NEUR3101 Lecture Notes on Central Fatigue PDF

Central fatigue Dr. Frederic von Wegner WARNING  This material has been reproduced and communicated to you by or...

Central fatigue Dr. Frederic von Wegner WARNING  This material has been reproduced and communicated to you by or on behalf of the University of New South Wales in accordance with section 113P of the Copyright Act 1968 (Act).  The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act.  Do not remove this notice Learning objectives - Give a definition of muscle fatigue and central fatigue - Describe twitch interpolation - Describe the behaviour of spinal motor neurons during sustained contractions (firing rates, excitability) - Explain the role of group III/IV and group I afferents - Describe changes in the motor cortex - Discuss the role of neurotransmitters - Given an overview of central vs. peripheral factors in muscle fatigue Literature Textbooks: - Purves, Neuroscience (Oxford University Press) - Guyton-Hall, Textbook of Medical Physiology Articles: - S. C. Gandevia, Spinal and supraspinal factors in human muscle fatigue. Physiological Reviews 81(4), 2001 - J. L. Taylor et al., Neural contributions to muscle fatigue: from the brain to the muscle and back again. Medicine and Science in Sports & Exercise, 48(11), 2016 Muscle fatigue remember from Lecture 16: Def. muscle fatigue: an exercise-induced reduction in the ability of muscle to produce maximal force or power (whether or not task fails) protocol: interrupt task and measure decline in maximum contractions (voluntary or electrical) - fatigue is not: task failure or complete exhaustion - fatigue: decrease in MVC force, submaximal force can often be sustained Central fatigue: - all changes proximal to the neuromuscular junction: brain, spinal cord, but also peripheral nerves Peripheral fatigue: - all changes distal to, and including the neuromuscular junction Maximal effort: really? - voluntary activity in “maximal” effort is actually submaximal - central (=brain) effects, lecturing shouldn’t affect max. muscle power! - electrical stimulation can recruit fibres that the brain could not Gandevia, Physiol Rev 2001 Maximal effort: really? - what else could you do to stimulate force production? Gandevia, Physiol Rev 2001 Maximal effort: really? - what else could you do to stimulate force production? - how to measure / quantify this effect? twitch interpolation Gandevia, Physiol Rev 2001 Twitch interpolation add supramax. electrical stimulus 1) during MVC = superimposed twitch (how much can stim. add on top?) 2) after MCV = rest twitch (how much can stim. get?) voluntary voluntary activation = (1-(superimposed/rest twitch)) x 100% Maffiuletti, J EMG and Kin., 2016 Twitch interpolation add supramax. electrical stimulus 1) during MVC = superimposed twitch (how much can stim. add on top?) 2) after MCV = rest twitch (how much can stim. get?) Example: super/rest = 1/5 vol. activ. = (1 – 1/5) x 100% voluntary = 80% voluntary activation = (1-(superimposed/rest twitch)) x 100% Maffiuletti, J EMG and Kin., 2016 Twitch interpolation: peripheral and central stimulation “rest” “rest”.../wiki/Transcranial_magnetic_stimulation Gandevia, Physiol Rev 2001 1. During central fatigue, the superimposed twitch will grow (I can add more…) 2. Voluntary activation decreases during central fatigue (the same, in other words…) 3. Twitch interpolation can measure central fatigue (practical use) Reducing central fatigue voluntarily voluntary electrical “super effort” Gandevia, Physiol Rev 2001 Training effects on MVC - training effects: - electrical stimulation: ~10% increase in max. force - MVC: >30% increase in max. force (??) - how can electrical stimulation be less effective? brain + spinal cord are smarter than the electrical stimulation! - no antagonist activation - activation of synergists, - stabilization of adjacent joints at optimum angles Gandevia, Physiol Rev 2001 Recovery from central and peripheral fatigue 1 2 3 1. isotonic MVC => fatigue 2. electrical stim. => larger force, restores central fatigue, not peripheral fatigue 3. complete rest (1 min.) => full recovery Gandevia, Physiol Rev 2001 Motor unit types and fibre types Purves, Neuroscience Fatigue: neuronal firing patterns - firing rate of a single motor unit (thumb) 1 minute MVC - observation: decrease of firing rate Gandevia, Physiol Rev 2001 Fatigue: neuronal firing patterns - firing rate of a single motor unit (thumb) 1 minute MVC - observation: decrease of firing rate but: not continuous Gandevia, Physiol Rev 2001 Motor unit firing - remember: force output is regulated by firing rates and recruitment of motor units (increasing size) - basic firing rate: 5-10 Hz, some bursts - large firing rates: 50-60 Hz - long endurance, low intensity: MU rotation motor units (MU) are de-recruited and re-activated later - during MVC: MU firing rates decrease (up to 50%) Stanfield, Principles of Human Physiology Motor unit firing - remember: force output is regulated by firing rates and recruitment of motor units (increasing size) - basic firing rate: 5-10 Hz, some bursts cerebral drive - large firing rates: 50-60 Hz - long endurance, low intensity: MU rotation motor units (MU) are de-recruited and re-activated later - during MVC: MU firing rates decrease (up to 50%) afferents - mechanisms: - less drive from the motor cortex - adaptation of the alpha-motoneuron in the spinal cord local - inhibitory feedback from the periphery adaptation Stanfield, Principles of Human Physiology Motor unit firing with increasing force 1. low intensity (50% MVC): all MUs finally show decreased firing rates Stanfield, Principles of Human Physiology Isolated motoneuron excitability 1. repeated current injection into motoneurons => firing rate decreases, excitability ↓ 2. recording of a single motor unit, subject maintains constant firing rate => other MUs are recruited interpretation: increasing descending drive needed to maintain the motoneuron firing rate 3. magnetic current stimulation of the cervical spinal cord during elbow MVC => reduced muscle response Summary: repetitive activation of motoneurons reduces excitability mechanisms unknown Gandevia, Physiol Rev 2001 III IV Purves, Neuroscience Group III IV afferents 1. group III sensitive to mechanical (contraction, stretch) group IV to chemical stimuli (lactate, ATP, H+) some only to “noxious” (damage) metabolites => increased activity during intense exercise (remember the muscle pain lecture!) 2. direct inhibition of motoneuron pools 3. indirect MN inhibition by inhibiting Ia (spindle) afferents 4. inhibition of descending drive from the brain and proximal spinal centres 5. activation of heart rate, respiration rate Baehr, Topical Diagnosis in Neurology Group Ia spindle afferents 1. basic function: activate motoneuron when muscle is elongated (length controller) 2. sustained submaximal isometric contraction => progressive decrease in afferent activity 3. normally: gamma-alpha-coactivation fatigue: less gamma activation => spindle sensitivity ↓ => H-reflex decreases during fatigue 4. other afferents: Golgi tendon organ (GTO) and Renshaw cells (inhibitory feedback) play no role, low firing rate in fatigue Boron, Medical Physiology Gandevia, Physiol Rev 2001 Gandevia, Physiol Rev 2001 Motor cortex role in central fatigue 1. surface EMG activity increases during submaximal contractions and motor evoked potentials (MEPs) increase => interpretation: motor cortex (M1) facilitation => possible compensation of spinal inhibition 2. but: increased drive from the motor cortex is transient, longer lasting activity: reduction and/or ‘suboptimal’ drive 3. using the superimposed twitch method, supraspinal fatigue might contribute ca. 25% to force loss in short MVCs, and up to ca. 60% in long duration, low intensity exercise ( fatigue - but: pharmacological interventions inconsistent: 5-HT - 5-HT has wide-ranging effects, numerous receptors - peripheral effects: vasoconstriction/-dilation, cardiac - 5-HT ‘spill over’ hypothesis small amounts 5-HT: excitation (synaptic receptors) large amounts 5-HT: inhibition (other receptors) DA - methylphenidate (DA↑) increases core temperature and performance, unaltered perceived effort/temperature => elevated risk (‘safety switch off’) Summary: pharmacological modulation of neurotransmitter NA states cannot reliably influence central fatigue Summary α-motoneuron activity 4 1. repeated motoneuron firing => excitability ↓ (mechanisms unclear) 1 5 2. afferents group III (Aδ) / IV (C): sensitive to mechanical and chemical stimuli, increased activity during intense exercise inhibition of most MN 2 3. Ia afferents from muscle spindles: decreased firing => decreased excitation of alpha-motoneurons 3 4. ‘supraspinal fatigue’: transient increase, then decrease from the motor cortex 5. serotonin (5-HT) hypothesis: ‘spill over’ Taylor, Med. & Sci. in Sports and Med., 2016 central fatigue M1 neuron excitability α-motoneuron excitability peripheral feedback peripheral fatigue muscle fibre excitability metabolic processes Gandevia, Physiol Rev 2001 Thank you!