I have read Dr Robergs’ article 1 with much enthusiasm, from the first to the last paragraph. He criticized my occasional piece article suggesting a probable Kuhnian paradigm shift in Exercise Sciences2. I was expecting comments and critiques to my provocative essay since its publication, approximately five years ago. Perhaps, as Philosophy of Science is complex and purely reflexive, just a few exercise scientists have devoted enough time to study it. I now have the opportunity to continue debating and applying some Philosophy in the Exercise Sciences perspective.
Reading Dr Robergs’ 1 article drove me back to the Philosophy of Science to reexamine some crucial academic works essential to a better understanding of how science operates. Since my first critical essay as a beginner student in science, about “The objective knowledge” of Karl Popper 3 during lectures on the Philosophy of Science by Emeritus Professor Michel Paty at the University of São Paulo, my thinking has evolved through different views of science, from Francis Bacon to Karl Popper, from Thomas Kuhn to Paul Feyerabend. Thus, the biased commentary promoted by Dr Robergs towards the falsification method did not surprise me because Karl Popper was one of the first philosophers I read as a beginner in science. Neither was Dr Robergs’ 1 claim in favor of the falsification criteria in Exercise Sciences entirely new 4. As a philosophy-oriented scientist I learned that we may benefit from a wider view of scie...
I have read Dr Robergs’ article 1 with much enthusiasm, from the first to the last paragraph. He criticized my occasional piece article suggesting a probable Kuhnian paradigm shift in Exercise Sciences2. I was expecting comments and critiques to my provocative essay since its publication, approximately five years ago. Perhaps, as Philosophy of Science is complex and purely reflexive, just a few exercise scientists have devoted enough time to study it. I now have the opportunity to continue debating and applying some Philosophy in the Exercise Sciences perspective.
Reading Dr Robergs’ 1 article drove me back to the Philosophy of Science to reexamine some crucial academic works essential to a better understanding of how science operates. Since my first critical essay as a beginner student in science, about “The objective knowledge” of Karl Popper 3 during lectures on the Philosophy of Science by Emeritus Professor Michel Paty at the University of São Paulo, my thinking has evolved through different views of science, from Francis Bacon to Karl Popper, from Thomas Kuhn to Paul Feyerabend. Thus, the biased commentary promoted by Dr Robergs towards the falsification method did not surprise me because Karl Popper was one of the first philosophers I read as a beginner in science. Neither was Dr Robergs’ 1 claim in favor of the falsification criteria in Exercise Sciences entirely new 4. As a philosophy-oriented scientist I learned that we may benefit from a wider view of science as there is no infallible mode to understand science whatsoever. The falsification method assumptions may have implications on how we conceive the scientific development in Exercise Sciences, nevertheless omitted by Dr Robergs.
It is beyond of this rebuttal to present all pros and cons relative to different views of science, thus beginners in Exercise Sciences are encouraged to read different views of science in full, in order to assume a more critical positioning in scientific debates. This would be of value to understand the points I highlight ahead about the weakness of Dr Robergs’ article.
Problems of the Falsification Principle
To criticize my earlier Kuhnian Paradigm Shift in Exercise Science essay 2 Dr Robergs classified Karl Popper as the most contemporary philosopher of science, the owner of “the single valid approach to scientific method in Exercise Sciences” 1. According to Dr Robergs, “Popper had a simplistic view of the delineation between science and pseudoscience, any non-critical application of science, that not based on efforts at falsification, was pseudoscientific”. Curiously, Dr Robergs did not warn readers about the important limitations of the falsification criteria.
Popper believed that the more falsifiable the hypothesis of a theory, the better the theory 5. However, the number of potential falsifiers for a given hypothesis is always infinite so that there is no measure to ensure asymmetric comparison between theories. In fact, some have argued that because falsification is never completely conclusive, the asymmetry of falsification principle proposed by Popper is actually impossible 5 6 7. For example, assuming the perspective I suggested for Exercise Sciences in 2012 2 that a “the growing acceptance of a centrally-regulated effort theory has replaced the dichotomized central vs peripheral fatigue theory”, exercise scientists guided by the falsification principle should know, a priori, all possible falsifiers between these two theories in order to choose the finest one. Because a given hypothesis of a theory can be false only if we take the theory as a whole in our test, the falsification of a theory is not a straightforward schema and, therefore, the application of falsification principle (in strict terms) in Exercise Sciences to test the Central Governor Model (CGM) is consequently impracticable.
Moreover, the need to know all conditions met by the theory before testing a hypothesis, forces scientists to oversimplify the theory since the knowledge of all conditions would be obviously possible only in simple conjectures. This controversy of falsification would drive the theory to a likely separation of its important components in order to create hypothesis possibly falsifiable. As a result, the application of the falsification method to test the CGM theory would lead, at least momentously, to an oversimplification of the exercise tolerance phenomenon. Remember, the CGM was formulated as a complex, non-linear, neurophysiological-psychological model of exercise performance 8-10. As stated by Duhem (apud Ladyman, 2002 5) using Physics as an example, “physical science is a system that must be taken as a whole; it is an organism in which one part cannot be made to function except when the parts that are most remote from it are called into play, some more so than others, but all to some degree”. Accordingly, Micklewright 11 stated that “the CGM cannot be adequately tested by observing its components in isolation”.
There are other two limitations of the falsification principle that readers must be aware. First, some statements cannot be experimentally falsifiable 5. A simple and embarrassing example is the following statement: “time and space are infinite”. Logically, the falsification of such a statement is experimentally impossible. Therefore, a theory asserting the existence of a phenomenon cannot be automatically classified as pseudoscience if someone fails to apply the falsification method over it. Another limitation is that the failure to find a phenomenon under some circumstances or to formulate refutable hypothesis in experimental setups may be a simple consequence of the lack of instruments to make crucial measurements 5. An exemplification of the need for instruments capable of measuring a given phenomenon was recently provided in Physics, as parts of the Gravitational Waves theory were only confirmed as a result of the investment into expensive technology. Accordingly, confirmation of the Heliocentric theory initially proposed by Copernicus was confirmed later, after the invention of the telescope 5. Regarding the CGM, some statements may not be momentously falsified due to the lack of means to falsify the theory. A technology capable of providing online feedback and feedforward measures integrated in the central nervous system, in a real-time exercise is a crucial limitation in attempts to refute the CGM.
Finally, some hypothesis may not be falsified simply because they can be part of a science that is seemingly unfalsifiable 5. For example, an unfalsifiable statement includes the Uncertainty Principle, which asserts that the more precise the determination of the position of a particle, the less precise the estimation of its momentum, and vice versa. This principle is apparently unfalsifiable, as results that do not match a given estimation cannot work to refute the theory. In fact, the falsification principle is unable to deal with probabilistic statements, being an inconvenient mismatch between logic and observation in the falsification perspective 5. Although one may argue that the CGM theory does not fit to probabilistic statements, the knowledge of such a limitation is important to highlight that falsification principle is far for being a universal principle for Philosophy of Science. In fact, incredible progress observed in Epidemiology and Pharmacy sciences (among others) cannot be explained by falsification.
We Benefit More by Using Different Philosophies of Science
I acknowledge that the Critical Rationalism embedded in the falsification method of Karl Popper could lead to a more critical and rational use of the scientific method in Exercise Sciences, as this may guide scientists to crucial questions and important investigations in some circumstances. Nonetheless, the falsification principle must be applied with balance, just as we should do with positive induction process. Otherwise, Popperian philosophy will be incompatible with the actual practice in science.
Different from Dr Robergs’ conclusion, Katch (1986) 12 seemed to have referred to Karl Popper just to highlight the importance of inductive inferences derived from exclusion research. In my opinion, Katch (1986) did not affirm that “Karl Popper was the philosopher who has contributed most to the understanding of the ideal tenants of the scientific method”. For example, when Dr Katch referred to experiments by Dr Brooks challenging the anaerobic threshold concept (page 594) 12, he suggested the use of “disproofability” as a vein to provide answers to important questions, instead of a method to decide between rival theories. Katch 12 wrote that “A new dimension to Wasserman hypothesis has been added that has made the hypothesis all the richer”. In my opinion, he indicated that refutation provided by Dr Brooks was of value to improve hypotheses of the theory, rather than refute the theory as a whole. Therefore, although recognizing that falsification principles may be of value to strengthen a given theory in some circumstances, we should be aware that they are only a critical approach to apply the scientific method occasionally. As argued above, this has nothing to do with a straightforward way to set a theory as acceptable/valid, once the choice between rival theories may involve a more complex dilemma. Accordingly, the best scenario of falsification method in Exercise Sciences is to guide scientists when using the scientific method in critical enquiries. Therefore, the acceptance or rejection of the CGM theory based exclusively on the falsification criteria is not practicable.
It is important to point out that Popperian scientists make their initial judgments about a hypothesis based on accepted knowledge derived from prior theories and experimentations. Hence, Popperian scientists must accept past experiences in order to formulate falsifiable hypothesis, thus falling back in induction. Actually, a scientist can believe in empirical consequences of a given theory only if he believes in the truth of the background assumptions. Popperian scientists should consciously admit the use of induction process in their observations when proposing balanced experimentation, because it is impossible to leave induction processes out from scientific scenarios. This is crucial for scientists intending to avoid novel assumptions when formulating a hypothesis and its experimentation, otherwise a purely naïve Popperian approach may lead them to reject a theory and its predictions before having a better theory for replacement. This is what happens if we take Dr Robergs’ suggestion integrally (despite arguing that CGM theory is a pseudoscience, he offered no alternative explanation for the phenomenon).
An important aspect that beginners in science should consider is that some have argued that the change of meaning of terms and logic is sometimes reasonable and more convenient than rejecting a particular theory 5. The Atomic theory provides a simple example of a change of meaning of a term, as this theory first defined the atom as the least indivisible particle, however when scientists found that atom was divisible they redefined the meaning of atom in order not to abandon the theory. In this example, the use of naïve falsification principles may have led scientists to abandon the Atomic theory, thus blocking an incredible scientific progress in Biology, Chemistry and other sciences. Therefore, rather than abandoning the CGM theory, perhaps is time to redefine the meaning of some terms to refine the theory, as recently suggested elsewhere 13 14. The final word about the acceptability of this theory belongs to the scientific community.
The Kuhnian Paradigm Shift in Exercise Sciences
I agree with Dr Roberg, “Kuhn did not write his text with the intention of presenting a model for how the scientific method, or science itself, should work”, accordingly neither I defended such a principle in my previous article 2. I am not sure about the implicit message left by him suggesting my Kuhnian approach as inadequate 1. As argued in my paper, there has occurred a change on how the Exercise Sciences community has focused on the limits of exercise tolerance 2. My suggestion of Paradigm Shift in Exercise Sciences was based on aspects that, together, may indicate a change of focus of the Exercise Sciences community and growing acceptance of a new theory.
Besides the omission of the work of Karl Popper, the most fundamental concern of Dr Robergs was the use of citations number in my essay (the argument that Exercise Physiology is not a discipline is irrelevant to this debate), since he conceived I used the number of citations by itself, to infer acceptance of a topic/theory. He correctly argued that “Journal citations or topical preference cannot be interpreted as evidence of acceptance or agreement” 1. Curiously, Dr Robergs omitted the fact that I used two other aspects together, to indicate a growing acceptance of a centrally-regulated effort model. Thus, he misunderstood that I used the number of citations to indicate “focus”, rather than “agreement or acceptance”. As I wrote in my previous article 2, “number of citations about a specific theme could indicate the focus of a particular scientific community along time”. Furthermore, in addition to number of citations I used the number of views on specific websites as an indication to where the Exercise Sciences community has its focus.
Besides the number of citations (1), I pointed out that the increased debate on issues challenged by the CGM (2) and the inclination of the scientific community to incorporate a new interpretation (3) could indicate, together, a growing acceptance. I argued that traditional important journals of Exercise Sciences had published specific contents about fatigue mechanisms, highlighting central mechanisms that could be involved in the exercise regulation. Furthermore, important researchers involved with mechanisms of the traditional central vs peripheral fatigue dilemma had started to recognize the importance of integrative explanations for the limits of exercise tolerance. I further assumed that “Perhaps, the most relevant is that scientists from different fields have highlighted mechanisms included in the CGM to understand the limits of exercise”. Therefore, different from what Dr Robergs suggested 1, I used three different aspects to indicate where the Exercise Sciences community has focused on, probably suggesting an intellectual trajectory towards the acceptance of a different theory.
According to a Kuhnian view of Science, the degree of confirmation given by experimentation is not objective, therefore no demarcation criteria can determine logically which theory is most justified by the evidence 6 15. The scientific community as a whole regards the theory as justified 5. I wrote on page 2 of my paper 2 that “the impossibility of performing neutral comparisons with standardized rules to determine the truth of a theory, labelled by Kuhn as “incommensurability of theories”, collective judgement is an important criterion to decide between rival theories in the Kuhnian process”. Thus, criteria 1, 2 and 3 together may suggest that the Exercise Sciences community has changed the focus toward a growing acceptance of a new, integrative theory.
Updating the Kuhnan view in Exercise Sciences
I agree that there is a flaw in my previous occasional piece, once I presented the number of citations of only two theoretical articles proposing the CGM theory. However, its proponents orchestrated this theory within five theoretical papers in an approach comparable to the elegant approach of Archibald V. Hill and colleagues almost hundred years earlier 16 17. First, proponents of the CGM theory presented sequential arguments rebutting the current paradigm 18, thereafter they suggested a novel model of integrative central neural regulation 8-10, 19. Thus, instead of using two of these five theoretical reviews arbitrarily determined, all five prepositional studies should have been used. Encouraged by this debate, I present now an updated number of citations of these works (Figure 1). It is important to warn readers that the number of citations by itself does not indicate too much, as others have presented relevant theoretical reviews with a high number of citations, but without changing the focus of the scientific community. Examples include the conservation of the traditional anaerobic threshold concept 20 as originally proposed by Wasserman and colleagues 21 22, even after evidences has accumulated against this traditional paradigm 23, as well as the lactate-derived acidosis dilemma promoted by Dr Robergs 24. Hence, rather than the number of citation by itself, other marks should be used together to strengthen the argument in favor a paradigm shift as proposed in 2012 2.
An important result predicted by the Kuhnian Scientific Revolution is the incorporation of new terms by scientific community to characterize the new paradigm 5. In this regard, new terms have emerged since the original proposition of the CGM theory. Thus, perhaps it is time to use new terms to verify how the Exercise Sciences community has incorporated the CGM. For example, “pacing strategy” and “decision-making” may reflect the original ideas promoted by the CGM theory, as both constructs has been related to a centrally-orchestrated neuro-psychological regulation 25 26. Although other terms could be also included to reflect the original CGM theory, it is beyond the aim of this article to present an updated list of new terms. Just as examples, I present the citation report having “central governor and exercise”, “pacing strategy and exercise” and “decision-making and exercise” as truncated keywords, therefore showing an increasing number of articles working with central, neuro-psychological regulation concepts (Figure 2). Thus, when compared to data presented in my first Kuhnian essay 2, it is possible to note that concepts derived from the CGM theory have been used, increasingly.
Furthermore, as originally suggested in 2012 2, there was an increased debate on issues challenged by the CGM (item 2 of the Kuhnian paper). Currently, important journals have still devoted relevant volumes to discuss concepts connected to this new paradigm 27 28. It is important to make clear that the present article is limited to discuss the probable Kuhnian Scientific Revolution in Exercise Sciences having the CGM as an example, thus it is beyond of this rebuttal to discuss other integrative interpretations to the exercise tolerance phenomenon 29 30, that appeared after the Kuhnian Scientific Revolution triggered by the CGM 8-10 19. Actually, the appearance of other ways to interpret the phenomenon may be indicative of a Kuhnian Scientific Revolution.
Additional Concerns of Dr Robergs
In his review 1 Dr Robergs included as an additional concern that proponents of CGM theory advocated the presence and function of a new brain location, which they referred to as the “teleoanticipatory central nervous system”. Then, he claimed that CGM proponents “provided no empirical evidence of this centre”. After several readings of the original theoretical CGM papers, I have never found such a reference, since my understanding of the CGM theory was that the integrative regulation involves multiple physiological systems under the control of brain regulatory mechanisms, in a dynamic and continuous interaction 13 19. The presence of a “new” brain location was never my understanding, as I always considered a central governor as the central nervous system as a whole. Therefore, despite of its helplessness utility, the name “Central Governor” seemed to be no more than a semantic choice.
Regarding the peer review process mentioned by Dr Robergs, from my perspective as an independent author, I have seen theoretical articles in favor 14 as well as against 31 this theory being published by this journal. Discussion about an “open, double-visible” review process in scholarly journals is fruitful and demanded, but it is beyond the aim of this review.
CONCLUSIONS
Thomas Kuhn predicted that scientists attached to the old paradigm would resist the acceptance of a novel paradigm. The skepticism of Dr Robergs to accept the CGM theory seems to belong to a different category, that based on naïve falsification principle. This category apparently matches with Thomas Kuhn’s view of science, that of “The scientist who pauses to examine every anomaly he notes will seldom get significant work done” 5 6. Therefore, rather than focusing the scientific debate on a biased-single view of science, the Exercise Sciences may benefit more from different views of science.
REFERENCE
1. Robergs RA. Lessons from Popper for science, paradigm shifts, scientific revolutions and exercise physiology. BMJ Open Sport Exerc Med 2017;3(1):e000226. doi: 10.1136/bmjsem-2017-000226 [published Online First: 2017/08/16]
2. Pires FO, de Oliveira Pires F. Thomas Kuhn's 'Structure of Scientific Revolutions' applied to exercise science paradigm shifts: example including the Central Governor Model. Br J Sports Med 2013;47(11):721-2. doi: 10.1136/bjsports-2012-091333
3. Popper KR. Objective Knowledge. Oxford: Claredon Press 1972.
4. Noakes TD. Is it time to retire the A.V. Hill Model?: A rebuttal to the article by Professor Roy Shephard. Sports Med 2011;41(4):263-77. doi: 10.2165/11583950-000000000-00000
5. Ladyman J. Understanding Philosophy of Science. London: Taylor & Francis 2002.
6. Kuhn T. The Structure of Scientific Revolutions. Chicago: University of Chicago Press 1962.
7. Feyerabend PK. Against Method: Outline of an Anarchistic Theory of Knowledge. Minneapolis: University of Minnesota Press 1970.
8. Lambert EV, St Clair Gibson A, Noakes TD. Complex systems model of fatigue: integrative homoeostatic control of peripheral physiological systems during exercise in humans. Br J Sports Med 2005;39(1):52-62. doi: 10.1136/bjsm.2003.011247
9. Noakes TD, St Clair Gibson A, Lambert EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans. Br J Sports Med 2004;38(4):511-4. doi: 10.1136/bjsm.2003.009860
10. Noakes TD, St Clair Gibson A, Lambert EV. From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans: summary and conclusions. Br J Sports Med 2005;39(2):120-4. doi: 10.1136/bjsm.2003.010330
11. Micklewright D, Parry D. The central governor model cannot be adequately tested by observing its components in isolation. Sports Med 2010;40(1):91-2; author reply 92-4. doi: 10.2165/11531360-000000000-00000
12. Katch V. "The burden of disproof...". Med Sci Sports Exerc 1986;18(5):593-5.
13. St Clair Gibson A, Swart J, Tucker R. The interaction of psychological and physiological homeostatic drives and role of general control principles in the regulation of physiological systems, exercise and the fatigue process - The Integrative Governor theory. Eur J Sport Sci 2017:1-12. doi: 10.1080/17461391.2017.1321688 [published Online First: 2017/05/06]
14. Venhorst A, Micklewright D, Noakes TD. Towards a three-dimensional framework of centrally regulated and goal-directed exercise behaviour: a narrative review. Br J Sports Med 2017 doi: 10.1136/bjsports-2016-096907 [published Online First: 2017/08/23]
15. Kuhn T. The Essential Tension. Chicago: University of Chicago Press 1977.
16. Hill AV, Lupton H. Muscular Exercise, Lactic Acid and the Supply and Utilization of Oxygen. The Quartely Journal of Medicine 1923;16:36. doi: 10.1093/qjmed/os-16.62.135
17. Hill AV, Long CN, Lupton H. The effect of fatigue on the relation between work and speed, in contraction of human arm muscles. J Physiol 1924;58(4-5):334-7.
18. Noakes TD, St Clair Gibson A. Logical limitations to the "catastrophe" models of fatigue during exercise in humans. Br J Sports Med 2004;38(5):648-9. doi: 10.1136/bjsm.2003.009761
19. St Clair Gibson A, Noakes TD. Evidence for complex system integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans. Br J Sports Med 2004;38(6):797-806. doi: 10.1136/bjsm.2003.009852
20. Meyer T, Lucía A, Earnest CP, et al. A conceptual framework for performance diagnosis and training prescription from submaximal gas exchange parameters--theory and application. Int J Sports Med 2005;26 Suppl 1:S38-48. doi: 10.1055/s-2004-830514
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22. Wasserman K, Whipp BJ, Koyl SN, et al. Anaerobic threshold and respiratory gas exchange during exercise. J Appl Physiol 1973;35(2):236-43.
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24. Robergs RA, Ghiasvand F, Parker D. Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol 2004;287(3):R502-16. doi: 10.1152/ajpregu.00114.2004
25. Renfree A, Martin L, Micklewright D, et al. Application of decision-making theory to the regulation of muscular work rate during self-paced competitive endurance activity. Sports Med 2014;44(2):147-58. doi: 10.1007/s40279-013-0107-0
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28. Hettinga FJ, Renfree A, Pageaux B, et al. Editorial: Regulation of Endurance Performance: New Frontiers. Front Physiol 2017;8:727. doi: 10.3389/fphys.2017.00727 [published Online First: 2017/09/21]
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31. Weir JP, Beck TW, Cramer JT, et al. Is fatigue all in your head? A critical review of the central governor model. Br J Sports Med 2006;40(7):573-86; discussion 86. doi: 10.1136/bjsm.2005.023028
I was surprised the authors did not take into consideration heel-to-toe height variances in SRSs, which can be significant (10+ mm). While this may have less effect on one's ability to land "softly" when running uphill, the opposite holds true on downward slopes; depending on the degree of slope, the heel is more likely to contact ground before or concurrent to the forefoot. At least, this has been my experience.
Secondly, while it may be true that a directive to "run softly" will effect the gait and form of a runner upon hearing the instructions, and may even hold sway for a few minutes, the truth is that we all tend to revert to habits after a time, and doubly so when fatigue sets in.
To the editor,
The postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of...
To the editor,
The postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of increase in pulmonary vascular pressure in IPE occurrence. They, furthermore, proposed several possible explanations for IPE and SIPE: 1) transient impairment of left ventricular (LV) systolic function, 2) reduced diastolic LV compliance. They suggested that redistribution from the periphery into the thorax combined with a less compliant LV would lead to a higher LV end-diastolic pressure and pulmonary artery pressure and pulmonary artery wedge pressure in SIPE-susceptible individuals. The authors proposed that, with augmented preload attributable to immersion in cold water, a greater LV wall stiffness in SIPE-susceptible individuals could be the cause of higher LV filling pressure during exercise in cold water.
We recently investigated the relationship between altered cardiac function and the development interstitial pulmonary edema in SCUBA divers. Fifteen healthy males performed a 30-min SCUBA dive in open sea. Echocardiography and lung ultrasound were performed before and immediately after immersion. We observed an increased preload and a right-left heart imbalance. Immediately following the dive the diameter of the inferior vena cava increased by 47 ± 5.2%, systolic pulmonary artery pressure increased by 105 ± 8.6%, left atrial volume increased by 18.0 ± 3.3% and left ventricle end-diastolic volume increased by 10.1 ± 2.4% suggesting both right and left ventricular filling pressures were elevated. Doppler studies showed an increased mitral E peak (+2.5 ± 0.3%) and E/A ratio (+22.5 ± 3.4%) with a decreased mitral A peak (-16.4 ± 2.7%), E peak deceleration time decreased (-14.5 ± 2.4%) consistent with rapid early left ventricular filling but there was no change in left ventricular stroke volume. There was an increase in right/left ventricle diameter ratio (+33.6 ± 4.8%) suggesting a relative increase in right heart output compared to the left.
We suggest the changes probably reflect rapid early LV filling driven by the higher pulmonary artery pressures secondary to increased work done by the right ventricle.3 It is unlikely our subjects had reduced left ventricular compliance due to an abnormality interstitial collagen or changes in intracellular titin (in the absence of known heart disease or hypertension). It is, however, plausible that the subjects reached the left ventricular/pericardial elastic limit towards the end of diastole, required higher end-diastolic pressures to achieve greater end-diastolic volumes in the presence of thick walled ventricle or developed abnormal intracellular calcium homeostasis during effort.4
Energy needs to be either added to the fluid or converted (say from kinetic energy) to create a higher pressure. A higher left ventricle end-diastolic pressure cannot be directly caused by diastolic dysfunction as the latter is not a form of energy. We think that the changes in left ventricle (LV) filling patterns are the result of an increased pulmonary venous pressure causing a rapid early diastolic filling due to the higher initial atrio-ventricular pressure gradient. The reduced A-wave velocity is a consequence of the higher end-diastolic pressure as the LV is already well filled. The “blood shift” induced by immersion will, sequentially, increases the right ventricular filling pressure, increasing right ventricle end-diastolic volume triggering the Frank-Starling mechanism, RV contraction and sequentially increasing pulmonary artery pressure, capillary pressure and, finally, LV filling pressure.3 At the same time, dilatation of the right heart might hamper filling of the left ventricle (ventricular interdependence) because of the limited distensibility of the pericardium and, so, may inhibit LV stroke volume.
We observed that increased preload and a right-left heart imbalance were correlated with the accumulation of extravascular lung water (EVLW). We showed that it was the changes in right ventricular physiology rather than changes in left ventricular indices that correlated with the development of interstitial pulmonary edema. The severity of interstitial pulmonary edema, was significantly correlated with measures of increased cardiac preload, right ventricular area change (a surrogate of right ventricle ejection fraction) and pulmonary artery pressure, but not left ventricle ejection fraction (LVEF) or left ventricle stroke volume (LVSV). Furthermore, the lung comet score correlated significantly with IVC diameter, systolic pulmonary artery pressure, right/left ventricle diameter ratio and E-wave deceleration time.
We have previously suggested acute pulmonary edema resulted from a mismatch or imbalance between the right and left ventricular stroke volume (SV)5. Although the pathophysiology of pulmonary (alveolar) edema (APE) is generally described in terms of a failing left ventricle, in reality, for APE to occur, there must be a mismatch between the right and left ventricular SV as fluid is lost from the circulation into the airspaces. The augmentation of right ventricular contractility increases stroke volume (and pulmonary pressures) relative to left ventricular SV which could then cause an increase in capillary hydrostatic pressure leading to transudation of fluid into the lung interstitium.5 A failure to increase LV stroke volume (relative to the RV stroke volume) due to a higher peripheral vascular resistance brought about by conditions such as systemic hypertension or cold water may increase the likelihood of occurrence of SIPE and IPE. The extravasation of fluid into the lung interstitium due to the RV/LV stroke volume mismatch is further exacerbated by higher heart rates explains interstitial pulmonary edema during exercise in divers.6
We provide a greater understanding to the pathophysiological mechanisms proposed by Moon and colleagues.1, 2 The altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema. Our findings may have implications for the pathogenesis of immersion pulmonary edema and could help reduce the deaths in swimming induced pulmonary edema.
We would be pleased to answer any request for further information.
Yours respectfully,
Olivier Castagna, M.D., Ph.D.
1. Moon RE, Martina SD, Peacher DF and Kraus WE. Deaths in triathletes: immersion pulmonary oedema as a possible cause. BMJ Open Sport Exerc Med. 2016;2:e000146.
2. Moon RE, Martina SD, Peacher DF, Potter JF, Wester TE, Cherry AD, Natoli MJ, Otteni CE, Kernagis DN, White WD and Freiberger JJ. Swimming-Induced Pulmonary Edema: Pathophysiology and Risk Reduction With Sildenafil. Circulation. 2016;133:988-96.
3. MacIver DH, Adeniran I, MacIver IR, Revell A and Zhang H. Physiological mechanisms of pulmonary hypertension. Am Heart J. 2016;180:1-11.
4. Adeniran I, MacIver DH, Hancox JC and Zhang H. Abnormal calcium homeostasis in heart failure with preserved ejection fraction is related to both reduced contractile function and incomplete relaxation: An electromechanically detailed biophysical modelling study. Frontiers Physiology. 2015;6:1-14.
5. MacIver DH and Clark AL. The vital role of the right ventricle in the pathogenesis of acute pulmonary edema. The American journal of cardiology. 2015;115:992-1000.
6. Castagna O, Gempp E, Poyet R, Schmid B, Desruelle AV, Crunel V, Maurin A, Choppard R and MacIver DH. Cardiovascular Mechanisms of Extravascular Lung Water Accumulation in Divers. Am J Cardiol. 2017;119:929-932.
I have read Dr Robergs’ article 1 with much enthusiasm, from the first to the last paragraph. He criticized my occasional piece article suggesting a probable Kuhnian paradigm shift in Exercise Sciences2. I was expecting comments and critiques to my provocative essay since its publication, approximately five years ago. Perhaps, as Philosophy of Science is complex and purely reflexive, just a few exercise scientists have devoted enough time to study it. I now have the opportunity to continue debating and applying some Philosophy in the Exercise Sciences perspective.
Show MoreReading Dr Robergs’ 1 article drove me back to the Philosophy of Science to reexamine some crucial academic works essential to a better understanding of how science operates. Since my first critical essay as a beginner student in science, about “The objective knowledge” of Karl Popper 3 during lectures on the Philosophy of Science by Emeritus Professor Michel Paty at the University of São Paulo, my thinking has evolved through different views of science, from Francis Bacon to Karl Popper, from Thomas Kuhn to Paul Feyerabend. Thus, the biased commentary promoted by Dr Robergs towards the falsification method did not surprise me because Karl Popper was one of the first philosophers I read as a beginner in science. Neither was Dr Robergs’ 1 claim in favor of the falsification criteria in Exercise Sciences entirely new 4. As a philosophy-oriented scientist I learned that we may benefit from a wider view of scie...
I was surprised the authors did not take into consideration heel-to-toe height variances in SRSs, which can be significant (10+ mm). While this may have less effect on one's ability to land "softly" when running uphill, the opposite holds true on downward slopes; depending on the degree of slope, the heel is more likely to contact ground before or concurrent to the forefoot. At least, this has been my experience.
Secondly, while it may be true that a directive to "run softly" will effect the gait and form of a runner upon hearing the instructions, and may even hold sway for a few minutes, the truth is that we all tend to revert to habits after a time, and doubly so when fatigue sets in.
PM
To the editor,
Show MoreThe postulated mechanisms of immersion pulmonary edema (IPE) or swimming induced pulmonary edema (SIPE) are not well understood. Most groups agree that an increase of cardiac preload plays a primary role. Several groups have assessed the effects of cold water and exercise on the increase of the filling of the heart right and pulmonary pressure.
In a recent report by Moon et al1, the authors investigated, in a series of sudden deaths during triathlon training. They identified 58 deaths, of which 42 (72.4%) occurred during the swim. They found that, when compared with healthy triathletes and the general population, individuals who died during a triathlon or in training had a higher prevalence of cardiac anomalies that could predispose to immersion pulmonary oedema (IPO). The authors suggested that triathletes susceptible to IPO may have abnormal myocardial diastolic compliance (lusitropy) -or stiff hearts. They proposed that abnormal left ventricle (LV) diastolic compliance is partly responsible for elevated LV end-diastolic pressure similar to that observed in patients suffering from heart failure with preserved ejection fraction.
It was shown, in a previous study by Moon et al. in this journal,2 that pulmonary artery and pulmonary artery wedge pressures are higher in SIPE-susceptible individuals during submerged exercise compared with the general population and these pressures are reduced by sildenafil. They confirmed the important role of...
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