Classically, a sprinter has the torso of an ox while a marathon runner has spindly legs and arms. Sprinters spend a substantial time in the gym lifting weights and afterwards eat a lot of protein; marathon runners spend even longer on the road depleting their muscle glycogen and then consume carbohydrate to replace it. When finishing a long run at a pace near to race pace, marathon runners are actually in danger of burning the protein from their own muscles. If they work with weights it is usually using high repetitions at moderate load to build up strength endurance rather than the power which a sprinter aims to develop with fewer repetitions with much heavier weights. These distinct training patterns have proven successful, on the one hand for many sprinters and on the other hand for many endurance runners. Clearly, the physiological needs of the sprinter, whose first requirements are muscle power and neuromuscular coordination, differ from those of the endurance runner, whose primary need is to supply oxygen and fuel to the muscles at a rate adequate to sustain aerobic metabolism for long periods.
However, it is interesting to note that sprinting speed is a good predictor of one’s ultimate performance in distance events. Nonetheless, a novice endurance runner will get best value from time spent training by working on building aerobic capacity. A powerful engine is of little use without oxygen and fuel. But once oxygen and fuel supply are more than adequate, perhaps it is time to focus more on muscle power.
There is an even more general rule about training and that is: repeating the same training stimulus time and time again yields diminishing returns. When the returns begin to diminish it is worth asking the question: what is now limiting my performance and what training stimulus might best break through the current limit?
In recent years several illnesses and also lack of time for training had been the most easily identified limitations, but the past year has been different. I been free of illness and injury, and have actually spent more time training than during any year of my life – even those years over four decades ago when I could run a marathon in less than two and a half hours, though it should be noted that in those days, other activities especially mountaineering, contributed a great deal to my basic fitness.
In the past year the time spent training has produced substantial gains. However, about three months ago, in the final few months of preparation for the Robin Hood Half Marathon at the end of September, it was clear that I had run up against a serious limitation. My aerobic fitness, as indicated by low heart rate when running at an easy pace, was good. My customary measure of aerobic fitness, the number of heart beats per Km, was typically in the range 630-640 b/Km during low aerobic runs, and there was very little upward drift of heart rate during long runs. I would have anticipated that such a level of aerobic fitness would allow me to maintain a pace in the range 4:35-4:45 min/Km for the duration of a half marathon, to produce a finishing time of 1:40 or less. But to my dismay, when I tried to maintain paces in this range, even for a few Km, I simply couldn’t muster the speed. I could not even maintain 5 min/Km pace for 4 Km. So it appeared that my limitation at that time was not aerobic fitness.
It was easy to identify the problem: the first factor is that I am in my late sixties, and suffering the general loss of muscle strength that accelerates alarmingly in the later part of the seventh decade. The second problem was that I had suffered an episode of acute arthritis two years ago that had affected several joints including my left knee. Painful movement leads to involuntary decrease in application of force, and as a result, my leg muscles, especially quads and hams, had atrophied even more than would be expected due to aging. The hopping test, in which I measure the total distance covered in 5 consecutive hops on one leg, had deteriorated dramatically from around 9.5 metres to 7.5 metres. In the subsequent two years lingering pain in the knee thwarted my attempts to introduce a program of plyometrics, while, ironically, marked pain in my arthritic left wrist made it difficult to lift weights. It was clear that I had to find some way around these problems.
Fortunately, around the time I received an email out of the blue from a runner named Kieren. Several years ago Kieren’s blog had inspired me both to run and to blog, and I had been saddened when he suffered an injury, stopped running, and eventually stopped blogging. I had discovered incidentally that he still posted occasionally on the Fetcheveryone website, and I had been interested to see that he had taken up resistance training a few months ago. Although his recent email to me was triggered by my posts on heart rhythm, we got to discussing resistance training. He emphasized the value of squats for building ‘whole body’ strength, but especially for strengthening the major muscles of the posterior chain: the glutes, hams and hip adductors. He recommended an excellent book by Mark Rippetoe which provided detailed clear guidance on how to squat safely and effectively.
As I mentioned in a previous post, at that stage I commenced a gradual progressive build up of weights and after four weeks was delighted by two outcomes: my painful arthritic wrist was much less painful, presumably due to increased support by stronger forearm muscles, and my pace during stride-outs at around 80% maximum effort, had increased, though of course, this is a rather imprecise measure of improvement. Nonetheless, the signs were encouraging. But by that point in my preparation for the Robin Hood half marathon, it was necessary to revert to predominantly aerobic training. However, I continued with body weight exercises and drills. Although there was not time to properly assess my ability to sustain a higher speed in those final few weeks before the race, short tempo runs during the taper suggested that I was now able to maintain a pace of 5 min/Km or even a little faster with reserve power. In the event, this proved to be the case. I crossed the line in 1:41:50, reflecting an average pace of 4:50/Km for the full 21.1 Km. Some of this improvement was no doubt due to a successful taper, but on balance, the prospects for further improvement with continuation of strength development looked promising.
But before committing myself to a major program of resistance training, it is necessary to consider the crucial issue of possible weight gain. For the sprinter, the greatest energy cost of running is the cost of re-positioning the swinging leg. But at the paces typical of endurance running, the greatest cost is the cost of elevating the body on each stride, and this cost is directly proportional to body weight. Irwin Stillman estimates that a long distance runner should weigh 15% less than the average non-athlete of the same height, though some coaches consider that 10% less than average is ideal. Until one reaches the state of emaciation where hormonal and immune function begins to be compromised, loss of fat is almost certainly beneficial to the distance runner. Weight training is potentially effective for promoting fat loss, and therefore, a substantial proportion of the weight change in early stages of a weight lifting program are likely to a beneficial loss of fat. I am currently about 9% below average weight for my height, so I do not need to lose much more weight. Some of this deficit is due to muscular atrophy, so I will probably profit from replacing fat by muscle.
But depending on the regimen adopted, gain in muscle mass from weight training might well overshadow the loss of fat, especially for a distance runner with little fat to spare. So if my running performance is to improve, it is crucial that any gain in muscle mass ‘pays its way’ by producing an increase in power output that more than compensates for the extra work I will have to do in order to get airborne on each stride. It will also be crucial to ensure that I maintain the ability to deliver enough oxygen and fuel to the muscles to sustain aerobic metabolism for several hours.
Muscle fibre types
This brings us to the key issue of types of muscle fibre. The sprinter relies largely on type 2B fibres, anaerobic fibres dominated by massive contractile machinery capable of rapid, and hence powerful contraction. Muscle contraction is produced by the ratchet-like interaction of actin and myosin fibrils that slide past each other as a result of making and breaking molecular bonds, employing energy provided by the energy molecule, ATP. Several different types of myosin fibrils exist. Type 2B fibres contain ‘heavy duty’ myosin capable of very rapid contraction. Thus, type 2B fibres are best equipped to utilise readily available ATP and creatine phosphate, which can be rapidly converted to ATP. Although oxygen is subsequently required to replenish the supply of ATP and creatine phosphate, this is usually done at a leisurely rate during recovery. Therefore, the development of type 2B fibres sacrifices capillary density for the sake of contractile machinery. These type 2B fibres are of limited use to a distance runner.
The distance runner relies largely on type 1 fibres in which there is a balance between contractile machinery and capillary density, and it addition, abundant mitochondria. The mitochondria contain the oxidative enzymes required to generate ATP by oxidizing fuels such as glucose. Thus type 1 fibres are well suited to aerobic metabolism. However, the variant of myosin in type 1 fibres can only contract at about 1/10th the rate of the variant found in type 2B fibres. Therefore the type 1 fibres are best suited to producing a modest power output for long periods using aerobic metabolism. But it is unlikely that lifting heavy weights will do much for the development of type 1 fibres.
The next question is: what fibres are enhanced by resistance training? The answer is perhaps a little surprising. Resistance training enhances mainly type 2A fibres. These are the aerobic fast twitch fibres. They contain a type of myosin fibril capable a fast contraction, but are also fairly well adapted to aerobic metabolism. They contain substantial numbers of mitochondria and a moderately high capillary density. Therefore, they are well equipped for tasks that require a moderately large power output sustained for a moderate duration, tasks such as running up long hills. As almost all cross country events and many road races include some hills, it is clearly desirable for the distance runner to have fairly well developed type 2A fibres. Unfortunately, I have poorly developed type 2A fibres. In my duel with Emily the Keyworth Turkey Trot two years ago, I could not match her on the ascents and had to rely on shrinking the gap during the descents. Similarly in a 5K parkrun two days ago, I was very evenly matched with a young man on the level stretches, but could not match him on the mild ascents, and again, had to rely on closing the gap during the descents. So, it is likely that further development of type 2A fibres will in itself improve my performance on hilly courses. But the cardinal question is: is it possible to convert type 2A fibres into other types of fibre? The answer to this question is still a subject of some uncertainly, but encouraging evidence is emerging
Conversion between fibre types
Before tackling the crucial question of the possibility of converting type 2A fibres to the type 1 fibres required by the distance runner, it is intriguing to ask how it is that weight training helps sprinters develop the type 2B fibres that are the key to speed. Enigmatically, the answer appears to be: by doing very little. It appears that type 2A fibres naturally revert to type 2B fibres when not subjected to repeated loading. It is probable that type 2B fibres are the default state to which other fibres regress if not required to work. This is illustrated by the fact that after a period of paralysis, the proportion of type 2B fibres is high. Thus, it is likely that the best strategy for a sprinter is marked periodization. In the pre-season, he/she should lift heavy weights, leading to the development of type 2A fibres. Then during the competitive season, the emphasis should be on sharpening neuromuscular coordination. Meanwhile the type 2A fibres developed during the pre-season weight lifting will revert to the required type 2B fibres.
But can an endurance athlete convert the type 2A fibres to type 1 fibres? The answer is less clear. It appears to depend on the initial fibre composition of the muscle. In a study of 21 cyclists who undertook training program in which volume of training was increased while intensity decreased, there was a significant decrease in proportion of type 2A fibres and a trend toward increased proportion of type 1 fibres, when averaged across the entire group. However, perhaps the most important finding emerged when the 21 cyclists were subdivided into a group with high initial proportion of type 1 fibres (the HPS group) and those with a low initial proportion of type 1 fibres the LPS) group. In the HPS group, the change to higher volume, low intensity training produced no appreciate change in fibre composition, whereas in the LPS group, there was a marked increase in type 1 fibres and a decrease in type 2A fibres. The question of whether or not the difference in initial proportion of type 1 fibres was determined by genes or by previous training was not addressed.
Thus, the study demonstrates that an increase in training volume and reduction in intensity is likely to produce a shift from type 2A to type 1 fibres in some endurance athletes, but not in others, and that difference in training effect is determined by the proportion of type 1 fibres at the beginning of the high volume training. Unfortunately, the question of whether it is the genetic influences on the initial fibre composition or previous training experience that determines the likely outcome remains unclear. However, it seems to me that prior training is the mostly likely factor, since cyclists with a genetic predisposition to a preponderance of type 1 fibres would have been more likely to be in the HPS group at the start.
I suspect that due either to my genes or to my childhood experience of running to and from school, I have a natural preponderance of type 1 fibres, and therefore, in my present state, further high volume. low intensity training will not increase my proportion of type 1 fibres. However, the available evidence indicates that a program of weight lifting might increase my proportion of type 2A fibres and subsequent high volume, low intensity training might lead to an increase in type 1 fibres.
The available evidence also indicates that the outcome of training depends on one’s initial state at the beginning of the training. There is no single answer to the question of how best to train. But after a careful evaluation of my own condition, I think that a program of weight training is a good bet in my case. However it is also noteworthy that in order to achieve the distance runner’s theoretical ideal of a very low amounts a type 2B, moderate proportion of type 2A and a large proportion of type 1 fibres, I need to revert from weight training to aerobic training well in advance of my next half marathon.
There are additional issues to consider. These include the effect of weight training on hormones, especially growth hormone, and also the question of what particular exercises I should include in my weight training program. I will return to each of these questions in future posts. I will finish this post with an account of how I plan to monitor progress.
I will monitor three ‘running specific’ variables: my time for a 5K, the distance achieved in 5 consecutive hops on one leg, and my weight.
With regard to 5K performance, I did my base-line test in a parkrun last Saturday. I achieved a time of 22:19. I was delighted with this, since in my first parkrun a year ago, run after about three months of systematic training, including both hills and intervals, I had achieved a time of 24:48. Thus, in the subsequent year, I have managed to reduce that time by about two and a half minutes. Whether this reduction can be attributed to the intervening aerobic training or to the resistance work and drills over the past few months in uncertain. The fact that I could not maintain 5 min/Km pace for 4 Km three months ago, at the end of a long period of predominantly aerobic training, suggests that it was a combination of both. Thus, I am cautiously optimistic that an appropriately periodized combination of weights, drills and aerobic training will lead to yet further improvement, though of course, reduction from a starting point of 22:19 is a greater challenge than reduction from a starting point of 24:48.
An finally, as a counterbalance to the somewhat gruesome photos of my efforts to conjure speed from my atrophied leg muscles in the RH half marathon, here are some photos taken during the two-lap parkrun on Saturday, by the husband of Plodding Hippo, a runner and doctor whose wisdom on running-related medical matters is much valued by readers of the Fetcheveryone website.