Saturday, March 23, 2019

Optimizing Lactate Clearance via Power Modulation

Have you ever been in the following situation?  You have just done a high power cycling climb, run or perhaps a cross country ski effort and have gone well into the high lactate zones.  The next part of the course is either flat or even downhill.  Do you coast, very lightly jog/cycle or keep up a near MLSS pace (max lactate steady state)?  What power profile is best to enhance endogenous lactate clearance so you can hammer hard again on the next climb or sprint?  Although your competition may have both superior genetic and acquired fitness attributes, other factors also play a major role in sports performance.  In some previous discussions, we reviewed the "fast start" strategy to reach peak VO2 faster, which theoretically can be of practical benefit in a race situation.  Certainly, in some activities (cross country skiing), the overall efficiency of technique could even outweigh a moderate VO2 peak handicap. 
During high intensity exercise, lactate production rises above that of disposal, leading to the predictable lactate excess and acidosis.  Given this situation it would be to our benefit if  there were ways to enhance the metabolic clearance of that excess lactate, possibly leading to better recovery and performance enhancements later on.  This post will be a review and discussion on how potential strategies to reduce lactate after a supra maximal effort.  We will be discussing optimal power modulation after reaching those high blood lactate levels, however there are other possible methods to mitigate lactate effects that will not be touched on (beta alanine, bicarb supplements etc).  

I would first like to review 3 papers (in order of publication) that have addressed this interesting subject.  The first paper came out in 2005.  Blood lactate was boosted by a supra maximal effort on a bike, then using different "recovery" loads, lactate levels were measured.  The idea was to see if lactate net clearance was better if the subjects pedaled at moderate power loads vs resting.  Both trained and untrained subjects were tested. 
Here is the protocol:

The recoveries are defined as follows:
The recovery conditions were passive recovery (PR), active recovery
at an intensity corresponding to the first anaerobic ventilatory
threshold minus 20% (VT1), active recovery at an intensity corresponding
to the second anaerobic ventilatory threshold minus
20% (VT2), and combined recovery (CR), that is 7 min at VT2 followed
by 13 min at VT1.
The VT2 is basically the lactate threshold power (MLSS).
The VT1 is a bit harder to pinpoint but corresponds to - "the point during exercise at which ventilation starts to increase" at a faster rate than VO2
The VT1 is about 50% of the VO2 peak, the VT2 (MLSS) is about 75% of the VO2 peak.

The subjects performed the supramax intervals (120% of the maximal aerobic power) then:
The recovery conditions were realized in the following order: 1)
passive recovery (PR): the subject sitting on the saddle; 2) active
recovery at an intensity corresponding to the first ventilatory
threshold minus 20% (VT1); 3) active recovery at an intensity
corresponding to the second ventilatory threshold minus 20%
(VT2); 4) active combined recovery which consisted of 2 min at
followed by 3 min at VT1 between supramaximal exercises
and 7 min at VT2 followed by 13 min at VT1 after SE3 (CR).

I bolded the combined recovery protocol.  It was the only one that had recovery time at the MLSS. The rest group just sat there, the VT1 minus 20% probably did about 120 watts, the VT2 minus 20% did about 180 watts to give you a ballpark. 

How did they do? 

The combined recovery group (who used the highest recovery power), had the best lactate clearance.  In the discussion the authors noted that other studies before this showed better lactate recovery at lower loads.  
The conclusion:
In conclusion, this study showed a significant difference between
the effects of recovery modes on peak lactate and lactate
disappearance. CR and VT2 conditions showed earlier peak blood
lactate (4th min of recovery) than PR or VT1 (7th min). We also
found that CR was more efficient for lactate removal than the
other modes for both groups.

The next study was done in 2010 and used running at 90% of the VO2 peak power for 5 minutes to generate lactate.  "Recovery" consisted of running at speeds of various percents of MLSS speed:
Immediately thereafter, participants continued
with the recovery bouts, at 100%, 80%, 60%,
40% or 0% (complete rest for passive recovery) of
the lactate threshold

The square boxes are the resting group who obviously had the worst lactate decay curve.
My only concern with the study conclusion is the failure to get higher lactate levels more consistent with those seen in supra max intervals.
It is also unclear why the subjects did not get more acidotic running at 90% MAP for 5 minutes (I know I would have).

Another look at the decay curves:
Both self regulated and 80-100% of the MLSS had superior blood lactate reduction, agreeing with the first study presented.
Finally the authors present an intriguing idea:
In other words perhaps the MLSS can shift upwards if ambient lactate levels are increased.

In a more recent paper regarding lactate kinetics, a detailed look at appearance and disposal was done at different exercise intensities.  The subjects were split between trained and untrained groups, but we will only speak about the trained.  Lactate kinetics were obtained by looking at radio isotope tracking.  Subjects cycled for 60 minutes at the MLSS, MLSS-10% and an interesting third trial.  This consisted of MLSS-10% power but infusing lactate to match the levels of the full MLSS trial.
Here are the fitness stats for the trained group with a highlight of the MLSS and % of VO2 max seen:
The MAP (maximal aerobic power or VO2 peak) was about 350+ watts - coincidentally close to mine.  The MLSS power was about 259 watts (in the results section).

The results are interesting.   
  • The lactate appearance rate increased with power as expected.
  • Disappearance of lactate was the limiting factor with a maximum that seems to be at the MLSS.

 From the discussion:
Fig. 8 illustrates the relationship between lactate MCR and absolute
and relative metabolic rates in the present and former studies
involving healthy men of variable fitness levels. The top curve
in Fig. 8 reflects the very high flux rates obtained in the present 

investigation on well-trained cyclists (5.0 l/min) VO2max
compared with the lower curves obtained on healthy men of 

variable but lesser fitness levels (2.6, 3.5, and 4.1 VO2max
l/min). In the present study, when PO was raised from LT-10%
to LT workloads, trained cyclists experienced a 60% increase
in [lactate]b, but only a 33% increase in Rd, resulting in a 30%
decline in MCR. These results suggest that at workloads
approaching the LT, lactate MCR declines rapidly
The infusion of lactate at power levels 10% below MLSS did improve the disappearance rate:

I included the power levels and circled the best disappearance rate which was at the lower power with infused lactate.
  • It does seem that a higher blood lactate may augment disappearance rates, although the authors did not specifically state this.  
  • This may indirectly support the supposition of the second study above where higher lactate levels may affect the MLSS to power measurement.

Finally the bottom line from this study:
We conclude that although endurance training increases the capacities for
lactate production, and disposal and clearance for higher absolute

and relative workload, the LT represents the point at
which clearance of endogenous lactate becomes limited.
A comment on this study: 
It may have been very helpful to have infused lactate at different rates to see if a higher serum level would have further enhanced the disappearance rate.  In addition, the final levels they did attain were not very high (4.3 in trained) and would not match levels post supra maximal efforts.

My data:
To try to best simulate some of the above studies, the "active recovery" was preceded by a 3 minute interval near the VO2 peak/max power also know as the maximal aerobic power or MAP.  
The procedure to boost lactate was:
  • to ride at MAP for 3 minutes, coast for 60 to 90 seconds (to recover from exhaustion) before a recovery bout of 5-6 min near or above the MLSS
  • or to do a 3 minute sub MAP with immediate continuation at a power well below the MLSS
MAP-10w then a recovery at MLSS-14%:
On the first trial below, no coasting was done between segments, after a priming segment of near MAP 340w x 3min, I immediately did an interval of 216 watts average (approx 86% of MLSS) for 5 minutes.  To demonstrate that indeed the ventilation, HR and HHb would shift with higher power, a mini sprint was done near the end.
  • During the 216w "recovery" session the ventilation rate progressively drops, possibly indicating declining lactate levels.  Toward the end of the recovery, a brief minute or so of 270w (MLSS+20w) caused the ventilation and HR to rise.  
  • Coupled with the literature studies above, lactate clearance seems to be good at 216w.  This combination of initial high power, then a (very) active recovery seems a good fit for a break away or hill climb.

NIRS, muscle HHb:
Since in certain situations, muscle HHb seems to track with lactate buildup, does this parallel the above?
Here is a tracing of costal, calf, rectus femoris and vastus lateralis HHb:

On first glance, the groups seem to track well except for the minimal change in the VL and mild changes in the calf.  So let take a better look without those two.

  • During the high power start there is a rapid, substantial rise in HHb.
  • There is a prompt drop in HHb during the start of, then stability during the active recovery.
  • Once MLSS+20w power is applied again, both RF and costal HHb rise promptly.

Full MAP then a recovery at MLSS plus minus:
The following series were done a bit differently.  The first 3 minute supra max effort was at VO2 peak power (about 350w), then a 60-90 second coast, followed by 5 to 6 minutes of a constant near MLSS power.  I will label each set by their recovery power.

Recovery just under MLSS (246 of 250w):
  • Both Vent rate and heart rate are stable during the active recovery period.

HHb tracings at just under MLSS:

  • Costal, Calf and forearm HHb remain stable.
  • There is a slight rise in RF HHb toward the end (reason or significance unclear).

Recovery at 250w:
  • Ventilation here was stable or even downward at the end of the active recovery (lower values could have been artifact since it does rise again afterward).
  • This series could also have been equivilant to the prior one at 246w given the 2% potential error in the power meter.

HHb tracings:
  • All curves are relatively flat with a mild rise toward the end (making the ventilation drop more likely artifact).
  • The statistical significance of that rise is not clear.

Recovery at 255w:
  • Here we see a stable ventilation rate throughout recovery even though it is above MLSS.

HHb tracings at 255w:
  • HHb tracings of all sites are relatively stable with a very slight rise at the end, similar to the 250w session.

Recovery at 262w:
  • Ventilation rate still stable despite power 12w above MLSS.  This was surprising.

HHb tracings at 262w:
  • All sites are still relatively flat despite being at 12w above MLSS.  Still similar to the 250 to 255 tracings above.

Recovery at 275w (here the term "recovery" is loosely applied):
I do not have ventilation data since the Hexoskin module did not record the ride.
Let's look at the HHb, especially the costal area which tracks well with ventilation.

HHb at 275w:
  • The costal and RF rise steadily throughout the 5 minute "recovery".  There is clearly no flat stable portion and the rise is rapid
  • Both calf and VL are not very helpful on this day.  A warning not to depend on these sites for exclusive insights.

Close up:
  • Here we finally see a significant rise in HHb at 25w above the MLSS.  I was beginning to wonder if this pattern would ever manifest as recovery power progressively rose in each trial.
  • This is Not a good zone to "recover" in.

One of the conjectures from the paper above was that a high existing ambient lactate would create a condition where "disappearance rate" would be higher than if a lower level was present.  In other words, would a recovery interval look different if it was preceded by a high lactate vs a lower lactate priming bout?

Since I did a 262w recovery (above) that had little in the way of ventilation and HHb change, let's compare to one I did on a prior post.  At that time I did a priming interval of only 235w (instead of 350), which should not have elevated lactate by much if at all.

           Low power prime                                                                    High power prime

  • Ventilation rate rises in the left panel (235w prime) but remains stable on the right (after a high power prime).  Perhaps there is an enhanced lactate disposal rate if the lactate is high.

Where does this leave us in regards to strategy?
It would seem that after a significant exercise effort above the MLSS, the best way to speed the disappearance of lactate would be to continue at a level between 80-100% of the MLSS.  It may also be possible to further enhance the clearance of lactate at power above the MLSS, if the ambient lactate levels are very high (conjecture).
So contrary to the method done by many of doing a high power interval (cycling or skiing up a hill) followed by a absolute rest (coasting down via the bike or ski), it should be more effective for performance and recovery to actually continue downward at a reasonable pace.
To further explore this strategy, let's examine a paper on recovery methods in alpine skiing.

We used highly trained alpine ski racers in a randomized
controlled trial to investigate the effects of on-hill active
recovery performed between training runs on blood lactate
clearance and fatigue. The skiers were randomized to either
an active recovery, comprised of a 3-minute walk with ski
poles, or a static recovery control group who remained
stationary in their skis.
Each participant performed 8 runs in their
respective training course and performed their randomly assigned
between-run recovery protocol, either active (ACT)
or static (CON) recovery, at the top of the training course
before each run. Blood lactate and perceived fatigue were
measured immediately before they started their run at the
top of the course and within 2 minutes of completing their
run at the bottom of the course
Recovery Strategy:
Participants were randomly assigned to either ACTor CON
recovery with equal men and women in each group. The
ACT condition walked along the road at the top of the
training course with their skis off for 3 minutes using their
poles to engage their arms at a slow to moderate pace
(250 m in 3 minutes). The CON condition remained
stationary in their skis at the top of the course for 3 minutes.
Comment - The active recovery was a a low level without measurement of "power". 


Better lactate at the top in the active recovery group toward the end of the runs.

Lower lactate at the bottom of the course in theactive recovery group:

Faster time to completion in many of the active recovery runs:
In addition:
Did not finish rates were recorded for all
participants. Eleven DNFs (incomplete runs) were recorded
in the CON group, of which 8 were in the last 2 runs, compared
with 0 DNFs in the ACT group (Figure 4).
  • The "did not finish" comparison was quite impressive 11 vs 0 in the control vs active groups.

Their conclusion:
Our findings show that on-hill active recovery performed between
training runs in alpine ski racers is effective at facilitating
lactate clearance from the blood.
The group performing
active recovery between runs showed faster average training
run times throughout the session and lower incompletion
rates, despite no differences in perceptions of fatigue.
addition to the improved performance (run time), the
importance of completion rates for technical and tactical
skiing ability, and the greater risk of injury that accompanies
incompletions, this is a critical implication of active recovery
performed between runs for alpine skiers.

Personalized Strategy:
  • After looking at my own data I can envision several different lactate recovery strategies.  
  • After a supra maximal effort (associated with very high lactate), cycling power near 85% of the MLSS could be done to both continue a reasonable pace as well as enhance resolution of acidosis.  Both ventilation and RF HHb improve at this power level.
  • Contrary to "common sense", a 3 minute MAP-10w (max aerobic power) interval does not handicap further exercise near the MLSS from the ventilation/HHb standpoint.  If doing a full MAP interval, a short rest followed by near MLSS power may also yield stable ventilation/HHb kinetics.
  • Raising the "recovery" pace to near the MLSS (post MAP interval) does not seem to worsen either ventilation nor RF HHb trends.  However, exercise near the MLSS will not lead to an improvement of ventilation/HHb toward more normal ranges.  MLSS pace is probably something that can be done for awhile if necessary.
  • For me, a short rest was needed to overcome exhaustion post MAP.  An interval just 10w below the MAP can be followed immediately by an active recovery.

Some concluding thoughts:
  • According to isotope tracer studies, the MLSS is determined primarily by the disappearance (clearance) of lactate and not by it's appearance (production).  This makes sense,since in a perfect scenario, one would simply metabolize any excess lactate, preventing it's rise with sufficient disposal.
  • The clearance of lactate is enhanced by an "active recovery".  
  • The "recovery" power performed to obtain a benefit can vary substantially from a very low level to that of the MLSS itself.  That's why I put a quote around the recovery, it's not necessarily a low power session (although it can be).  Power up to the MLSS (or a tad higher) can provide for a higher lactate clearance.
  • Depending on the current blood lactate concentration, the ability to clear lactate may be altered.  It is possible that clearance rates are higher at very elevated lactate levels.  There is precedence for this in many biologic systems, a higher concentration of substrate can enhance subsequent metabolic pathways.  Expanding on this further, perhaps part of the "fast start" strategy benefit is to quickly elevate lactate which in turn enhances it's disposal.
  • Improving blood lactate clearance should provide benefits to exercise performance and recovery.  
  • Power modulation strategies during a race could be optimized to take advantage of accelerated lactate clearance with continued exercise at or below the MLSS.
  • Observation of ventilation and/or muscle O2 dynamics may be helpful.  Both ventilation and some regions of muscle HHb (costal, RF for me) seem to track well for steady state conditions around the MLSS.  Real time visualization of either parameter could provide rapid feedback to optimize lactate recovery.
  • Individualized testing of lactate recovery zones for each athlete may be of further value.  Given the acquired and genetic variations in lactate handling, it is certainly plausible that some people will have different beneficial load ranges.
  • Other causes of fatigue and exercise performance decline that are not lactate related, may or may not optimize in a similar power modulation profile.  
 Lactate related posts

Friday, March 1, 2019

Determining MLSS with long intervals

A concern about using ramp associated breakpoints is the issue of what protocol was used.  For instance, one may do a power escalation of 25w/min or 25w/3min and get totally different results.  One could argue that the ideal way to look for patterns and breakpoints would be longer, steady state sessions.  The problem with that of course is that it may take a very long overall time, as well as inducing fatigue toward the end.  However, after looking over my data, I feel that some intriguing insights can be obtained by looking at NIRS and respiratory data of intervals near the MLSS.  The laboratory determination choices of MLSS are controversial and subject to a given amount of error.  According to a review on the subject, at least 2 trials are needed and even so the the coefficient of error can be as high as 3-4%.  
In comparison to HRmax and VO2max, the range of CVs
reported for threshold measurements is large, spanning
1.5–10.4 % for AerT and 1.2–11.9 % for AnT (Table 1).
This may be partly attributed to differences in protocol and
study design, including, in some cases, the reliability with
which investigators are able to identify threshold measurements
by visual inspection [118, 119]. It is also
apparent that the reliability of threshold measurements
varies according to whether the threshold is reported as a
workload, an HR, a VO2, or a blood lactate concentration.
Of six examples [109, 111, 112, 115, 120] of a threshold
reported according to the corresponding HR, speed or
power output, and VO2, four found threshold HR to be the
most reliable with CVs of 1.5–3.8 %
Here is the summary table of studies:

The lactate strips themselves can introduce an element of random error since no two readings will be exactly alike.  In addition, depending on what parameter (Heart rate, power, lactate, running speed, percent of VO2) is indexed, further error can occur.  Since many athletes use this as a fitness status benchmark or a training workload target, significant error can lead to erroneous strategy and conclusions.
While there is a strong theoretical basis for using
threshold-based exercise prescription, the challenges of
determining thresholds in practice may partially explain
why many researchers continue to favor the use of
%VO2max, %HRmax, %VO2R, or %HRR. For instance,
when derived from a blood lactate curve, neither the AerT
nor the AnT can be assumed to pinpoint the true thresholds
of metabolic response in all individuals without
verification. Verification of threshold measures on an
individual basis would require two or three additional visits
to the laboratory and is highly uncommon. Nevertheless,
failure to verify threshold measurements may create the
same individual variation in blood lactate accumulation for
which %VO2max and %HRmax have been criticized. It
follows that VO2max and HRmax, which can be measured
and verified within a single laboratory visit, have a definite
practical, if not theoretical, advantage over threshold
measurements for prescribing exercise intensity.

What is generally agreed upon though, is that once lactate accumulation becomes non steady state, a compensatory ventilation increase will occur that will continue to rise.  
As is well known, different exercise
intensity domains are associated not only with a shift in
blood lactate responses but also with changes in ventilation
[44], oxygen uptake kinetics [45], and catecholamine
responses [46, 47]. For example, constant-intensity exercise
within the ‘‘severe’’ exercise intensity domain ([AnT)
is characterized by a continuous increase in ventilation and
VO2, progressive acidosis, and metabolite accumulation,
whereas constant-intensity exercise equal to or below the
AnT is associated with a physiological steady state
Further investigation into the NIRS behavior of both the RF and VL at the MLSS and above comes from Dr Murias' group again.  This was covered in a previous post, but let's look at this from a different perspective this time.

They were looking at long sessions (30 min) of cycling at the MLSS as well as MLSS+10w in regards to NIRS changes in HHb dynamics of the RF and VL along with cardiac-respiratory parameters. Given the differences in recruitment, fiber characteristics between sites, they felt that a change would be apparent in the MLSS+10 tracings.

The subjects cycled for 30 minutes at MLSS and MLSS+10w.
Some observations-
Ventilation and Heart rate:
It was plainly seen that the ventilation rate remained relatively stable in the MLSS group, but progressively rose in the MLSS+10 trials.  Despite the buildup of lactate and higher locomotor+respiratory load in MLSS+10, the heart rate rose, but to a fixed degree above MLSS.  The VO2 response did mirror the heart rate as well (which makes sense).  A take home lesson is that heart rate by itself seems a poor metric to demarcate MLSS, as opposed to ventilation rate (if available) which is a good marker.

HHb of VL vs RF:

In the left column, both RF and VL HHb values remain stable throughout the 30 minute trial (the end >30 minutes is a time to exhaustion sprint).  The right sided figure is the HHb pattern during MLSS+10.  It is a bit difficult to see which muscle group rises more from the figure but here is a table breakdown:
It seems that the RF HHb value (footnote c) does have a statistical change from minute 10 to 30 in the MLSS+10 where the VL does not.  During MLSS, both RF and VL HHb values remain stable.
Some of their comments:
Concomitantly with the accumulation of lactate, a greater
ventilatory response when exercising at MLSSp+10 was also
observed. Multiple factors might have contributed to this exacerbated
response, such as augmented metabolic acidosis,
body temperature, respiratory muscle fatigue, and perception
of effort. The greater increase in V.E, along with the accumulation
of lactate, seems to be a defining characteristic of
exercising slightly above MLSS (compared to “at” MLSS).
So the Ventilation response was felt to be a good indicator of loads above MLSS. 

After exercising in the severe-intensity domain at a PO
substantially above MLSS a reduction in performance is to
be expected. The findings from the present study are notable
as they demonstrate that even a very small increase in PO
(+10 W, ~3%-5%) above MLSS, reflected in a ~100 mL/min
increase in V.O2, results in a progressive rise in [La−]b and
disproportionately impairs subsequent exercise performance.
This is an important observation, as most methods utilized to
estimate the PO associated with MLSS, and similar thresholds
or critical intensities (supposedly eliciting stable [La−]b
and V.O2 responses) generally have an error in their estimate
that is greater than 10w
What they are saying is that it relatively easy to misjudge the MLSS (even with good testing), but exercising at MLSS+10 leads to severe reduction in performance later on.  In other words, setting your pace according to "measured" MLSS may lead to disappointing results with endeavors such as time trialing (if the measurement is off by just 10w).  Remember that a part of their study was devoted to showing the significance performance hit incurred by a MLSS+10 pace.

Overall, these data corroborate previous evidence highlighting
the diverse relative contribution of each of the muscles
(or muscle portions) engaged in the exercise task
the whole-body arteriovenous O2 difference which
arises from the heterogeneity in motor unit recruitment patterns, fiber-type
expression, and the resulting vascular
dynamic controls that characterize the active muscles.
the different dynamics in the behavior of the
[HHb] signal confirms that the regulation of the delivery
and utilization of O2 is different across the quadriceps muscles,
and may reveal that metabolic perturbations of exercising
in the severe-intensity
domain may be greater in
some muscles compared to others 
The RF behaves differently both in a ramp and at steady state at moderate to high power outputs.  Given the difference, it would seem that the RF would be a much better "target" for observation in distinguishing the MLSS transition.


Practical value of the above:
Expanding on the concept of looking for the point where steady state is no longer present let's look at a 10 min session comprised of 5 min of cycling about 15w below my measured MLSS (or 4 mmol threshold) immediately followed by a 5 min segment boosting power to 15w higher than MLSS.  Note that the "measured" MLSS could be over or under whatever the true MLSS is.  
What I would like to consider here is the use of NIRS measurements of various locations as surrogate markers of MLSS.  The costal muscle O2 response would be expected to track with ventilation rates, making that an attractive metric.  However, as seen in the last post, other muscle areas have similar breakpoints and could be helpful.  Yes, I have generally been skeptical of NIRS for MLSS or breakpoint monitoring but perhaps there is an effective use case scenario if done with long segments.  

Here is the overall breakdown from
On this day, sensors were on the costal, deltoid, biceps and calf areas.

To "verify" loss of steady state after the power shift, a look at ventilation data should be helpful:
I drew a blue line through the relatively stable Vent rate during the first 5 minutes, then a gradual rise over the next segment.

As a side note, I did have both the Moov sweat heart rate sensor and the Hexoskin recording to separate devices, heart rate correlation was excellent:
  • It is interesting that although heart rate did rise during the second segment, there was not a continuous rise as there was in ventilation.  This was also seen in Dr Murias' paper.

Costal HHb and saturation:

  • It seems pretty clear that both costal (serratus) HHb and O2 sat remain stable during the first segment (below MLSS).  
  • It is also apparent that the desaturated hemoglobin rises, with a fall in O2 saturation during the second half (above MLSS).
If one was training or racing, it would not be particularly difficult to track this in real time.  The absolute value is not critical, however the 5 minute curve shape is.   Acidosis leads to a respiratory rate/ventilation rise, increasing respiratory muscle activity along with costal O2 usage and extraction.  Absolute change in HHb is substantial.

Are these changes present in other sites?
According to the ramp testing, they should be.


  • The deltoid response is very similar to the costal despite that location having little to do with respiration.  This is presumably cardiac output redistribution, as the legs and now respiratory system use a larger piece of what cardiac flow is available, restricting flow elsewhere (to preserve blood pressure), increasing extraction.  
  • There is a stable HHb pattern below MLSS, with a continuous rise above it.


  • Very similar to deltoid, for the same reasons.
  • HHb stable below MLSS.
  • HHb continually rises above it.


This was a surprise.  I record the calf on many occasions but usually don't look at the data since it's generally not a recognized site for cycling.  In addition, the previous ramp data (for me) did not show a clear breakpoint.  
  • In this case, there is a clear demarcation of both HHb and O2 sat at the point of wattage change above MLSS.  HHb is stable below MLSS.
  • As in the other tracings, the HHb continues to rise throughout the MLSS+15 power.

Session summary of differences between MLSS-15w vs MLSS+15w (approx):
  • Mild elevation of HR that does not continue to rise despite rising ventilation in MLSS+15.
  • Initial stable ventilation during MLSS-15, then take-off of ventilation rate closely following change in power that continues throughout the MLSS+15 interval.
  • Stable costal O2 during MLSS-15 power, then continued rise in costal (serratus) HHb, fall in O2 sat after power boost to MLSS+15.
  • Stable calf, deltoid, biceps HHb/O2 sat during the MLSS-15w, then all rise continually after MLSS+15w.

Absolute HHb changes (approx):
                                         Costal                Biceps             Deltoid                 Calf         
        Total change         1.7 (9.0-7.3)      2.5 (9.3-6.8)     1.1 (9.1-8.0)       1.3 (10.3-9.0)

  • The biceps seems to have the best absolute change in this comparison followed by the costal.  The calf is just a bit higher than the deltoid and has a very nice looking curve.  
  • Despite the lack of a noticeable breakpoint on the ramp (possibly from the Hex sensor smoothing), the calf seems like a valid site for lactate change after all!

Another day with different sites:
Sensors were placed on the costal, biceps, forearm and rectus femoris.  The first 5 minutes were done at 240w with the next 5 minutes at about 275w.  So lets call them MLSS-10w and MLSS+25w (even though the MLSS may not be exactly 250w).

Ventilation/Hexoskin HR response:
 Ventilation only:

  • After a rapid rise, the ventilation and heart rate remain stable toward the mid to end of the MLSS-10 interval.  
  • The MLSS+25 results in a steady rise in ventilation throughout.  Heart rate rises but stabilizes during the last half of that interval.

Costal HHb and O2 sat:

  • During the MLSS-10, costal HHb and saturation remain stable.
  • During the MLSS+25, the HHb rises, with the O2 sat falling in a similar fashion to the MLSS+15.
  • The absolute increase in HHb is slightly higher than the MLSS+10 shown above this, but this could be related to placement rather than effort of course.  I don't think anyone would dispute the curve slope shifting (which occurs rather quickly).

Biceps HHb and O2 sat:

  • During the MLSS-10, the biceps HHb and O2 sat remain stable.
  • Shortly after MLSS+25, biceps HHb rises and O2 sat fall progressively as in MLSS+15.  Absolute HHb rise is higher than MLSS+15 (same disclaimer as in costal).

Forearm (inside/volar surface):

This is an interesting location since on the ramp test, it had a breakpoint at a lower power than the other sites. 
  • Although I may be over reading, the HHb and O2 sat seem to be somewhat less than stable on the initial MLSS-10.  Perhaps the last stable power range is below MLSS-10.
  • Certainly after MLSS+25, the curve markedly changes slope.
  • There seems to be an overshoot of HHb rise after pedaling stops.  The significance is unclear, but this has occurred after other high load intervals.

RF HHb O2 sat:

  • The rectus femoris response is in keeping with the concepts outlined above (higher recruitment with load), as well as the ramp tests done in a prior post.
  • The HHb, O2 sat remain stable in the MLSS-10 segment.
  • Both HHb rise and O2 sat fall steadily with the MLSS+25 interval.
  • There is a bit of an overshoot in HHb after pedaling stops.

Absolute HHb changes (approx):
                                         Costal                Biceps             Volar Forearm           RF         
        Total change         2.3 (9.8-7.5)      2.7 (10.9-8.2)      3.7 (10.3-6.0)       2.0 (9.8-7.8)

The forearm (which did have the earliest ramp takeoff) did have the largest absolute HHb rise.  Absolute values of HHb change were higher than in MLSS+15 testing.

Riding at MLSS and MLSS+18
Another 5-6 minute pair of intervals closer to the MLSS:
In this session, the sensors were on the costal, RF, VL and calf areas, giving a comprehensive view of both respiratory and locomotor areas in one session.  The first 5 minute segment was done close to the MLSS (247w) with the next part (6 minutes) done about 18w higher.  Considering the MLSS may not be exactly 250w, the first section may already exceed this, however the second part definitely should.

Ventilation, Power and Hexoskin heart rate:

Here things get a bit more interesting.  The first segment done at just under MLSS did have a stable ventilation rate.  However the second segment of MLSS+18 was not done at a steady power output.  The first part was done at 270w, then dipping down to an average of 255w during the last 2 minutes before coming back up (this was not intentional).  This lead to an increase in ventilation that peaks during the higher power section, but falls as power is cut back.  
  • This is a great example of how sensitive ventilation is to ongoing power fluctuations.  The question will be if this is seen in the NIRS tracings.

Costal HHb and O2 sat:

  • The MLSS pace seems to produce a stable costal HHb and O2 sat.  This actually looks even more stable than the raw ventilation rate curve.
  • The higher power segment is associated with a rising HHb that has a decrease in slope around the time of power decline.
  • The O2 sat generally follows HHb pattern (in reverse).

Calf HHb and O2 sat:

  • Calf HHB seems to remain steady during the MLSS pace.
  • During the higher power segment there is a steady rise in HHb that appears to follow the fluctuation in cycling load later on.  Whether this is real or random is unclear.  There is no doubt though that the HHb is rising in MLSS+18.
  • The O2 sat generally follows HHb pattern (in reverse).

VL HHb and O2 sat:

  • The HHb seems stable in the last part of the first section of MLSS power.
  • There seems to be a small but steady rise in HHb during the MLSS+18 segment.
  • However this is of a small absolute magnitude and there is no slope change associated to the power dip/rise.
  • The O2 sat generally follows HHb pattern (in reverse).

RF HHb and O2 sat:

  • The RF HHb response seems stable during the MLSS phase.
  • There is a steady rise in HHb during MLSS+18.
  • There is a HHb slope change associated with cycling power fluctuation toward the end of MLSS+18 (like the calf).
  • The O2 sat generally follows HHb pattern (in reverse).

Absolute HHb changes (approx):

                                         Costal                Calf                     VL                 RF         
        Total change         1.1 (7.9-6.8)      .9 (9.4-8.5)         .4 (7-6.6)       .7 (8.2-7.5)

On this day, the costal and calf sites still had decent absolute range of value change that could be distinguished in real time, but the VL did not have changes that would be noticeable while riding outside on the road.   

What about a longer interval at the MLSS?

Here is a session composed of an initial 30 seconds at 400w (well above maximal aerobic power) then a steady 253w for 10 minutes.  This type of effort would presumably accumulate a fair amount of lactate initially, then allow a slow rise (while riding at the MLSS+3).   Sensors were on the costal, VL and RF areas.  The RF placement was different than the above, hence the difference in saturation numbers.

 Ventilation and Heart rate:

 Close up of Ventilation only:
  • Although the rise is not as sharp as in some of the above tracings (MLSS+25), there is a steady rise throughout.
  • Heart rate remained stable past midway.

Costal HHb and O2 sat:

  • There is a steady rise in HHb, fall in O2 sat (parallel to ventilation) starting about minute 3.

Vastus HHb and O2 sat:

  • There is a rise in VL HHb, fall in O2 sat that is of a much smaller magnitude than the Costal site.
  • Although there is a trend, the limited dynamic range may obscure any practical use in real time on the road.  
  • This makes sense in view considering the VL has a blunted desaturation response at high loads, therefore not much should happen to the HHb in this zone

Rectus Femoris HHb and O2 sat: 

  • There is a steady rise in HHb, fall in O2 sat past the 3 min mark of a reasonable magnitude.
  • This seems a better locomotor site (than the VL) to look for MLSS associated change, or worsening acidosis in general. 

Summary of absolute change in HHb ((nadir at about 2-3 min) - (end value)):

                                         Costal                        VL                         RF         
        Total change         1.1 (8.2-7.1)         .35 (7.25-6.9)         1.1 (7.6-6.5)

Absolute value change is not much different to the set of figures immediately above this one.  The VL again shows poor absolute range in saturation and HHb magnitude.

Although lactate was not measured, given the initial, then steady state power, the gradual rise in ventilation, this interval probably was done somewhat past MLSS.  The absolute amount over is less important than the behavior of each metric.  In either road training, racing, time trialing, one won't be able to perfectly modulate their pace to maintain an exact MLSS power output.  If ventilation was available as a viewable value (with graph), that would give a good indication whether a lactate buildup was occurring, or if MLSS was exceeded.
  • In the absence of ventilation data the next best measure seems to be the various muscle HHb/O2 sat measures reviewed above.  Unfortunately, heart rate is not very helpful and remains stable (and submaximal, although higher) at MLSS+10 or even MLSS+25 (my data).

  • Measurement of the true MLSS is quite difficult and prone to error.  Multiple separate studies are needed.  
  • The MLSS (even if noted exactly) can fluctuate over time depending on training and conditioning status.
  • Consequences of exercise minimally above the MLSS are significant.  This includes impairment of performance later in the session.  Therefore, unintended exercise time above MLSS can be counterproductive in a race.
  • Ramp testing using NIRS of locomotor muscles has been used to estimate MLSS.  Unfortunately, this has a substantial error, well above the 10 watts shown to adversely affect performance. 
  • Longer steady state intervals have the potential to identify the MLSS power with proper sensor placement.
  • Many MLSS ramp tests use the VL since it is "active" in cycling.  But, it's ramp breakpoint curve is blunted at that intensity.  Therefore, this site is not optimal for steady state MLSS identification.
  • The RF NIRS response has been shown to have potential to indicate power above the MLSS using long interval observation.
  • Ventilation rates have also been noted to be useful in the demarcation between steady lactate versus accelerating rise in lactate values.
  • Alternate NIRS sites including the respiratory muscles and non locomotor areas have potential to indicate power above MLSS.

Practical Considerations:
Although multiple studies have shown some correlation between NIRS breakpoints and MLSS, most suffer from the following:
  • Use of the VL which has a blunted HHb response at high load.  This in turn will limit the dynamic range of HHb/O2 sat values making trend analysis difficult.
  • If one were to use a locomotor area, either the RF or perhaps the calf would be better choices given the ramp behavior and net change in HHb/O2 sat.
  • Usual method to determine MLSS was a ramp test.  Depending on the ramp protocol and interpretation of NIRS curves, substantially different results can be claimed.  Ramp tests are not practical for the average user.  In addition, even small changes in sensor placement may have effects on the values obtained.
  • Little to no exploration of HHb/O2 sat behavior with longer, steady state intervals.
  • Sensor placement on locomotor muscles only.  In view of the excellent correlation of MLSS with ventilatory rate change, the respiratory muscle seem a logical choice as a marker of respiratory effort.  Other non locomotor sites (deltoid, forearm, biceps) may also be useful in sports that do not generally engage these muscles.  In these areas, cardiac output redistribution with resultant blood flow reduction would be expected to lead to higher net O2 extraction.  My (anecdotal) data does indicate the potential usefulness of these sites particularly in view of the large absolute saturation/HHb changes that occur.
  • Instead of short discontinuous intervals (moxy 5-1-5), athletes should consider doing their own longer, continuous steady state, HHb/O2 sat trials.  A limited number of segments may be all that is needed to see where NIRS values begin to lose a stable pattern.  Given individuals may have different insights depending on their own best site for sensor placement as well as interval time.  "One size may not fit all" for both site and length of interval required.
  • During a long segment of exercise, tracking the direction of the O2 saturation slope (not the absolute values) may provide important feedback in regards to not exceeding MLSS.  Limiting long time periods above MLSS may allow one to have better performance and reserve power at the end of a long session.

 Lactate related posts