stroke volume in athletes

It all has to do with stroke volume. I think some of the gains in stroke volume that athletes get is attained through muscle stretch, from what I’ve read over the years. Again I'm thinking along the lines of "too much of a good thing".

So a parameter that increases volume will increase blood flow and the stroke volume is increased with an increase in contractility. Higher EF stronger contractility. The converse is true a reduction in volume the lower the contractility and lower stroke volume. Your question seems to be addressing the control factors to maintain integrity of a balance of blood flow between the left and right side of the heart....

Your heart is slower than the average, probably due to fitness. You will have a larger stroke volume if this is the case, which is why it can beat slower. Basically it pumps a higher volume of blood with each beat than the average person. When you stand, you lose a lot of your blood into you legs, due to gravity, and you have to wait for the next beat to start getting blood back up to the brain.

The heart is a muscle, and like all muscles in our body, when worked hard they build mass. When the heart enlarges, it can cause problems with the efficiency factor of how your heart expels blood from one chamber of the heart to the next. If you received that information, I'm guessing you had a procedure that made that determination. You are entitled to receive a written procedure report.

t just make a blanket interpretation of the LVEF based on the number. For all we know, I bet when you run your stroke volume goes much higher than someone who leads a sedentary lifestyle. Studies have shown that in hyper trained athletes, LVEF can become lower or higher. A piece I've read that makes sense is that when you compare athletes to sedentary people, the at-rest *stroke volume* will usually measure the same as sedentary people when studied.

Ultimately, ventricular remodeling may result in diminished contractile (systolic) function and reduced stroke volume". To Jim: I agree with Jon. Finding the underlying cause and successfully treating will/can reverse remodeling (depending on the cause). A diseased hypertrophied heart tend to relax more slowly after contraction (slower recovery), reduces filling space, and develop less power, whereas the athletic heart is capable of performing normally.

The only way I know of to lower resting heartrate is to strengthen your heart through exercise (it improves the efficiency of your muscles including the heart and also increases the stroke volume of the heart so that you pump more blood with every beat) but I don't know how issues like age, heart disease etc affect that process.

For a more definitive measurement a right heart catheterization is necessary because the exercise echocardiogram has limitations, namely the inability to measure left-sided filling pressures and cardiac output (stroke volume) that is in part needed for evaluation.....

5 % reference 54-74(LV end-diastolic volume/bsa (H) value 148 ml/m\s\2 reference 29-61(LV end-systolic volume/bsa (H) value 122ml/m\s2 reference 8-24(LV ejection fraction, 1-p A4C (L) value 16.3% reference 46-78(Stroke volume, 1-p A4C value 30 ml (Stroke volume/bsa, 1-pA4C value 16.1 ml/m/s\2(LV end-diastolic volume 2-p (h) value 189 ml reference 46-106(LV end systolic volume 2-p (H) value 158 ml reference 14-42(LV ejection fraction 2-p (L) value 16.

m not sure why EF remains at 30%. It seems to me an increase in stroke volume would increase EF? The formula is blood volume in the LV at end of diastole minus volume at end of systole divided by LV end diastole. As your record indicates there is an increase of stroke volume! ____________________________________________________________________ QUOTE: This time a remark is added-" AV sclerosis+". The cardiologist who did echo says it is not serious.

The calulation for EF is volume of blood in the left ventricle at systole (pumping) phase. Subtract the volume left in the ventricle after diastolic (filling) phase. Then divide the volume of blood during systole for a fraction...that would be EF. Your EF idicates you have a normal pumping heart. Normal is 50 to 70%. Do you have any heart valve regurgitation (leakage)?

In fact you may have heard that athletes have low heart rates.. Their high ef is what allows this.

s has a physical change that is a thickening of the heart wall, thereby a stronger contraction with each stroke...this increase in stroke volume enables a dcrease in heart rate to meet system demand for blood oxygen at rest. It is not pathological due to the alignment of the heart cells different from the pathophysioloical with hypercardiomyopathy heart cell arrangement...but both condition can enlarge the left ventricles.

As is the heart rate, blood pressure, etc. the EF (ejection fraction) is an estimate and measurement that is always in flux to maintain a balance of blood flow between the right and left side. The simple, every second/minute dilation of the left ventricle increases the EF, reduction decreases EF. An athlete's heart muscle increases contractility strength...a resting heart rate can be less than 60 bpm.

t see how my stroke volume could be 60.2. I am a college runner, and although my value is considered normal, 70 is the average normal, so shouldn't I be more up there or at the high end of normal given that I can run faster than the average person over long distances?

It's been 2yrs since my stroke and I have no voluntary movement in my left arm or hand. Is there any possibilty that i could recover any movement? My neurlogist told me that if within 6month of the stroke if I didnt have any movement that my hand will stay paralyzed?

A faster heartbeat does not provide enough time to fill as at rest, and the timing of contractions are less. The percent of blood pumped with each heartbeat is less reducing stroke volume (lower EF). The heart rate has increased to provide the necessary blood/oxygen to meet the system's demand for the diminished stroke volume. The CT scan indicates there is substanital soft plaque buildup within the linings of the vessels.

Ejection fraction (Ef) is the fraction of the end-diastolic volume that is ejected with each beat; it is stroke volume divided by end-diastolic volume. Normal in a man is 50-68%. With a given sized ventricle and its volume, and its ability to contract, I fail to see how a faster or slower heart rate will affect the volume of blood leaving the chamber. If the heart pumps faster, the volume leaving the ventricle will always be the same.

These mechanisms would be interrrelated. The low blood supply (volume in circulation) the kidneys will increase the volume (an example would blood loss, or a low cardiac output). The left venticle will dilate to increase blood flow with each stroke and the heart rate will increase the cardiac output (amount of blood pumped per minute). If the system is dysfunctional, medication, etc. can change the dynamics.

d expect the stroke volume to be inverse to the Heart Rate - e.g. a well-conditioned person would have a low HR with a low BP but a high stroke volume with every beat. As far as poisoning, it'd seem natural for the system to go into high gear to remove the poison - but 4 months would sure be a long time for that, unless it created some semi-permanent change in you somehow.

Stroke volume in athletes

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