– restoration of force with external stimulation of muscle -indicates
central fatigue
– NH3, hypoglycemia, reticular formation
• Peripheral - PNS to muscle - EC coupling, energy supply
and force generation
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Exercise Metabolism - Human Kinetics - 2006
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Exercise Metabolism - Human Kinetics - 2006
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Identifying site of Fatigue
• fatigue can be identified specifically - eg.
Glycogen, Ca++ depletion
• Compartmentalization within the cell
increases the difficult of determining the
source of fatigue
– eg. ATP may be depleted at the myosin head, but
adequate elsewhere in the cell - is this detectable?
• Often the origin of fatigue is diffuse
– eg dehydration
– several factors then contribute to a disturbance of
homeostasis
– Often easier to identify correlations to fatigue,
rather than causal contributions to fatigue
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Environment and Fatigue
• Heat and humidity - can affect endurance
performance
• inc sweat, heat gain, dehydration, changes in
electrolytes results in
– redistribution of Cardiac Output
– Uncoupling of mitochondria - less ATP with same VO2
– changes in psychological perception of exercise
• Fatigue is cumulative over time
– dehydration yesterday can influence performance today
– Glycogen depletion cumulative as well
• Reduced circulation to muscle may result in
glycogen depletion
– Reducing endurance capacity
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Central Fatigue
• possible to have fatigue w/out the muscles itself
being fatigued
– eg pain may affect drive to continue
• Compare force output during fatigue with force
output during maximal external stimulus (eg
electrical impulse on motor nerve)
– An ability of this external stimulation to restore force
would indicate central fatigue
• Psychological Fatigue
– understanding is minimal
– With training - athletes can learn to minimize influence of
sensory inputs
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– Able to approach performance limits
Central Fatigue
• Central fatigue - Stechnov Phenomenon
• Fig 33-9 - faster recovery of strength with distraction or
“active pauses” during recovery from exhaustion
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Peripheral Fatigue
• Fig 33-6 - ulnar
stimulation is
constant - force
development
decrease over
time - indicating
peripheral fatigue
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Peripheral Fatigue
• Fig 33-7 - large increase in EMG signal - no increase in
force - also indicates peripheral fatigue (see slide 5)
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Peripheral Fatigue
• Two hypothesis for peripheral fatigue
• a) Exhaustion - depletion of energy substrates - eg
ATP, CP, glycogen
– Phosphagens are present in low quantities
– Must match use with restoration from other metabolic
pathways - or fatigue
• b) Accumulation of metabolic byproducts - eg H+,
Ca++, Pi
• Likely a combination of factors with contributions influenced
by the specific conditions of the activity
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Exhaustion Hypothesis
• Depletion of
metabolites
• Phosphagens
• Fig 33-2a - CP
levels decline in
two phases - drop
rapidly, then
slowly
• Rate of ATP
synthesis by CK
decreases along
with decrease in
CP content - rate
is fastest at rest
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Exhaustion Hypothesis
• both severity
of first drop
and extent of
final drop
related to
work intensity
– fig 33-3
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Exhaustion Hypothesis
• Fig 33-2b - ATP well
maintained
– compartmentalization?
– Down regulation /
protection theory?
• ms cell shuts off
contraction - with ATP
depletion in favor of
maintaining ion
concentration
gradients and cell
viability
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Depletion (continued)
• Glycogen
– depletion associated with fatigue
– moderate activity - uniform depletion from different fiber
types
• Also activity specific fiber depletion
– Carbohydrate loading can improve performance
– Caffeine (inc FFA mobilization) can also offset fatigue
• Blood Glucose
– During short intense exercise bouts - blood glucose rises
– With prolonged activity- blood glucose may fall
• Fatigue at blood glucose below 3.5 mM
• Anapleurotic substrates
– Krebs cycle intermediates - decline results in reduced
capacity of Krebs
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Accumulation Hypothesis
• H+ (acidity)
• Lactic acid accumulates during short term high
intensity exercise
– As production exceeds removal
– exported into blood from muscle
• As it is a strong acid -blood pH decreases
– H+ in blood - affects CNS
• pain, nausea, discomfort, disorientation
– inhibits O2 / Hb combination in lung
– reduces HS lipase - dec FFA oxidation
– **still unsure if this induces fatigue**
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Accumulation Hypothesis
• muscle acidosis
– all glycolytic intermediates are weak acids
– ATP breakdown also produces H+
• may inhibit PFK - slowing glycolysis
• may interfere with calcium binding TnC
• may stimulate pain receptors
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Accumulation
• Phosphate( Pi) and Diprotenated phosphate
(H2PO4)
• phosphagen depletion (CP) - results in Pi
accumulation
– behaves like proton
• inhibiting PFK
• interfering with X-bridge attachment, detachment and
force production
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Accumulation
•Fig 33-4 H2PO42- acid and Pi
–indicative of non steady state - fatigue
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Accumulation
• Calcium Ion Accumulation
• mitochondrial coupling efficiency
–
–
–
–
some Ca++ stimulates Krebs cycle
accumulation - requires energy to remove the calcium
Creates oxidative phosphorylation uncoupling in test tube
exacerbated by reduced Ca++ sequestering by SR with
fatigue
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Calcium (cont)
• Fig 33-5 changes
in Ca++
flux and
signaling
in fatigued
muscle
– Po refers
to max
isometric
force
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Calcium (cont)
• symptoms of fatigue (fig 33-5)
– decreased force generation - with single or tetanic stimulation
– related to SR Ca++ release, and/or pH affects on opening of SR
channels
• 1. dec free calcium
–
–
–
–
May be EC coupling at T tubules, sarcolemma, or SR channels
Accumulation in mito, dec SR uptake
Lactate anion interference with ryanodine receptor
Pi precipitation with free calcium
• 2. Responsiveness - down shift
– H+ interference with Ca++ binding
• 3. Sensitivity - small L-R shift
– given free Ca++ - less force
– less impact than dec release or responsiveness
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Potassium (K+)
• Foss p 65
• K+ is released from contracting muscle resulting in
– reducing cytosolic and an increasing plasma K+ content
– Release high enough to block nerve transmission in T
tubules
– Concomitant increase in Na+ intracellulary disrupts
normal sarcolemmal membrane potential and excitability
• High Na+/K+ pump activity improves performance
• Rapid recovery of K+- 2-5 minutes
– Complete in ~30 minutes
– During exercise inactive tissues take up K+
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O2 depletion and Mitochondria
• O2 depletion and Mito density
– dec in ms O2 or circ O2 can lead to fatigue eg altitude, circulation impairments
– low O2 often indicated by lactate accumulation, CP
depletion or both
– exercise depends on integration of many functions
- any upset -- fatigue
• Doubling of oxidative capacity with training
– increases use of FFA -sparing glycogen
– Minimizes impact of the damaging effects of free
radicals
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Heart Fatigue
• Heart as site of Fatigue
– no direct evidence that heart is site of fatigue
– Arterial PO2 is maintained during exercise, heart
gets Q priority
– heart can utilize lactate or FFA
– ECG - no signs of ischemia at maximal effort or
fatigue
– if there are signs- heart disease is indicated
– With severe dehydration... Cardiac arrhythmia is
possible
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Future of Fatigue
• Technology is making available new devices - further
investigation of fatigue
• NMR
– possible to determine [ ] of Phosphagens, protons, water,
fat, metabolites
– without breaking the skin
– Fig 33-11
– a at rest - before fatigue
– b after fatigue
– area under curve represents [ ] of metabolites (ATP, CP, Pi)
– Clear indication of declines and accumulations at fatigue
• Table 33-1 comparison of values
– NMR vs muscle biopsy
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Fig. 1. Estimation of critical power (CP) in a representative subject
Critical Power highest constant
work rate
that can be
maintained
without fatigue
Jones, A. M. et al. Am J Physiol Regul Integr Comp Physiol 294: R585-R593 2008;
doi:10.1152/ajpregu.00731.2007
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Copyright ©2008 American Physiological Society
Exercise Metabolism - Human Kinetics - 2006
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