During the past three years I have been working on a PhD at the Sport and Exercise Science Research Centre of South Bank University. My area of research has been the influence of thermoregulation on central fatigue, and I have arrived at the view that this issue is highly pertinent to endurance cycling performance - so I thought that coaches and riders should know about it. Hence this article.

First, a definition - what exactly is 'central fatigue'? Traditionally, fatigue has been viewed as being sited in the exercising muscle - that is, as being peripheral in origin. This is not surprising; we know from first-hand experience that when we exercise hard, fatigue feels as though it occurs in the muscle. But what if the ability to activate the muscle is impaired, or the perception of effort increased, by processes going on in the brain during prolonged strenuous exercise? Might not the ultimate limitation to performance then be sited in the brain, rather than in the muscle?

Muscle contracts optimally when all the links in a long chain of command (from the motor centres in the brain to the sliding actin/myosin cross-bridges in muscle cells) function appropriately. There are several well-recognised peripheral mechanisms (substrate depletion, acidosis, and so on) by which muscular power output may be compromised during prolonged exercise. There are also other, less well understood, peripheral fatigue mechanisms such as depletion of the sodium and potassium ions which are required to broadcast the 'command to contract' across the muscle fibre, and the failure to keep up with the demand to recycle calcium (necessary to allow cross-bridging to take place) within the muscle cell. All of these mechanisms operate in the muscle - that is, at points on the muscle side of the neuromuscular junction. There are also links in the generation and transmission of the 'command to contract' at which failure could occur, in which case fatigue would be classed as central, i.e. sited in the central nervous system (CNS). A good definition of central fatigue is: 'failure to generate the required muscular power, the cause of which originates on the CNS side of the neuromuscular junction'.

That central fatigue is a real phenomenon has been convincingly demonstrated by numerous studies in which subjects have maintained maximal voluntary isometric contractions (MVCS) of single muscles or muscle groups for periods of -1 minute or longer. By intermittently supplementing the CNS drive to the muscle with a brief artificial stimulus via skin electrodes, the muscular force achieved can be temporarily increased, indicating that the supposedly maximal neural drive does not in fact elicit all the force the muscle is capable of generating - even though the subject believes himself to be making the greatest effort of which he is capable. In untrained individuals, attempted MVCs are seldom truly maximal, but there are numerous anecdotal reports of ordinary people achieving in extremis remarkable feats of strength by overriding the normal inhibition of maximal effort - for example, the mother who frees her baby, trapped under an overturned car. In a sports context, elite weight-lifters may be elite because they have superior ability to access their available strength.

Central fatigue is frequently demonstrated in another type of effort. Most cyclists, on terminating a continuously progressive VO2max test (a ramp test), will give as their reason for stopping 'l couldn't maintain my pedalhng rate against the increasing power demand'. That is, they perceive the failure to keep up with the ergometer as being sited in the exercising muscle. Could the subject keep going longer if he absolutely had to - say, if a gun were held to his head? There is a school of thought in exercise physiology which argues that the fundamental reason for termination of a ramp test is normally that the central 'drive' to the muscle is inhibited. According to this view, there is potential remaining in the muscle to generate more power at the point of fatigue, but this muscle power cannot normally be accessed, because to do so might cause damage. This suggests that central fatigue could be an evolved protective mechanism, designed to prevent organ damage resulting from overexertion. There would have to be some sort of signal to the brain to inform it that conditions necessitated the inhibition of central drive. It is likely that neural feedback from the muscle, brought about by changes in its metabolic or mechanical state, serves such a purpose. An explanation along these lines could also account for central fatigue in the MVC trials described above.

Another potential hazard of exercise against which a protective mechanism could have evolved, and which could therefore be a contributory factor in central fatigue, is thermoregulatory stress. There is evidence from animal studies to support this idea. Muscle metabolism is approximately 25% efficient at using stored energy to do work, producing considerable excess heat which, in warm conditions, must be dispersed. At their maximum running speed of about 68mph, cheetahs generate very large amounts of heat - about 54 times resting levels. Their pursuit of prey is limited by their ability to store that metabolic heat: when their safe heat storage capacity is reached, they abandon the chase. But why? After all, they don't make a conscious decision. Perhaps their perception of effort is increased, or their ability to activate muscle maximally reduced, as the safe limit to heat storage is approached, causing them to stop running.

There is also evidence from studies in humans that heat stress per se causes fatigue, independent of any other fatigue factor associated with prolonged exercise. Cyclists (the exercise physiologist's favourite subjects) exercising at a fairly modest 60% V02max worldoad reach exhaustion when they attain a critical core temperature of -39.7degC, irrespective of their initial core temperature and of the rate at which heat was accumulated. However, when core temperature is lowered prior to exercise by immersion in cold water, exercise capacity is increased; there appears to be more 'headroom' for core temperature increase. You may remember that Peter Keen sprayed Chris Boardman with a water/ isopropyl alcohol mixture prior to his 1992 Olmpic Pursiot rides and hour record attempts, the reasoning behind this being that alcohol evaporates more readily than water (i.e. sweat) and so enhances cooling - or at least delays heat accumulation. Boardman also had a minimal warm-up, a subject to which I shall return later.

My own belief (and it remains that, rather than established scientific fact, at the moment) is that in hot conditions thermoregulatory stress is the main factor underlying central fatigue during sustained exercise, and that in events lasting between -15 and 90 minutes central fatigue is a major determinant of performance. A useful study in which cyclists rode to exhaustion at -70% VO2max in controlled temperatures of 4, 11, 21 and 31degC found that exercise capacity was greatest at 11degC, and was markedly reduced at 31degC. Subsequent analysis of blood samples collected during these trials revealed that the circulating level of the hormone prolactin was elevated at fatigue only in the trial at 31degC - which was also the only trial in which the subjects' core temperattire exceeded the putative critical core temperature of 39.7degC. Prolactin is interesting not in itself, but because it is widely accepted as a marker of the activity within the brain of the neurotransmitters serotonin and dopamine (since even cyclists are not so obliging as to allow us to look inside their brains during exercise, we depend on measurement of circulating hormones for evidence of what is happening there) and it is thought that it is via these neurotransmitters that central fatigue is mediated.

To summarise what happens in the brain during heat stress, and why it impacts on exercise performance, my grand unified theory of thermoregulatory stress-induced central fatigue (current version) runs like this:

1. warmed blood and signals from thermoreceptors in the skin feed back information on thermoregulatory status to the brain's main controller of homeostatic mechanisms, the hypothalamus

2. the hypothalamus activates the heat-dissipating mechanisms (sweating, and redistribution of blood flow to the skin) in a coarse manner, like an on/off control

3. serotonin is involved in the regulation of heat loss mechanisms as a 'gain control' which fine tunes their activity

4. increased activity of serotonin within the brain (or possibly an increase in the ratio of serotonin to dopamine activity) has a side effect, which may have evolved as a safety mechanism, of limiting exercise

5. exercise limitation could be effected via inhibition of output - from the motor centres and/or by an increase in the perception of exertion

Does training confer resistance to central fatigue? That is a difficult question, and one which is beyond the scope of this short article. At a given absolute submaximal workload, trained individuals are certainly better thermoregulators than sedentaries - as might be expected, since if your maximum power output is 40OW then 20OW represents a modest stress, whereas if you are only capable of 22OW, then 20OW is a substantial stress. Added to this, athletes have a greater cardiac output capacity than sedentaries, so they can afford to increase blood flow to the skin to disperse heat at absolute workloads which would require less well-trained individuals to devote most of their cardiac output to the transport of oxygen to, and carbon dioxide away from, the exercising muscle. In practice, this is less beneficial than it might at first appear - after all, the whole point of endurance training is to increase the absolute workload a cyclist can maintain, and during exercise of a given relative intensity (e.g. 70% V02max), most evidence suggests that the ability to regulate body heat is similar regardless of training status.

So, what practical relevance has all this to the coaching of cyclists - in what circumstances is thermal stress-induced central fatigue likely to limit performance, and what can we do about it? The need and ability to disperse heat are governed by a combination of metabolic, environmental and behavioural factors:

• exercise intensity

• ambient temperature and humidity

• airflow (which influences convective heat loss and the rate of sweat evaporation)

• clothing (i.e. the amount of exposed skin)

• hydration status

• fitness

Any combination of circumstances in which the rate of metabolic heat production closely approaches or exceeds the ability to disperse excess heat is likely to result in a significant impact of central fatigue on performance. So for example a ten-mile time trial, although short in duration, is such an intense effort that even on a merely warm day heat stress could significantly affect performance. In a 12-hour time trial on the other hand, speed (and thus the metabolic heat load) is lower, so environment and hydration status are more important - each 1% of dehydration compromising the ability to defend core temperature by -0.3degC.

How can we influence these factors in our athletes' favour? I am not suggesting that we should necessarily follow the Australians by taking baths of cold water along to events (although where there are showers ... ) but it is simple to spray competitors with 50:50 water/isopropyl alcohol prior to short time trials, something which I now do as a matter of course on warm days. We can also influence behavioural factors, for example hydration. We should consider whether an aero helmet, with its lack of ventilation, represents an advantage or a performance penalty. The scalp is heavily vascularised with blood vessels which lack the ability to constrict (as you will have noticed if you have ever cut your head); this makes it a very effective radiator of heat. The aerodynamic advantage represented by the helmet (and the positive psychological effect of wearing it?) have to be weighed against its impairment of heat-dissipating capacity, taken in the context of the duration and speed of the event, and the environmental conditions on the day. The same argument applies, to a lesser extent, to the wearing of long-sleeved skinsuits and track mitts in time trials. In road races and long distance time trials in warm conditions, riders should consider carrying plain water to spray over exposed skin, as well as a supply of energy/rehydration drink. The whole body acts as the brain's radiator, so maximising evaporative heat loss will stave off central fatigue. Some research indicates that ingestion of branched-chain amino acids during exercise could delay central fatigue in the heat, but more experimental evidence is needed to support this intervention before it becomes accepted as a valid nutritional strategy for competition.

Our new knowledge also puts current pre-event warm-up practice in a rather different light, at least in warm-to-hot weather conditions. A long, intense warm-up for a short event will impose its own thermal stress, so that central fatigue during the event itself will occur earlier - just as taking a hot bath prior to the race would bring forward the point at which the critical core temperature is approached. I suggest that the objective of the warm-up should be to protect muscles and joints from injury, and match metabolic rate to the anticipated demands of the event, while increasing core temperature to the smallest extent compatible with those objectives. As an example, before a10ml time trial on a warm day I currently recommend that athletes prepare their joints and muscles for the demands of the race effort by pedalling a low gear for about 10 minutes. In the last five minutes of the warm-up, I have them do three or four 30-second intervals at race pace in an attempt to 'warn' their muscle metabolism of what is about to be demanded of it; they then go from warm-up to start line with the smallest practicable delay. Truly optimal warmup strategies for each event and set of conditions remain to be evolved.

As coaches, we strive to ensure that our athletes are well prepared by their training and diet, that they adopt effective nutritional strategies during events, that their tactics or pacing strategy are well founded... If we fail to take heat stress and its role in central fatigue into consideration, we may be missing out on giving our athletes an important competitive edge.

References
BOOTH j et al. (1997) Improved running performance in hot humid conditions following whole body precooling. MSSE 29(7):943-949

GALLOWAY SDR and MAUGHAN Rj (1997) Effects of ambient temperature on the capacity to perform prolonged cycle exercise in man. MSSE 29(9):1240-1249

GONZALEZ-ALONSO j et al. (1999) Influence of body temperature on the development of fatigue during prolonged exercise in the heat. JAP 86(3):1032-1039

MITTLEMAN KD et al. (1998) Branched-chain amino acids prolong exercise during heat stress in men and women. MSSE 30(l):83-91