🩸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
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/
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
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/
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/
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/
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
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/
🩸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
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
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
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
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
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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👇)
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/
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/
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🧵
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/
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/🧵
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/
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/
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💭🧵👇
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/
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/
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
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
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/