Lecture 5 activation hisotry.pdf

Activation history: potentiation and neuromuscular fatigue Michael Paris School of Kinesiology and Health Science York University, Toronto, ON Learning objectives Explain muscle potentiation and its effects on force output and motor unit firing rates Define neuromuscular fatigue Describe the central...

Activation history: potentiation and neuromuscular fatigue Michael Paris School of Kinesiology and Health Science York University, Toronto, ON Learning objectives Explain muscle potentiation and its effects on force output and motor unit firing rates Define neuromuscular fatigue Describe the central and peripheral components of neuromuscular fatigue Muscle twitch potentiation Post-Activation Potentiation Same input to muscle (twitch), significantly more force output in the potentiated state – why? How will MU firing rates be affected by potentiation? Changes in MU firing rate (@20% MVC), and twitch potentiation after a 5s, 75% MVC Activation history: muscle potentiation Brief (3-10s) high intensity (50-100%) tetanus, or voluntary contractions enhance the active state Assessed by twitch potentiation of 150-200%, exponential decline with time for several minutes Result: larger twitches summate to greater forces than smaller twitches; thus a given force can be achieved with less neural input to the system Effects only submaximal levels of effort 2 likely mechanisms: (there may be others) Ca2+ kinetics at the SR level Myosin light-chain phosphorylation during actin/myosin interaction Neuromuscular Fatigue What is limiting the ability to continually flex the finger under a fixed load? Reduced ROM due to fatigue Task terminated – unable to voluntarily flex finger Activation history: Neuromuscular Fatigue Any reduction in the ability to exert force or power in response to voluntary effort (exercise), regardless of whether or not the task can be performed successfully. Weakness: Inability to generate an initial force appropriate for the task Exhaustion: Endpoint of performance Fatigue processes begin almost immediately, but what part(s) of the system are failing? Depends on the task Why is it not possible to keep it up indefinitely? Compensatory mechanisms to minimize fatigue? Task Specificity and Fatigue Isometric Concentric Eccentric Sustained Intermittent Fast Slow High Intensity Low Intensity Trained Untrained Healthy Unhealthy Male Female Younger Older Need to define a task to understand the outcome Different outcome depending on the task and population Strength / duration relationship Possible sites of fatigue in the neuromuscular system PERIPHERAL Muscle blood flow Motor cortex E-C coupling Intracellular milieu (metabolism) CNS drive to LMN Contractile apparatus NMJ MU activation Metabolic substrates Maximal or high intensity (>50% MVC) exercise is associated with reduced force and contractile slowing STIMULATED Muscle response: reduced force AND slowed contractile speed What is causing the decrease in peripheral force generating capacity? Many force-generating factors affected by metabolic perturbations 1) Reduced force/cross-bridge 2) Reduced Ca+2 sensitivity 3) Reduced Ca+2 release from SR Big controversy on the relative contributions of these metabolites and their impact on the fatigue response Why limit force output in the presence of a high metabolite? Prevent catastrophic consequences of ATP depletion! Finger can still be flexed, but only with electrical stimulation… limitations also within central systems Reduced ROM due to fatigue Task terminated – unable to voluntarily flex finger Recovery period – some restoration of fatiguerelated impairments Superimposed twitch is increasing throughout a fatiguing task Remember… the superimposed twitch technique evaluates the degree of musculature active 1. Motor units not recruited 2. Motor units not firing maximally More force will be observed (interpolated) during the stimulation Decreasing ability to fully activate muscle indicates fatigue within central systems Motor unit firing rates during sustained maximal contraction They decline Possible factors that decrease muscle activation (reduced firing rates) with fatigue increased inhibition decreased excitability from supraspinal centres peripheral feedback from exercising muscle decreased intrinsic excitability Some combination depending on task Decreased descending drive from corticospinal tract during sustained MVC Is it good or bad that firing rates decline as muscle contractile speed is slower? Firing rates seem to be reduced in relation to slowed muscle: speed / firing rate match is maintained. No benefit to having firing rates higher than needed for full tetanus Sub-maximal tasks - Motor units and fatigue Combination of recruitment and rate coding from voluntary contraction 35% MVC - submaximal Task specificity Submaximal intermittent exercise Maximal sustained exercise EMG Force Force 100% MVC – for 60s 35% MVC 2s 2s 2s … for 5 minutes What accounts for loss of force? It depends on the task! (and population…. more on this later) E-C coupling: 1) Ca+2 impairments: reduced sensitivity and release 2) Myofibrillar impairments: reduced force/cross bridge Spinal and supra-spinal activation 1) Motor unit firing rates decrease during sustained maximal contractions Muscle wisdom – is the decreased firing rate a beneficial adaptation?? 2) BUT motor unit output still may not be enough to ensure maximal activation…. How much does it affect the actual force output? 3) Sub-maximal efforts EMG increases, until contraction becomes maximal