Why endurance athletes cannot afford to ignore the vital contribution of fast-twitch muscle fibres
In last month’s issue, I offered the lowdown on maximising fast-twitch muscle fibre potential for speed and power (PP201, August 2004). This article focuses on getting the most out of muscle fibre for endurance activity.
Biopsies are used to determine what types of fibres exist within our muscles. A special needle is pushed into the muscle and a grain-of-rice-size piece of tissue extracted and chemically analysed. Two basic fibre types have been identified via this process: slow-twitch (also known as type I or ‘red’ fibres) and fast-twitch (aka type II or ‘white’ fibres). Type II fibres, as we shall see, can be further sub-divided into type IIa and type IIb variants.
Slow-twitch muscle fibre contracts at almost half the speed of fast-twitch fibre – at 10-30 twitches per second compared with 30-70. Slowtwitch fibre has a good level of blood supply, which greatly assists its ability to generate aerobic energy by allowing plentiful supplies of oxygen to reach the working muscles and numerous mitochondria.
Mitochondria are cellular power plants; they function to turn food (primarily carbohydrates) into the energy required for muscular action, specifically adenosine triphosphate (ATP). ATP is found in all cells and is the body’s universal energy donor. It is produced through aerobic and anaerobic energy metabolism and, consequently, through the associated actions of both slow and fast-twitch muscle fibre.
Slow-twitch fibre is much less likely than its fast-twitch counterpart to increase muscle size (hypertrophy), although well-trained endurance athletes have slow-twitch fibres that are slightly enlarged by comparison with sedentary people. The most notable training effects, however, occur below the surface.
Subject to relevant endurance training, these unseen changes include:
An improved aerobic capacity caused by fibre adaptation. Specifically this involves an increase in the size of mitochondria, boosting the ability of the fibres to generate aerobic energy;
An increase in capillary density, which enhances the fibres’ capacity to transport oxygen, and thus to create energy;
An increase in the number of enzymes relevant to the Krebs cycle – a chemical process within muscles that permits the regeneration of ATP under aerobic conditions. The enzymes involved in this process may actually increase by a factor of two to three after a sustained period of endurance training.
Blood lactate plays a crucial role in energy creation which is not, as many people mistakenly assume, restricted to the latter stages of intense exercise.
Lactate is actually involved in energy production in our muscles at all times, although response to lactate generation varies according to fibre type. A brief consideration of this process will begin to explain why the relationship between fast and slow-twitch fibre is crucial to optimum endurance.
Fast-twitch fibres produce the enzyme lactate dehydrogenase (LDH), which converts pyruvic acid (PA) into lactic acid (LA). The LDH in slowtwitch muscle fibre however, favours the conversion of LA to PA. This means that the LA produced by the fast-twitch muscle fibres can be oxidised by the slow-twitch fibres in the same muscle to produce continuous muscular contractions.
When LA production reaches a level where it cannot be recycled to generate steady-state aerobic energy, endurance exercise moves into anaerobic territory – with less reliance on oxygen and more on stored phosphates for energy production.
There will come a point, under these conditions, when an athlete reaches his or her ‘lactate threshold’, at which point further exercise becomes increasingly difficult and the athlete is forced to slow down and ultimately stop.
As we shall see later, this ‘anaerobiosis’ and its exercise-halting effect may be as much a consequence of brain activity as of muscular limitations, especially under extreme endurance conditions.
Well-trained endurance athletes are able to generate blood lactate levels that are 20-30% higher than those of untrained individuals under similar conditions. This makes for significantly enhanced endurance as their muscles no longer drown in lactate but rather ‘drink’ it to fuel further muscular energy. To continue the analogy, the untrained individual’s muscles would get ‘drunk’ on lactate after just a few intervals – or should that be rounds!
As noted, failure to train fast-twitch fibre to contribute to endurance performance will result in lactate threshold being reached – and performance arrested – at a much earlier point. Unlike the 100m sprinter, who can ignore his slow-twitch fibres altogether in training without damaging performance, the endurance athlete has to train all fibre types in order to maximise sustained muscular energy.
Athletes are made rather than born
As I pointed out in my previous article, most people are born with a relatively even distribution of fast and slow-twitch fibres, suggesting that power and endurance athletes are made’ rather than born. As exercise physiologists McKardle, Katch and Katch point out, ‘studies with both humans and animals suggest a change in the biochemical-physiological properties of muscle fibres with a progressive transformation in fibre type with specific and chronic training’(1).
Table 1, below, shows the extent to which fibre type can be ‘altered’ after training for selected endurance activities, although whether these changes are lasting is open to debate, as we shall see.
We have shown how slow-twitch fibre adapts to endurance training. Now let’s take a look at how fast-twitch fibres respond.
Type IIa or ‘intermediate’ fibres can, in elite endurance athletes, become as effective at producing aerobic energy as slow-twitch fibres found in non-trained subjects. Like slow-twitch fibres, these fibres (and their type IIb counterparts) will benefit from an increase in capillary density. In fact, it has been estimated that endurance training that recruits fast and slow-twitch muscle fibre can boost intramuscular blood flow by 50-200%(2);
Type IIb fibres can play a much more significant role in sustained energy release than had been assumed, according to research carried out by Essen-Gustavsson and associates(3). These researchers studied muscular enzyme changes brought about by endurance training and concluded that type IIb fibres were as important to endurance athletes in terms of their oxidative energy production and the clearance of exerciseinhibiting phosphates as type IIa fibres.
A raft of relatively recent research indicates that intense training efforts – eg three-minute intervals at 90-95% of max heart rate/over 85% of VO2max, with three-minute recoveries – are great ways to boost lactate threshold (as well as VO2max, economy and strength). These ‘lactate-stacker’ sessions, by their very nature, rely on fast-twitch fibre to generate power. Note, though, that these workouts are very tough and stressful and should be used judiciously (see PP 100, Feb 1998; 163, April 2002 and 179, April 2003 for detailed descriptions of lactate stacker workouts).
Endurance gains can be made much more quickly through capillary adaptation in fast and slow-twitch fibre with anaerobic training methods, such as the lactate stacker workouts, than with less intense aerobic training.
Although it is possible to train fast-twitch fibre to take on more of the slow-twitch blueprint, taken to extremis – especially through the use of slowtwitch steady state training – this may not actually be the best strategy for endurance athletes.
The marathon runner Alberto Salazar once said that he aimed to train aerobically hard enough to lose his ability to jump(4). In other words, he was trying to convert all his fast-twitch fibres into slow-twitch ones in terms of their energy-producing potential so that they could contribute all their energy to his marathon running.
However, for a variety of reasons, losing all fast-twitch speed and power ability may not actually be a good idea. For example, at the end of a closely-fought marathon there may be a need for a sprint, requiring fast-twitch fibre input.
Even more specifically, there is the anaerobic/aerobic component of an endurance activity to consider, and the speed required to complete it competitively. An 800m race or a 2k row calls for an anaerobic energy contribution of around 40%, and athletes in these disciplines must be fast and powerful to succeed.
Fast-twitch fibres have to be trained accordingly; it’s no good turning them into plodders with an emphasis on slow-twitch, steady state work, if they are needed to produce a short or sustained kick and a sizeable energy contribution.
The recent research into lactate stacker sessions and the vital role of lactate threshold as the key endurance performance variable further substantiates the need for the development of a high-powered endurance contribution from fasttwitch fibres.
Despite virtually undisputed evidence that all muscle fibre types will adapt to a relevant training stimulus, it is less certain whether these changes are permanent. One of the few studies concerned with the long-term effects of endurance training was conducted by Thayer et al, who looked at muscle-fibre adaptation over a decade(6). Specifically, they compared skeletal muscle from the vastus lateralis (front thigh) in seven subjects who had participated in 10 years or more of high intensity aerobic training with that of six untrained controls.
They found that the trained group had 70.9% of slow-twitch fibres compared with just 37.7% in the controls. Conversely, the trained group had just 25.3% fast-twitch fibre, compared with 51.8% in the controls. The researchers concluded that endurance training may promote a transition from fast to slow-twitch fibres, and that this occurs at the expense of the fast-twitch fibre population.
Fibre reversion after inactivity
However, it seems that slow-twitch (and fasttwitch) muscle fibre tends to revert back to its pre-training status after a period of inactivity (although aging may provide an exception to this rule, as we shall see later). In fact, the theory is that muscle fibre has a fast-twitch default setting. This is entirely logical: since we use our slowtwitch fibres much more than our fast-twitch ones on a daily basis, a period of inactivity would detrain slow-twitch fibre and allow fast-twitch fibre to regenerate and convert back to a faster contraction speed. The interesting and slightly less logical aspect of this process is that it does not necessarily require speed training, as demonstrated by research on muscle tissue rendered inactive by accident or illness(7).
When it comes to recruiting winning muscle, it is impossible to overlook the vital role of the brain. Muscle fibre can only function at the behest of our brains, and it is possible that athletes ‘learn’ how to tolerate the pain associated with lactate build up, for example, and consequently become better able to recruit their muscle fibres.
Recently, research has begun to appear on the so-called ‘central governor’, which is seen to be the determinant of the body’s ability to sustain endurance activity by tolerating increasing intensities of exercise. It has been argued that the governor’s setting can be altered through the experience of intense exercise and a corresponding shift in willpower to permit greater endurance perseverance. This theory has been substantiated by evidence that muscles can still hold onto 80-90% of ATP and some glycogen after intense endurance efforts – ie when the athlete has ‘decided’ to stop exercising.
It has been suggested that the body – and, for our purposes, its muscles – will always hold onto some crucial energy-producing materials, just in case it is called upon to react in an emergency. This is seen as a legacy of the unpredictable past that confronted our prehistoric ancestors, who never knew if they would need a bit more energy to flee from a sabre-toothed tiger after a long day’s hunting and gathering!
The central fatigue hypothesis
Closely related to the thoughts on the ‘governor’ is the ‘central (nervous system) fatigue hypothesis’, postulating that the brain will ‘shut down’ the body under certain conditions when there is a perceived threat of damage to vital organs, irrespective of an individual’s fitness. The conditions specifically identified to trigger central fatigue are high altitude and high temperatures, although researchers believe it could also swing into play under less taxing conditions.
The famous exercise physiologist and runner Tim Noakes states: ‘There is no evidence that exhaustion under these conditions is associated with either skeletal muscle ‘anaerobiosis’ or energy depletion…. There is sufficient evidence to suggest that a reduced central nervous system recruitment of the active muscles terminates maximum exercise’(8).
Various methods have been used to try to trick the brain into keeping muscle fibre recruitment going under extreme conditions. With regard to high temperatures, these involve ‘pre-cooling’ strategies, such as ice baths or ice helmets. These and similar strategies are designed, quite literally, to cool the brain and extend the body’s ‘heat stop switch’ threshold.
As mentioned previously, aging also has an influence on the development of endurance muscle fibre, with fast-twitch fibre declining much more rapidly than its slow-twitch counterpart – by as much as 30% between the ages of 20 and 80.
By contrast, endurance athletes can expect to maintain their slow-twitch fibres and even increase them by as much as 20%, over a sustained training career. The trouble is, though, that without fast-twitch fibres endurance performance will inevitably decline.
In summary, then, developing your endurance capacity relies on a number of adaptations, as follows:
Enhancing the already high oxidative capacities of slow-twitch fibres;
Improving the capacity of fast-twitch fibres to contribute to endurance activity, taking account of distance and the need for both sustained and ‘kicking’ power. This process may, in fact, hold the physiological key to optimising endurance performance;
Working on mental strategies to develop increased endurance tolerance and the sustainable contractile properties of all muscle fibre types;
Using pre-cooling techniques to delay physiological shut-down.
John Shepherd
References
McArdle, Katch and Katch, Exercise Physiology, Williams & Wilkins, 1994
Acta Physiol Scand 1984 Apr: 120(4):505-515
J of App Phys, vol 62, 438-444, 1987
Salazaar – Nike lecture, Nike HQ Oregon October 2002
Dick FW, Sports Training Principles, A&C Black 4th edition, 2002
J Sports Med Phys Fitness 2000 Dec;40(4):284-9
Pflugers Arch 2003 Mar; 445(6): 734-40 E Pub 2003 Jan 14
Sports Performance Bulletin keynote lecture, September 2000