Mechanism of fatigue in the 100m dash…

Posted In: The Classics

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    jjh999 on #8314

    Ok, I figured I’d christen this forum since I’ve been lurking for a while…

    As Mike knows, I have a strong interest in further elucidating the mechanism of fatigue in the 100m dash.

    I have a strong suspicion (and I believe others share it) that the etiology of the fatigue has less to do with lactate (old-school thinking) and is much more a question of “bioelectricity”. I think that the fatigue is either occuring peripherally/post-synaptically at the level of the Na+/K+ pump or centrally/pre-synaptically-decreased neural drive.

    My own personal bias (with no data to support it) has been that it could be a firing rate problem. From that stance, I think that the problem could be in the refractory state of the Na+/K+ pump at the neuromuscular juntion. As maximum velocity is reached, the Na+/K+ pump is unable to maintain a bioelectrical gradient across the cell membrane and therefore unable to propagate an action potential.

    If that is true (which is a HUGE if), then why are the pumps “failing”? Insufficient ATP to drive the pumps? Not enough pumps?

    I’m interested to hear your thoughts. I know we have some great minds out there, so let’s have at it…

    (…I know, I know…more decaf…):)

    Mike Young
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    Mike Young on #19414

    JJ-
    How many times do I have to tell you….decaf is the one of the devil’s tools to keep us unproductive….drink as much coffee as you like! :D.

    Here’s what I’m thinking as of tonight…..I don’t think we can totally discount lactate as a source of fatigue (I’m not talking about soreness and lactate which is a whole other issue). In fact, I think lactate may play a role in fatigue but not as is commonly thought. Several studies have even shown a clear link between lactic acid accumulation and fatigue. However, I don’t think it’s the lactate itself that causes the fatigue but rather the chemical environment that the lactate accumulation creates. I can think of two ways lactate could possibly hinder muscle function. In the first possibility, an increased lactate concentration would cause a decrease in pH (increase in H+ concentration). The increase in H+ ions might hinder the excitation-coupling process by decreasing Ca++ released from the sarcoplasmic reticulum and possibly interfere with Ca++ and troponin binding (which wouldn’t be too far from your idea). In the other possibility, increased H+ concentration might inhibit enzyme activities that are important for anaerobic glycolysis. This would in turn reduce the ATP available for immediate energy.

    I’ll think about it some more later…..I need to go home now though.

    ELITETRACK Founder

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    Todd Lane on #19415

    Mike
    I’m no damn scientiest like kebba, but,,

    In the other possibility, increased H+ concentration might inhibit enzyme activities that are important for anaerobic glycolysis. This would in turn reduce the ATP available for immediate energy.

    is this impairment of enzymes, also same impairment of enzymes that will affect acetylcholine from being recycled at neuromuscular junction?

    still doesn’t answer question, just curious.

    thanks.

    Mike Young
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    Mike Young on #19416

    Todd-
    Consider yourself a quasi-scientist or even an honorary scientist because that was exactly what I was thinking.

    ELITETRACK Founder

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    jjh999 on #19417

    Hey Scientists,

    I think that you are referring to acetlycholinesterase as the enzyme that recycles ACh…

    I need to look this up, but I don’t think that over a 10s period that ACh levels would drop by a degree that muscular contraction speed would decrease. That enzyme is pretty plentiful and I have a hunch that H+ ion levels would need to be higher or elevated for a longer period of time before you witness the deformation of the enzyme binding sites for ligands or cofactors. I think that decreased effectiveness of acetylcholinesterase may be an issue after about 30-40s of sprinting, though…

    I need to pull out the neuromusc. phys. text so I speak more intelligently…

    🙂

    Mike Young
    Keymaster
    Mike Young on #19418

    I wrote Dan Pfaff and asked what he thought about this question since he’s coached quite a few decent 100m guys (that’s a huge understatement if you don’t know who he’s coached). Here’s his reply:


    I am positive that it is neurochemical and or pathway propagation problems……Your hypothesis is and has been looked at by some of the leading researchers in this area but alas technology limits hinder the exploration. Pumps fail because of osmotic gradient environments and or ion concentration levels……….despite the lack of concrete answers I think this track is correct so the ergonomic solution is to build bigger batteries and develope additional pathways and routing mechanisms……….I think the same thoughts and never drink coffee after noon……..dan

    ELITETRACK Founder

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    lumberjack on #19419

    [i]Originally posted by mike[/i]
    despite the lack of concrete answers I think this track is correct so the ergonomic solution is to build bigger batteries and develope additional pathways and routing mechanisms……..dan[/i]

    Interesting question JJ. That is about the answer I expected from Dan. Now the obvious next question is what are the best methods of building a bigger ‘battery’?

    I would think the simplest and most direct method would be to ensure that you are working on maximum velocity sprints in that time frame of 8-12 seconds or from 80 to 120m as the racing season approaches. But are there other forms of training that could have some carryover?

    At one point in my running career, when I ran 10.56/20.90, I worked on all of the parts of the 100m in isolation but not the whole thing except during races. For example my speed work consisted of isolated work on top end (max velocity with a long easy buildup), Accelerations up to 30m, and maximum speed runs mainly around 150m. When I trained like this I found I could have strong sections of 100m races, but I could never put a whole run together.

    When my training had more work at maximum speed between 60 and 120m I felt like I could run the 100m from start to finish and my times dropped to 10.37 and interestingly enough my 200m time also improved to 20.51 without running anything beyond 120m in training.

    Granted some of these improvements were due to some technical changes implemented by Dan Pfaff and my coach Stu McMillan. But I really feel that once I regularly included that type of work between 60 and 120m I could ‘run the whole 100m race’. As if I could open the throttle and keep it open longer.

    Does anyone have any more ideas of how you could ‘build bigger batteries and develope additional pathways and routing mechanisms’ other than the obvious putting in more work in that specific time frame of max effort for 8-12 seconds?

    Carl Valle
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    Carl Valle on #19420

    Any shift to improve a neurochemical/enzyme repsonse is based on on two primary training paths. One is increase the intensity of the stimulus, and the other is to increase the tolerance to the fatigue of race conditions. Dan suggests we do the following.

    (1) Create a bigger battery
    (2) Add more wires from the existing battery

    I agree with this statement since tollerance is an addaptation to 80-140m work. Speed endurance is a well known training aspect but nobody can explain how it works well enought beyond just stating the obvious. Take a look of some of the research of antalopes. They are running at near speads of 68 mph and maintain that speed far longer then a cheetah (minutes vs seconds). I don’t think it is all neurochemical, perhaps a part the old school lactate theory has some influence since the onset of that byproduct can be changed based on 3 factors.

    (1) Antagonist relaxation- allowing the fibers to rebound instead of contracting the whole time. This can be learned from both coaching and repetitiion.

    (2) The power shift of having a better strength to weight ratio from general and specific means.

    (3) The lactate shift from acceleration work, speed, and speed endurance work.

    After listening to Dan speak I felt that the nervous system can be improved by a carefull balance of various submaximal contractions such as medball throws, cleans, and jump training. This will expand the battery “envelope” so that such high velocity runs can resist fatigue.

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    Kebba Tolbert on #19421

    Originally posted by Lumberjack

    Does anyone have any more ideas of how you could ‘build bigger batteries and develope additional pathways and routing mechanisms’ other than the obvious putting in more work in that specific time frame of max effort for 8-12 seconds?

    given my experience i think that a few of the following (by themselves, but even more so in the “right combination) can make hug differences in the manifestation of fatigue in sprints/hiurdlles.

    1) we all know that elastic energy is cheaper and more efficient. so training that promotes the ability to “endure” (used very loosely) elastically is crucial. this is why i really like to do endurance bounding in various modes and volumes throughout the year.

    it’s impt to remember that posture plays a *hugh* role in how elastic force is generated and used so sometimes simply by correcting errorsa here you get a gain in terms of the abiility to sustain high level efforts.

    i think that Glenn’s thoughts about “longer” runs is interesting in that by doing stuff from 60-120 it can help teach you how to wait and what to do. if you’re doing competetive 70’s or 90’s or 120’s and you blow your wad too soon you just suffer the last 1/3 or so. so some of the longer runs force you to distribute evenly and progressively because of the price you have to pay (physically and psychologically if you don’t)

    [i remember Leroy Burrell commenting at a clinic about SMTC practices – “if you came out and were playing around or weren’t on top of your game you’d simply get embarassed”}

    2) wt room – the firing rates, angular changes, postural demands, timing considerations, psychological pressure (getting pysched up to move a heavy, challenging load) can be huge here. So even though everyone says that the loads and speed of movement are too slow to be specific there’s a lot of stuff going on that building capacity to withstand the challenges of sprints/hurdles. there are a bunch of diff capacities required in the sprints and a lot of it can be addressed in the wt room in at least a remedial fashion.

    i think that the “bigger battery” theory is huge… it’s similar to the “energy envelope” theory that was being discussed on Charlie’s website last summer

    so bigger battery/bigger envelope to me is creating more potentiall… gotta run to practice, but will post more on this later.

    Mike Young
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    Mike Young on #19422

    Clemson welcome to the board. I didn’t quite follow what you said in your last post. Specifically, this statement……

    [i]Originally posted by Clemson[/i]
    I don’t think it is all neurochemical, perhaps a part iold school lactate since the onset of that byproduct can be changed based on 3 factors…….

    Did you think lactate is a possible cause or is not a cause?

    ELITETRACK Founder

    Mike Young
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    Mike Young on #19423

    I don’t really think we can so much train to increase our elastic qualities as we can teach (in an obviously implicit manner) to take advantage of the potential elastic properties of the musculo-tendinous unit. From my understanding the elastic properties of the muscle-tendon unit should be somewhat fixed. Small gains may be seen in:

    1. The ability to sustain / handle quasi-static muscular contractions under high loads and velocities.

    2. Soft tissue remodelling to create tendons that respond more elastically to a given force vector.

    Overall though I think the most beneficial gains would be in training or teaching an individual to tap into the elastic energy (reliance on tendon elasticity but dependent on muscular quasi-static strength) rather than relying on muscular contraction to produce force.

    ELITETRACK Founder

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    Kebba Tolbert on #19424

    [i]Originally posted by mike[/i]
    I don’t really think we can so much train to increase our elastic qualities as we can teach (in an obviously implicit manner) to take advantage of the potential elastic properties of the musculo-tendinous unit. ……Overall though I think the most beneficial gains would be in training or teaching an individual to tap into the elastic energy (reliance on tendon elasticity but dependent on muscular quasi-static strength) rather than relying on muscular contraction to produce force.

    i think we’re basically thinking along the same lines, you just worded it better:)

    Carl Valle
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    Carl Valle on #19425

    Mike, I think that lactate is part of the fatigue formula, but I am eager to see what biochemical pathways and neuropeptide channels cause the loss of power at the end of the race. Is is something we can train besides sprinting, or is a general element that can be worked on by many different submax aspects? This thead rexamines a old concept with a far different light.

    CNS fatigue is like what lactate work was in the 70s and early 80’s. Getting closer to better answers.

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    jjh999 on #19426

    Hey guys,

    I’m on the road right now, so I just skimmed the responses, but they look fantastic. I’m going to talk to Dan today (in Austin) and hopefully get more of his thoughts re: building a better battery.

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    carson on #19427

    Very interesting topic. I am skeptical about big pH changes in the muscle over 8-10 seconds, and think many of the points made so far are worth looking into.

    What has always fascinated me is that when one looks at energy systems from an old school perspective, the 200m really throws a wrench into the theory of ATP-CP pool, pH changes etc.

    Look at Lumberjack´s post. 10.37 and 20.51. Then look at Mennea´s 200m record – 19.72, and MJ at 19.32. Don´t know how fast MJ and Mennea were over 100m, but I doubt that Mennea was much faster than 10.00.

    I have no answers, but the 200m seems to make this topic even more challenging.

    I tend to think along the lines of neurotransmitters, harnessing and utilizing elastic energy, and maintaining coordination and rhythm.

    Charlie Francis has also discussed breathing pattern changes later in a 100m and how they may affect the speed curve.

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