Why do marathon runner slow down – the role of muscle damage

While planning the next few months of base-building for a marathon in the autumn, I have been pondering the question of what are the most important foundations for marathon running.   The marathon is run in the upper reaches of the aerobic zone, so at first sight, the most important goal of training is extending the duration for which one can maintain a pace in the vicinity of lactate threshold.   This requires a good capacity for metabolizing lactate, so developing that capacity will be part of my base-building.

Perhaps the most infamous feature of the marathon, at least in the mind of many recreational runners is the ‘wall’ that awaits somewhere near the 20 mile mark.   It is often assumed that this wall reflects the point at which glycogen stores are exhausted, and all available glucose is shunted away from muscle to the brain.  For the ill-prepared runner, that might well be a major issue, but dealing with the risk of serious glucose depletion should be relatively straightforward.   A large volume of low to mid-aerobic running and sensible nutrition in the preceding months should ensure that a good proportion of the fuel at marathon pace is derived from fat, thereby conserving glycogen, which together with adequate ingestion of carbohydrates during the race itself, should minimise the risk of a shortage of glucose.

While it is true that for many marathoners the gruelling memories are centred on the final few miles, in my own memories of the times when I have run a marathon with inadequate preparation, the  point at which I became aware that I was not running well occurred shortly after half-way.   At that stage, the problem wasn’t breathlessness, or agony.  It was a loss of fluency in my stride.   I was therefore intrigued by Reid Coolsaet’s account of his tribulations in Fukuoka in December.   Reid’s blog provides the best personal account of elite marathoning available on the web.

Reid Coolsaet in Fukuoka, 2013

Reid had arrived in Fukuoka better prepared than ever and was aiming for sub 2:10; a PB and a Canadian national record.  He started in the leading pack behind the pacemakers, Collis Birmingham and Ben St. Lawrence from Australia, running 3 min Kms (2:07 pace).  When the lead pack split on an upward slope just before 16Km Reid sensibly opted to stay back with the second group, which included one of the current leading Japanese marathoners, Arata Fujiwara, who has a PB of 2:07.  However Fujiwara was having a bad day and the second group slowed too much so Reid left them at 18Km and ran on alone.   He was still comfortable maintaining his target pace when he reached half-way in 1:04:11.  He then lost a few seconds as a consequence of grabbing the wrong bottle at the 25.8Km water station.  He covered the 5Km from 30 to 35 Km in 15:51 but was not too worried at that stage. He reports that after 35km the going got really tough and he began to ‘lose it mentally’.  He eventually finished in 6th place in a very creditable 2:11:24, just over 5 minutes behind the winner, Martin Mathathi of Kenya.

Reid had again demonstrated that he is not very far behind the best of the current North American marathoners, despite lacking the resources of Nike’s Oregon Project.   In his own analysis, the problem was running solo from 18Km to the end.  That was almost certainly part of the problem.  However, despite the seconds lost as a result of the confusion with the wrong bottle at 25.8Km, I think that the crucial evidence that the wheels were coming off was the 15:51 split from 30 to 35 Km. I suspect that the damage had been done in the first 15 Km, which he had covered about 1 minute too quickly.   But what was the damage he had done?   I doubt that the burning a little more glucose in the first 15 Km nor the confusion with his re-fuelling had left him in a glycogen depleted state by 30Km.

Running pace decrease and markers of muscle damage during a marathon

I think perhaps a clue is to be found in the recently published study of marathon runners by Juan Del Coso and colleagues from Madrid.  Del Coso performed a variety of physiological measurements on a group of 40 amateur runners immediately before and after the 2012 Madrid Marathon.  The investigators retrospectively divided the runner into two groups according to how well they maintained pace during the race.  The group of 22 runners who exhibited a decrease in pace of less than 15% from the first 5Km to the end were classified as having maintained their speed, while the group of 18 runners who slowed by more than 15% between the first 5Km and the end were classified as having a pronounced decrease in speed.  The decreased speed group slowed their pace by an average of 29% while the group classified as having maintained speed exhibited an average decrease of 5%.

The most interesting feature of the 5Km split times over the course of the race was the fact that the group with a pronounced pace decrease began to slow-down  markedly shortly after half way.  The difference in pace between the two groups became statistical significant for the split from 20 to 25 Km.  But even more interestingly, the most significant difference in the physiological measurements was a much greater increase in the blood levels of the muscle proteins, myoglobin and lactate dehydrogenase, between the start and finish in the group who slowed.  These proteins are markers of muscle damage.    Both group exhibited a decrease in counter move jump (CMJ) height from before to after the event, but this decrease was greater in the group who slowed substantially.  The group who maintained their speed exhibited a 23% decrease in CMJ height, while the group with pronounced slowing suffered a 30% decrease.

Both groups of runners exhibited a decrease in weight of approximately 3%, assumed due to dehydration.   There was no evidence of decrease in blood glucose in either group.  The runners had been allowed to take fluids and carbohydrates according to their own inclination during the race.  There was no appreciable group difference in body temperature.  Thus, there was no evidence that dehydration, decrease in blood glucose, or hyperthermia, accounted for the different degree of slowing of the groups.  It is also noteworthy that there had been no significant difference in prior training volume between the groups. In fact the group who showed the most pronounced slowing has actually performed a slightly larger volume of training.

Thus the findings from this study suggest that for reasonably well- trained amateur runners who are allowed to re-hydrate and re-fuel according to their own inclination during the race, the major feature that is associated with deteriorating pace is muscle damage.  Furthermore the deterioration becomes manifest shortly after the half-way point.

The observation of appreciable loss of strength and power, together with increased levels of muscle proteins in blood indicating skeletal muscle damage during endurance events, has been reported previously.  For example, the year previously Del Coso and colleagues had studied 25 triathletes participating in a half-ironman event.  They found that after the event, the capacity of leg muscles to produce force was markedly diminished while arm muscle force output remained unaffected.  Leg muscle fatigue was correlated with increases in blood levels of the muscle proteins, myoglobin and creatinine kinase, suggesting that muscle breakdown is one of the most relevant sources of muscle fatigue during a half-ironman.

My own experience

Looking back to my own experience in the half marathon in September, I was aware of aching legs though much of the race. Indeed I had been experiencing pronounced aching of the legs following most of my long runs during the preceding months.  In my recent post I had discussed the possible role of elevated cortisol in my mediocre half marathon performance.  While a link between cortisol and muscle damage is speculative, it is perhaps plausible that sustained elevation of cortisol had left me in a catabolic state with reduced capacity to repair muscle damage following long runs, for a period of several months.

What are the implications for base-building this year?  The first implication is that I should build up the length of long runs cautiously to minimise the risk of developing a catabolic state. I am even considering adopting Geoff Galloway’ s run/walk approach to see if I can build-up to a weekly training volume of 50 miles or more without persistent aching of my legs.   A far as I can see there has been little good independent scientific investigation of the run-walk strategy though I think there are reasons to think that it might be a sound approach – and not just for elderly runners such as myself.   I will discuss this in a future post.

An alternative approach is to include more sprint training.   In a study of the muscle damage produced by drop-jumping (which is often regarded a good model f the eccentric stress produced by running, Skurvydas and colleagues compared sprinters with long-distance runners and a group of untrained controls.  Following 100 maximal effort drop-jumps, the sprinters experienced a smaller reduction in counter-movement jump height than the other two groups, while there was no appreciable difference in evidence of damage suffered by the distance runners and the untrained controls.  It appears that sprint training might protect against muscle damage much more effectively that long-distance training.


25 Responses to “Why do marathon runner slow down – the role of muscle damage”

  1. Ewen Says:

    Interesting topic Canute. With Coolaset’s marathon, do you think he would have mainted even 5k splits further into the race had the initial pacing group been running at 2:08:30-2:09 pace? I think a very small misjudgement on goal pace in a marathon can cause big problems later in the race. Could the muscle damage have been forestalled to 35k if the earlier pace had been slower?

    On the drop-jumping study, couldn’t it be that the sprinting group suffered less muscle damage because that type of movement is closer to the movement that they use in their event (than the distance runners)?

    • canute1 Says:

      I agree that a small misjudgement of pace in the early stages makes a big difference later in the race. This was evident in London 2013 when the first half was about a minute too fast and the entire elite field subsequently hit the wall. Interestingly Tsegaye Kebede realised what had happened and eased off early in the second half enabling him to pick off the leaders one by one in the final few Km, but even Kebede’s winning time was somewhat slower than his winning time in Chicago in 2012.

      I think that Reid Coolsaet might well have deferred the damage if he had run a minute slower over the first 15 Km. In my one marathon in middle age – the Robin Hood in 2004 – which I ran after a very inadequate preparation mainly to get a sense of what starting in a field of 10,000 runners would be like, I was tempted to run too fast to escape the melee in the early stages. By 25 Km I was not running fluently and when I hit a patch of rough road surface approaching Holme Pierrepoint at about 29Km I could feel that my leg muscles were shredded.

      Yes, almost certainly drop jumping was less damaging for the sprinters than distance runners because the eccentric loading of drop jumping is more like the loading experienced during sprinting, but the point is that Del Coso’s study of the half iron-man suggests that reduced CMJ height is associated with the type of muscle damage experienced during endurance events, and his study of the marathon suggests that similar muscle damage is associated with substantial slowing during the marathon.

  2. Mike Says:

    The runners that slowed down considerably in the marathon study – did they not just set off that bit too fast for their ability on the day – the commonest mistake that amateur marathon runners make?

    • canute1 Says:

      Thanks for your comment. Yes, the runners who slowed substantially did set off too fast. The question I am addressing could be re-framed: ‘What physiological system cracks first when you start too fast and is there any way of training to reduce this problem? ‘ Is it running out of glucose; or dehydration or over-heating or something else? Del Coso’s studies suggests that the limiting factor might be muscle damage, and Skuvydas’ data suggests that sprint training might help reduce this. But I accept that this is speculation. Nonetheless it is noteworthy that the runners who slowed more than 15% in Del Coso’s study had done a slightly larger volume of training than those who didn’t slow as much.

      Nonetheless, there were two other possibilities that I think might be important that Del Coso did not address. Did those who slowed excessively accumulate too much acidity or alternatively, did they lose too much intra-cellular potassium? I think that both of these are plausible issues.

  3. Robert Osfield Says:

    Happy New Year Canute 🙂

    Your post touches on stuff I’ve been thinking about and has spurred me to pen down my thoughts on a model I’m working on to try and encapsulate all that goes into achieving a good race performance in marathon and ultra-marathons races. I did start writing it out as reply on this post, but after a couple of paragraphs realized that it’d be far better to just put up a post on my own blog.


    It’s getting late here now so I’ll pen reply specific to your blog entry tomorrow.

    • Robert Osfield Says:

      In my post “Introducing the Concept of Aerobic Resilience” I’ve categorised muscle damage under the Structural Resilience.

      Pacing strategies have an effect on muscle damage, if you go out too fast then you’ll accumulate more muscle damage early in a race that you then have to accommodate for the rest of the race. Muscle damage impacts our running economy so our speed for a given intensity level goes down, and the pain it produces also puts greater strain on our Mental Resilience, as does the extra effort required to maintain pace, so eventual Mental Resilience can crumble and if it does will loose any will to keep pushing on through the discomfort.

      Runners with good Structural and Metabolic Resilience are likely to be able to cope with errors in pacing far better than runners that are weak in these areas. High Mental Resilience can go some way for making up with weaknesses in Structural and Metabolic Resilience but it’s hugely stressful on the body and mind.

      I believe that Structural Resilience is probably best built up during long runs, downhill running and other forms of exercise that stress eccentric loading of muscles and ligaments. Strength training and high intensity training is likely to put more strain on soft and hard tissue as well and should help develop stronger and more resilience.

      Metabolic Resilience is fundamentally about how well you body can cope running off fats rather than limited stores of carbohydrates. Basic aerobic fitness is obviously crucial, but you also need the enzymes to specifically handle fat metabolism. Training that maximizes aerobic fitness and a diet that enables naturally high levels of fat metabolism are key.

      Training specifically to improve your ability to metabolize lactate via the Cori cycle would help with Metabolic Resilience but it’s something I’d only see as a small contribution to performance at the marathon and longer distances. I believe it’s far more important to build you basic aerobic fitness and fat metabolism so you are burning more fat and generating less lactate for a given pace.

      However, training at lactate threshold and faster is an important part of building overall aerobic fitness so still has an role in training.

    • canute1 Says:

      Happy New Year and thanks for your detailed comment. I agree with most of the points you make. While I agree with the importance of increasing your capacity to utilize fats, I think you under-estimate the importance of lactic acid. Even at paces well below lactate threshold a substantial amount of recycling of lactate occurs. I believe that the heart utilises lactate preferentially even at sub LT paces.

      As to why it is that starting either a marathon or an ultra too fast causes muscle damage, I suspect that there is a substantial metabolic component to the mechanism of the damage. In particular, I suspect that metabolic factors account for the evidence that maintaining a pace near to LT for a sustained period is associated with marked muscle damage. The generation of acidity might be an important contributor. The catabolic state induced by increase in cortisol might play a synergistic role.

      • Robert Osfield Says:

        I doubt lactate will be a large source of fuel at marathon pace. Published values I’ve seen for aerobic vs anaerobic contribution puts the values at 98 to 99% aerobic and 2% to 1% anaerobic. So at most you’ll be 2% anaerobic and generating associated lactate, but likely less, especially as non elite runners at likely to be running at a lower percentage of their lactate threshold.

        With aerobic contribution 50 to 100 times higher than anaerobic at marathon pace I believe that aerobic conditioning is the key. As part of your training to maximize aerobic fitness you’ll be doing training sessions at or above lactate threshold and here you’ll develop your ability to use lactate, I can’t see any reason to go beyond this. Focus on what you need for aerobic fitness and let the lactate take care of itself.

        On the topic of what causes muscle damage, the combined stress of acidity, loading itself, vibrations that shoot through the leg on landing, dehydration and the catabolic state all have role to play. While all of these factors are impossible to measure as a lone runner training, it’s easy to feel the extra stress of doing a fast half marathon vs one at an easy pace. Even backing off pace a little helps a lot in reducing the perceived stress.

        With a marathon you don’t get to stop and recover at the half way point, you just have solder one with whatever damage you’ve built up already. On race day thanks to adrenalin it’s a lot more difficult to access the stress you are putting on your body as it accumulates. I suspect once you start getting near exhaustion of glycogen race focus begins to get distracted by the first serious signs of discomfort and adrenalin levels drop and then not long after you are in a world of hurt, struggling to keep even a jog going.

    • canute1 Says:

      Even at aerobic paces lactate is an important fuel. Lactate is an aerobic fuel – when the heart or any other organs uses lactate to generate energy it does so via aerobic metabolism.

      In the resting state organs such as the heart use fat as their main fuel. However, when skeletal muscle begins to consume a moderate amount of glucose, some lactate is produced as an inevitable by- product. Much of this lactate is transported into the blood and onwards to other organs such as liver and heart. The heart uses it as a source of energy and the liver converts it to glucose.

      Provided the rate of lactate production in muscle is fairly low, the blood level of lactate rises only gradually, typically rising from around 1mM in the low aerobic zone to near 4 nm in the upper aerobic zone. Once oxygen supply is inadequate, lactate production rises rapidly, but this should be avoided during a marathon. At marathon pace, oxygen supply is usually adequate, though lactate level might well rise to around 3 mM. It is therefore beneficial to utilise as much of this lactate as possible, especially as a source of energy in the heart and for the synthesis of glucose in the liver.

      As lactate is removed, hydrogen ions are also removed. Thus efficient utilization of lactate at marathon pace keeps the level of acidity relatively low, thereby minimising the harmful effects of acid. Training the body to utilise lactate efficiently in the upper aerobic zone is an essential part of marathon training.

      • Robert Osfield Says:

        Do you have any figures as to just how much lactate we generated at marathon pace?

        I’ll have a stab at guessing. Would the following roughly apply?

        We derive 1% of energy at marathon pace from
        anaerobic metabolism,

        Aerobic metabolism generates 18 times more ATP’s
        than anaerobic metabolism then 17/18th of the
        glycogen used would become lactate.

        So… 1% of pure anaerobic fuel usage would generate
        17% lactate surplus.

        If this is even approximately right then indeed lactate is significant fuel even at marathon pace and I stand surprised and corrected 🙂

        However, at marathon pace we are still 99% aerobic metabolism, processing lactate being aerobic requires aerobic development as well as specific mechanisms associated with just lactate metabolism.

        I do wonder if the lactate generation will vary through a race. As muscle glycogen is exhausted there is less potential for generating power anaerobically so less potential for lactate generation and subsequent reuse. Conversely as we fatigue if we start to call upon our fast twitch fibres more then perhaps there could be an up tick.

    • canute1 Says:

      One further point to note about use of lactate as fuel for heart muscle during aerobic running, lactate is the fuel that is most easily converted to acetyl CoA – the essential input to the Krebs cycle during aerobic metabolism (as shown in the figure in my post of 5th Dec 2013). At rest, the rate of oxidation of fat is adequate to supply enough acetyl CoA to meet the heart’s demand for energy. However when the heart is required to beat much faster, during aerobic exercise, I suspect that the heart preferentially uses lactate. I do not have to hand any data that demonstrates this in athletes, but it is noteworthy that in the infant heart, which beats much faster than the adult heart, lactate is the main fuel. So while I agree with your emphasis on the importance of deriving as much energy from fat as possible, I suspect that for several purposes, including generation of lactate for use by the heart and for the production of glutamine in muscle, it is beneficial to maintain at least a moderate amount of glucose metabolism in skeletal muscle.

    • canute1 Says:

      Robert, Your calculation of the lactate surplus generated by anaerobic metabolism even when anaerobic metabolism provides only 1% of the energy is an interesting illustration of the fact that lactate turnover associated with even a small proportion of anaerobic metabolism can be substantial. As you demonstrate, because more much more fuel is required to generate specific amount of energy via anaerobic metabolism than via aerobic metabolism, even when the fraction of energy is derived from anaerobic metabolism is small, a much larger fraction of the fuel consumed is undergoing anaerobic metabolism. However, lactate plays an important role even at lower work rates where net anaerobic metabolism is negligible. Under fully aerobic conditions lactate is formed and utilized continuously. Shuttling of lactate between different compartments within cells and between different cells plays a part in facilitating many metabolic processes. As discussed previously, lactate shuttling can help ensure a supply of readily accessible fuel for heart muscle during aerobic exercise. Within skeletal muscle lactate formed in anaerobic fast twitch fibres can be taken up and oxidized in adjacent aerobic fibres, thereby allowing the use of powerful fast twitch fibres without net anaerobic metabolism leading to harmful accumulation of acidity. Lactate plays a role in facilitating the beta oxidation of fats.
      The marathon places heavy demands on the function of many tissues in the body. In light of the complex network of metabolic processes occurring in these various different issues it is not easy to draw clear conclusions about which metabolic adaptations that are most important for a marathon runner. Since lactate is a crucial intermediary in numerous metabolic processes in the body, the ability to shuttle lactate and utilise lactate efficiently does appear to be an important aspect of fitness for running at paces extending throughout the aerobic range, but I am inclined to think that this capacity becomes most crucial in the vicinity of marathon pace because the balance between lactate production and utilization is finely balanced at this pace.

      • Robert Osfield Says:

        If we are generate and using lactate when we run at all paces, just in different amounts I’d be inclined to suggest one probably doesn’t need to specific train to handle lactate efficiently, it will just come as part of training well balanced training plan.

        My current inclination is that if your are training for a marathon then you probably want to train to metabolize efficiently all the fuels that you will use at marathon pace. Training around marathon pace for a decent number of miles during your training cycle will probably achieve this, as well as all one to improve the neurological tuning required to maximize the running economy at this pace.

        Since it’s common for runners to run out of glycogen at end end of marathon it would seem important to builds one capacity to burn fats so that the fuel mix you use will ensure you get over the line without hitting the wall.

        Since one also want to optimize running economy and metabolic efficiency for the fuels you use on race day I would inclined to believe that one should develop ones fat burning potential first, then once this is done start spending more time at race pace to achieve the final optimization.

    • canute1 Says:


      I agree that a well-balanced training plan is what is required but there is debate about what a well-balanced marathon plan entails. In general terms, most coaches recommend a mixture of types of session, but recommended programs differ greatly in the relative emphasis on volume and intensity.

      I also strongly believe that developing a good ability to metabolise fats is a very high priority but programs ranging from high volume/ low intensity programs to high intensity interval programs have been shown to enhance ability to utilise fats.

      To some extent, each person has to find what mixture of types of session suits best for him/her, but establishing this is not straightforward because there are so many variables that might be adjusted. So if one wants to devise a program that it likely to meet one’s own needs well, I believe it is best to combine information from prior personal experience; information for reputable coaches and information derived from scientific studies. There has been a huge amount of potentially relevant information generated by scientific studies in the past decade. One of the goals of this blog is to examine the relevant evidence from scientific studies.

      My focus in this post has been primarily on the issue of muscle damage, which until recently has been largely ignored while the focus has been on aerobic capacity, lactate threshold and fat burning. All of these factors remain important but I believe it is potentially useful to look more widely at the nature of both the mechanical and metabolic stresses that the marathon runner faces.

  4. Mike Says:

    Is there any evidence that support/compression leg wear can reduce muscle damage in the marathon? Or conversely, by wearing such clothing on a regular basis, is damage/repair reduced, so that the muscles are damaged more in really stressful events like the marathon?

    • canute1 Says:

      That is an interesting question. Although Del Coso’s study indicates that muscle damage contributed to the slowing of those runners whose pace decreased by more than 15%, the relative contribution of mechanical and metabolic factors to the mechanism of damage remains unknown. It is very likely that the eccentric contraction is one of the key mechanical factors. Accumulation of acidity and the catabolic state induced by high cortisol levels are plausible metabolic contributors. I do not know of any compelling evidence that the mechanical support offered by compression clothing would limit this damage, though I think it remains an interesting possibility.

  5. Pete Says:

    Hi Canute,

    I have followed your interesting blog for some time already and enjoyed it a lot. I hope that you will have a successful training and racing year ahead of you!

    Could one factor in the accumulation of muscle damage be the deterioration of the running form during long races. This could partly be caused by neuromotoric fatigue, but possibly also by the premature running-out of glycogen from some fast-twitch fibers which are important for maintaining the running form, especially in e.g. some swerves and other corrective movements that occur irregularly and unexpectedly in the course of the race. In most discussions the leg muscle glycogen stores are treated as a single entity which lasts until it is depleted. More likely, different fiber populations in different muscles run out of fuel at different stages of the run. It is known that there are huge individual differences between persons in the fast/slow twitch fiber composition in the muscles. Maybe this could also be one explanatory factor between the two groups in the Del Coso study. And maybe the personal fiber composition should be taken into account in devising a training programme to combat the fatigue-associated muscle damage.

    • canute1 Says:

      Thanks for your comment. You make a very good point about the fact that muscle glycogen stores cannot easily be shared between all the fibres within a muscle. When glycogen is broken down to yield usable fuel, it is broken down to glucose-1-phosphate, which then undergoes glycolysis to produce pyruvate and lactate. Glucose-1-phospahe cannot be transferred from one muscle fibre to another. However, lactate can be transported out of and into muscle cells. Therefore, the most efficient way to transfer fuel from one muscle fibre to another is via lactate. It can also be transferred via glutamine but that is a complex pathway.

      Aerobic type 2 fibres almost certainly make a substantial contribution to generating the muscle power required to maintain marathon pace. Because these fibres generate more power, they tend to exhaust their glygogen store more quickly than type 1 slow twitch fibres. Once they run out of glycogen they rely on transport of glucose for the blood (derived largely from liver stores) or on lactate from other muscle fibres. When cortisol is high, transport of glucose from blood into muscle is inhibited. So if the pace is to be maintained, the type 2 aerobic fibres would need to be refuelled via lactate geenrated by anaerobic metabolism in other fibres. Thus muscle levels of lactate and the associated acidity become moderately elevated, potentially impeding the efficiency of muscle contraction, and possibly promoting muscle damage. This suggests that it is helpful for a marathon runner to have moderately abundant aerobic type 2 fibres that are fully stocked with glycogen at the beginning of the race.

      Therefore, a runner who naturally has a small proportion of type 2 aerobic fibres compared with type 1 fibres should train a way that favours development of aerobic type 2 fibres. I think that I have a natural tendency towards higher proportion of type 1 fibres and therefore, I am likely to benefit most from training that favours development of type 2 aerobic fibres. In support of this, forty five years ago, I ran some fairly fast marathons based largely on training for 5000m track events.

      On the other hand, an athlete who has too few type 1 fibres faces the opposite problem. If the type 1’s become exhausted they would have to be refuelled via anaerobic metabolism in type 2 fibres. The best strategy is having to optimum balance of type 1 and type 2 aerobic fibres.

      As for the relationship between deterioration in form and muscle damage, there is good evidence that form deteriorates during marathon in many runners. The poor form might either cause or be caused by damage. Whatever the primary cause , it very likely that impaired coordination of muscle contractions will increase the damage.

  6. EternalFury Says:

    Maybe the inverse-square law applies to distance running. In the sense that your body will allow you to run much faster than you should at the beginning of a certain distance. You will be able to do so initially, but you will pay the price before you are done covering the entire distance.

    That would bring back this problem to a matter of pacing. And it is likely that most predictors out there overestimate the pace one should target for a distance race.

    Damage is damage. It leads to adaptation up to a point, and that point is probably not too far from the point where no real damage occurs.

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  8. Otherwise Says:

    Very helpful stuff, Canute1. I, too, find the answer “because you went out too fast” to be tautological. Yes, I got that, but “WHY?” You reframed that question nicely.

    Just ran my second marathon in Indy. I’m 61 years old, 172 lbs, no athletic background. Ran steady 7:45’s until mile 14, then slowed evenly to a final 9:00 pace, a degradation of 18%.

    Whatever happened, happened just after halfway and was caused by distance/time. I went from no correlation at all between mileage and pace to an almost perfect correlation.

    So what was the cause? I can think of five possibilities–heat, course, cardio drift, nutrition or something muscular.

    It wasn’t heat. The race started at 32 and finished mid-forties, although it was sunny.

    It wasn’t the course. The course was pretty flat, and actually a bit downhill after mile 17 or so. There was also a strong headwind out and tailwind back.

    It wasn’t cardio– my HR actually dropped from 152 to 146. My new Garmin has a “marathon predictor” function, which I’ve inferred is based on HR Zones (cardio,) and it says I could have run much, much faster than I actually did (a 3:11 vs. a 3:32.)

    It might have been nutrition related–I didn’t do a great job of fueling. But if so, it certainly wasn’t a case of hitting a “wall,” since the degradation was remarkably even, about 6 sec per mile. If it was nutrition, then I just sort of leaked energy out.

    I think the idea of muscle damage makes a lot of sense, particularly given the soreness that followed the race.

    My guess, and this is purely a guess, is that it was a mixture of both nutrition and muscular deterioration. My time was about 7 minutes higher than predicted by my pre-race sims, so I’m going to make the working assumption that the gap between my actual performance and potential best performance was 1/3 nutrition and 2/3 muscle related.

    Nutrition is (relatively) easy to fix. I’ll have to research and ponder the muscle problem. My first stab will be to increase training volume and lengthen out my training period. For the last few years, I’ve started training for running after triathlon season is over. Basically, that means a ten week training cycle for the marathon.

    Will let you know if it works.

    Thanks again.

    • canute1 Says:

      Sorry to hear about the slow-down. You analysis of the problem makes sense. I think that a gradual increase in the volume of slow running and then a gradual increase of speed up to marathon pace for a substantial proportion of some of the long runs is probably the best way to increase leg muscle resilience. To achieve a gradual build-up, the total duration of marathon preparation must be fairly long.

      As described in my post, some evidence suggests that sprinting might also help – but I think that the volume of sprinting should be very small

      In principle, weight training should also help though on the basis of my own experience, I think it is less effective than gradual build-up of running.

      I look forward to hearing how things work out next time.

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