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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

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Fatigue During Muscular Exercise

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  1. 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?

  2. 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 • glycogen depletion - dec endurance • Metabolite depletion • ATP/ CP - low quantity in cell • must match use with restoration • otherwise - can not maintain exercise

  3. 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

  4. 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

  5. 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**

  6. 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 • some Ca++ stimulates TCA cycle • accumulation - energy to remove • ox phosph uncoupling in test tube • exacerbated by reduced Ca++ sequestering by SR with fatigue

  7. 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

  8. 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

  9. 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”

  10. 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

  11. 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

  12. 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 • 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

  13. 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

  14. 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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