I need once again to re-build my aerobic base. Last year, I enjoyed a year free of ill-health, and after averaging a little over 40 miles of predominantly low aerobic training each week in the spring and summer, was pleased to run half marathon in 101:50. By mid-summer it appeared that I was mainly limited by lack of strength rather than aerobic fitness. Therefore, following the half-marathon, I began regular resistance sessions: three sessions per week in which the major focus was on 5 sets of 5 squats with the goal of building up my 5 RM to at least 150% of body weight. Although I did not know it at the time, Alberto Salazar had set a very similar target for Mo Farah in preparation for the London Olympics. Mo achieved a 5 RM of 200lbs for squats. My program of lifting went well, and to my amazement, I built up to a 5 RM of 230 lbs over a period of four months. Since I am a little lighter than Mo and substantially more than twice his age, I felt quite pleased with my progress. I am afraid that I will no longer be able to blame my atrophied elderly muscles for my poor running speed. Furthermore my creaky joints appeared to cope with the lifting well. By the end of the year I had less arthritic pain than at any time in recent years. So I was looking forward to redirecting my focus onto running in the new year
However, shortly after I started running again, my former arthritis returned. As on previous occasions, the problem started in my neck and left wrist, before extending to my knees, so I do not think it can be attributed directly to the impact at foot-strike when running. I do wonder whether running led to a build-up of circulating inflammatory molecules in the blood stream that inflamed the joints, but that is speculation. The unfortunate consequence was curtailed training and loss of fitness. In recent weeks, my joints have settled and now only my neck is painful – though my knees still feel fragile. But my endurance and aerobic capacity have deteriorated. I have deferred my target of a sub-100 minute half marathon in the spring to the autumn.
So once again I am facing the cardinal question: what is the best training strategy for base-building? For an endurance runner, a sound base has two key components: resilience of the connective tissues (ligaments, tendons, bones, fascia) and ability to utilise fuel efficiently. The simple rule of thumb for building up resilient connective tissues is a gradual increase in volume and intensity of training over a sustained period, though there is a paucity of detailed information about this topic. On the other hand, there is abundant information about the topic of improving the efficiency of fuel utilization, but some crucial issues remain a topic of debate.
The major determinant of endurance running performance is the maximum pace that can be sustained without accumulating appreciable lactic acid. Loosely speaking, that is the pace at lactate threshold. The problem with this terminology is that there is no precise threshold. Although lactate level in the blood begins to rise fairly rapidly after a certain point, the graph of lactate concentration against pace does not show a single sharp kink between two straight lines. Instead there is an initial upward trend typically occurring at a lactate concentration above 2mMol and then a steeper up-slope beyond 4 mMol. From the practical point of view, there are two fairly clear thresholds. The first corresponds to maximum pace that can be sustained for several hours (provided your connective tissues have the necessary resilience, and you can avoid running out of glucose). At this pace, the rate at which lactate is cleared from the blood matches the rate at which it is produced. Typically this is at a lactate level of 2 mMol. Roughly speaking, this is marathon pace. Because blood acidity is a major influence on the urge to breathe, it also corresponds approximately to the point at which breathing becomes a noticeable effort. Because I link my breathing rate to my step rate, I become aware that I have crossed this ‘aerobic’ threshold when I find I am more comfortable taking one breath every 4 steps rather than one breath every 6 steps. This ‘aerobic’ threshold is what Hadd refers to as the lactate threshold.
The second threshold is the pace beyond which lactate builds up to an intolerable level on a time scale measured in minutes. I know I have crossed this ‘anaerobic’ threshold when breath rate increases to one breath every two steps – but I avoid this except in the final few hundred metres of a race (or occasionally on steep hills). Races from 5K to HM are run at a pace somewhere between the aerobic and anaerobic thresholds, while the marathon is run at aerobic threshold. So for the endurance runner, the success of the base building phase can best be quantified by measuring the pace at aerobic threshold, or as Hadd described it, the pace at lactate threshold.
Capillaries and VEGF
To re-iterate the key point, the late threshold is the point at which the rate of removal of lactate balances the rate of generation of lactate. Therefore, a major goal of base-building is reducing the rate of generation of lactate. Since no lactate is produced when fuel is metabolised in the presence of sufficient oxygen, the first requirement is delivery of a copious supply of oxygen to the muscle. This requires enhancement of cardiac output and the development of capillaries in the muscle. Both of these developments will be enhanced by running at a pace that is adequate to place the heart and muscles under some stress, but not too much. The production of various growth factors, such as Vascular Endothelial Growth Factor (VEGF) that is responsible for stimulating the development of new capillaries, is promoted by a shortage of oxygen, so a degree of oxygen deprivation is required to maximise the development of capillaries. The first major challenge is determining just where this ‘goldilocks’ level of stress occurs. The answer is still a matter of controversy, but before attempting to answer it, we need to consider several more issues.
Oxidative enzymes in mitochondria
Maximising power output at lactate threshold also requires the development of the oxidative enzymes in mitochondria that carry out the process of burning fats or glucose, and transferring the energy released to the high energy molecule, ATP, that is the direct source of energy for muscle contraction. The required development of oxidative enzymes will occur if the system is appropriately challenged. Running in the aerobic zone stimulates the development of oxidative enzymes, but it is also of interest to note that High Intensity Interval Training (HIIT) also leads to increased production of mitochondrial oxidative enzymes.
In order to minimise accumulation of lactate when running near the threshold, we also need to maximise the ability to remove lactate. This is done by a process that converts lactate back to glucose in the liver. The process of transporting lactate to the liver, conversion to glucose and then transporting it back to muscle where it can be used again as fuel, is known as the Cori cycle. It is likely that training at a pace that generates at least a moderate level of lactate will promote development of the enzymes of the Cori cycle. However, the Cori cycle is not a source of ‘cost-free’ energy for muscle because conversion of lactate to glucose in the liver consumes energy. Therefore, while it is beneficial to develop the enzymes of the Cori cycle, it is far more effective to minimise the production of lactate in the first place.
So far, the various issues we have considered emphasize the importance of training at a sufficiently high intensity to produce adequate stress on the system to stimulate production of growth factors such as VEGF; enzymes such as the mitochondrial oxidative enzymes and to a lesser extent, the Cori cycle enzymes.
The recruitment of different types of muscle fibre
However, this is only one side of the equation that must be balanced. Muscles contain slow twitch and fast twitch fibres. The slow twitch fibres are specialised to function aerobically for long periods at low intensity. The fast twitch fibres are designed to generate high power output for a relatively brief time. The fast twitch fibres occur in two types: aerobic and anaerobic. The anaerobic are capable of generating the power needed for explosive movement. They can develop power on a time scale that is rapid compared with the delivery of oxygen to tissues. For this purpose, fuel efficiency is usually less important that speed of contraction. These fibres generate their ATP via the rapid but uneconomical conversion of glucose to lactic acid. Thus, when the anaerobic fast twitch fibres are engaged, acidity develops rapidly.
However, the nervous system is canny in the way it recruits muscle fibres. As the requirement for increased power output increases, fibres are recruited in the order: slow twitch, aerobic fast twitch and finally anaerobic fast twitch. At low power, slow twitch fibres are recruited and little acidity is generated. Training at an intensity that puts a little bit of pressure on the slow twitch fibres will lead to further development of capillaries and mitochondria, thereby providing an increase in the power output that can be generated by these fibres.
If at the other extreme, you demand that your muscles generate a high power output, the anaerobic fast twitch fibres are recruited and the muscle is flooded with lactic acid. Acidity makes muscle contraction less efficient and ultimately, the muscles shut down. It appears that the slow twitch fibres shut down first, although do not know of direct evidence for this,. Whether or not the slow twitch fibres shut down first, when you run at a pace that preferentially recruits the anaerobic fast twitch fibres there is little opportunity for the prolonged activity that promotes the development of mitochondrial enzymes in slow twitch fibres.
Two options for increasing oxidative capacity
An unresolved issue of major practical importance is what happens if you do multiple brief bursts of high intensity activity, separated by recovery periods in which lactate is cleared, as in high intensity interval training. As mentioned previously, measurement of mitochondrial oxidative enzymes before and after HIIT reveals an increase in oxidative capacity. The question of whether this occurs preferentially in aerobic fast twitch fibres or occurs also in slow twitch fibres is not clearly established. Nonetheless, if you want to increase oxidative capacity, you have two options: run slowly, though the gains are likely to be most rapid near to the point where appreciable recruitment of fast twitch fibres begins; or do high intensity interval training in which the recovery intervals are sufficient to clear lactate between the effort epochs.
Developing fat utilization
However, we should not focus only on developing the capacity to metabolise glucose. At least in longer races such as the marathon, it is essential to derive a substantial proportion of the required energy from fat, simply because the glucose supply is inadequate. The amount of energy that can be derived from fat increases up to a certain power output, but then decreases rapidly to near zero. The power output at which the maximum rate of fat utilization is achieved varies between individuals, though on average, in trained athletes it occurs at around 63% of VO2max. However, the level at which maximum fat utilization occurs can be increased by appropriate training (and perhaps also by diet). A marathon runner will be limited to an average pace that is not much greater than the pace at which maximum fat utilization occurs. Therefore, in preparation for a marathon, increasing the proportion of VO2max at which fat utilization is maximal, is crucial.
Although several key questions remain unanswered, the above considerations provide a basis for rational planning of base-building. In my next post I will address the question of the optimum practical strategy.