Anaerobic Threshold on a Bike versus Treadmill – Q&A
Q: Question that I’ve been asking around and can’t find a good, solid answer: I recently did a metabolic test at my gym to determine my anaerobic threshold and my VO2 max. The trainer who conducted the test told me, as they tell everyone who takes the test, that my AT would be 10 bpm lower on a bike or in a cycle class than it was on the treadmill when I took the test. Why might that be true?? A: I should probably define at least one term so that the above question and my answer will even make sense. Anaerobic threshold, which is often equated or called lactate threshold, OBLA, ventilatory threshold and probably others (note: technically these all describe slightly different things but they are conceptually similar enough that the distinction isn’t relevant) is a term that has been floating around for a good 40 years and is usually taken to indicate the period where an exerciser shifts from primarily aerobic to anaerobic metabolism. Now, for a variety of reasons I don’t want to get into, this turns out to be a poor description of what’s going on, there is no abrupt switch from aerobic to anaerobic metabolism and scientists have been very busy not only studying the topic, but arguing with each other about what in the hell is actually going on. The same can be said for the other concepts I listed above such as lactate threshold; originally conceptualized at the point where lactate starts accumulating massively and causing fatigue….well, it’s more complicated than that. But all of this is physiological pedantry that even I get bored with. And that takes a lot. Ultimately, the mechanism or nomenclature of what’s going on isn’t what I think is important; the practical implications are what are valuable here. And practically speaking, all of the above concepts (AT, LT, OBLA, VT) essentially represent the following: the highest exercise intensity that can be sustained for extended periods of time without rapid fatigue. So consider someone who has a (pick one) AT, LT, OBLA, VT while running 10mph. Conceptually they should be able to run 10mph for quite some time (various cutoffs such as an hour are often thrown around, at least in cycling). It might be a hell of an effort but it can be done. Below that speed and the duration that can be sustained goes up and up. But above that (say 11 mph), fatigue will set in fairly quickly. Hopefully that makes sense. AT, etc. are tested in a variety of ways but all ultimately attempt to determine the maximum intensity that can be sustained for extended periods without fatigue. As above, what you call this or think it represents is a lot less important in my mind than what it practically represents. So, back to the question: the trainer in question claimed that AT on a bike will be lower than while running, following what I presume to be a running test. Frankly, I’m not 100% sure that this is true but, searching through my resources, I can’t find anything either way on the topic. Different types of training will show different lactate levels at the same percentage of VO2 max (my own sport, speedskating, shows the highest lactate levels at any given percentage of VO2) and that would tend to imply differences between activities. That is, there is generally a decent relationship between percentage of VO2 max. and heart rate and if there are then differences in lactate accumulation at a given percentage VO2, you’d expect that to end up showing a difference in heart rate at that level. A better question might be why this is the case. Part of it is simply specificity, folks tend to test better in the activities that they typically do. So if you have an athlete who runs all the time, and you test their AT on a bike, they will show a much lower value than if you tested them on running. Beyond that, the only physiological reason I can think of why running might show a higher heart rate at AT, etc. would be that more muscle mass is active, several pieces of research certainly support this. For example, comparisons of rowing (using a large muscle mass, including both upper and lower body) to cycling or speed skating show a higher maximal lactate steady state (MLSS, another concept akin to AT, LT, etc. above) for rowing. Probably due to the greater amount of muscle mass being utilized. In cycling, only the legs are moving (unless you’re doing something very strange on the bike), in running the upper body is active and this might shift the relationship between HR and LT. Will it be exactly 10 beats? I honestly can’t say.
Jens Bangsbo & Lars Michalsik brings up the subject in their book “aerobic and anaerobic training” (it’s Swedish). They also claim that peak heart rate and maximum heart rate will differ between different activities. They don’t give a generic answer to why this is but they do write that when it comes to biking the lower heart rate comes from the loading being so high making it hard to pedal.
Unfortunately there are no references in the book so I can’t tell where they got the information from. Bangsbo & Michalsik are solid guys though…
I also found this in the book Cardiovascular Physiology Concepts
“The point at which increased heart rate begins to decrease stroke volume varies considerably among individuals because of age, health, and physical conditioning. Furthermore, this point can vary within an individual depending on the type of exercise and the environmental conditions.”
Regarding the gravity stuff that I wrote in a previous comment I learned that from the book Cardiovascular Physiology Concepts (http://www.amazon.com/Cardiovascular-Physiology-Concepts-Richard-Klabunde/dp/078175030X/).
Body posture also influences how the cardiovascular system responds to exercise because of the effects of gravity on venous return and central venous pressure (see Chapter 5). When a person exercises in the supine position (e.g., swimming), central venous pressure is higher than when the person is exercising in the upright position (e.g., running). In the resting state before the physical activity begins, ventricular stroke volume is higher in the supine position than in the upright position owing to increased right ventricular preload. Furthermore, the resting heart rate is lower in the supine position. When exercise commences in the supine position, the stroke volume cannot be increased appreciably by the Frank-Starling mechanism because the high resting preload reduces the reserve capacity of the ventricle to increase its end diastolic volume. Stroke volume still increases during exercise although not as much as when exercising while standing; however, the increased stroke volume is resulting primarily from increases in inotropy and ejection fraction with minimal contribution from the Frank-Starling mechanism. Because heart rate is initially lower in the supine position, the percent increase in heart rate is greater in the supine position, which compensates for the reduced ability to increase stroke volume. Overall, the change in cardiac output during exercise, which depends upon the fractional increases in both stroke volume and heart rate, is not appreciably different in the supine versus standing position.
Now that I’ve had time to think about it for a day or two I regret bringing up the gravity stuff in my previous post since the explanation from Bangsbo & Michalsik and the one you bring up about more active muscle mass makes a lot more sense than gravity differences between biking and running