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.