Base-building, muscle damage and adaptation

One of the challenges of training is getting the right balance between the principle of specificity and the need to build a base.  The principle of specificity dictates that if one wants to run a mile in 4 minutes one should train the body to be able to maintain a pace of 15 miles per hour for 4 minutes.  Hence one might imagine that the best approach is to start by running ¼ mile repeats in 1 minute, and gradually build up the distance at this pace to the stage of running ¾ miles in 3 minutes, before attempting the goal of a 4 minute mile.  Perhaps Zatopek’s famous rhetorical question: Why should I run slowly when I want to learn how to run fast?’ captures the idea of specificity most elegantly.  And perhaps this would be a sensible approach to the final stages of preparation for an assault on the 4 minute mile.

 

However, to start with a training program based on running at 15 mph is likely to be a prescription for injury and frustration.  To prepare for the rigors of specific training for an event that might test one’s body to its limits, it is necessary to lay a foundation in which many of the tissues of the body are prepared to handle the demands that will be placed upon them.  This is the purpose of base-building.

 

The goals of base-building

In building a base for middle and long distance running, the two tissues that require the greatest development are skeletal muscles and heart muscle.  However many other tissues require an adequate level of development:

  • lungs to transfer oxygen from air to blood and carbon dioxide from blood to air;
  • ligaments to transmit the force of muscle contraction to joints;
  • bone and joints to withstands the forces generated by muscle, gravity or ground reactions;
  • liver to remove lactate from the blood and regenerate glucose, and replenish glycogen stores;
  • kidneys to assist the lungs in maintaining acid base balance, and to maintain electrolyte levels;
  • the endocrine system to produce the hormones that balance anabolism (building up of tissues) with catabolism (breaking down);
  • and the brain to couple motivation to action and orchestrate all of these actions.  

Base-building prepares all of these tissues, in addtion to skeletal muscle and heart.

 

Construction v demolition

The essence of base-building is construction, not demolition.  The way in which we build the tissues of the body is by challenging them.  Applying stress stimulates the body to react by strengthening the function that is challenged.  But if we present a challenge that is too great, the net effect is destruction.  The art of base-building is getting the balance right.

 

From time to time in recent weeks I have mentioned my intention to review the processes that transform muscle during training.  It is in muscle that we can see most clearly the way in which a challenging stress can result in strengthening if applied appropriately, but the process is fraught with risk of both short term damage and possible long term damage.  As with all physiological processes, the topic is complex, and the outcome of the interaction between the processes of destruction and construction is difficult to predict.  I have held back from tackling this topic because the available evidence must be drawn from many sources: historical anecdotes; scientific studies of groups of athletes undergoing specific training routines, and the extensive and rapidly growing body of knowledge about the physiological processes involved.

 

Reviewing the historical evidence

Much of the information we have to guide training is based on the inspired observations of coaches such as Gerschler in the 1940’s and 50’s and Lydiard in the 1960’s and 70’s who transformed training in their own eras.  Gerschler’s introduction of interval training led, via Franz Stampfl, to Bannister’s four minute mile in 1954, and perhaps also contributed indirectly to Zatopek’s gold medals in the 5000m,10000m and marathon in Helsinki in 1952, though it appears Zatopek developed his training technique independently of Gerschler.  Lydiard’s emphasis on building a base by a large volume of aerobic running followed by a period of intense event-specific training led not only to the middle distance triumphs of Snell but also the longer distance achievements of Halberg, Clarke and others. 

 

However, world records have continued to improve and in the past decade or so, many African runners, most notably Hicham El Guerrouj in the 1500m and mile, Kenenisa Bekele in the 5000m and 10000m and Haile Gebrselassie in the marathon, have left the records of Bannister, Zatopek, Snell, Halberg and Clarke in tatters.  While there is still some debate about the genetic endowment of African runners, it is more likely that better training provides the main explanation.  However the question of which aspects of training are responsible remains controversial.  Training at altitude is part of the story but more likely a childhood spent building a base, and a large amount of quite high intensity training in the competitive years, are the crucial ingredients.  However, higher intensity training brings with it risks, making it all the more important to understand the mechanisms of both the benefits and of the potential damage.

 

Historical evidence v. recent scientific evidence

First, we should re-examine the evidence we have touched on in reecent weeks suggesting that Lydiard was wrong to maintain that aerobic capacity could only be developed by aerobic training  There is little doubt that at least in the short and medium term, high intensity training can improve aerobic capacity while providing a more efficient use of time than traditional endurance training.  In the study by Gibala and colleagues comparing 6 sessions of high intensity sprint cycling consisting of 4 to 6 30second sprints with 6 session of endurance training consisting of 90-120 minutes of cycling at 65% of VO2max, over a two week period, similar improvements in performance; muscle oxidative capacity; muscle buffering capacity; and muscle glycogen content were produced even though the total training time commitment was only 2.5 hours for the sprint training compared with 10.5 hours for the endurance training (J Physiol Vol 575, pp 901-911, 2006).

 

Although the acidity produced by anaerobic training might limit the capacity for aerobic conditioning within a particular training session, I can find no substantial evidence that a reasonable mixture of aerobic and anaerobic sessions damages aerobic development.  In a study mentioned in my recent comparison of Maffetone and Lydiard, Ingjer demonstrated that 24 weeks of training that included one predominantly aerobic session and two interval sessions per week, resulted in an increased proportions of type 2A fibres (fast twitch, aerobic) at the expense of type 2B fibres (fast twitch anaerobic), but without changing the proportion of Type 1 (slow-twitch fibres).  Ingjer also reported that this training program produced substantial improvement in other indices of aerobic function. The mean number of capillaries per muscle fibre increased by 29%   There was a major increase in mitochondrial density in both type 1 and type 2A muscle fibres.  During training the proportion of type 1 fibres that were described as rich in mitochondria increased from  59 to 95%., while the proportion of mitochondria-rich type 2A fibres increased from 21 to 77 % . These increases in proprtion of aerobic fibres, capillary density and mitochondria were associated with an average increase in maximal oxygen uptake capacity of 25% (J. Physiol, vol 294, pp. 419-432, 1979).

 

Several subsequent studies have confirmed that training can convert fast twitch anaerobic fibres to aerobic fibres.  For example Hather and colleagues demonstrated that a program of eccentric and concentric resistance training increased the proportion of type 2A fibres (fast-twitch aerobic) at the expense of type 2B (anaerobic) fibres, while also increasing the size of type 1 (slow twitch) fibres and increasing capillary density in both type 1 and type 2A fibres ( Acta Physiologica Scandinavica, Vol 143,Pages177–185).  Staron and colleagues demonstrated that heavy resistance training in women produced hypertophy of all three fibre types (European Journal of Applied Physiology, Vol 60, pp1439-6319,  1990).

 

I am aware of only one study that showed a reduction in type 1 fibres  during training.  That was a study of intense sprint cycling training that resulted in a 7% reduction in proportion of  type 1 fibres and a 6% increase in the proportion of type 2A (aerobic fast twitch fibres) (Jansson and colleagues. Acta Physiologica Scandinavica, Vol 140 pp359-363).  Even in this study, the aerobic slow twitch fibres were replaced by aerobic fast twitch fibres and hence provide no evidence for loss of aerobic capacity.

 

Thus, recent scientific evidence demonstrates that both aerobic and anaerobic training can lead to enhanced aerobic capacity.  This perhaps explains why coaches and athletes employing quite different strategies have in some instances achieved spectacular success.  There is no single path to success.  However, the large numbers of injured athletes and of athletes who have exhibited great promise early in their careers, but failed to deliver on that promise, demonstrates that despite the multiplicity of paths to success, there are also multiple paths to stunted growth, frustration or outright failure.  Therefore rather than being guided simply by anecdotal evidence of the success of Olympians, or alternatively by scientific studies that reveal group-average benefits in small groups of athletes who have undergone a particular training regime under quite specific circumstances, we might be well advised to understand also what physiological science has revealed about the mechanisms of tissue damage and adaptation.

 

Use it or lose it

Living tissues are dynamic structures which degenerate unless continuously renewed.  Many of the major functions of living tissues are mediated by proteins. Usually, the process starts when receptor proteins embedded in membranes that enclose the cells in all types of body tissues receive either electrical or chemical messages, arising from the external environment or from within the body, that cause them to adapt their shape in a way that promotes the function of that type of tissue. 

 

For example, the electrical message from a nerve to a muscle releases a chemical messenger called acetylcholine that binds to receptor proteins on the muscle surface membrane in a region known as the muscle end-plate.  These receptors change their shape when the messenger molecule binds to them, triggering a cascade of signaling processes within the cell.  These signals involve additional chemical messengers which bind to other proteins within the cell, triggering further signaling until ultimately, the proteins that perform the main functions of the cell are activated.  Within muscles, the final signaling messenger is calcium released from a membranous structure surrounding each myofibril known as the sarcoplasmic reticulum.  The calcium acts on the actin and myosin within the myofibril to produce contraction.  Actin and myosin are long chain-like protein molecules that are aligned in parallel and linked by cross-bridges.  In the presence of calcium, the cross-bridges reform creating a ratcheting action that pulls the actin and myosin fibres past each other, producing contraction of the muscle fibre.

 

However, activation of the receptor proteins on the cell surface not only initiates a cascade of signalling that results in other proteins within the cell executing the function of the cell, the process of activation of the receptor proteins also results in an additional cascade of chemical signals that ultimately act on the DNA in the cell nucleus triggering the genesis of proteins within the cell.  In the case of muscle, binding of acetylcholine triggers the translation of DNA to produce proteins that replace any that have suffered degradation and provide new building material for hypertrophy of the muscle.  Thus muscle, and indeed virtually all body tissues, experience continual repair and remodelling as they are used.  However, if they are not used, they eventually decay due to the inevitable degradation of biological materials.  

 

It should be noted that the process that leads from the electrical message in the nerve via release of acetylcholine onto receptors on the muscle endplate and subsequent release of calcium from the sarcoplasmic reticulum to the ratcheting of the actin and myosin molecules that results in contraction, occurs on a time scale of milliseconds, whereas the translation of the DNA code and production of new protein takes many hours or even days.  Thus consumption of protein-containing foods which are broken down to produce the amino acids which are the basic building blocks for construction of new protein can occur over a period of hours after exercise; similarly the natural anabolic hormones that promote regeneration and hypertrophy are required to act over a period of many hours.

 

Mechanisms of muscle damage and adaptation

While processes such as the translation of the DNA code and production of new proteins as a consequence of use, occur in almost types of tissue in the body, the processes of damage and repair are even more dramatic in muscle due to the forceful nature of muscle contraction.  The phenomenon of delayed onset muscle soreness appears to be overt evidence of the damage due to use, and the subsequent increase in strength is an illustration of the hypertrophy due to synthesis of new muscle protein.

 

The most marked damage to muscle occurs following eccentric contraction – when the muscle attempts to contract while it is actually undergoing stretching due to external forces.  This is a situation that occurs at foot-strike when running.  As the foot contacts the ground, with knee and ankle flexed, the necessity of arresting the free-fall under the influence of gravity in the airborne phase results in stretching of quadriceps and the calf muscles.  This stretching facilitates the storage of gravitational energy as elastic energy which can be recovered at lift off from stance. However, the inevitable eccentric contraction of the quads and calf muscle produces quite marked damage.  Electron microscopic images of muscle fibres after running, especially down-hill running, reveal visible disruption of the points where the actin and myosin chains are attached to the framework of the myofibril.  This manifest evidence of structural damage is known as Z-line streaming.  (For photographs, see for example, Gibala and colleagues, Journal of Applied Physiology, Vol 78, 702-708, 1995).  It is possible that it is due to shorter myofibrils being torn asunder by the powerful contraction of adjacent longer fibrils in the same bundle.

 

This dramatic damage appears immediately after exercise and is associated with loss of strength that is maximal in the period 24-48 hours after exercise and resolves slowly over a period of up to 96 hours.  Satellite cells appear to play a key role in the recovery from this damage.  Satellite cells are small specialised stem cells found in close association with skeletal muscle fibres. In response to injury they become activated and fuse with the myofibrils promoting repair and regeneration.  They have also been observed to become active during periods of heavy muscle loading and fuse with apparently undamaged myofibres as part of the hypertrophy process  ( GE Adams Satellite cell proliferation and skeletal muscle hypertrophy, Appl Physiol Nutr Metab Vol 31, pp782-790, 2006).  Various factors, including hormonal and nutritional status regulate this process.

 

In future posts I will review the evidence regarding the likely effect of different training programs on the nature and extent of this damage to muscles, and on the repair and adaptation processes mediated by satellite cells, though there are of course many outstanding questions that remain unanswered.

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12 Responses to “Base-building, muscle damage and adaptation”

  1. canute1 Says:

    I have received a message from a friend saying that comment box is in the blink, so I am posting this to see what happens.

    I am sorry if anyone else has tried to post a comment and has had problems. I will do what I can to sort out the problem

  2. canute1 Says:

    As far as I can tell, the comment box is now working.

  3. Jason Says:

    From my memory (which is likely to be wrong) the study by Jansson and colleagues, claiming a 7% reduction in Type I fibres was measured as the proportion of cross-sectional area of muscle, not as the number of fibres. Further this was only as a relative measurement, not in absolute terms. ie. The overall cross-sectional area of muscle increased overall, there was significant increase in the proportional area (not number) of type II fibres. The study wasn’t clear if there was any absolute reduction or if this percentage reduction in type I fibres was simply as a result of bigger gains in the various type II fibre size increases over the term of the study.

    In my view this leads towards further supporting the rest of the evidence of development in type I and IIa fibres from training, even when the training is based on intense sprint training.

    My favourite part of your post is:
    “There is no single path to success. However, the large numbers of injured athletes and of athletes who have exhibited great promise early in their careers, but failed to deliver on that promise, demonstrates that despite the multiplicity of paths to success, there are also multiple paths to stunted growth, frustration or outright failure. ”
    An absolutely awesome observation.

  4. rick Says:

    Hi Canute,
    With a history of 10 years cycle training and now 15 years running I have tried just about every type of training possible and my only unscientific conclusion has to be that you can’t get away from the fact that building a massive aerobic base first before starting high intensity anaerobic training [ boring that it my be] always produces the best long term benefits!
    I find it quite worrying that many clubs put their youngsters through year round interval training with little concern for base building !
    However unappealing spending hours and hours running might seem, in the real world away from the white coats and the laboratory’s it works, one needs to look at the evolution of the human on the African planes back in the mists of time to understand why!

  5. Ewen Says:

    I’ll be interested to read more about the satellite cells and muscle damage repair and hypertrophy.

    I’m just throwing a figure in the air, but I’d say that 80% or more of the distance running athletes that follow a path to “to stunted growth, frustration or outright failure” are those that train with too much intensity, not enough consistency and insufficient base. Even elite runners (I’m thinking of some Kenyans and Ethiopians) who now run lower volume/higher quality mileage of around 140-150k/week had many years previously of running mileages in the 180-220k range.

  6. canute1 Says:

    Jason, As you state, Jansson reported changes in proportions of fibre types, though they did interpret their findings as evidence of transformation between fibre type. As we both agree, however one interpets the numbers they report, their study appears to confirm that anaerobic training can increase aerobic capacity.
    Rick and Ewen, I agree that the safest path to success almost certainly involves fairly high volume, relativley low intensity base-building, though even high volume training has some risks – which I will attempt to address in a later post.

  7. rick Says:

    EVOLUTION OF THE DISTANCE RUNNER!
    http://news.bbc.co.uk/1/hi/health/4021811.stm
    maybe the best way to train is like are distant ancestors use to run, long steady runs with the odd sprint to catch prey or run away from danger!!!

  8. Ewen Says:

    Canute, I came across a link to a study that shows that high acidosis may interfere with mitochondria production:

    http://tiny.cc/KDz35

    Could it show that Lydiard may have been right aerobic and anaerobic training don’t ‘mix’?

  9. canute1 Says:

    Ewen, That is very interesting, and is consistent with the proposal that maximal production of mitochondria might be achieved near the upper end of the aerobic zone. It also is consistent with the proposal that acidosis during a session might decrease the efficiency of aerobic development in that session. I do not think it demonstrates that anaerobic training reverses the benefits of aerobic training, or that aerobic development cannot occur during a phase of mixed anaerobic and aerobic training.
    What the authors report was a comparison of the effect of 10×2 min cycle intervals at 80% VO2max intensity on two separate occasions: once after consumption of ammonium chloride, which causes an artificial acidosis and once after the consumption of calcium carbonate which does not cause acidosis. On both occasions there was a marked increase in translation of the DNA that codes for a protein that regulates the generation of mitochondria. However, the increase was less marked in the presence of the acidosis induced by ammonium chloride. Thus even in the presence of an artificially induced acidosis the production of mitochondria is likely to be increased by vigorous exercise, but mitochondrial production is likely to be greater during vigorous exercise in the absence of acidosis.
    Overall this study suggests that intervals at 80% VO2max (which would be likely to be upper aerobic for many athletes) promote marked increase in mitochondrial production, while at anaerobic levels mitochondrial production would be expected but might be less marked. This study did not look at mitochondrial production when exercising in the lower aerobic zone, so it does not assess whether the production of mitochondria during vigorous exercise in the presence of acidosis is greater than or less than that during less vigorous lower aerobic training

  10. Ewen Says:

    Canute, thanks for that summary. I’m still unsure as to whether mitochondrial production is equally pronounced in upper and lower aerobic training. Perhaps in the lower aerobic zone it is if the duration of the exercise is sufficient?

    Does the study show that anaerobic training within an aerobic session (for example, hard fartlek training, or very fast intervals within a long run) is detrimental to mitochondrial production during that session?

    Perhaps mixed training where the anaerobic sessions are kept separate from the aerobic sessions is the best way to go for athletes using a mixed program?

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