Lactic acid and running: myths, legends and reality - the ABC Lactic acid and running: myths, legends and reality - the ABC
Most runners still believe that lactic acid is released during hard or unaccustomed exercise and that this is what limits running performance, as well as being the cause of stiffness. Neither is correct. But not even is the terminology of “lactic acid”.
Lactic acid does not exist as an acid in the body: it exists in another form called “lactate”, and it is this that is actually measured in the blood when “lactic acid” concentration is determined, as is done from time to time. This distinction is important not only for the sake of correctness, but more importantly, because lactate and lactic acid would have different physiological effects.
The greatest myth is that lactic acid is the cause of the stiffness felt after an event such as a marathon. Stiffness is due mostly to damage to the muscle, and not an accumulation of lactic acid or lactic acid crystals in the muscle.
Another misconception is that lactate is responsible for acidifying the blood, thereby causing fatigue. To the contrary, lactate is actually an important fuel that is used by the muscles during prolonged exercise. Lactate released from the muscle is converted in the liver to glucose, which is then used as an energy source. So rather than cause fatigue, it actually helps to delay a possible lowering of blood glucose concentration, a condition called hypoglycemia, and which will cause a runner to feel weak and fatigued if it occurs.
A more recent addition to the muddled thinking is that of the anaerobic threshold. Pictures are seen of athletes having a blood sample taken with an accompanying caption indicating that the workout is being monitored by measuring “lactic acid”. The supposed rationale is that as running speed is increased, a point is reached at which there is insufficient oxygen available to the muscle and energy sources that do not require oxygen contribute to the energy that is needed. This results in a disproportionate increase in the blood lactate concentration, a point identified as the anaerobic threshold. This is also known as the lactate threshold or lactate ‘turnpoint’. There are two problems with this. Firstly, the muscle never becomes anaerobic: there are other reasons for the supposed disproportionate increase that is measured in blood lactate concentration. Secondly, the so-called disproportionate increase causing a ‘turnpoint’ is not correct, in that the increase is actually smooth and incremental. This led to another way of using blood lactate concentration to monitor running performance.
If blood lactate concentration is measured at different, increasing running speeds, it is possible to eventually draw a curve depicting the continued increase in concentration as the running speed gets faster. The position of this curve changes as fitness level changes. Particularly, the fitter a runner gets, the more the curve shifts to the right, meaning that at any given lactate concentration the running speed is higher than before. Often, the running speed at a lactate concentration of 4 mmol/l is used as a standard for comparison. This can also be used as a guide for training speed i.e. a runner could do some runs each week at the speed corresponding to the 4 mmol/l lactate concentration, some runs above this speed, and recovery runs at a slower speed. Of course, as fitness changes and the curve shifts, these speeds will change, and so a new curve will have to be determined. This is all very well, but the problem is to know how much running should be done below, at, and above the 4 mmol/l concentration. Remember, 4 mmol/l is a fairly arbitrarily chosen amount. Thus the real value in determining a “lactate curve” is to monitor how it shifts with training. The desirable shift is one in which a faster running speed is achieved at a given lactate concentration than before. This regular testing can be done in the laboratory with the athlete running on a treadmill or on a track in which running speed can be carefully controlled, such as by means of pace lights. Both types of testing are done at the Sports Science Institute, usually for research purposes.
While useful information can be gained from regular testing to determine a runners’ lactate curve, it is important to keep in mind what is fact and what is fiction.
Post run stiffness - the ABC - the Andrew Bosch Corner Post run stiffness - the ABC - the Andrew Bosch Corner
Lactic acid build-up is the cause of post hard-run stiffness ……. Wrong! Most runners believe that the stiffness and muscle pain felt after a marathon or hard run is caused by lactic acid. While this was believed correct some decades ago, we now know that lactic acid, or more correctly, lactate, is not the cause of stiffness.
Although the precise cause of delayed onset muscle soreness remains unknown, all runners are aware that the degree of pain depends on the intensity and duration of the run. For example, you have probably noticed that your muscles are more painful after a long or hard downhill run than after running over flat terrain. Comrades runners, particularly, will have noticed that the post-race stiffness is worse after a “down” run than an “up” run. In fact, it is this very phenomenon that begins to exclude a build-up of lactic acid as a cause of the pain. In downhill running the concentration of lactate in the blood and muscle is very low compared to running at the same speed on the flat. Thus, the most painful post-race stiffness occurs when the lactate concentration is lowest.
If we take a blood sample from a runner the day after a marathon, especially an ultra-marathon such as the Two-Oceans or Comrades, we find that the levels of an enzyme called creatine kinase are very high. This is a marker of muscle damage as this particular enzyme “leaks” from damaged muscle. The “damage” is in the form of minute tears or ruptures of the muscle fibres. We can see this trauma to the muscle if a sample of muscle is examined microscopically. However, it is not just the muscle that is damaged. By measuring hydroxyproline, it is possible to show that the connective tissue in and around the muscles is also disrupted. What this shows is that stiffness results from muscle damage and breakdown of connective tissue.
Running fast or running downhill places greater strain on the muscle fibres and connective tissue compared with running over a flat route. Downhill running is particularly damaging because of the greater so-called eccentric muscle contractions that occur. When your foot contacts the ground after the air-borne phase of the gait cycle, the muscles in the thigh contract to support you. But the nature of the running action is such that although the muscle is contracting, it is forced to lengthen at the same time. It is this simultaneous contracting while lengthening that is called an eccentric contraction and is most damaging to muscle fibres.
What does this mean for the runner? Firstly, after the muscles have recovered from the damage that caused the stiffness and the adaptive process is complete, the muscle is more resistant to damage from subsequent exercise for up to six weeks. It may therefore be beneficial to include a short downhill race or training run 4 to 6 weeks prior to a race such as the Two-oceans or Comrades. Secondly, allowing adequate recovery after a marathon that has resulted in post-race soreness is important so as to allow complete healing to take place so that you can benefit by being “stronger” than before. Thirdly, a well-trained muscle is less prone to damage than a lesser trained one, so hard but scientific training is important.
It has been suggested that vitamin E may help to reduce muscle soreness, but there is little evidence to support this idea. Vitamin E is thought to act as an antioxidant that may blunt the damaging action of free radicals that attack the cell membrane of the muscle fibre. It has also been suggested that stretching the painful muscle or muscles may be beneficial, but this has not consistently been shown to alleviate delayed onset muscle soreness. Similarly, an easy “loosening up” run “to flush out the lactic acid” is unlikely to speed up recovery. To the contrary, running when the muscle is still damaged may delay full recovery. I often tell runners that while it is possible to run when there is still some post run stiffness, they will be running better some weeks later if they delay their return to full training until they no longer feel sore.
The real cause of muscle stiffness after a hard run is clearly not due to lactic acid in the muscle. Once this is well known, runners will be in a better position to manage their return to normal training after a marathon.
The Great VO2 max Myth by Doctor Andrew Bosch The Great VO2 max Myth by Doctor Andrew Bosch
I often receive telephone calls from runners wanting to know if it would be possible to measure their VO2 max. My standard answer is something along the lines that it is, indeed, possible. However, I then go on to ask why they want to have their VO2 max measured? There is usually one of two replies. Firstly, I am told, by knowing his or her VO2 max the runner will know that esoteric time that he or she is ultimately capable of running for some particular race distance, and therefore their ultimate potential as a runner. Secondly, once their VO2 max is known it will be possible to prescribe the ultimate personalised training schedule. My response to both is that knowing the VO2 max of a runner does not answer either question.
It is widely believed that the VO2 max is genetically determined and unchanging and that an individual is born with either a high or low “max”. Someone with a high value has muscles that are capable of utilising large amounts of oxygen and a cardiovascular system capable of delivering this volume of oxygen. The athlete is able to run at a maximum aerobic speed that this oxygen supply can sustain. In this paradigm it does not appear to matter whether the runner is unfit or superbly fit, the outcome of a VO2 max test remains the same. However, it is intuitively obvious that when fit the athlete can run much faster on the treadmill than when unfit. Thus, since VO2 max is genetically determined and does not change (in this model), VO2 max would be reached at a relatively slow running speed when a runner is unfit compared to when very fit, when a much higher speed can be reached on the treadmill. This means that in a totally unfit world-class runner we would measure a high VO2 max (say 75 ml/kg/min or higher) at a speed of maybe 17 km/hr on the treadmill. When very fit the same athlete will reach the same VO2 max at a speed of about 24 km/hr. The problem is that such a high VO2 max is never measured at a speed of just 17 km/hr. This would be almost impossibly inefficient. The theory of a genetically set and unchanging VO2 max therefore begins to appear a little shaky.
This concept of VO2 max evolved from misinterpretation of the data of early experimental work. It was believed that as an athlete ran faster and faster during a treadmill test, the muscles needed an increasing volume of oxygen, a process, which continued until the supply of oxygen, became limiting or the ability of the muscle to utilise oxygen was exceeded. At this point there would be no further increase in oxygen uptake. This plateau in oxygen utilisation was regarded as the VO2 max of the runner. If high, then the athlete had great genetic potential. However, in addition to the problem described in the previous paragraph, half of all runners tested in exercise laboratories never have a plateau in their oxygen uptake. Instead, the oxygen uptake is still increasing when the athlete cannot continue the test. The conventional view of VO2 max now appears to be even more suspect.
Consider a different scenario. A runner on a treadmill requires a certain amount of oxygen to run at a given speed. When the speed is increased, there is a corresponding increase in the volume of oxygen needed to run at the higher speed. The runner runs faster and faster, with corresponding increases in the oxygen required, until something other than oxygen supply to the muscle prevents any further increase in running speed. The volume of oxygen being used by the muscle when this occurs is at a maximum value, which is then termed the VO2 max. With this theory, oxygen requirement merely follows the increase in running speed, until a peak running speed and therefore peak oxygen requirement (VO2 max) is reached. It is easy to see why the VO2 max value will change as a runner gets fitter and can run faster. Within this framework, the genetically determined limit of VO2 max is determined by the highest running speed that can be reached, or in some instances a true limit in the supply and utilisation of oxygen by the muscle.
The inability to use the VO2 max test as a predictor of future performance in someone who can still improve his or her running by using a scientifically designed training programme becomes obvious. A great training-induced increase in running speed will result in a substantial change in VO2 max.
Knowing a VO2 max value is not going to assist in the construction of a training programme any more than will knowing current race times. There are, however, some potential uses of a VO2 max test. When constructing a training programme for someone who has not run any races and who therefore has no race times, a VO2 max test will help give an indication of the current ability of the athlete on which to base training schedules. Secondly, if done regularly, the test can provide information about the efficacy of a training programme. Finally, its fun to compare ones’ own VO2 max value with that of elite runners, who have VO2 max values higher than 70 ml/kg/min. What is yours in comparison ?
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