Q - Power

Indoor Rowing Team

Intensity (5 of 6)

So that is the first of the two physiologically significant marker points. Let’s move on to the second. Unfortunately whereas this one starts simply enough, it becomes a little more complex. We will take it one step at a time.

As we continue to move the intensity up very gradually from HR151 (being the example athlete's VT1), blood lactate levels continue to slowly rise further above resting level. The muscle cells are put under ever increasing load and as much they might “try” to work aerobically, more and more acid is produced. This moves into the blood and the buffering system starts to reach breaking point. As the bicarbonate buffering system is overwhelmed, blood pH starts to fall (i.e. the blood becomes more acidic) and the relationship between ventilation and carbon dioxide now breaks as well, with a disproportionately large amount of carbon dioxide being produced for the level of ventilation. It might also be described as the “gasping threshold” and can be particularly unpleasant if you have not done much high intensity work for a while – the body is not used to these excessive amounts of carbon dioxide and it can feel as if you are drowning.

VE/VCO2 is plotted in Diagram 7 below and there should be a clear inflection point in the line which defines VT2. Unfortunately real world data does not always appear in “textbook” form so an element of judgment is needed to drop the line in the right pace. The data in this test is not perfect, but it is easy enough to make out a clear inflection. As it happens, there is a second way of finding VT2 which involves plotting VCO2/VO2 which will also show an inflection at the same point. (This ratio can be used to determine how much fuel is coming from fat and how much is coming from glucose. At VT2 you expect to see a marked reduction in fat contribution towards zero). A third and final way of doing it is to look for an inflection in HR against power output (i.e. the one which may or may not exist as we  considered on page 3 of this article).

From Diagram 7, VT2 is determined to be HR172. There is also a fairly clear inverse deflection in HR at the same point (take a look back at the same line in Diagram 6 without the perpendiculars and it is even easier to see). For James, VT2 represents an oxygen consumption of about 4,600ml/min being about 79%VO2max and a heart rate of 88%HRR.

Now we have to determine what we are going to call this threshold. So far in this article I have been calling it VT2 since it is the second inflection point with respect to ventilation. It is worth noting that sometimes in articles, studies and textbooks reference is made just to "VT" and it is not always absolutely clear which one of the two ventilatory thresholds is being talked about which can be a little frustrating.  

Now I warned you that this second threshold was going to get a little more complicated. Here we go. The problem is one of terminology in that there are two other terms which are sometimes used to refer to this point: "lactate threshold" (LT) and the onset of blood lactate accumulation (OBLA). What makes it tricky is that sometimes these terms are being used to refer to something else! 

Let's start with lactate threshold. It has previously been described in various publications as the intensity of exercise where blood lactate rises to levels no more than 1.0mmol/l greater than that at rest. Sometimes it is said to be a blood lactate level of 2.0mmol/l although I have also seen it described as 2.5mmol/l (see for example "Exercise Physiology: Nutrition, Energy and Human Performance" by McArdle and Katch).

In fact they go on to say that lactate threshold essential refers to the same concept as OBLA (which they themselves define as being at 4.0mmol/l) and the respiratory compensation threshold (by which they clearly mean VT2, since they define VT1 as ventilatory threshold). They even say that LT is the same concept as metabolic acidosis, which occurs at VT2 since prior to that buffering successfully maintains blood pH. All in all, absolute chaos.  

So when someone refers to lactate threshold, if you want to understand exactly what they are saying then you need to understand exactly how they are using this term. If they mean the point at which you start gasping or producing uncontrollably large amounts of lactic acid then they are talking about VT2. If they are talking about the point at which blood pH starts to fall then they are also talking about VT2. That is what most people mean most of the time when they talk about LT. However if they are talking about the point at which lactate levels rise above normal levels or to 2-2.5mmol/l then they are talking about VT1. Given that in our example VT1 occurred at 75%HRR and VT2 occurred at 88%HRR, the difference is very important and the confusion in terminology sometimes employed is unhelpful to say the very least.

So what then is OBLA. Well this brings yet more controversy. Sometimes it is used to describe the intensity correlating to maximum lactate steady state (MLSS). However others prefer to define it at a fixed lactate level (being 4mmol/l). OBLA tends to occur at a similar point to VT2 (but, since one is a ventilatory threshold and one is a lactate threshold, by definition they are not precisely the same thing). For example, those with McArdle’s disease lack the enzyme phosphorylase such that they are incapable of producing lactic acid, yet they still show a ventilatory threshold.

MLSS is a useful concept from a performance perspective, and since it seems to occur at about the same point as VT2 then that works quite nicely. However it is not accurate to describe this point as equating to a blood lactate level of 4mmol/l. The justification for using 4mmol/l as the definition originated out of work done by Heck.H. et al, “Justification of the 4mml/L lactate threshold”, Int. J. Sports Med. 6 (1985) 117-130. It is worth just considering Table 2 of that paper which appears below relabelled as Diagram 8. What one sees here are the maximal lactate steady state figures for 16 individuals, the average being 4.02mmol/l (yes, that’s where the 4mmol figure comes from). However you will also note the lowest figure is 3.05mmol/l and the highest is 5.52mmol/l. The 4mmol figure would not work too well for them.

The article itself in fact goes on to identify some of the shortcomings is using step testing to determine lactate levels because it shows quite effectively that as you lengthen the time spent at each speed (or power output) step, the lactate level is higher for the same workload.

So, all in all, given that these days we can determine VT2 fairly easily with modern testing equipment, there seems no particular reason to hang on to 4mmol/l as definitive of anything. That is not to say it is not useful to know your power output at 4mmol/L one year so that you might compare it a year later, but you could just as well use 3.5mmol/l or 4.5mmol/l.

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Diagram 7. VT2 occurs at the inflexion of VE/VCO2, in this case at HR172.

(Below) Diagram 8. An extract from Heck's justification of the 4mmol/l lactate level.

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