Dr. Winkle wrote: "As was explained to you several times, the etiology of the incomplete filling is the fact that the heart can't relax fast enough to reach maximal end systolic volume (which is normally restrained by the pericardium). Since beta blockade results in increased stroke volume (although reduced cardiac output) at VO2max, the "precipitating factors" seems to be excessive ionotropic and chronotropic stimulation of the heart by the sympathetic nervous system."
Thanks. Finally some iinformation that actually might support the cardiac point of view. Couple of questions as I see a couple of "problems" with the explanation. Since it requires energy for muscle to relax, is the failure to relax due to inadequate energy supplies or something else. What is the basis of the inadequate relaxation. You state that SV is constrained by the pericardium, but then state that beta blockade will allow increased SV. Is it constrained by pericardium or not? Is there a reference where this data was reported? Did they also report what was going on with electrolytes, filling pressure, and pH when all of these changes were occuring?
Anyhow, it makes sense that the changes you describe probablyt occur (although your explanation has some contradictions) but they, in and of themselves, do not prove your argument that the basis of these changes are entirely cardiac as these changes could just as well come from lack of energy due to pH changes interfering with energy production, leading to poor relaxation. The argument here, again, is what is the trigger that starts all of these changes.
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Frank,
An original Ironman and the Inventor of PowerCranks
Thanks. Finally some iinformation that actually might support the cardiac point of view. Couple of questions as I see a couple of "problems" with the explanation. Since it requires energy for muscle to relax, is the failure to relax due to inadequate energy supplies or something else. What is the basis of the inadequate relaxation. You state that SV is constrained by the pericardium, but then state that beta blockade will allow increased SV. Is it constrained by pericardium or not? Is there a reference where this data was reported? Did they also report what was going on with electrolytes, filling pressure, and pH when all of these changes were occuring?
Anyhow, it makes sense that the changes you describe probablyt occur (although your explanation has some contradictions) but they, in and of themselves, do not prove your argument that the basis of these changes are entirely cardiac as these changes could just as well come from lack of energy due to pH changes interfering with energy production, leading to poor relaxation. The argument here, again, is what is the trigger that starts all of these changes.
--------------
Frank,
An original Ironman and the Inventor of PowerCranks