My previous post discussed evidence indicating that training in the vicinity of lactate threshold (LT) can lead to sustained elevation of cortisol which has the potential to damage to the neuromuscular system and suppress immune responses. In particular, the study by Balsalobre-Fernandez indicates that frequent training at or a little above lactate threshold is more damaging than a lesser amount of training at a higher intensity. This might be the key to understanding why a growing body of evidence favours polarized training, which includes a large volume of low intensity training, a small amount of high intensity training and a similarly small amount of threshold training, in preference to a training program with a higher proportion of threshold training.
As distance races from 5 Km to marathon are raced in vicinity of lactate threshold, pace at LT is a crucial determinant of performance. Enhancing the ability to delay the onset of lactic acid accumulation as pace increases is one of the key goals of training. The effectiveness of polarised training raises the question of how a program with only a small about of threshold training might nonetheless be effective in enhancing ability to minimise lactate accumulation.
Lactate accumulation might be minimised by decreasing the rate of production and /or increasing ability to remove it. The rate of production can best be minimised by increasing the capacity to generate energy aerobically, which in turn might be enhanced by increasing the capacity of aerobic enzymes in mitochondria and/or increasing delivery of oxygenated blood to muscles.
Developing Aerobic Capacity
While a large volume of low intensity running would be expected to increase the aerobic enzymes in slow twitch fibres, the more challenging question is how to enhance the aerobic capacity of fast twitch fibres. Low intensity running beyond the point of exhaustion of slow twitch fibres might help achieve this, but frequent very long runs create the risk of excessive stress. For many years followers of Arthur Lydiard’s approach to periodization, in which the base-building phase is almost exclusively devoted to relatively low intensity aerobic running, have maintained that when you bring speed work into the program, you halt the development of aerobic enzymes. The size of the engine is now fixed; the task of speed work is to tune this engine.
This claim was associated with a widespread belief that the acidity generated above LT prevented development of aerobic enzymes, and perhaps even damaged them. This belief is ill-founded. Extensive research into high intensity interval training (HIIT) in recent years has demonstrated that HIIT is a very efficient way to increase the capacity of aerobic enzymes. The available evidence indicates that HIIT achieves the enhancement of mitochondrial enzymes via the increasing the activity of the messenger molecule, PGC-1alpha, the same messenger as appears to mediate mitochondrial development in response to lower intensity endurance training
HIIT research is largely focussed on comparing high intensity training with low intensity training and has not so far investigated the potential benefits of a polarised approach. It would be anticipated that in a polarised approach the rate of gain in aerobic capacity would not be a rapid as with HIIT, but it is scarcely credible that diluting the high intensity session with low intensity sessions would abolish the aerobic gains of the high intensity sessions, provided there is adequate opportunity for recovery.
Not only does HIIT produce efficient development of aerobic enzymes, but it is also effective in enhancing the development of the enzymes that metabolise fats, thereby promoting the generation of energy from fat, a processes that does not generate lactate
With regard to increasing the supply of oxygenated blood to muscle, sprint interval training is as effective as endurance training in promoting development of capillaries. Although the effect of HIIT on development of cardiac output has been less thoroughly studied, it is noteworthy that the Gerschler’s rationale for the introduction of interval training was the stimulation of cardiac output. In his word interval training provides “a stimulus particularly powerful to reach the heart.”
Transport of lactate
The alternative approach to minimizing lactate accumulation is removal of lactate from muscle and blood. With regard to the relative efficacy of polarised training compared with threshold training, the important issue is whether or not this is better promoted by brief surges of intensive lactate production or by sustaining a moderate level of lactate. The mechanisms by which lactate is removed from muscle include the transport of lactate from fast twitch fibres, where it is produced, to slow twitch fibres, which have the capacity to metabolise the lactate; the transport to other organs such as heart muscle which are well adapted to metabolising lactate; or transport to the liver where the process of glycogenesis converts lactate to glucose and subsequent storage in the form of glycogen.
The transport of lactate across cell membranes is mediated via a set of transport molecules, the monocarboxylate transporters (MCTs) that transport lactate together with protons. Transport by MCT’s involves diffusion and the rate is determined by the transmembrane gradient of either lactate or acidity (protons). It is likely that under most conditions, lactate flux is determined mainly by the gradient produced by metabolism-driven uptake, while the availability of MCTs is rate-limiting only after the establishment of large transmembrane gradients. Therefore, the first goal in enhancing the capacity to clear lactate during distance running is enhancing the ability to metabolise lactate. In heart and slow twitch fibres, this is achieved by enhancing vascularization and aerobic enzyme activity. The evidence discussed above suggests that polarized training is an effective way to do this. Nonetheless, it is desirable to ensure that MCT’s are maintained at an adequate level. Because MCT-mediated transport is rate-limiting only in the presence of large transmembrane gradients, it would be expected that brief surges of lactate will be more effective in promoting development of MCTs than sustained moderate levels.
Buffering of acidity
The role of acidity in stimulating training effects is ambiguous. On the one hand rising acidity eventually halts metabolism in muscle, but on the other, some degree of stress is likely to be necessary to promote adaptation. Ingestion of sodium bicarbonate (baking soda) which neutralises acid has been shown to diminish the secretion of anabolic hormones, such as growth hormone, following intense exercise. Thus rise in acidity appears to facilitate at least some of the desired effects of training. In contrast, sodium bicarbonate ingestion augments the increase in activity of the messenger molecule PGC-1alpha in skeletal muscle during recovery from intense interval exercise in humans, and therefore might promote the development of mitochondria.
This raises the question of the role of natural buffering mechanisms in the blood. During intense exercise there is a transient rise in the body’s natural buffers, phosphate ions and bicarbonate ions, that helps neutralise the rise in acidity despite the rise in lactate concentration. Thus it is plausible that one of the advantages of interval training compared with threshold training is that the transient natural buffering during interval training allows more intense exercise and hence allows greater lactate production without excessive acidity. Perhaps this would act as a greater stimulus to PGC-1 Alpha activity and perhaps MCT production as well. On the other hand, natural buffering might diminish the potentially beneficial increase growth hormone activity. Overall, on account of the competing antagonistic effects, I doubt that buffering is an important adjunct to training. The issue is similar to the debate about the value of cold baths to reduce inflammation after training.
Nonetheless, the possibility that buffering might increase tolerance of lactate production, together with the substantial evidence for improved endurance performance in rats and humans, reviewed McNaughton and colleagues, has led to the proposal that bicarbonate doping might enhance race performance. I am intrinsically opposed to the ingestion of substances in marked excess of the amounts present in a normal healthy diet for the sake of enhancing performance, but some athletes might argue that provided it is not illegal it is acceptable. However, the dose required to produce an appreciable effect (20-30 gm) can cause vomiting or diarrhoea. I would regard this is too great a risk to take.
Long term improvement
It is clear that many of the physiological adaptations required to minimise the rate of accumulation of lactate can be achieved very efficiently by HIIT. This evidence undermines the principle that enhancement of the ability to handle lactate is achieved most effectively by specific training in the vicinity of LT.
Unfortunately, most of the HIIT research so far has focussed on the contrast of HIIT with lower intensity training, delivered over a time scale of several weeks. There is some evidence that the benefits of HIIT do plateau after a period of a few months. The study by Stoggl and Sperlich demonstrated that for athletes who have a history of regular training, polarised training produces greater benefits than either threshold training or predominantly high intensity training. It is plausible that the adaptations produced by HIIT can also be achieved, perhaps more gradually but with the potential for steady improvement over a prolonged period, by a polarised program. Hitherto there have been too few studies that have examined the development of physiological capacities such as aerobic enzymes, delivery of blood to muscle and the transport of lactate, during training programs sustained over a full season or longer.
Injury is an issue of perennial importance to athletes. In general, muscle injury is likely if a large force is exerted unexpectedly, or if muscles are fatigued. Protection against injury is minimised by the strengthening promoted by anabolic hormones on the one hand, or diminished by the breakdown of tissues promoted by sustained elevation of catabolic hormones such as cortisol. In the next post in this series, I will address the question of whether injury is more or less likely with a polarised program than with threshold training.