Dear Editor

I read the recent article by Paul Boyle [1] regarding the longevity of English test cricketers with interest. In this paper the authors linked length of international cricket career (‘success’) with lifespan, suggesting that a successful life lead to a longer life. The hypothesis that quality of life grants one a physiological advantage and therefore increases length of life is well accepted in the medical field and its mechanisms deserve closer examination.

However, I feel that the author has potentially overreached with this conclusion by dismissing the effect of physical activity on lifespan. The author states that the increased levels of physical fitness we would expect in world class athletes are unlikely to affect lifespan because “cricket is not a sport which requires physical strength”. In this conclusion the author has incorrectly regarded fitness as musculoskeletal strength alone, ignoring the important aerobic component. Cricket is primarily an aerobic sport, and the fitness of its players is often underestimated [3]. Several studies in both animals and humans have demonstrated a link between aerobic activity and lifespan. Rats subjected to only 10 minutes walking a day live 25% longer than sedentary littermates [4]. The classic London busmen study [2] and several others [5] all demonstrated that people who worked in physically active positions lived significantly longer then workmates who had more sedentary positions.

It is reasonable to assume that those who were honored to represent their country for longer had a higher level of physical activity for a longer period of time than those who did not, therefore likely having an effect on longevity.

Bradley Elliott, Centre de recherche de l'Hôpital Laval, Québec, Canada bradley.elliott@crhl.ulaval.ca

References

[1] Boyle, P. J. (2008). "Does occupational success influence longevity among England test cricketers?" Br J Sports Med: bjsm.2007.041566.

[2]Heady, J. A., J. N. Morris and P. A. Raffle (1956). "Physique of London busmen; epidemiology of uniforms." Lancet 271(6942): 569-70.

[3]Noakes, T. D. and J. J. Durandt (2000). "Physiological requirements of cricket." J Sports Sci 18(12): 919-29.

[4]Retzlaff, E., J. Fontaine and W. Furuta (1966). "Effect of daily exercise on life-span of albino rats." Geriatrics 21(3): 171-7.

[5]Warburton, D. E., C. W. Nicol and S. S. Bredin (2006). "Health benefits of physical activity: the evidence." Cmaj 174(6): 801-9.

Dear Editor

I read with concern the recent review of Noakes[1] accepted for publication in the journal. Noakes suggests that there is no “biologically plausible explanation” for the observation of lower oxygen uptake (VO₂) values in supramaximal exercise compared to incremental exercise.[2] Noakes further argues that those supramaximal data are therefore questionable and should be excluded, thus resulting in the conclusions of the original authors being disproved. Noakes’ first assertion (biological implausibility) is incorrect. His second assertion is at best biased, and at worst could be viewed as endorsing unethical practices.

The observation of lower VO₂ values at exhaustion during supramaximal exercise could be attributed to normal biological variation (random error). However, the kinetics of VO₂ dictates the rate at which VO₂ rises to meet the energetic demand. In situations where exhaustion occurs before the kinetics drive VO₂ to the maximum (so-called “extreme intensity exercise”[3]), VO₂ will be lower than that measured in an incremental test performed to exhaustion. The boundary between “severe intensity exercise” (wherein VO₂ reaches VO₂max before exercise termination) and “extreme exercise” has been estimated to be ~110-135% VO₂max,[3,4] providing the “biologically plausible explanation” Noakes wishes to deny.

To argue exclusion of the supramaximal data is ethically troubling. Such exclusion, in this case solely for the purpose of interpretation, results in grossly biased conclusions. For any scientist, particularly one as influential as Noakes, to adopt such an approach does a disservice to students of exercise science. It would be tragic indeed if these impressionable proto-scientists use Noakes’ precedence to endorse unethical data manipulation techniques to promote their own subjective opinions. Accordingly, I call upon Noakes to retract these statements to prevent further misleading interpretations from entering the literature.

References

1. Noakes TD. Peer review/fair review: How did A.V. Hill understand the VO2max and the “plateau phenomenon”? Still no clarity? Brit J Sports Med, in press. DOI: 10.1136/bjsm.2008.046771.

2. Hawkins MN, Raven PD, Snell PG, Stray-Gundersen J, Levine BD. Maximal oxygen uptake as a parametric parameter of cardiorespiratory capacity. Med Sci Sports Exerc. 2007;39:103-107.

3. Hill DW, Poole DC, Stevens JC. The relationship between power and the time to achieve VO2max. Med Sci Sports Exerc. 2002;34:709-714.

4. Wilkerson DP, Koppo K, Barstow TJ, Jones AM. Effect of work rate on the functional ‘gain’ of Phase II pulmonary O2 uptake response to exercise. Respir Physiol Neurobiol. 2004;142: 211-223.

Dear Editors,

The altitude training study of Friedmann et al. reported a 6% increase in haemoglobin mass (Hbmass), but this result warrants close scrutiny, particularly without a corroborating measure of augmented VO2max, nor of corresponding measures in a matched control group. The authors’ contend that “there exist no studies in which the changes in total haemoglobin mass following treatment with recombinant human were measured…”. But in 2001, we reported increased Hbmass after 4 weeks of injections with recombinant human EPO (r HuEPO) at doses of 50 IU/kg, thrice weekly [1]. When combined with weekly iron supplements either intra-muscularly or orally, the mean (SD) increase in Hbmass was 7 (2)% and 12 (2)%, respectively [1]. In comparison, by interpolating from Friedmann’s Figure 2A, we calculate a mean (SD) expansion of Hbmass of 6 (7)%, reinforcing the authors’ conclusion of large individual variability.

Although we commend the authors for providing individual percent changes in Hbmass, rises of 24, 18 and even 13% (interpolation from their Figure 2A) after 3 weeks at 2100-2300m are disconcerting. Collectively, these three subjects contribute more than half of the overall group increase in Hbmass. Moreover, perturbations as large as these are extreme given the relatively attenuated EPO response of altitude compared with r HuEPO injections [2]. What else might contribute to such large increase in Hbmass? From our experience, the most common source of error with the CO- method is a leak by a subject around the mouthpiece or noseclip, or a leak in the rebreathing apparatus itself. An inadvertent leak substantially increases, never decreases, the estimated Hbmass. Secondly, a small rebreathing volume and large dose of CO (~1.5 ml.kg-1 for men and 1.25 ml.kg-1 for women) ameliorate the magnitude of error for Hbmass, but the smaller dose used by Friedmann (0.85 ml.kg-1) and the larger rebreathing volume (5L) are sub-optimal [3].

References

1. Parisotto R, Gore CJ, Emslie KR, et al. A novel method utilising markers of altered erythropoiesis for the detection of recombinant human erythropoietin abuse in athletes. Haematologica 2000;85:564-72.

2. Ashenden MJ, Hahn AG, Martin DT, et al. A comparison of the physiological response to simulated altitude exposure and r-HuEpo administration. J Sports Sci 2001;19:831-7.

3. Burge CM, Skinner SL. Determination of hemoglobin mass and blood volume with CO: evaluation and application of a method. J Appl Physiol 1995;79:623-31.

Dear Editor:

I now better appreciate Prof. Noakes' reasons for using the words he used following his response to my eletter posted on the BJSM Blog, and consider the issue of "data exclusion" settled. However, I would like to make the following points to clarify my position and respond to Noakes' interpretation of the physiology:

1. I do not consider myself "wedded to the Hill model" because the "Hill model" as presented by Noakes bears no relationship to my understanding of the physiological response to exercise. It is my contention that the "Hill model" is an erroneous caricature of the physiology of exercise that Noakes uses as a straw man in contrast to his central governor model. Few scientists are likely to defend the view that cardiac output and VO₂ must always be identical at exhaustion, for the evidence against this proposition is overwhelming! In short, the “Hill model” is not a contemporary model of exercise physiology, it is a vehicle invented by Noakes.

2. “Oxygen consumption" or, more correctly, pulmonary oxygen uptake, is not a "surrogate measure of cardiac output and the state of muscle oxygenation". To claim this indicates a misunderstanding or misrepresentation of basic physiological measurements. Pulmonary VO₂ is useful because in both the non-steady state and the steady state it closely reflects muscle VO₂, which itself reflects energetic events occurring in the cell. If one accepts that the rate of energy transfer is an important consideration during exercise, then measuring the most quantitatively significant energy transfer process is worthwhile. Furthermore, the phrase “state of muscle oxygenation” is hopelessly vague. Does Noakes mean “muscle O₂ extraction”, “arterio-venous oxygen difference” or “intracellular [or mitochondrial] PO₂”? The first two measures are difficult to make, whilst the latter is currently impossible to make during whole-body exercise.

3. I do not “believe” that exhaustion occurs before VO₂max is attained during "extreme" exercise, it is an experimental fact: exercise is terminated whilst VO₂ is still rising in a futile attempt to meet the energetic demand.[1] Exercise under these conditions is terminated because the subject is no longer able to sustain the power requirements of the task (in my experience not because the subject is unwilling), but this says little of the mechanism. Classic works on the aetiology of muscle fatigue acknowledge that fatigue processes occur at a number of sites within the neuromuscular system,[2,3] and I certainly embrace this. Exhaustion at these “extreme” work rates is attended by falling [PCr] and pH and rising [Pi] and [ADP], amongst other derangements known to cause a fall in tension produced by the myocyte.[4] However, measurements of these processes in whole-body exercise are presently too spatially or temporally crude to be definitive – but that is certainly not a reason to reject the periphery as a plausible or even pivotal contributor to task failure (exhaustion). Note also that the identification of metabolites involved in substrate-level phosphorylation does not imply that the conditions within the cell are “anaerobic”: the concentrations of these metabolites will change progressively during exercise above the so-called “critical power”[5] irrespective of cellular PO₂.[6]

4. Noakes argues that the “simulaneous [sic] measurement of muscle activation” is required to test the alternate (central governor) theory “that maximal exercise always terminates before there is 100% activation of all the available motor units in the exercising limbs”. However, this is impossible to verify with current technology. Even if electromyographic recordings are taken from the surface of a large number of muscles and normalised to some measure of maximal voluntary muscle function (such as an MVC), this will not provide an estimate of the fractional number of motor units that are active. The EMG signal is determined, in part, by the number of active muscle fibres in the region of interrogation, their firing frequency, and the conductivity of the tissues between the fibres and the electrodes, not simply by the number of active motor units. A method of determining the total number of active motor units during whole-body exercise would be very useful but does not currently exist.

The processes leading to additional motor unit recruitment during rhythmic whole-body exercise are far from understood. However, it is logical that in conditions where the rate of O₂ delivery is maximal (i.e., when cardiac output is maximal) the recruitment of additional motor units will lead to worsening metabolic conditions within the exercising muscles, as those newly recruited fibres will also extract O₂ from the microvasculature. The consequent fall in microvascular PO₂ will make the appropriate matching of O₂ demand and supply (essential for the continuance of exercise) increasingly difficult. Additional motor unit recruitment is thus likely to yield diminishing returns in terms of sustaining the required power output. In this scenario, task failure will occur before all motor units are activated even in the absence of a “governor”.

In summary, Prof. Noakes’ representation of the physiology of exercise could be charitably described as inaccurate. The “Hill model” is not one that any physiologist is “wedded” to because it does not exist. Therein lay the “misleading interpretations” to which I referred in my first letter. One final point needs to be made:

If the “absence of any such catastrophe [myocardial ischaemia or rigor during exercise] suggests the presence of an anticipatory, complex, regulatory control system”[7], then surely the presence of myocardial ischaemia during exercise[8] suggests the absence of an anticipatory, complex regulatory control system? How long can the central governor theory survive with this elephant in the room?

“It does not make any difference how beautiful your guess is. It does not make any difference how smart you are, who made the guess, or what his name is - if it disagrees with experiment it’s wrong. That’s all there is to it.” Richard P. Feynman.

References

1. Hill DW, Poole DC, Stevens JC. The relationship between power and the time to achieve VO₂max. Med Sci Sports Exerc. 2002;34:709-714

2. Bigland-Ritchie B, Woods JJ. Changes in muscle contractile properties and neural control during human muscular fatigue. Muscle Nerve. 1984;7:691-699.

3. Gandevia SC. Spinal and supraspinal factors in human muscle fatigue. Physiol Rev. 2001;81:1725-1789.

4. Fitts RH. The cross-bridge cycle and skeletal muscle fatigue. J Appl Physiol. 2008;104:551-558.

5. Jones AM, Wilkerson DP, DiMenna F, Fulford J, Poole DC. Muscle metabolic responses to exercise above and below the “critical power” assessed using 31-PMRS. Am J Physiol Regul Integr Comp Physiol. 2008;294:R585-R593.

6. Richardson RS, Newcomer SC, Noyszewski EA. Skeletal muscle intracellular PO₂ assessed by myoglobin desaturation: response to graded exercise. J Appl Physiol. 2001;91:2679-2685.

7. Noakes TD. Peer review/fair review: How did A.V. Hill understand the VO₂max and the “plateau phenomenon”? Still no clarity? Brit J Sports Med, in press. DOI: 10.1136/bjsm.2008.046771.

8. Bogaty P, Poirier P, Boyer L, Jobin J, Dagenais GR. What induces the warm-up ischemia/angina phenomenon: exercise or myocardial ischemia? Circulation. 2003;107:1858-1863.