Jem Arnold Profile picture
Jan 21, 2024 17 tweets 6 min read Read on X
🩸Blood lactate [BLa] does NOT increase exponentially during high intensity exercise 🧑‍🔬

Why do we make this common mistake?

I think because we have focused too much on the lactate test

And forgotten what information that test is trying to give us about real exercise
🧵1/14 Image
We are probably familiar with the🩸BLa curve during an incremental exercise test

As intensity increases 🩸BLa accumulates at a faster rate, approximating an exponential increase

We can estimate a 'threshold' in this curve, but what is this threshold telling us?
2/ Image
We don’t actually care about the deflection point in a lactate curve on its own

True exponential curves don't have deflections. it's like finding the corner of a circle

There are lots of corners depending on our operational definitions 🫣

3/
DOI: 10.1371/journal.pone.0199794 Image
We care about what our lactate curve predicts about our *constant workload* performance at every intensity

What happens to 🩸BLa if we clamped workload during a lactate test and continued exercising at that constant workload?

At lower intensities, something like this 👇
4/ Image
If we continued our incremental lactate test and clamped workload above the lactate threshold, would it continue to increase exponentially?

Nope! 🩸BLa accumulation *decelerates* over time, even at high intensity

Because⬆️V̇O₂ and ⬆️BLa oxidation
(science incoming 🧑‍🏫👇)
5/ Image
Wasserman et al (and others before them) observed this waaaay back in the mid-1900’s

MOD & HVY intensity are characterised by transiently⬆️🩸BLa, before settling back to a low baseline over 5-10 minutes

SVR intensity sees a rapid increase toward an upper ceiling
6/ Image
Standard schematic representation of constant workload 🩸BLa response below, at, and above the maximal lactate steady state looks like this

At higher intensity 🩸BLa response is *logarithmic*, not exponential!

7/
DOI: 10.1007/s00421-017-3795-6 Image
What about during high intensity intervals?

A good example from Stepto et al 2001, highly trained cyclists completed a workout of 8x 5min / 1min rests, averaging 86±2% V̇O₂max

🩸BLa across work bouts followed the same logarithmic response

8/ Image
🩸BLa observed during a lactate test is the product of whole-body balance of:

La⁻ production & release from working muscles into blood

La⁻ oxidation/disposal by other tissues: muscle, heart, etc

9/
DOI: 10.1113/jp280955 Image
La⁻ production & release is greatest at the start of exercise

V̇O₂ (OXPHOS) is still ramping up, and substrate (“anaerobic”) glycolysis must buffer the immediate energetic demand

10/
DOI: 10.1113/jp279963 Image
As OXPHOS spins up during the first ~2min V̇O₂ onset kinetics, this also reflects ⬆️rate of La⁻ oxidation at a cellular level before it ever reaches the blood, and at the whole-body scale

Net 🩸BLa begins to slow and reverse at lower intensity

11/
DOI: 10.1002/cphy.c100072 Image
So why do we care about lactate testing? Two reasons:

☝️to monitor change over time

The major thing that matters for monitoring is consistency of the test

LTs are reliable within around 5-10% (10-15 W)
12/
DOI: 10.1371/journal.pone.0199794
✌️to predict real world performance

LTs can be useful to extrapolate / predict transitions between intensity domains, or race performances

This 2018 study found that differences in LTs could explain 30-60% of the variance in TT performance

13/
DOI: 10.1371/journal.pone.0206846 Image
We need to keep in mind what information the test is trying to give us

Try to picture *logarithmic* 🩸BLa responses during your exercise sessions, instead of exponential

This might improve how we apply information from our tests to our training!
14/14 Image
Turns out hearing that "BLa increases exponentially at high intensity" is a bit of a pet peeve of mine 😅

Hopefully this thread can help how we think about this

If you chose 'exponential' were you thinking about a lactate test? Or were you thinking about it some other way?
couldn't fit the DOI to Wasserman et al, 1967:
10.1152/jappl.1967.22.1.71

Fitting in the 'late 1900s' meme was more important 😂

I should have added: this is why stage duration matters in a lactate test protocol: the kinetics of La⁻ production & disposal change during the first 5-10 min of exercise

When we take the observation at each stage will change the shape of the curve

DOI: 10.1123/ijspp.2017-0258 Image

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More from @jem_arnold

Jul 29
Can mNIRS muscle oxygenation be used to estimate peripheral 🦵training load/stress?

Similar to using time >90% VO2max for central 🫀cardiovascular stress

A new paper provides some descriptive data for runners performing HIIT and SIT 1/12🧵 (study 🔗 in alt text👇) An example of the muscle deoxygenation responses for the 1 km (a) and 400 m (b) session. An ischemia/hyperaemia calibration was performed prior to each session to normalize the NIRS signals, whereby the deoxygenation signal was scaled from 0-100% corresponding to the minimum and maximum during the ischaemia and hyperaemia periods, respectively. Average deoxygenation was greater during 400m than in 1km intervals. Bellinger et al 2025. Maximizing Muscle Deoxygenation during Interval Training in Middle-Distance Runners. https://doi.org/10.1007/s00421-025-05903-1
In an exploratory study, @Phil_Bellinger et al compared 1km vs 400m running intervals with @Artinis_MS Portamon on gastroc (calf)

They found greater peripheral muscle deoxygenation in the shorter, higher speed session, and greater central stress in the longer distance session 2/ Time spent with values > 60% muscle deoxygenation and time spent with a heart rate > 90% peak heart rate throughout each session. a = Significantly different from 1 km session. 400m sprints had greater time >60% deoxygenation, while 1km intervals had greater time >90% HRmax. Possibly indicating greater peripheral and central stress, respectively. Bellinger et al 2025. Maximizing Muscle Deoxygenation during Interval Training in Middle-Distance Runners. https://doi.org/10.1007/s00421-025-05903-1
They speculate time >60% deoxygenation might be a valuable estimate of peripheral muscle training load/stress, similar to >90% VO2max for central adaptations

I’d also be curious about AUC (area under the curve) metrics for deoxygenation (see prev👇) 3/
The consensus from the interval training literature concerned with improving VO 2max is that the interval training prescription variables should be manipulated to maximize the time spent with VO 2 above 90% VO 2max which may maximize the stimulus for central physiological adaptations to improve VO 2max and high-intensity endurance performance (Midgley and Mc Naughton 2006; Buchheit and Laursen 2013a). Akin to maximizing the time spent with VO 2 above 90% VO 2max , we could also speculate that maximizing the time spent with a high level of muscle deoxygenation may provide a similar stimulus ...
Read 12 tweets
Feb 18
In our recent meta-analysis with trained athletes, did the athletes who improved their VO2max more also improve their endurance performance more?🤔

No! 😮
In this dataset, +1% change in VO2max was associated with only +0.04% change in TT performance. But why? 1/15🧵 A one-stage linear mixed effects model meta-analysis based on our individual participant dataset (but not peer reviewed) showing individual athlete percentage change scores for both VO2max (maximal oxygen uptake) and time-trial (TT) performance, for 236 trained athletes in 6 studies. The relationship (correlation) between change in VO2max and change in performance was not significant and not meaningful. The overall change in VO2max only explained around 25% of the total variance in the change in endurance performance, across athletes.
This is the third thread about our recent meta on training intensity distribution (TID)

The last thread was about our secondary findings 👇. This one is about some interesting exploratory observations
🔗Links below, more details in the 📊Alt text 2/
Conceptually, endurance performance is an integration of many interrelated physiological components

VO2max is only one piece, and may not be the limiting factor to improving performance 3/
Read 17 tweets
Feb 10
In our recent meta-analysis we found:
🔴Higher level competitive athletes improved VO2max modestly more with Polarised training
🔷Lower level recreational athletes modestly more with Pyramidal training

This is what those differences looks like 👇
But is this meaningful? 🤔1/🧵 A density plot using {ggdist} showing distribution of individual observations for the change in VO2peak pre to post training intervention. For the full meta-analysis sample (bottom grey figure) the mean difference of 0.11 ml/kg/min was not significant between polarised vs pyramidal training intensity distribution (TID) models. For recreationally trained vs competitive athletes, the contrast was significant such that competitive athletes improved more following polarised training (top), and recreational athletes improved more following pyramidal training (middle). But the mean differences wi...
This is the second thread about our recent meta on training intensity distribution (TID)

Start with the first thread 👇for main findings. Keep reading here for more of the story!
🔗Links below, and more detail on figures in the 📊Alt text 2/

~350 trained athletes improved both VO2max and TT performance each by ~ +2% average during their study interventions

But individual variation was very wide, as we see here

Only 60% participants improved VO2max, and 80% improved TT performance at all, over 3-18 weeks training 3/ Box plot of simple mean differences (%Δ) for peak oxygen uptake (VO2peak) and endurance time-trial (TT) for 348 participants in 13 studies captured by the current individual participant data meta-analysis. The simple mean difference is around +2% for each VO2peak and TT performance, however, it is unclear (from this figure) how well associated is improvement in VO2peak with improvement in TT performance. Paired lines for individuals at the outliers of increase (or decrease) in either VO2peak or TT tend to regress toward the mean for change in the other variable.
Read 13 tweets
Jan 31
Polarised🆚Pyramidal🆚Threshold

Which training model is best?🏆
It might matter how trained you are🤔

Our new meta-analysis tries to answer which training intervention produces the greatest improvements in endurance performance in trained athletes

Thread🧵 & 🔗links below👇
Article link:


Keep reading for a summary of our main findings and questions 📚🧵2/18

Alt text in images have additional details & links. Full access link at the bottom🔗👇 link.springer.com/article/10.100…Image of article title, authors, abstract, and key points. Key points reads: 1. When training load was quantified by time in heart rate zone, our results indicate that the adaptations to maximal oxygen uptake following different training intensity distribution (TID) interventions is dependent on performance level. Athletes at a more competitive level may benefit from a polarized (POL) TID intervention and recreational athletes from a pyramidal (PYR) TID intervention.  2. A pooled analysis using different methods to estimate borders between training zones among the included studies did not a...
This was a huge collaborative effort led by Dr. Michael Rosenblat with 20+ institutions 🏫across 10 countries 🌎🌍🌏 and 20 years worth of published data 🧑‍🔬🧑‍🏫

This project is a model of multi-centre cooperation strongly needed in #SportScience 👏Thanks to all co-authors 3/ A collage of profile pictures from co-authors involved in this study: Michael A. Rosenblat, PT, PhD. Jennifer A. Watt, MD, PhD. Jem I. Arnold, PT, PhD(c). Gunnar Treff, PhD. Øyvind B. Sandbakk, PhD. Jonathan Esteve-Lanao, PhD. Luca Festa, PhD. Luca Filipas, PhD. Stuart D. Galloway, PhD. Iker Muñoz, PhD. Domingo J. Ramos-Campo, PhD. Patrick Schneeweiss, PhD. Sergio Sellés-Pérez, PhD. Thomas Stöggl, PhD. Rune K. Talsnes, PhD. Christoph Zinner, PhD. Stephen Seiler, PhD.
Read 21 tweets
Oct 21, 2024
Here's a strange new study discussing doping and cyclist's iliac syndrome (FLIA/endofibrosis). I don't think I can take it literally, but I will take it seriously

Can doping increase risks in endofibrosis? Likely yes
Is FLIA/endofibrosis caused by doping? No
Let's discuss💭🧵👇 Image
Although not entirely clear, and entirely un-cited, this sentence speculates on the mechanisms relating PEDs to exacerbated pathological remodelling of the iliac artery. This more or less conforms to my understanding of the risks of PEDs on peripheral vascular health 2/ Image
Here is my wall-of-text summary of mechanisms from my thesis

More simply: endofibrosis develops in response to pathological shear stress from large blood flows during exercise through an artery being repeatedly compressed/kinked/bent/twisted with hip flexions (pedalling) 3/ Image
Read 12 tweets
Sep 19, 2024
Just published from my (eventual) PhD thesis 🔖

Review of conservative treatment (CTx) for Flow Limitations in the Iliac Arteries (FLIA, endofibrosis) and proposal of Return to Sport (RTS) guidelines after surgery

Here is what we learned🧵/14 Image
Briefly, FLIA is an uncommon vascular condition where the iliac artery is compressed/kinked during exercise and performance is impaired by ischaemia & claudication. Often seen in cyclists in an aero racing position

Good background thread here 2/
Not enough is known about non-operative management for sport-related vascular conditions like FLIA

62 articles mention CTx modalities in FLIA. We categorised them by perspective on effectiveness (colour) and either theoretical discussion or results of direct case application 3/ Image
Read 17 tweets

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