Cardiac Stroke Volume

[Joel J]

Happy 2011 everyone!

As I sit hear pondering what to include in the looming trainer ride I have only one question... How to stimulate cardiac stroke volume?

Andrew has mentioned that Hiking and Riding around LBP have shown a tendency to maximize stroke volume, but why? Is there a correlation between body position, diversity and number of muscle groups used, eccentric loading, higher intensity and the desired SV increase?

It makes sense that with the increase in demand- upright position leads to more vertical displacement of blood, more muscles require a more efficient cardiac output, higher intensity- the SV will rise.

If these theories are true, then I have a new idea for SV stimulus while riding. Out of the saddle rides will increase the vertical displacement strain on the heart and require a more efficient method of circulation- higher SV. Integration of full body stimulus such as riding the trainer with free weights, et cetera.

If we had access to blood pressure monitors... It might be easier to extrapolate our polar data into SV numbers and track improvement based on Systolic and Diastolic BP with polar heart rate and variability. I would love to test all these thoughts with the fitmate one day soon!

Joel J

[MartinC]

I would also be interested in any developments regarding cardiac stroke volume training as it seems to have been identified as my limiter.
Any news on when the fitmate will be available? I would like to get tested to see if the training plan I have been following since Jeurg was in town has had any effect on this parameter.

[Andrew]

We can set up Fitmate testing any time, just give us a ring, or wait until Chris hits the runway next week.

In response to the SV idas Joel has put forward. Fantastic thoughts and ideas. Our only problem is we are currently working with VERY SMALL case studies looking at what is the best way to address SV in training. Juerg is doing more and more research and finding more and more variability between athletes. This means that what might work for Joel, could backfire for Martin, and leads us to the desire to have our own equipment to help guide us.

The good news, is we have data on Joel and Martin that can be compared later. The other good news is we may have an opportunity to meet with Juerg in J.Tree to follow up on some of our crazy ideas. And lastly, we can certainly make some observations with the Fitmate and LBP data to give us an answer regarding how the recent training has affected Joel's and Martin's physiology.

I am looking forward to follow up testing. Give us a ring and lets set it up!

[PeterW]

What are we trying to increase when we are training "stroke volume"?

I understand that when training around balance point, SV is increased as there is increased sympathetic stimulation, causing the Ventricles to contract more forcefully. In turn, strengthening the heart. But is the increase in SV only coming from a decrease in ESV, as compared to an ESV you'd see at rest?

Since the heart is beating more rapidly at LBP, there is less time for ventricular filling, as compared to a lower HR, yes? so at LBP are we only increasing the amount of blood the heart can squish out? rather than actually increasing volume??

Are there any SV gains at a lower intensity. training with less peripheral resistance... and in a position with better venous return? say on a recumbent bicycle, where the body is horizontal, and gravity has less effect on blood pooling?
Increased venous return, with a longer Diastole, would mean a higher EDV. The ventricular walls would be stretched, stimulating a more forceful contraction of the heart (starlings law I think).

secondly, with less peripheral resistance, afterload would be decreased (amount of pressure in the aorta the heart has to pump against). So would the heart be able to push more blood out. Or, because of the lower workload, would sympathetic stimulation be too low to stimulate a "complete" contraction?

[GordM]

Ditto to peter's questions. I am confused about ESV in comparitive terms. When I am lying in bed, my HR is around 60. I would think that because there is almost a full second for the heart to fill, that ESV would be highest at that point? (I realize the lack of sympathetic system here, but force does not equal volume?) Am I way off here? During jeurg's tests, is there a constant pattern to ESV? or is there an 'optimal range' so to speak.

I think it would be cool to look at stroke volume during a respiratory workout. When I do spiro, near the end of the workout (no matter the rate, etc.) My heart rate is always above 120-130. Because the respiratory and circulatory systems are so closely linked, would an increased respiratory rate mean an increased venous return from the lungs to the heart, which would be more effective in creative a 'positive' pressure on the Left ventricle??

My thinking here is that when i 'lose control' of my resp, system, RR goes up and HR drifts up with it... I'm curious what ESV would look like then.?

Better yet! (to take things way out of proportion) A spiro workout lying down with legs raised!

I like peter's ideas... all i can picture now is a BPR session where everyone has wacky recumbent bikes. haha

[MartinC]

From my understanding there are two factors that play a role here to improve SV (and, I believe it is ESV that is measured). The two factors that I believe we have been using to stimulate change are peripheral resistance and the sympathetic stimulation described by Peter.
To increase PR I have been training using multiple muscle groups at different intensities. So, hiking/snowshoeing/xc sking, all using poles. I think the theory being that multiple contracting muscles increase PR in order to cause a more forceful contraction thereby increasing the load on the heart to stimulate adaptive change.
Venous return has not been mentioned as a factor in the information I have seen. I think the pre-load stretch of the ventricle before contraction which is also a factor in the SV might need something more forceful driving it than gravity driven return of blood.
From what I understand despite the more rapid beating of the heart during exercise in some well trained athletes the SV increases despite there being less time for "filling". I believe this is where Starlings Law comes into effect causing the stretch and contraction Peter has described.

[Andrew]

It is a little more complex than we are all trying to describe. I love that the athletes are putting their brains to good use, and feel this is so much more valuable than a coach "telling" you what to do, and you blindly following the instructions.

However, we may not have been able to give a full picture yet, and are still learning every day, so please don;t be surprised if we find that the ideas we are working on today turn out needing some adjustment or rethinking in the future.

Here is a good article to stimulate some more ideas and questions:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1725174/pdf/v039p00190.pdf

I think we will take some time to discuss the implications of our current level of knowledge on the ideas of SV training this Saturday at the EES session. Unfortunately, Tom Stewart, who was expected to be a guest speaker, will be attending the funeral of an old cycling friend. He will join us another week-end.

Remember when reading the article, that in our small number of subjects tested, we have seen a wide variety of responses. That is, one of the best athletes ever tested, had a plateau in stroke volume just below LBP, while in other well-trained athletes, we saw a continued rise in SV right through LBP to maximum effort achieved.

The questions that are being asked here are valid, and I will try to work through some of them this week, but will need to do some more reading before I commit my thoughts to this forum. Be patient, I am learning also.