I’m not sure a variation in stroke volume, per se, explains HR drift at or below AeT.
A certain pace, once warmed up, demands a certain amount of oxygen (VO2), which is individual specific. VO2 and VO2max are determined by cardiac output, muscle vascularity, and mitochondrial efficiency/density. Cardiac output (CO) is stroke volume (SV) times heart rate (HR)–so for a certain VO2 demand, as one’s intrinsic SV increases (with training) then a lower HR is required to produce the same CO. Once SV is maximized, however, which occurs at abut 50% of VO2max, further increases in CO is only possible by increasing HR.
The theory purported in the article is that after a certain amount of time at AeT (say 15min) one’s SV naturally starts to decline, which is compensated for by the drifting up of one’s HR to maintain a constant VO2. The article goes on to review some preliminary data about how best to train at maximal SV, because maybe training at maximal SV may allow your SV to not decline. The main confounder, in my opinion, is that an increase in HR reduces SV (when exercising at a CO at or above maximal SV). Because of this, its a chicken or the egg conundrum: did a decrease in SV (due to some unknown fatigue in unconditioned athletes down-regulating one’s SV) cause the HR to drift up, or did the HR drift up (due, for example, to an increase in the VO2 required to maintain a steady pace).
SV is determined by heart muscle contractility, as well as by preload (how much blood is in the heart before it pumps)–both of these factors increase with training. This, in part, explains why one’s resting heart rate decreases with exercise. Nevertheless, SV appears to max out quite early during exercise, even in conditioned athletes (whether this is actually true is the crux). Data varies, but most think it maxes out at about 50% of VO2max (for simplicity, VO2max is about 10 beats below maxHR). My point is that for most Z2, at or below AeT, exercise one is mostly functioning well above maximal SV. For example, maximal SV occurs at a heart rate of 90-100 for someone with a max HR of 190. In summary, I don’t think SV can be increased to the extent where training to potentially stay below maximal SV can explain the absence of a HR drift in conditioned athletes. Furthermore, as mentioned, increasing HR decreases SV. This is because a fast HR does not give the heart enough time to to fill (reducing preload and therefore CO). I am not sure at what point HR starts to hinder SV, but I assume it’s gradual after a certain threshold. This explains why, after a certain point, an increase in HR does not increase VO2 (or CO) to the same degree as it did at lower HRs; or even at all when one exercises above VO2 max.
SV optimization to reduce HR drift is an interesting concept, and who know, I may be wrong, and it may be where the money is. But other factors that cause one’s oxygen requirement to increase over time, or for the CO to increase over time, despite a constant pace, may be the true causes of HR drift, or in effect a SV down-drift (as an epiphenomenon).
Thank you for posting that article, I found it very interesting. For me it raises as many questions as it answers.
