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Skeletal Muscle Fatigue Common Definition

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Reduction in Physical performance

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Skeletal Muscle Fatigue Physiology Definition

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Failure to maintain the required or expected force

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Fatigue for Isometric Contractions

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Decrease in force

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Fatigue for Isotonic Contractions

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Decease in contractile response decrease in force decrease in velocity of shortening decrease in power

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Skeletal Muscle Fatigue Endurance Exercise Definition

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Effort required to maintain a constant submaximal task increases -increased MU recruitment -increased firing frequency

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Skeletal Muscle Fatigue Site: Central NS

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Motor Cortex Brainstem Spinal Cord Descending Motor Pathways Interneurons Pain Mental Fatigue

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Skeletal Muscle Fatigue Site: Peripheral NS NEURAL

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Motor Neuron Neuromuscular Junction

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Skeletal Muscle Fatigue Site: Peripheral NS MUSCLE -Cell Membrane -T Tubule -Ca Uptake -Actin/Myosin Interaction -DHP/Ryanodine

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1) Cell Membrane> potential altered, harder to depolarize and generate AP 2) T Tubule> potential altered as well, harder to depolarize and generate AP. 3) Ca+ uptake (Ca ATPase activity) 4) Actin Myosin Interaction -force per crossbridge -turnover of crossbridges (velocity, depends on ATP) 5) DHP and Ryanodine receptors> Channel for Calcium on the T Tubule and SR. Elevation in Calcium release in response to AP in T Tubule.

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Evidence for Skeletal Muscle Fatigue due to Central Factors -Ikai and Steinhaus (1920) Classic study

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-Max voluntary contractions decline with exercise over time. -If unexpected gun shot fires, muscle tension (force generated) rises significantly -declining force can also be reversed (increased) by asking subject to scream. -external motivation helps! -capable of generating more force -limiting factor then probably Central Factor (CF)

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Evidence for Skeletal Muscle Fatigue due to Central Factors: -MVC (Maximum Voluntary Contractions) vs. electrically stimulated ones

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-MVC decrease over time -submaximal, forced electrically stimulated contractions do NOT decrease in tension over time -muscle fibers themselves not fatigued -force of MVC can be increased by asking subject to work harder

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Evidence for Skeletal Muscle Fatigue due to Central Factors: -Repeated submaximal isotonic contractions continued until voluntary tension reaches nearly 0 -How can we increase force now?

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-Peripheral median nerve can be stimulated electrically to increase force. -1/2 force recovered! -must be CNS -probably pain -If we stop stimulated it electrically, voluntary contractions can resume and reach initial force but this rapidly declines back to 0 -shows interaction between CNS and PNS.

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Evidence for Skeletal Muscle Fatigue due to Motor Neutron: What happens to motor neuron firing?

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MN firing rate decreases proportionate to decline in force

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Evidence for Skeletal Muscle Fatigue due to Motor Neutron: Can some fibers no longer be activated?

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Yes- with direct electrical stimulation of a MN, some muscle fibers are no longer activated after several minutes.

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Evidence for Skeletal Muscle Fatigue due to Neuromuscular Junction: -What happens with APs?

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Amplitude of motor-endplate potentials decreases during fatiguing exercise -eventually dont cause APs

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Evidence for Skeletal Muscle Fatigue due to Neuromuscular Junction: -What happens with AcH?

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Decrease in amount of AcH released by each nerve ending. Reduction in (at nerve terminal): 1) number of exocytotic vesicles 2) amount of AcH released per vesicle 3) number of AcH receptors on the motor endplate. 4) Sensitivity of ACh decreased with prolonged exposure to ACh. More time required for ACh to bind to receptor.

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What happens to ACh in synapse when not taken up at motor endplate? -ACh esterase

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-if not taken up because of fatigue: 1) sensitivity decreased 2) less ACh receptors AcH esterase enzyme in the synapse (neuromuscular junction) starts to break down AcH. It is destroyed.

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Evidence for Skeletal Muscle Fatigue due to Neuromuscular Junction: -What happens with intracellular calcium within nerve endings?

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-decrease in intracellular calcium concentration within the nerve endings plays a key role (via exocytosis) in the quantity of neurotransmitter released. -may be not enough signal to cause exocytosis

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Skeletal Muscle Fatigue: Substrate Depletion

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-ATP -CP (Creatine Phosphate) -Glycogen -Glucose all depleted. all supply ATP.

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Skeletal Muscle Fatigue: Metabolite Accumulation List PPS MHL

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1) Potassium 2) Sodium 3) Phosphate 4) Hydrogen (h+) 5) Lactate 6) Mg

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Substate Depletion- PCr

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-PCr keeps ATP levels stable -Without it, impairment in force because loss of buffering capacity -ATP levels fall a little but remain fairly stable even after PCr gone, though (?). Small fall in levels causes extreme drop in force -Meanwhile, Lactate rising as we use glycolysis to generate ATP.

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Essential role of PCr -creatine kinase

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-PCr gives phosphate to ADP to form ATP. Creatine Kinase is the enzyme that helps this happen. -inhibiting Creatine Kinase prevents buffering of ATP concentrations by PCr.

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Two CK inhibitors (creatine kinase)

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1) DNFB 2) Iodoacetamide Treating a muscle with these leads to a 50 percent reduction in Po during contractions (rapid contractions)

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Glycogen Depletion -which type of exercise? -modifying diet.. what happens when you increase glycogen input?

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-fatigue for long term exercise (1-2 hours) -glycogen essential for maintaining submaximal exercise (70 percent of VO2) -manipulating glycogen levels via diet. more glycogen in diet increases performance time. less glycogen in diet decreases performance. This, however, doesn't change glycogen depletion rate, just changes how much you start with (still negative, linear relationship with negative slope_

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Blood Glucose Depletion -Which type of exercise

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-extreme fatigue for prolonged (3 hour) exercise

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Threshold for hypoglycemia and symptoms

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-less than 3mM (54 mg/dl) of blood glucose -immediate onset of fatigue -impairment in motor performance -sweating -decreased reaction time -this fatigue can be delated by supplying carb during exercise to prevent hypoglycemia

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Changes in Intracellular/extracellular concentrations of sodium (mM) during rest and exercise in motor neuron

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Intracellular Increases ^^^ 10 mM ---> 20 mM Extracellular Decreases 140 mM -----> 130 mM notice gradients are weakening

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Changes in Intracellular/extracellular concentrations of potassium (mM) during rest and exercise in motor neuron

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Intracellular Decreases 160 mM----> 130 mM Extracellular Increases*** 5 mM------> 11 or even 12 mM result: accumulation of K in the interstitial fluid (extracellular) notice gradient is weakening

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What happens when K accumulates in extracellular space? in MN

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-Extreme drop off in force at around 7-11 mM -AP impaired -Force impaired severely

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How do changes in Na and K during exercise affect RMP? -what happens to the APs now? in MN

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Increase in extracellular K and increase in intracellular Na results in an ELEVATION of RMP from -80 to -50 mV. but wouldn't this make it easier to depolarize it and cause AP? No -sustained changes in these concentrations actually leads to the desensitization in the voltage gated sensor of Na and K -even MORE depolarization required for them to open (to propagate AP) -when they DO open, influx of ions is less because the gradient has decreased for both Na and K. -\"mini\" AP generated that generates LESS FORCE.

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Curve for Tetatanic Tension vs. Extracellular K content. -shift to the left...why? -shift to the right...why? in MN

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-downward, sigmoidal curve. dramatic drop off at around 10. Curve Shift to the LEFT: becomes more sensitive to extracellular potassium, more likely to fatigue at lower levels (dropoff at around 8 mM K) 1) This occurs when the ratio of intracellular to extracellular Na+ rises (this occurs normally, see previous) Curve shift to the RIGHT: becomes less sensitive to extracellular potassium, less likely to fatigue at lower levels (dropoff occurs at around 11) 2) This occurs when Lactate levels RISE or when pH falls and H+ rises... not what you would normally think. Lactate is actually preventing fall in force..delaying onset of fatigue as is the decrease in pH.

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K and Na changes in the Transverse Tubule 1) Accumulation of K Why is it more dramatic? What happens to RMP?

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Accumulation of extracellular K even more dramatic than the motor neuron values (4-5x greater). as much as 50 mM of K+ extracellular! AND further accumulation of intracellular Na+ near surface of TT, making it more sensitive to K. Why? -large surface area of TT -small volume of TT So effects are even greater. Reduce membrane potential even further. (to, say, maybe -30 mV). -even harder to generate AP. -so even if AP able to be generated in MN, may not make it along the TT

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What happens when AP not propagated down TT?

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-DHP receptors (voltage dependent) won't release Ca -actin and myosin will remain inhibited

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Skeletal Muscle Fatigue: Accumulation of Pi -how does it accumulate?

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accumulates with breakdown of ATP.

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Skeletal Muscle Fatigue: Accumulation of Pi -effect on myofibrils (muscle fibers)

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1) Decrease cross-bridge interaction -myosin heads release Pi to ratchet forward -when too much myosin, can't release Pi. 2) Decrease force production during power stroke 3) Decrease Ca 2+ sensitivity -by decreasing troponin sensitivity to calcium -calcium removes troponin inhibition, allowing interaction of thick and thin

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Skeletal Muscle Fatigue: Accumulation of Pi -effect on sarcoplasmic reticulum (SR) -Ca 2+ handling

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1) Inhibits ATP-driven SR Ca uptake, so large calcium transient now isn't set up. 2) Reduce SR Ca for release. Ca trapped inside SR by Pi-Ca complex SR can't release this complex No cross bridge interactions

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Skeletal Muscle Fatigue- Ca sensitivity graph -shift to the right (less force, more Ca)

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1) calcium transients reduced 2) decrease in myofibril sensitivity to Ca (because troponin TnC unit doesn't have strong affinity for Ca) -more Ca, less force

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Skeletal Muscle Fatigue H+ accumulation

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1. NO effect on crossbridge production 2. NO effect on Ca release from SR 3. NO effect on fatigue resistance 4. Mild effect on RT 50% 5. Modest reduction in rate of crossbridge cycling. This causes decrease in velocity (Vmax) and Power. This effects type I fibers more than type II.

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Skeletal Muscle Fatigue Lactic Acid accumulation

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1. NO effect on crossbridge production 2. NO effect on fatigue resistance 3. NO effect on rate of crossbrige cycling (Vmax and power are unchanged) 4. PREVENTS force reduction (and fatigue) that are caused by increased extracellular K+************

Muscle Physiology- Skeletal Muscle Fatigue

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