Fatigue During Muscular Exercise
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Transcript Fatigue During Muscular Exercise
Fatigue During
Muscular Exercise
• Fatigue- inability to maintain a given
exercise intensity
– rarely completely fatigued - maintain
lower power output
• often fatigue identified specifically
• other times, diffuse - eg dehydration
• several factors disturb homeostasis
– easier to identify correlation than
causal relationship between factors and
fatigue
• Compartmentalization - more
difficult to identify site of fatigue
– eg. ATP depleted at myosin head, but
adequate elsewhere?
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Fatigue
• Environmental factors - can affect
endurance performance
– eg. Heat - redistribution of CO
– uncouple mitochondria - less ATP with
same VO2
• inc sweat, heat gain - dehydration body fluid and electrolyte shifts
– affect psychological perception of
exercise
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glycogen depletion - dec endurance
Metabolite depletion
ATP/ CP - low quantity in cell
must match use with restoration
otherwise - can not maintain exercise
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Phosphagens
• Fig 33-1a - CP levels decline in two
phases - drop rapidly, then slowly
– both severity of first drop and extent of
final drop related to work intensity – fig 33-2
• fatigue - in super-max cycling coincides with CP depletion in ms
– tension development related to CP level
- therefore CP related to fatigue
• Fig 33-1b - ATP well maintained
– why ? - compartmentalization
– Down reg / protection theory
– ms cell shuts off contraction - with ATP
depletion in favor of maintaining ion
gradients
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Fatigue
• Free energy of ATP declines 14% in
physiological pH range - Fig 2-7
– also depends on ATP/ADP ratio
– consequence-less energy available for
work with given VO2 flux
– fatigue also influences ATP binding in
X-bridge cycle
• Glycogen
– depletion associated with fatigue
– moderate activity - uniform depletion
from different fiber types
– low resistance- type I - high type II
• Blood Glucose
– short intense ex bouts - bld gluc rises
– prolonged - bld glucose may fall
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Metabolite Accumulation
• Lactic acid accumulation
• short term high intensity exercise
– production exceeds removal
– strong organic acid - pH decreases
– accumulates in blood - exported
• muscle acidosis
– actually all glycolytic intermediates and
ATP breakdown - weak acids
– may inhibit PFK - slow glycolysis
– may interfere with contraction
– may stimulate pain receptors
• H+ in blood - CNS - pain, nausea
– inhibits O2 / Hb combination in lung
– reduces HS lipase - dec FFA oxidation
– still unsure if it stops exercise**
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Metabolite Accumulation
• Phosphate and Diprotenated phosph.
• With phosphagen depletion - get
phosphate accumulation
– behaves like proton - PFK inhib
– calcium binding interference
• Fig 33-3 H2PO42- acid and phosh
– indicative of non steady state - fatigue
• Calcium Ion
• mitochondrial coupling efficiency
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some Ca++ stimulates TCA cycle
accumulation - energy to remove
ox phosph uncoupling in test tube
exacerbated by reduced Ca++
sequestering by SR with fatigue
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Calcium accumulation
• Ryanodine receptor Fatigue
• Fig 33-4 - changes in Ca++ flux and
signaling in fatigued muscle
– Po - max isometric force
• symptoms of fatigue - dec force
generation - single or tetanic stim
– dec related to SR ca++ release
• 1. dec free calcium
• 2. Responsiveness - downward shift
– H+ interference with given Ca level
• 3. Sensitivity - small L-R shift
– given free Ca - less force
– less impact than dec release or
responsiveness
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Fatigue
• O2 depletion and Mito density
– dec in ms O2 or circ O2 - fatigue
– low O2 - indicated by lactate accum or
CP depletion (causes of fatigue)
• Homeostasis
– exercise depends on integration of
many functions - any upset -- fatigue
• Central and Neuromuscular Fatigue
– many sites require adequate functioning
- decrement at any --fatigue
– possible to have fatigue w/out ms itself
being fatigued
– eg painful inputs - affect willingness to
continue activity
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Central and
Neuromuscular Fatigue
• Fig 33-5 - illustrates fatigue in ms
– ulnar nerve stimulation – full stim indicated by ms AP
– force production absent - ms fatigue
• EMG - often distinct changes - fatigue
• Fig 33-6 - inc in EMG signal failure in muscle to respond
• Fig 33-7shift to left - PFS
– Power Frequency spectrum
– slow fibers recruited at fatigue
• Central fatigue - Stechnov Phenomenon
– Fig 33-8 - faster recovery with
distraction - “active pauses”
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Fatigue
• Psychological Fatigue
– understanding of mechanisms is
minimal
– training - athletes can learn to minimize
influence of afferents
– approach performance limits of ms
• Heart as site of Fatigue
– no direct evidence that heart is site of
fatigue
– art PO2 maintained, heart gets CO
– heart can use lactate or FFA
– ECG - no signs of ischemia
– if there are - heart disease is indicated
– severe dehydration... Cardiac
arrhythmia possible
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VO2 max and Endurance
• Relationship between Max O2
consumption and upper limit for
aerobic metabolism important
• 1. VO2 max limited by O2 transport
- CO and Art content of O2
• 2. Vo2 max limited by Resp capacity
of contracting ms.
• Conclude - VO2 max set by O2 tx
– endurance determined by resp capacity
• Muscle Mass - influences VO2max
• but, at critical mass utilization
• VO2 max is independent of ms mass
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Muscle Mitochondria
• Correlation observed between VO2
max and Mito activity - 0.8
• Henriksson - observed changes in ms
mito and Vo2 with Tx and detraining
– ms mito inc 30%, Vo2 19%
– VO2 changes more persistent with
detraining than resp capacity
– illustrates independence of these factors
• Davies - CH 6
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Correlation's VO2 and End Cap .74
Ms Resp and Running endurance.92
Training 100% in in ms mito
100 % inc in running endurance
15% inc in VO2 max
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VO2 and Mito
• Davies study 2 - iron deficiency
• Fig 33-9 restoration of iron
– hematocrit and VO2 max responded
rapidly and in parallel
– ms mito and running endurance - more
slowly also in parallel
• other experiment
– anemic blood replaced with rbc
– immediately raised Hb - restored VO2
max to 90%
– running endurance was not improved
• strongly suggest - VO2 max function of
O2 transport
– Endurance - more dependant on ms
mito capacity
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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 33-10a - before fatigue - b after
– area under curve representative of [ ]
of metabolites
• Table 33-1 comparison of values
– NMR vs muscle biopsy
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