4 e-Letters

  • Leucocyte Rich and Poor Platelet Concentrates and Tenocyte Proliferation

    We read with interest the article by Parrish et al, “Normal platelet function in platelet concentrates requires non-platelet cells: a comparative in vitro evaluation of leucocyte-rich (type 1a) and leucocyte-poor (type 3b) platelet concentrates.”(1)

    Parrish et al define PRP as a preparation with a platelet concentration of at least 5x over baseline, yet the LP-PRP they prepared (Arthrex Autologous Conditioned Plasma) was significantly lower at 2x over baseline, while the LR-PRP (Mitek Sports Medicine PEAK PRP) was significantly higher at 8x over baseline. We might reasonably expect that the ratio of growth factors between their LR-PRP and their LP-PRP to be approximately 8x/2x or 4:1, and this was indeed the case as seen in their Figure 4.

    Subsequently, the authors grew tenocytes (tendon cells) exposed to serum derived from LR-PRP and LP-PRP preparations. Given that their LR-PRP was approximately 4 times richer in growth factors than their LP-PRP, we might reasonably expect that the 2.5% solution of serum derived from their LR-PRP have approximately the same effect as the 10% solution of serum derived from their LP-PRP. However, their 10% LP-PRP solution actually resulted in higher growth of tenocytes (2656 light units) than their 2.5% LR-PRP solution (1001 light units), as seen in their Table 5, but not discussed by the authors. The fact that their 10% LR-PRP-derived serum caused tenocytes to grow to confluence while their 10% LP-PRP-derived serum did...

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  • Lessons from a broad view of science: a commentary on Dr Robergs’ article

    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...

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  • What, no consideration of heel-to-toe drop?

    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.


  • The altered right/left heart stroke volume balance could play an essential role in the development of immersion pulmonary edema.

    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...

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