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Pushing and Pulling: the importance of zones 2 and 3 for raising the lactate threshold

Preparation for the season requires considerable time developing your endurance ability; and the most common way to do this is to train in the zones of 2 and 3 (see the separate factsheets on training in zone 2 and zone 3). Used in combination, they are the most effective way to build endurance – and therefore, the foundation to race fitness. Miss these stages out, and you risk being unable to cope with the training load in the pre season build period, and also, blunting the peak in fitness you can attain.

The traditional measure of endurance ability is the lactate threshold: and it is this parameter that forms the border between zones 2 and 3. By using both of these training zones, training improvements ~ 10% over a course of 6 to 8 weeks are regularly cited in the scientific literature. While it is true that training above the LT may bring on more rapid increases (certainly, in short term research studies, bigger improvements in LT are seen if you train above LT), we suggest a two stage process:

  • Working below the LT (zone 2) pushes LT up from below
  • Working above LT (zone 3) pulls LT up from above

This factsheet explains why the two stage process, while seemingly time consuming, is needed for the athlete hoping to excel in endurance events.

What causes the lactate threshold?

Pushing_and_PullingBefore explaining the rationale for the ‘push / pull’ process, it is worth considering what causes the LT, the sudden and sustained increase in blood lactate concentration as exercise intensity increases. The increased blood lactate concentration is brought about by an imbalance between the rate of appearance of lactic acid from the muscle into the blood (at which time the lactic acid dissociates into lactate and hydrogen) and the rate of its disappearance from the blood. In other words, the amount of lactate in the blood at any given time is the result of lactic acid production and its clearance. So, our lactate threshold could be caused because:

  • Production increases
  • Clearance mechanisms cannot keep up

Why might this happen? Research suggests the following mechanisms might contribute.

a) Inadequate muscle blood flow and local pockets of low oxygen (hypoxia)

You may come across the term ‘anaerobic threshold’ when reading about the concept of the lactate threshold. This phrase was originally assigned by Wasserman and co-workers1 on the assumption that blood lactate increases were generated by oxygen deficiency in the working muscle. When oxygen delivery is reduced and becomes insufficient to meet the required rate of energy production, anaerobic sources are needed and therefore increased lactate production results. Endurance training causes capillary and mitochondrial proliferation enhance muscle O2 delivery and utilisation. These adaptations delay the onset of substrate level phosphorylation, and may explain, in part, the increase in LT observed with training2.

b) Decreased lactate removal

When discussing blood [lactate], it is not uncommon for consideration to be restricted to its rate of production therefore neglecting rate of removal. During exercise however, lactate is continually removed alongside its production: A mechanism presented for causing the LT is a decrease in this removal rate. One reason for a decreased removal of blood lactate is the redistribution of blood flow as exercise becomes progressively harder. As an individual progressively works at higher intensities, blood flow to the active muscles is increased, thus reducing flow to potential sites of lactate oxidation3. Tissues involved in the uptake of lactate include the heart, the liver, and the kidney. This may lend itself to training induced improvements in the LT.

c) Metabolic substrate utilisation

Fatty acids are the preferred muscular fuel at low intensities. As exercise intensity increases, the ability of the contracting muscle to oxidise fat becomes limiting, necessitating increased carbohydrate metabolism to maintain or increase power output4. At this point, [lactate] will increase. Training improvements to the LT support this reasoning with the increased oxidative capacity of muscle enabling an increased contribution of fat oxidation and therefore reductions in lactate production. Manipulations of carbohydrate stores also support a substrate linked mechanism for the LT. Both glycogen depletion5 and augmented dietary fat intake6 increase the LT. Of note, this illustrates how important it is for the athlete to come into the lab for testing when well fed and rested!

d) Hormone response

At exercise intensities of approximately 60% VO2max, adrenalin and other hormones are seen to rise steeply7. As this value generally coincides with the LT, hormones have been linked to the increase in muscle lactate concentration. Adrenalin is known to stimulate splitting of muscle glycogen and therefore increase muscle lactate concentration8. Training studies again support the hormone hypothesis with lower blood lactate concentration concurrent with lower adrenalin concentration following endurance training9.

e) Muscle fibre recruitment patterns

Fibre_contributionsHuman muscle can generally be divided broadly into three fibre types, based on biochemical characteristics:

  • Slow twitch, or type I muscle fibres contain a large number of mitochondria, are surrounded by a large number of capillaries, and have a high myoglobin concentration. These fibres have a high oxidative capacity and are fatigue resistant.
  • Fast twitch, or Type II muscle fibres have a relatively small number of mitochondria and are therefore less resistant to fatigue. However, they are rich in glycogen stores and glycolytic enzymes giving them a large anaerobic energy production capacity.
  • Intermediate, or Type IIb fibres represent a continuum in their characteristics between the type I and type IIb fibres.

Studies using electromyography (EMG) suggest that increasing lactate concentration is linked to the progressive recruitment of motor units with a greater glycolytic / lower oxidative capacity10. Increased type II recruitment is necessary to meet force production demands as the type I fibre pool becomes fatigued. Furthermore, glycogen depletion studies show depletion of type II fibres to occur during exercise above LT11. As a consequence of their low oxidative capacity, the recruitment of type II fibres ultimately leads to lactic acid production.

So why ‘push and pull’?

So, we have learnt that blood lactate concentration is the sum of production and removal. Any training we do to shift the LT must therefore impact on one, or maybe both, of these sides of the equation.

Training in zone 2 emphasises the following physiology:

  • As the power outputs are low, you recruit mainly slow twitch fibres – increasing the time they have to contract by lengthening session duration challenges their metabolism, and the fibres will begin to grow more machinery to help that.
  • The low intensities mean that circulating adrenalin is low, allowing the slow twitch fibres to use their preferred fuel: burning fat. Lots of oxygen is needed as a result.
  • In order to process oxygen, the body will produce more mitochondria.
  • More oxygen around means a decrease in local pockets of hypoxia.

Result: Zone 2 training decreases muscle blood production. On the other hand, let us look at zone 3 training. During sessions in zone 3 because of the higher exercise intensity, greater reliance is placed on the fast twitch fibres and circulating levels of adrenalin have increased. In the untrained athlete, exercising in zone 3 will use a lot of muscle glycogen for energy production. Over time, the body will adapt to zone 3 work by:

Because of the challenge zone 3 brings to fuel metabolism (glycogen use), the body will respond by growing more machinery to help oxygen delivery i.e. a more dense capillary network is generated in the muscle tissue.

  • Using the now better equipped muscle to oxidise lactate (capillaries, mitochondria) – slow twitch fibres will take lactate out of the blood and use it as fuel.

In other words: Zone 3 training increases blood lactate clearance. Another benefit of zone 3 training is that it enables the body to store more glycogen – so, although the body still develops the ability to use this ‘high octane’ fuel, alongside that, it is also adapting to cope with the consequences.

Perhaps the best way to appreciate the importance of building these two systems in a stepwise manner is to consider your athletic ability in terms of the rate of energy turnover you can deal with. Training in zone 3 allows you to improve your use of glycogen (more fast twitch fibres, release of glycogen through the hormone response and a better storage of glycogen at rest) – in some ways, this is counter intuitive to a building of aerobic base. BUT, because the athlete has also established good clearance mechanisms in zone 2 training (more oxidising capacity) the body can operate at higher revs, a higher metabolic rate. Therefore, energy turnover is higher i.e. more watts are achieved, for a given metabolic stress.

Message to take home:

Hopefully, this explains why you start with base training before moving up the training levels:

  • Time spent in zone 2 pushes up the LT because you are creating systems to delay lactate production to a higher intensity.
  • Time spent in zone 3 will at first cause a greater challenge to the balance, but with time, your body gets better at clearing the circulating lactate

Without zone 2 work, you have not prepared the systems to cope with increases in lactate production that occur above the lactate threshold i.e. have more mitochondria to oxidise the lactate. It might seem a circular argument, and in some ways it is! An appreciation that physiological responses are on a continuum will help your understanding. For instance, don’t leave this factsheet thinking things suddenly switch from below to above LT –they don’t! You will still build mitochondria through training in zone 3, but why take a sledgehammer to a walnut? Rather, use the least fatiguing, more manageable training and squeeze out as much adaptation using that method first. To some, training in zone 2 feels time inefficient – but long term, it’s worth the investment.

REFERENCES

1. Wasserman & McIlroy. Am J Cardiol 1964, 14, 844-852.

2. Yoshida et al. Eur J Appl Physiol Occup Physiol 1982, 49, 223-230.

3. Donovan & Brooks. Am J Physiol 1983, 244, E83-92.

4. Walsh & Banister. Sports Med 1988, 5, 269-302.

5. Heigenhauser et al. J Appl Physiol 1983, 54, 470-474.

6. Ivy et al. Int J Sports Med 1981, 2, 139-142.

7. Podolin et al. J Appl Physiol 1991, 71, 1427-1433.

8. Febbraio et al. J Appl Physiol 1998, 84, 465-470.

9. MacRae et al. J Appl Physiol 1992, 72, 1649-1656.

10. Nagata et al. Jpn J Physiol 1981, 31, 585-597.

11. Vollestad & Blom. Acta Physiol Scand 1985, 125, 395-405