Transcript Fatigue During Muscular Exercise

Fatigue
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Brooks Ch 33
Outline
Definitions
Central Fatigue
Peripheral Fatigue
Exhaustion (depletion) Hypothesis
– Phosphagens
– Glycogen / glucose
• Accumulation Hypothesis
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pH
Phosphate
Calcium
Potassium (Foss p 65)
Oxygen
• VO2max and endurance
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Fatigue During Exercise
• Fatigue- inability to maintain a given
exercise intensity
– 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
• The effect of exercise at an absolute or
relative exercise intensity will be more
severe on an untrained individual
• 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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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
– An ability of this external stimulation to
restore force would indicate central
fatigue
• Central fatigue - Stechnov Phenomenon
• Fig 33-8 - faster recovery of strength
with distraction or “active pauses” during
recovery from exhaustion
• Psychological Fatigue
– understanding is minimal
– With training - athletes can learn to
minimize influence of sensory inputs
– Able to approach performance limits
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Peripheral Fatigue
• Fig 33-5 - ulnar stimulation is constant force development decrease - peripheral
• Fig 33-6 - large increase in EMG signal no increase in force - 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+, NH3, Pi
• Likely a combination of factors from both.
Contributions of factors are influenced by
the specific conditions of the activity
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Exhaustion Hypothesis
• Depletion of metabolites
• 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
– 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
• 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**
• 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
• Fig 33-3 H2PO42- acid and Pi
– indicative of non steady state - fatigue
• 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 33-4 - changes in Ca++ flux and
signaling in fatigued muscle
– Po refers to max isometric force
• symptoms of fatigue
– 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 sarcolemma, T
tubules, or SR channels
– Accumulation in mito, dec SR uptake
• 2. Responsiveness - downward 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 CO 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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VO2 max and Endurance
• Relationship between Max O2
consumption and upper limit for
aerobic metabolism is important
• Two possibilities – 1. VO2 max limited by O2 transport
• CO and Arterial content of O2
– 2. VO2 max limited by Respiratory
capacity of contracting ms.
• Conclude – VO2 max set by O2 transport capacity
– endurance determined by respiratory
capacity of muscle
• Evidence
– Muscle Mass used- influences VO2max
• Minimum of 50% of total ms mass for true
value of VO2 max
– but, at critical muscle mass VO2 max is
independent of muscle 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 respiratory capacity
– illustrating independence of these
factors
• Davies - CH 6 - Correlation's
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VO2 and End Cap .74
Ms Resp and Running endurance.92
Training 100% increase in ms mito
100 % inc in running endurance
15% inc in VO2 max
Again illustrating independence of VO2
max and endurance
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VO2 and Mito
• Davies study 2 - iron deficiency
• Fig 33-9 restoration of iron in diet
– hematocrit and VO2 max responded
rapidly and in parallel
– ms mito and running endurance - more
slowly, but also in parallel
• further experiments
– anemic blood replaced with healthy
blood containing red blood cells
– immediately raises Hb - and restores
VO2 max to 90% of pre anemic levels
– 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 33-10
– a at rest - before fatigue
– b after fatigue
– area under curve representative of [ ]
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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