Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Fatigue • • • • • • Brooks Ch 33 Outline Definitions Central Fatigue Peripheral Fatigue Exhaustion (depletion) Hypothesis – Phosphagens – Glycogen / glucose • Accumulation Hypothesis – – – – – pH Phosphate Calcium Potassium (Foss p 65) Oxygen • VO2max and endurance 1 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 2 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 3 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 4 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 5 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 6 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 7 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 8 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 9 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 10 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 11 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+ 12 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 13 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 14 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 15 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 – – – – – – 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 16 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 17 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 18