Could you clarify what you mean by “what I’ve seen” exactly? Like are you talking about live measurements of cardiac output in athletes with like a Swan Ganz or maybe ECHO? Or are you just kind of saying things?
Because cardiac output is directly proportional to heart rate… up until you overwhelm diastolic function and stroke volume starts to fall because of incomplete filling. The point at which this happens (via carotid baroreceptors) is what we think determines max HR.
Heart rate is a major determinant of cardiac output, particularly in the later phases of exercise when stroke volume augmentation plateaus [3]. It is, however, inefficient for the heart rate to increase such that LV filling is impaired. Thus, although the factors which determine maximal heart rate during exercise are incompletely understood, it is likely that cardiopulmonary baroreceptor activation contributes to maintaining an appropriate balance between LV preload and heart rate during exercise [51].
But as suggested by word choice of the authors here, this is not completely settled science.
If you do have experimental data to the contrary (ie: that cardiac output significantly drops by the time max HR is reached, not peaks), could you be more specific about how you were testing, etc. as this is an area of academic interest for me and I’d be interested in hearing about it. Especially given that it contradicts our current model of human cardiovascular physiology during exercise, which is why it would be really interesting.
