To the Editor: In my opinion the negative influence of Nobel Laureate AV Hill on subsequent generations of exercise physiologists is not about the plateau in VO2 or other physiological concepts criticized by Professor Tim Noakes in his article. Hill’s influence is much deeper than that. It is about the fundamental assumption over which the current physiological model of exercise tolerance has been built over the years: In well-motivated subjects used to physical exertion, exercise is terminated because the subject, due to muscle fatigue, is no longer able to produce the force/power required by the task.

Hill thought that muscle fatigue during intense whole-body exercise in athletic subjects was caused by “oxygen want and lactic acid in their muscles” (Gandevia, 2000). As correctly pointed out by Dr. Mark Burnley in his letters, since then many more central and peripheral mechanisms of muscle fatigue have been identified (McKenna and Hargreaves, 2008), and some of the conclusions reached by Hill in the early XX century have now been proven wrong. However, the main assumption of Hill’s model has remained unchallenged for many years, and the vast majority of exercise physiologists accept as true the proposition that athletic subjects stop exercise not because of motivational factors but because of muscle fatigue (Sejersted and Sjøgaard, 2000; Allen et al., 2008; Jones et al., 2008). The problem with this fundamental assumption is that it has never been proven valid. Furthermore, available scientific evidence suggests it is very likely to be invalid.

Indeed, in the literature there is plenty of evidence (Millet and Lepers, 2004) suggesting that after exhaustion, despite significant muscle fatigue, maximal voluntary force produced with the locomotor muscles is well above the force required by even maximal intensity aerobic exercise (less than 20% of resting MVC) (Löllgen et al., 1980). These findings do not provide conclusive evidence against Hill’s basic assumption because MVC tests are usually of isolated muscles in isometric conditions, and performed few minutes after exhaustive exercise. Therefore, these MVC tests are not specific to dynamic whole-body exercise, and some recovery of muscle fatigue may occur. However, scientists interested in muscle fatigue of isolated muscles have measured MVC in a specific manner immediately after terminating prolonged isometric contractions to exhaustion, and found very similar results: MVC at exhaustion (about 80% of resting MVC) is well above the force required by the submaximal task (5-30% of resting MVC). Therefore, these scientists have now concluded that the duration of sustained tasks is not necessarily limited by fatigue of the principal muscles (Enoka and Duchateau, 2008). The same may be true for even very high-intensity endurance exercise.

For how long can traditional exercise physiologists live with this elephant in their room? Given that their model of exercise tolerance is based on the assumption that central and/or peripheral muscle fatigue causes exhaustion, why nobody has checked, in more than 80 years, whether this assumption is true or not?

As Richard P. Feynman would certainly agree, the mere presence of muscle fatigue and/or its mechanisms (e.g. falling [PCr] and pH and rising [Pi] and [ADP]) does not prove that muscle fatigue directly limits time to exhaustion during incremental or constant-workload exercise tests.

Samuele M Marcora

REFERENCES

Allen DG, Lamb GD, Westerblad H. Skeletal muscle fatigue: cellular mechanisms. Physiol Rev. 2008; 88: 287-332

Enoka RM, Duchateau J. Muscle fatigue: what, why and how it influences muscle function. J Physiol. 2008; 586: 11-23.

Gandevia SC. Spinal and supraspinal factors in human muscle fatigue. Physiol Rev. 2001; 81: 1725-89.

Jones AM, Wilkerson DP, DiMenna F, Fulford J, Poole DC. Muscle metabolic responses to exercise above and below the "critical power" assessed using 31P-MRS. Am J Physiol Regul Integr Comp Physiol. 2008; 294:R585-93.

Löllgen H, Graham T, Sjogaard G. Muscle metabolites, force, and perceived exertion bicycling at varying pedal rates. Med Sci Sports Exerc. 1980; 12: 345-51.

McKenna MJ, Hargreaves M. Resolving fatigue mechanisms determining exercise performance: integrative physiology at its finest! J Appl Physiol. 2008; 104: 286-7.

Millet GY, Lepers R. Alterations of neuromuscular function after prolonged running, cycling and skiing exercises. Sports Med. 2004; 34: 105-16.

Sejersted OM, Sj�gaard G. Dynamics and consequences of potassium shifts in skeletal muscle and heart during exercise. Physiol Rev. 2000; 80: 1411-81.

Dear Editor,

Travel fatigue and jet-lag are not synonyms

We were pleased to see the ‘original article’ by Milne and Shaw (2008) offering advice for those travelling to the Beijing Summer Olympics Games in August later this year in a professional or participatory capacity. The authors are to be complimented on their endeavours to accommodate a comprehensive range of environmental aspects that might influence health and performance. Their experiences in China in particular should be of interest to other groups, especially those hitherto unable to make reconnaissance visits to its competitive venues and training camps to experience and monitor the challenges to be faced. Besides they are in good time to be of use for devising travel strategies and general advice to be circulated to all athletes selected to participate and their support staff.

There is one area that we would wish to comment on, the issue of travel fatigue and jet-lag. These problems will be worse for European, frican and American athletes than for those from Australia and New Zealand in view of the difference in time–zone transitions. Furthermore, some of the advice about dealing with jet-lag should not be based on the previous report of Milne and Fuard (2007) in this journal. The interpretation of anecdotal information, on one individual, was flawed. It is easy to beat an opponent who does not exist and the conditions that provoke jet-lag may not have applied in the trip they described.

In the original report, a brief account was given about one subject who travelled between Europe and New Zealand and back within a few days. The itinerary focused upon constituted a net zero time-zone transition by which time body-clock time and local time were desynchronised. The root cause of jet-lag is the desynchronisation that occurs between the endogenous circadian rhythm and local environmental time. Prior to undertaking the last trip before the critical final game, the athlete would not have been in France long enough to adjust to European time, is unlikely to have experienced anything more severe than mild jet-lag, even if travel fatigue was severe.

The authors made no attempt to measure jet-lag, either subjectively or by means of an appropriate biological marker. Jet-lag is likely to have been minimal by the time of the criterion match since there would have been limited adjustment before the last 12-hour time-zone transition and hence no need of a further re-adjustment. Besides, there was no valid measure of performance used. Evidence consists of an anecdotal comment that the player’s performance was up to its usual high standard (open skills) and that he kicked a conversion and three penalty kicks (closed skills). Finally, the cocktail of soporifics that were advocated are not recommended as a panacea for jet-lag in recent reviews (Waterhouse et al., 2007) or in consensus statements about alleviating jet-lag (Reilly et al., 2007a).

Lastly, the notes about travellers’ diarrhoea and on food are to be welcomed. Whilst the notes are necessarily brief, an appropriate further reference would be that of Reilly et al. (2007b). In this consensus, supported by the International Association of Athletics Federations, more detailed advice on food and nutrition is given, as is an account of other gastrointestinal problems that travelling athletes face.

Thomas Reilly, Greg Atkinson, Ben Edwards, Jim Waterhouse

Liverpool John Moores University

References
Milne C. Fuard MH. Beating jet lag. Br J Sports Med 2007; 41: 401.

Milne CJ. Shaw MTM. Travelling to China for the Beijing 2008 Olympic Games. Br J Sports Med 2008; 42: 321-326.

Reilly T. Atkinson G. Edwards B. et al. Coping with jet lag: a Position Statement for the European College of Sport Science . Europ J Sport Sci 2007a; 7: 1-7.

Reilly T. Waterhouse J. Burke LM. Alonso JM. Nutrition for travel. J Sports Sci 2007b; 25: S125-134.

Waterhouse J. Reilly T. Atkinson G. Edwards B. Jet lag: trends and coping strategies. The Lancet; 2007 ; 369: 1117-1129.

Dear editor

I read with interest the study by Panics et al on the effect of proprioceptive training on joint position sense (JPS)at the knee. The authors report a significant improvement in JPS in terms of reduction in mean absolute error after the training. I have several concerns, however, regarding the methods used by the author to assess JPS. First, looking at Fig 1, one can ask as to how the positioning of the electrogoniometer was properly controlled between sessions and between participants. Reports have shown that even slight change in reference points with regard to anatomical landmarks can lead to substantial error in measurements (see Szulc,et al (2001) Med Sci Monit, 7(2), 312-315). Second, given that the leg was moved passively by one experimenter, how tactile feedback arising from contact with the skin was controlled? And what about the speed of mobilization? One can easily see the difficulty for accelerating the leg at the reported constant speed (ie., 10 deg/s) at 10 vs 80 deg in the range tested. Such factors, when not properly controlled, can lead to spurious cues influencing participants' ability to report joint angle. It is also not clear to me as to why the intervention group initially displayed poor JPS as compared to control. In the same vein, the range of errors for JPS reported by the authors (8.21 -9.78 deg) is quite at odds with the range reported in previous studies for normal young adults (typically <5 deg, see Barrett et al (1991). J Bone Joint Surg Br, 73- B(1), 53-56.). I think the issue of measuring the impact of proprioceptive training on proprioception is important for rehabilitation of sport injuries, but we also need to be careful as to how we measure this complex sensation.

Dear Editor

Utter nonsense. The study laughably considers WG , Ranji, Jardine & Larwood to have been failures, whilst Reg Simpson, Peter Richardson & Bob Barber – batsmen who all averaged in the mid 30s - were bizarrely thought of as successes.

The flaw was in the chosen criteria for success ( 25 Tests). Far fewer Test matches were played years ago thus those born in the 1900s - who died, on average, 10 years younger than their 20th Century counterparts - are categorised, virtually en masse, as failures. So, of course successful ( ie modern day) cricketers live longer than unsuccessful ( Victorian) players.

That aside, cricketers that play 25 Tests should live slightly longer as England don’t select dead players. Colin Blythe in 19 Tests took 100 wickets at 18 – what a failure - but was killed in the war, aged 38. Admittedly he’d retired but he still had time to reach the 25 benchmark - Wilfrid Rhodes played until he was 52 . The correct conclusion should have been ‘Cricketers that live longer play more Tests’.