Fatigue During Muscular Exercise Fatigue inability to maintain

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Fatigue During Muscular Exercise • Fatigue- inability to maintain a given exercise intensity –

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? 1

Fatigue • Environmental factors - can affect endurance performance – eg. Heat - redistribution

Fatigue • Environmental factors - can affect endurance performance – eg. Heat - redistribution of CO – uncouple mitochondria - less ATP with same VO 2 • 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 2

Phosphagens • Fig 33 -1 a - CP levels decline in two phases -

Phosphagens • Fig 33 -1 a - 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 -1 b - ATP well maintained – why ? - compartmentalization – Down reg / protection theory – ms cell shuts off contraction - with ATP depletion in favor of maintaining ion gradients 3

Fatigue • Free energy of ATP declines 14% in physiological p. H range -

Fatigue • Free energy of ATP declines 14% in physiological p. H range - Fig 2 -7 – also depends on ATP/ADP ratio – consequence-less energy available for work with given VO 2 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 4

Metabolite Accumulation • Lactic acid accumulation • short term high intensity exercise – production

Metabolite Accumulation • Lactic acid accumulation • short term high intensity exercise – production exceeds removal – strong organic acid - p. H 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 O 2 / Hb combination in lung – reduces HS lipase - dec FFA oxidation – still unsure if it stops exercise** 5

Metabolite Accumulation • Phosphate and Diprotenated phosph. • With phosphagen depletion - get phosphate

Metabolite Accumulation • Phosphate and Diprotenated phosph. • With phosphagen depletion - get phosphate accumulation – behaves like proton - PFK inhib – calcium binding interference • Fig 33 -3 H 2 PO 42 - 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 6

Calcium accumulation • Ryanodine receptor Fatigue • Fig 33 -4 - changes in Ca++

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 7

Fatigue • O 2 depletion and Mito density – dec in ms O 2

Fatigue • O 2 depletion and Mito density – dec in ms O 2 or circ O 2 - fatigue – low O 2 - 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 8

Central and Neuromuscular Fatigue • Fig 33 -5 - illustrates fatigue in ms –

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 -7 shift to left - PFS – Power Frequency spectrum – slow fibers recruited at fatigue • Central fatigue - Stechnov Phenomenon – Fig 33 -8 - faster recovery with distraction - “active pauses” 9

Fatigue • Psychological Fatigue – understanding of mechanisms is minimal – training - athletes

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 PO 2 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 10

VO 2 max and Endurance • Relationship between Max O 2 consumption and upper

VO 2 max and Endurance • Relationship between Max O 2 consumption and upper limit for aerobic metabolism important • 1. VO 2 max limited by O 2 transport - CO and Art content of O 2 • 2. Vo 2 max limited by Resp capacity of contracting ms. • Conclude - VO 2 max set by O 2 tx – endurance determined by resp capacity • Muscle Mass - influences VO 2 max • but, at critical mass utilization • VO 2 max is independent of ms mass 11

Muscle Mitochondria • Correlation observed between VO 2 max and Mito activity - 0.

Muscle Mitochondria • Correlation observed between VO 2 max and Mito activity - 0. 8 • Henriksson - observed changes in ms mito and Vo 2 with Tx and detraining – ms mito inc 30%, Vo 2 19% – VO 2 changes more persistent with detraining than resp capacity – illustrates independence of these factors • Davies - CH 6 – – – Correlation's VO 2 and End Cap. 74 Ms Resp and Running endurance. 92 Training 100% in in ms mito 100 % inc in running endurance 15% inc in VO 2 max 12

VO 2 and Mito • Davies study 2 - iron deficiency • Fig 33

VO 2 and Mito • Davies study 2 - iron deficiency • Fig 33 -9 restoration of iron – hematocrit and VO 2 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 VO 2 max to 90% – running endurance was not improved • strongly suggest - VO 2 max function of O 2 transport – Endurance - more dependant on ms mito capacity 13

Future of Fatigue • Technology is making available new devices - further investigation of

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 - before fatigue - b after – area under curve representative of [ ] of metabolites • Table 33 -1 comparison of values – NMR vs muscle biopsy 14