This year has been frustrating in an undramatic but challenging way. Undramatic because I have remained free of overt injury apart from some persistent though relatively mild problems with my joints and ligaments, but challenging because it has not been easy to identify why my fitness improved so slowly and then degenerated so rapidly. I achieved a greater volume of training – approximately 2000 miles (including the mileage equivalent of my elliptical cross-training sessions estimated on the basis of 100Kcal = 1 mile) than in any year in the past four decades. Taking account of my slower training paces, it is probable that I have actually spent more time training this year than during any year in my entire life. Yet through the summer I was frustrated by the tardy rate of improvement in fitness.
There were few occasions when I experienced the exhilaration of running fluently and powerfully. I felt tired much of the time and experienced persistent aching of the connective tissues in my legs. My short term goal was a half marathon time faster than 101:50. Despite the fact that I was unable maintain a pace of 5 min /Km (corresponding to 105:30 for the HM) for even a few Km as the date of the event approached, I nurtured the hope that a three week taper with some drills and faster running to sharpen my pace, would allow me to defy any rational prediction based the evidence of my limited fitness. However, in the event, rational prediction was indeed confirmed and despite a spirited finish, I recorded a time of 107:45.
In the aftermath I took some consolation from the fact that I had coped with a large volume of training without injury, though I was aware that I would need a few easy months to allow my body to recover. I cut my training volume to an average of slightly less than 30 (equivalent) miles per week, including an increased proportion of elliptical cross-training. After a month or so, I added a modest plyometric program as described in my previous post. The encouraging outcome was a modest improvement in hopping and jumping, indicating some gain in musculo-tendonous resilience and eccentric strength, but the dominating feature of the final few months of the year has been a devastating loss of fitness. Although I had cut my training volume substantially, the cut was less ruthless than the cut forced upon me by an episode of arthritis a year ago, yet the loss of fitness has been far greater. I am now at my lowest ebb since summer 2011 when a hectic and exhausting six months at work had left me with neither the time nor energy for solid training. In 2011, my lack of fitness illustrated the fact that for the elderly, fitness is hard won and easily lost. But in 2013, I am facing the disconcerting question: has fitness become even more difficult to gain and easier to lose as I have moved from my mid to late 60’s, or did I do something wrong this year?
I had used submaximal tests throughout the summer to ensure that I was just one step short of over-training, as indicated by autonomic measures of stress, such as heart rate at submaximal effort and resting heart rate variability. However, perhaps I should have taken more notice of the chronic tiredness and aching legs. I suspect that my mediocre half marathon performance demonstrated that I was not merely over-reaching but that a least a mild degree of over-training had interfered with my ability to benefit from training. This lurking suspicion has been strongly re-enforced by the devastating loss of fitness since September. It is clear that I had not built a sound base.
In the past few months, I have continually questioned whether or not I simply needed a bit more rest, but on the occasions when I have cut back the training volume even more drastically for a few weeks, the deterioration in fitness has accelerated. So the evidence suggests that I was not merely in a state of functional over-reaching from which the body bounces back with renewed vigour after a brief respite. I had almost certainly over-trained. I was in need of a more profound rest. Yesterday, I ran 11 Km, the longest distance I have run in recent times. My pace was very slow – around 6:30 min/Km – but for the first time since September, my legs did not ache. I hope this indicates that I have now passed the nadir, and can again begin re-building, but very cautiously.
Do miles make champions?
Arthur Lydiard’s simple dictum, ‘miles make champions’ is undoubtedly true. Indeed the rapid crumbling of my fragile fitness base as I have cut back the training volume since September confirms the crucial role of training volume. But just as every wise proverb can be countered by one that draws the opposite conclusion, miles can also undo would-be champions. In the summer, the most striking contrast with my training of recent years was the much greater proportion of long runs, mainly at a quite slow pace. I think it is likely that I did too many long runs this year. As I discussed in a post in October, Dudley’s studies of rats who ran at various intensities for various durations, showed that the increase in the mitochondrial enzymes that are essential for aerobic metabolism reaches a plateau after a sufficiently long duration of running. The plateau was achieved late, and was highest, in the rats that ran at the modest pace of 30 metres/min which they could maintain comfortably for over 90 minutes. A somewhat faster pace of 40 m/min, which was near to the peak pace that they could maintain for 90 minutes, produced a slightly lesser gain in aerobic enzymes. Paces below 30 m/min achieved an even lower plateau. On the other hand, at paces faster 40 m/ min the gains in fitness were more rapid but the duration for which the animals could sustain the pace was less and consequently the total gain in fitness was less than that achieved at 30 m/min.
Rats differ from humans in many respects, and the actual paces of animals with legs of only a few centimetres in length are of little relevance to humans, but the muscle physiology of rats is essentially similar to ours. It is likely that similar principles govern the effects of training. There appear to be two major conclusions. First, the greatest gain in aerobic capacity is achieved by a ’good aerobic pace’ that can be maintained comfortably for 90 minutes. Second, there is a limit to the benefit in aerobic capacity obtainable by increasing the length of training sessions. There may be other benefits of long runs, such as strengthening of connective tissues. But the occurrence of the plateau in development of aerobic enzymes suggests that at that beyond around 90 minutes something inhibits the further development of aerobic enzymes. Perhaps the most plausible limiting factor is the accumulation of cortisol.
Skoluda and colleagues have demonstrated that endurance athletes exhibit a sustained elevation of cortisol, and furthermore, the magnitude of the increase correlates with greater training volume, measured in either hours per week or distance per week. Cortisol is a catabolic hormone that promotes the breakdown of body tissues, including muscle, while inhibiting the synthesis of new protein. To evaluate the plausibility of the proposal that cortisol limited the synthesis of aerobic enzymes in Dudley’s rats and also played a part in my mediocre half marathon and the subsequent crumbling of my aerobic base, it is necessary to re-examine some of the details of role of hormones in the regulation of energy metabolism discussed in the first of my posts comparing the Paleo diet with a high carbohydrate diet.
At the commencement of exercise, there is an acute elevation of cortisol, together with adrenaline, that mobilizes the body’s resources to meet the demand for increased energy. The generation of glucose from glycogen is stimulated, thereby releasing the fuel that can be utilized most rapidly for muscle contraction. Cortisol also stimulates the metabolism of fats and of amino acids. Conversely, protein synthesis from amino acids slows down and body systems that serve longer term survival needs are put on hold. The immune system and the gut suffer first, though as long as the muscle continues to generate the amino acid glutamine, which helps sustain both immune cells and the lining of the gut, these body systems continue to function reasonably well. However, as the duration of exercise extends into the period when glycogen stores show signs of depletion, cortisol level rises further. Now the body’s priority is ensuring adequate supply of glucose for the brain. The increased level of cortisol inhibits the glut 4 carrier proteins that transport glucose into muscles. The muscles are increasingly reliant on the relatively slow production of energy via fat metabolism. Meanwhile, synthesis of glutamine drains the pool of intermediate metabolites that participate in the Krebs cycle, the closed-loop of metabolic transformations that plays a central role in energy metabolism and also in the synthesis of amino acids. Although fat metabolism can keep the Kreb’s cycle going, it cannot top-up the pool of intermediate metabolites. This topping-up requires input from pyruvate which is generated by the metabolism of glucose. In the absence of concurrent glucose metabolism, glutamine levels begin to fall, impairing the function of both the immune system and the gut.
Thus, the immediate effect of the elevation of cortisol is the provision of fuel for exercise, but as glycogen supplies diminish the priority is provisioning the brain, and the rest of the body suffers. How long does it take for this to occur? Cook and colleagues recorded salivary cortisol levels in recreational runners both during and after a marathon. The highest level was almost 6 times higher than typical morning levels, recorded 30 minutes after completion of the event, but the level had risen steadily throughout and was already very high by 25 miles. Similar levels were recorded following a non-competitive marathon. Thus, an appreciable elevation of cortisol is likely even during long training runs, consistent with Skoluda’s finding that endurance athletes have chronic elevation of cortisol that rises in proportion to training volume.
What are the potential adverse medium and long term consequences? The acute anti-inflammatory effect of cortisol is likely to hinder the repair and strengthening of muscles and other body tissues. In particular, the synthesis of aerobic enzymes is inhibited. Suppression of immune function creates the risk of infections. Sustained elevation of cortisol will sustain a balance that favours breakdown rather than building up of tissues, and thereby promote further loss of fitness. Furthermore, prolonged exposure to high levels of cortisol decreases the sensitively of the receptor molecules that mediate the effects of cortisol on body tissues, and might ultimately promote chronic inflammation, harming joints and connective tissues while promoting the deposition of atheroma in blood vessels.
In my own situation, I suspect that a continuing bias towards catabolism rather than anabolism has hastened my loss of fitness, while the continued aches in my legs probably reflected chronic inflammation in the ligaments. On the other hand, I have been pleased to note that I have not suffered any exacerbation of asthma this year. I hope that any tendency towards increased formation of atheroma in my blood vessels has been minor.
Next year, I plan to train for a marathon. But if I am to achieve a more robust fitness base and even more importantly, to enhance rather than harm my long term health, I need to adopt a different training strategy. I should start with a more careful scrutiny of the past year.
Closer scrutiny of the training log
While the most immediately apparent feature of my training during summer of 2013 was the relatively high proportion of long runs, a more careful inspection of my training log reveals a potentially more significant issue. After the resolution of arthritis in the early months of the year I had gradually increased my training volume up to 30 (equivalent) miles per week, and was coping well. Then, in March I increased the volume quite rapidly, by almost 15% each week for 4 weeks, up to 50 (equivalent) miles per week by early April. The submaximal test revealed that my fitness continued to improve fairly steadily until mid-April, but then suffered a slight decline in May, so I reduced the weekly volume back to 45 (equivalent) miles per week. Once again fitness began to improve, albeit slowly and I was feeling tired much of the time. I continued at that level of training until mid-August when I once again increased to 50 (equivalent) miles per week, but that produced only a marginal further increase in fitness by late September. At the time, it appeared that I had pushed myself to the limit but had not quite over-stepped the mark. However, in retrospect, I think I had overdone it. The damage was probably done in March and early April when I had increased training volume by 15% per week. At that time, all had appeared well, as my fitness continued to improve. Indeed from mid-March to mid-April I saw the greatest gain in fitness in any month of the year. It appeared I had got away with a relatively minor infringement of the 10% rule. But the increases in weekly volume reflected another feature, an increase in the number of long runs. By late April, I was occasionally slipping in two moderately long runs within a single week. I suspect I was accumulating a surfeit of cortisol that led to the transient decline of fitness in May, the mediocre half marathon in September and the subsequent devastating loss of fitness.
Plans for the future
I have about nine months until my target marathon next autumn. This gives me five months to build a solid base, leaving four months for specific marathon preparation. The cardinal goal of the final four months will be developing the capacity to sustain marathon pace for 26.2 miles. The goals of the preceding five months of base-building are more varied.
First, I need to ensure that my connective tissues are well conditioned and free of any trace of lingering inflammation. I will need to adjust my training over the next few months according to how well the recent recovery is maintained. I will continue with moderately demanding weight sessions and some mild plyometrics. It is likely that I will do a greater proportion of my aerobic training on the elliptical cross trainer next year, and I will build-up the long runs very gradually, aiming to increase from the current 11 Km to 25 Km by late spring.
Secondly I aim to develop the ability to utilise fat in preference to carbohydrate at low and mid-aerobic paces, thereby minimising the risk of excessive elevation cortisol during long training runs. The main element of the strategy to achieve this goal will be a gradual increase in training volume, especially in the low and mid-aerobic zones. I will also maintain my current nutrition, consuming a diet that matches the Mediterranean diet as described in my post two weeks ago.
My third goal will be the development of aerobic capacity, including the ability to utilise lactate. The gradual increase of training volume in the low and mid-aerobic zones required to promote utilization of fat will also contribute to this goal. In addition, I will do regular sessions similar to Hadd’s 25×200/200 sessions, in which brief epochs that are effortful enough to generate a modest amount of lactate, alternate with recovery periods long enough to allow the metabolism of the lactate. Because there is minimal accumulation of acidity the session is only moderately stressful.
Fourthly, I will attempt to build up the strength to maintain a reasonable marathon pace without the need to increase cadence to an inefficient level. At present, my cadence exceeds 200 steps per minute even at 5 min/Km. My strategy for developing the strength required to lengthen my stride includes a mixture of short hills, long hills and sprinting in addition to weights and plyometrics. A key feature of all of these sessions will be generous recovery after each effortful epoch, to maximise the stimulation of anabolic hormones and minimise cortisol production.
Above all these specific goals, I will aim to start the marathon specific training in a robust and relaxed state.