The following data is from a road ride using BSX sensors on the L VL, R RF, L costal area, Hexoskin shirt, Assioma DUO power meter. After about an hour warm up, a 5 min relatively constant interval at my previously measured lactate threshold was done, followed immediately by another 5 minutes at that power +25 watts. Although I could have used a smaller power increment, I wanted the results to be obvious and as shown on the prior post, 10 watts over the limit did not show much in the way of change (but only over 4 minutes).
In addition, I wanted to get closer to (or exceed) the RCP (respiratory compensation point). This should cause a substantially higher respiratory rate/ventilation, work of breathing, thus taxing the costal muscles to a greater extent.
Two views of the same data (Cycling analytics and Garmin):
The RF did drop in each case, but only from a baseline of 60% to 54% in the first, 52% in the second interval. So although probably real, within the noise range somewhat.
The VL data is here:
The VL also drops, with the second interval downsloping, but the net percent change is again quite small, curve slope shallow.
Hexoskin data:
The green arrow is the LT interval and the orange arrow LT+25 watts.
I attempted to put straight lines under the numbers to indicate some degree of stability over 30 seconds or so.
Minute ventilation was a steady 172 +- in the LT effort vs 222 at the end of LT+25. As seen in the prior post, minute ventilation appears to be a very sensitive indicator of effort around the lactate threshold.
There was a change in end interval heart rate of about 10 bpm. The extra 25 watts definitely caused a difference here as opposed to just 10 watts.
A close up of the ventilation data:
I drew a green line showing how steady minute ventilation was on the LT interval.
The yellow line is tracking ventilation toward the end of the LT+25 effort, rising rapidly then plateaus at about 220 is my historic max.
What does all this indicate?
- Although locomotor muscle O2 does drop from LT to LT+25, it is a minimal amount. The information is not particularly useful while riding since it's so trivial.
- Both minute ventilation and costal O2 change in predicted direction as the RCP is approached (or exceeded). Both are visibly significant and can give the rider real time clues on loss (or regaining) steady state kinetics
- There is a change in heart rate with LT+25, but given effects of heat, hydration and cardiac drift, it may or may not be reliable. As noted with the previous post, a 10 watt boost above LT does not seem to change it.
A few comments about the RCP
There have been attempts to equate the MLSS/CP as somewhat equal to the RCP.
A recent excellent "rebuttal" to that was recently published. The authors argue that the RCP must appear after the LT by definition (you need an acidosis to cause the RCP which occurs after LT).
Here are the relevant passages:
First, the important understanding of the RCP
Second, they also address the use of NIRS, namely muscle O2. The difficulties and pitfalls of using this are discussed:
Lastly, the order of breakpoint occurrence:
Interestingly, they mention that the RCP generally occurs about 20% higher than the MLSS. That coincidentally is near the LT+25 power tested above (I used 10%). When I performed my lactate threshold, 10 watts (5 percent) did not seem to cause the changes noted here.
Conclusions:
- The Costal O2 desaturation curve appears to relate to the RCP. As seen in the previous post, 10 watts above or below the LT do no change the costal O2 to a noticeable degree. However, with 25 watts above LT (10%), a very obvious drop in costal O2 and curve shape downslope will occur. This may provide a real time indicator of respiratory compensation, acidosis and alert the rider to adjust their pace or prepare for the consequences.
- Minute ventilation again provides a nice stratification for zones of effort as well as the loss of steady state work. Although I was looking at this parameter after the fact, it does show promise for real time monitoring.
- Locomotor muscle O2 does not have the dynamic range to be helpful for a given single individual in real time interested in avoiding loss of steady state, reaching either LT or RCP. There are numerous papers showing a lactate threshold can be calculated from this metric, but on a practical basis, it does not have the ability to discriminate RCP/LT while actually on the road.
Lactate related posts
- Issues in using Muscle O2 for lactate testing
- Lactate Kinetics, Cycling power, Muscle O2 and Minute ventilation
- Observations just above the lactate threshold...the RCP
- MLSS +10 watts, a journal review plus personal data
- Determining MLSS with longer intervals and a NIRS device
- Optimizing Lactate Clearance via Power Modulation
- MLSS retest by both blood lactate, Vent and NIRS
- Ventilatory thresholds and Heart rate variability testing
- First and second Lactate thresholds, why the confusion, how to measure?
- VO2 max by gas exchange and official lactate testing - my data
Do you get the same results when using a Moxy Monitor instead of a BSX? I saw a video of a comparison between the two in a Blood Flow Restriction circumstance and the BSX was not nearly as sensitive as the Moxy.
ReplyDeleteI don't have a Moxy, but I have 4 different BSX sensors and they are virtually identical in the SmO2 numbers they measure. However, they may not be "gold standard" accurate to a Portamon, and certainly may be different than the Moxy. In strength training, the BSX (in my experience) does change with very minimal alteration of lifting load, validating the sensitivity somewhat.
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