So why does HRmax decrease in trained individuals? Would it be because delivering O2 via higher stroke volume/bpm isn’t now the limiting factor rather it becomes lactate accumulation at the duration needed to create that high of HRmax?
In my class, we’ve touched on this. There’s no real conclusive conclusion but my thoughts are this. As we train, our overall cardiac output increased dramatically. Along similar lines, we observe left ventricular hypertrophy which allows for an increased end-diastolic volume (more filling) and decreased end-systolic volume (more ejection of blood into aorta). This means that the increased EDV will take more time. Even though HR max is lower (because it takes more time to fill the ventricle), the SV is so much greater which allows for CO to remain large. (Again the fick equation relays cardiac output to heart rate and strove volume: CO = HR x SV)
Very useful an informative.
Great video!
So why does HRmax decrease in trained individuals? Would it be because delivering O2 via higher stroke volume/bpm isn’t now the limiting factor rather it becomes lactate accumulation at the duration needed to create that high of HRmax?
In my class, we’ve touched on this. There’s no real conclusive conclusion but my thoughts are this. As we train, our overall cardiac output increased dramatically. Along similar lines, we observe left ventricular hypertrophy which allows for an increased end-diastolic volume (more filling) and decreased end-systolic volume (more ejection of blood into aorta). This means that the increased EDV will take more time. Even though HR max is lower (because it takes more time to fill the ventricle), the SV is so much greater which allows for CO to remain large. (Again the fick equation relays cardiac output to heart rate and strove volume: CO = HR x SV)