Week 4 Notes - Fatigue PDF

Fatigue Powers & Howley Chapters 1, 3 and 19 Learning Objectives Define fatigue, central and peripheral fatigue Outline the factors that may influence the ability to identify mechanisms contributing to fatigue List and explain the possible sites of fatigue Define central and perip...

Fatigue Powers & Howley Chapters 1, 3 and 19 Learning Objectives Define fatigue, central and peripheral fatigue Outline the factors that may influence the ability to identify mechanisms contributing to fatigue List and explain the possible sites of fatigue Define central and peripheral fatigue and discuss factors that contribute to each Explain the accumulation and depletion hypotheses Describe and discuss central and peripheral factors affecting exercise performance durations 4 hours Factors Affecting Performance Fatigue is associated with each factor affecting performance Impair/ limit exercise performance  Outline the factors that may influence the ability to identify mechanisms contributing to fatigue Mechanisms Underlying Fatigue There is no single mechanism that accounts for a decline in performance as a result of fatigue under all conditions of exercise (Enoka & Stuart, 1992) https://www.youtube.com/watch?v=liCRrheKIOI https://www.youtube.com/watch?v=lBasZWjd92k  Mechanisms Underlying Fatigue cont.. Fatigue is task dependent Mechanisms underlying fatigue vary as the details of the task vary: Subject motivation Neural strategy (pattern of muscle activation and motor command) Intensity and duration of activity Speed of contraction Extent to which activity is continuously sustained (i.e. type of activity) (Enoka & Stuart, 1992)  Enoka & Stuart, 1992 CNS motor neurons muscles and motor units activated (neural strategy) neuromuscular propagation excitation-contraction coupling availability of metabolic substrates intracellular milieu (interstitial fluid) contractile apparatus muscle blood flow Enoka, R.M. and Stuart, D.G., 1992. Neurobiology of muscle fatigue. Journal of applied physiology, 72(5), pp.1631-1648. Mechanisms Underlying Fatigue cont.. Ability to determine mechanisms underlying fatigue are also influenced by: Fibre type (Type I or II) and distribution Training status of individual Trained individuals have greater resistance to fatigue than untrained/ lesser trained individuals (i.e. greater muscle glycogen stores, strength and lactate tolerance) Mechanisms Underlying Fatigue cont.. Environmental factors (heat, humidity, altitude etc) Whether voluntary or involuntary (i.e. electrical stimulation) Use of animal models (single muscle fibres or isolated muscle fibres) Muscles studied outside their normal environment may change how a muscle interacts with its surroundings and alter the level, type and source of fatigue Types of Fatigue Immediate – fatigue produced by a specific training stimulus e.g. fatigue experienced during events, reps/sets and immediately after competition/training session Residual – the general fatigue resulting from the total training session i.e. fatigue that continues after the cessation of a training session for a period of hours (e.g. 24-48 hours) Cumulative – long-term fatigue that results from entering the "stage of exhaustion" in the overall stress adaptation syndrome due to inappropriate rest between training sessions resulting in fatigue state being compounded (repeated stimulus too soon) Define fatigue, central and peripheral fatigue  Fatigue Inability to maintain power output or force during a prolonged muscle contraction or repeated muscle contractions Central fatigue: Brain and central nervous system Peripheral fatigue: Neural factors, mechanical factors and energetics of contractions Need to understand the mechanisms of fatigue across different types of exercise in order to: Prevent overreaching and/or overtraining, injuries etc Maximise training adaptation List and explain the possible sites of fatigue Sites of fatigue https://www.google.com/url?sa=i&source=images&cd=&cad=rja&uact=8&ved=2ahUKEwionuqT1KHkAhU OVH0KHcQBAmkQjRx6BAgBEAQ&url=https%3A%2F%2Fsimplifaster.com%2Farticles%2Fcentral- nervous-system-fatigue-effects-speed-power-athletes%2F&psig=AOvVaw2_Vv5eTiz9G8- __HgJ7hfG&ust=1566947163686413 Central Fatigue Refers to fatigue in the CNS (brain and spinal cord motor neurons). Central fatigue is indicated if: a) Reduction in number of motor units activated b) Reduction in motor unit firing frequency CNS arousal can alter the state of fatigue 160 140 By facilitating motor unit recruitment 120 Force (Nm) 100 Stim 80 Voluntary drive: motivation- less motivation reduces No Stim 60 40 level of signals to muscles 20 0 1 101 201 301 401 501 601 Physical or mental diversion= increased work output in Time subsequent bouts Central Fatigue cont.. Excessive endurance training (overtraining) Reduced performance Altered HR (resting & exercise) Altered mood, soreness Unmotivated, depression** Related to brain serotonin (neurotransmitter) activity, cortisol Exercise begins and ends in the brain Anticipation, recruitment of motor units and continual feedback Peripheral Fatigue Although evidence exists both for and against the CNS being a site of fatigue, greater body of evidence points to peripheral fatigue Neural factors Neuromuscular junction Sarcolemma – action potential Transverse tubules (T-tubules) Mechanical factors Cross-bridge cycling (actin-myosin interaction) Availability of Ca++ (SR) Energetics of contraction ATP availability Peripheral Fatigue: Neural Factors Neuromuscular Junction (NMJ) questioned as a site for fatigue axonal branch point conduction block action potential appears to (blockage of action potential) reach NMJ even when fatigued failure of excitation-secretion coupling; reductions in quantal release of ACh receptor desensitization, reduced sarcolemmal excitability Peripheral Fatigue: Neural Factors cont.. Sarcolemma Hypothesized sarcolemma might be the site of fatigue due to its inability to maintain Na+ and K+ concentrations during repeated contractions Na+/K+ pumps unable to maintain pace which results in K+ accumulation outside cell and a decrease inside the cell Can be improved by training result = depolarization of cell and a reduction in action potential amplitude K K + + Na + Peripheral Fatigue: Neural Factors cont.. Transverse tubules (T-tubules) under certain conditions like gradual depolarization of sarcolemma, altered T-tubule function (blocking of T-tubule action potential) can occur hence a reduction in Ca++ release from SR and a reduction in myosin cross bridge activation result = reduced ability of muscle to develop tension Peripheral Fatigue: Mechanical Factors Cross bridge cycling= primary mechanical factor Cross bridge cycling and tension development influenced by: Cross-bridge formation of actin and myosin Ca2+ binding to troponin ATP availability for binding and disassociation Fatigue may be due to: H+ interference with Ca2+ binding to troponin Reduced force per cross bridge Inability of SR to take up Ca2+ i.e. physical disruption/damage of sarcomere resulting from eccentric contractions Inhibition of Ca2+ release from SR Peripheral Fatigue: Energetics of Contraction Fatigue is due to a mismatch between the rate of ATP production and utilisation Fatigue results in slowing of ATP utilisation to preserve homeostasis (preventing cell damage) Accumulation of Pi ( P + ADP = ATP) Muscle fibre recruitment in increasing intensities of exercise (size principle) Type 1 to Type IIa to Type IIb/x Progression from most to least oxidative fibre types Exercise> 75% VO2max requires IIx fibres Results in increased use of glycolysis to maintain ATP production resulting in lactate/ H+ production Summary: Sites of fatigue CNS PNS H+ Models of Fatigue Catastrophic Model: Assumes that humans exercise automatically until metabolic failure in muscle or brain (1920’s AV Hill) Central Governance Model: Fatigue as a conscious sensation of changes in subconscious homeostatic control systems (St Clair Gibson and Noakes) Awareness Model: Brain is continuously in a conscious state At low intensities, actions are automated At higher intensities, actions require higher conscious involvement (Edwards & Polman 2013) Explain the accumulation and depletion hypotheses Possible Mechanisms- Accumulation Hypothesis High intensity exercise recruits Type II glycolytic fibres Accumulation of lactate and relationship with buffering capacity? Accumulation of H+ concentration that accompanies lactate accumulation Possible Mechanisms- Accumulation Hypothesis cont.. Influences muscle intracellular environment: inhibits phosphofructokinase (PFK) thus glycolytic rate, lactate dehydrogenase (LDH) and myosin-ATPase activity inhibits the SR ATPase reducing Ca2+ re-uptake and subsequent Ca2+ release which in turn reduces ability of muscle to produce tension (Davis & Fitts, 1998) H+ also competes for Ca++ binding sites reducing force capabilities reduced pH also inhibits FFA mobilisation resulting in a greater depletion of glycogen stores Type II fibres influenced more by acidic conditions than Type I fibres (lactate also used as a fuel) – why? (based on the above) glycolysis Possible Mechanisms- Accumulation Hypothesis cont.. Accumulation of inorganic phosphate when ATP production cannot keep pace with ATP utilisation inorganic phosphate (Pi) accumulates in the cell not converted to ATP accumulation of Pi can inhibit force production seems to act directly on cross bridges and their ability to bind to actin higher the concentration of Pi, the lower the force production Possible Mechanisms: Depletion (exhaustion) Hypothesis rate of glycogen utilisation dependent on: intensity and duration of exercise low intensity exercise = predominately fat metabolism as exercise intensity increases, CHO usage increases (think RER) as exercise duration continues, shift from CHO to fat 1 hr high intensity can reduce liver glycogen by 50-60% 2 hours at same intensity can nearly deplete liver and exercising muscle stores (Type I & Type IIa first) can reduce work output dramatically – rely heavily on fat metabolism as primary energy source (slow energy release) state of fitness of individual fit individuals have greater muscle glycogen stores and deplete them at a slower rate than unfit individuals Possible Mechanisms: Depletion (exhaustion) Hypothesis Fatigue occurs when exercise continues to the point where liver and muscle glycogen supply compromised even though ample fat supplies available hitting the wall or bonking hypoglycaemia (muscle stores and liver’s output fails to keep pace with muscle glucose use results in a reduction of circulating blood glucose) exact mechanism for low/depleted muscle glycogen coinciding with fatigue is not clear but may be due to: use of blood glucose for optimal CNS function muscle glycogen’s role as a primer in fat breakdown significantly slower rate of energy release from fat than CHO fatigue in endurance exercise may be related to degree of muscle use not necessarily glycogen depletion Describe and discuss central and peripheral factors affecting exercise performance durations 4 hours Ultra-short Duration Performance Events lasting