kay, this is my last word on the subject. For reference, you can find much of the following information in Costill (1999), Chapter 7, entitled Cardiovascular Control During Exercise. It can also be found in Astrand, and some of it in Guyton (my med school text…sorta weak on the phys of exerecise, but usefull none the less).
Cardiac output is determined by a few factors: preload (how much venous return blood is hitting the heart) Contractility (which is how hard the heart is squeezing), and afterload (the blood pressure in the aorta which the heart must overcome to eject blood).
Cardiac output is increased in a few ways as exercise is increased. When muscle units are activated, they are perfused with blood. The heart must respond to maintain blood pressure in the face of an increased volume. Cardiac input increases by increased contractility, by increased rate via the sympathetic system, and also because afterlaod has been reduced, allowing the heart to eject more blood. Finally, the heart begins to receive more blood per unit time because of increased return. This stretches the heart more, and by the frank-starling mechanism, the heart ejects what is put into it. This is that part frank has been harping on.
Frank's argument would hold water IF and only IF the heart was able to increase it's output indefinitely. He keeps talking about "reserve". The problem is this: As heart rate increases, and the heart stretches to accept more blood, there is a problem. The heart is beating so fast that it does not have time to fully fill any more. Thus, cardiac output levels off. There is a nice graph of this on page 228 in Costill, where cardiac output is graphed against treadmill speed for a runner from 4 km/hr to 30 km/hr. Around 14 km/hr, cardiac output begins to level off, maximal output is finally reached at 17 km/hr, and then cardiac output finally begins to FALL because it is beating so fast that it is not filling fully anymore.
Vo2 max occurs somewhere around the point of maximal cardiac output, and certainly BEFORE the point that cardiac output begins to fall because the rate has gone too high. The reason why muscles are going anaerobic and generating high levels of lactate is because the heart is unable to provide them with any more oxygen, because it has reached it's maximum output. They are thus less reliant on oxidative phosphorylation, and more reliant on anaerobic metabolism.
Now, frank may propose whatever he likes to argue with this. This will be his opinion. It is not what is accepted in the field of physiology, and is not what I or any other physician or physiologist I know to be based on data. I refuse to argue the point any more. Please note I am not arguing about powercranks. I stated my position earlier, which is that I have no position until I see a good study. I am arguing that Frank is obviously not familiar with what is understood about the physiology of exercise. If he does not belive this information is true, he is free to argue his opinion and write his own treatise on the subject, after doing the appropriate research. He will then most likely win a nobel prize because he will have undone quite a bit of previous work and revolutionized the science.
Please frank, tell me I am wrong. I have gone through my texts and written a thorough response. I'm on call today, and I have the whole medical library of my hospital at my disposal. I would LOVE to read things that contradict what I just wrote. Problem is, I can't find any, because all three phys texts texts I have access to agree on this. So do the anesthesisologist and cardiologist I had lunch with.
Over and Out,
Philbert.
Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!
Cardiac output is determined by a few factors: preload (how much venous return blood is hitting the heart) Contractility (which is how hard the heart is squeezing), and afterload (the blood pressure in the aorta which the heart must overcome to eject blood).
Cardiac output is increased in a few ways as exercise is increased. When muscle units are activated, they are perfused with blood. The heart must respond to maintain blood pressure in the face of an increased volume. Cardiac input increases by increased contractility, by increased rate via the sympathetic system, and also because afterlaod has been reduced, allowing the heart to eject more blood. Finally, the heart begins to receive more blood per unit time because of increased return. This stretches the heart more, and by the frank-starling mechanism, the heart ejects what is put into it. This is that part frank has been harping on.
Frank's argument would hold water IF and only IF the heart was able to increase it's output indefinitely. He keeps talking about "reserve". The problem is this: As heart rate increases, and the heart stretches to accept more blood, there is a problem. The heart is beating so fast that it does not have time to fully fill any more. Thus, cardiac output levels off. There is a nice graph of this on page 228 in Costill, where cardiac output is graphed against treadmill speed for a runner from 4 km/hr to 30 km/hr. Around 14 km/hr, cardiac output begins to level off, maximal output is finally reached at 17 km/hr, and then cardiac output finally begins to FALL because it is beating so fast that it is not filling fully anymore.
Vo2 max occurs somewhere around the point of maximal cardiac output, and certainly BEFORE the point that cardiac output begins to fall because the rate has gone too high. The reason why muscles are going anaerobic and generating high levels of lactate is because the heart is unable to provide them with any more oxygen, because it has reached it's maximum output. They are thus less reliant on oxidative phosphorylation, and more reliant on anaerobic metabolism.
Now, frank may propose whatever he likes to argue with this. This will be his opinion. It is not what is accepted in the field of physiology, and is not what I or any other physician or physiologist I know to be based on data. I refuse to argue the point any more. Please note I am not arguing about powercranks. I stated my position earlier, which is that I have no position until I see a good study. I am arguing that Frank is obviously not familiar with what is understood about the physiology of exercise. If he does not belive this information is true, he is free to argue his opinion and write his own treatise on the subject, after doing the appropriate research. He will then most likely win a nobel prize because he will have undone quite a bit of previous work and revolutionized the science.
Please frank, tell me I am wrong. I have gone through my texts and written a thorough response. I'm on call today, and I have the whole medical library of my hospital at my disposal. I would LOVE to read things that contradict what I just wrote. Problem is, I can't find any, because all three phys texts texts I have access to agree on this. So do the anesthesisologist and cardiologist I had lunch with.
Over and Out,
Philbert.
Dr. Philip Skiba
Scientific Training for Endurance Athletes now available on Amazon!