Nutrition Low carbs - The Oxygen Problem

[Wesker11]

Found this study really interesting, thought others might as well. With my current diet, slow carb/fasting, I sort of unintentionally cycle carbs. A couple weeks ago I tried testing S&S time with my 24KG. I've hit the time multiple times before. After I was a couple sets in I was gassed...and pissed that it was so hard. Now usually I test later in the week, this week I decided to test on a Monday after a fast day. I am now wondering if that is why it seemed so hard.

Low-carbing for endurance: the oxygen problem | Examine.com

 

[offwidth]

From what I've read adaptations to fat as an endurance fuel take a while.

 

[pet']

Hello,

@Wesker11
I noted that 3 weeks - on average - permit to adapt to a new diet.

Kind regards,

Pet'

 

[Al Ciampa]

First:

After I was a couple sets in I was gassed...and pissed that it was so hard.

@Anna C ... this is an unhealthy attitude toward physical training, and why I don't recommend focusing primarily on goals, especially for GPP.

With my current diet, slow carb/fasting

How long have you been running this; and what is your total carb intake?

I am now wondering if that is why it seemed so hard.

I don't know which "why" you are asking about. The O2 efficiency thing discussed in the study? Or, that you changed your training day closer to the end of a fast?

This study is not interesting because it was run too short to say anything without much doubt.

 

[North Coast Miller]

This study is not interesting because it was run too short to say anything without much doubt.

What I did find interesting is the correlation between fat utilization and increased demand for oxygen, and how it is hypothesized as the limiting factor.

Is there any research indicating a drop off in oxygen demand for fat utilization with longer adaptation to a LCHF diet?

One would think for a given amount of ATP production from fat there would be a required amount of oxygen and that this formula is relatively static. I've found a fair amount of literature describing the process, but not much about where the bottlenecks are in practice.

 

[Matts]

Not reading much of the study in OP, but would say that all the carb vs. fat studies have to read with a grain of salt in light of the efforts of lobbies to protect shares of the billions of dollars involved in affected industries. Here's an article about that aspect:
https://www.nytimes.com/2016/09/13/well/eat/how-the-sugar-industry-shifted-blame-to-fat.html?_r=0
https://www.nytimes.com/2016/09/13/well/eat/how-the-sugar-industry-shifted-blame-to-fat.html?_r=0

 

[Al Ciampa]

What I did find interesting is the correlation between fat utilization and increased demand for oxygen, and how it is hypothesized as the limiting factor.

IMO, its not interesting because it is to be expected. You're supplementing less ATP through glycolysis. Moreover, through my lens, I see muscle fiber type as the common thread. And, if the smaller fibers are more aerobic/faster fibers less aerobic, LC nutrition would elicit less faster fibers.

What's really interesting is that after only 3 weeks of the intervention, the LC athletes lost no performance.

Is there any research indicating a drop off in oxygen demand for fat utilization with longer adaptation to a LCHF diet?

I don't believe its been looked at, but I am no longer immersed in that study. Check out Volek and Phinney, if anything.

One would think for a given amount of ATP production from fat there would be a required amount of oxygen and that this formula is relatively static. I've found a fair amount of literature describing the process, but not much about where the bottlenecks are in practice.

I would expect the LC athletes to use more O2, but I don't see how the authors concluded that it is the bottleneck.... because they did not improve? If you remove excess anaerobic contribution of ATP through less faster fiber and lower glucose use, and, performance remains constant, this IMO indicates an improvement.... especially to the longer term health of the athletes.

 

[North Coast Miller]

@ aciampa

Let me make sure I'm understanding what you are expressing here.

The real bottleneck as far as this study goes was that the LC subjects didn't alter their training methods to take advantage of increased ATP supply from fat. They are trying to power the system with a less effective fuel. Hence the surprise that the LC lost no performance over such a short adaptation period.

My speculation - they showed up with a muscle composition that was a reasonable fit and already possessed good potential for metabolic fat utilization, though perhaps not as good as it could be?

Presumably if the study were run longer and the training were tailored to the intended fuel source, performance would have been comparable (at the least) across all the study groups and in terms of metabolic by products, the LC group would have come out ahead.

Are there any studies that show a muscular composition adaptation based only on dietary changes, or is the current understanding that this can only be done primarily thru intentional training ie A&A? I wouldn't expect such to be the case but without research who knows?

https://www.strongfirst.com/community/members/aciampa.1014/

 

[Al Ciampa]

The real bottleneck as far as this study goes was that the LC subjects didn't alter their training methods to take advantage of increased ATP supply from fat. They are trying to power the system with a less effective fuel. Hence the surprise that the LC lost no performance over such a short adaptation period.

This might also be the case, but it wasn't what I was trying to explain. Without writing a book here, this is my theory to explain the literature about metabolism and biochemistry:

The energy systems are not separated from muscle fibers; i.e., the slower fibers are mostly aerobic, and the faster fibers are mostly anaerobic. What this means is that the traditional model of the energy systems (alactic, lactic, respiration working in their time periods) doesn't apply to the end of the spectrum fibers, only the middle ones at best. IOW, the slowest fibers are incapable of glycolysis, and the fastest ones incapable of respiration. This might explain why we see unhealthy folks with certain conditions lose all but the fastest muscle fibers.

Moreover, muscle fiber types probably exist on a spectrum of slow-to-fast, with their being more than the 4 types that the textbooks report. If you "see" the biology through this lens, then, even though there is evidence that fibers can share acid load and substrates, if you use the fastest fibers, you will be anaerobic because they can't produce force aerobically. If your contractions contain so little force that only the slowest fibers need be employed, you will be aerobic.

Overuse of sugar and carbs, among other things, motivates anaerobic activity regardless of the contractile force. You can experience this when you're sitting still and you get spooked, or otherwise anxious. If you don't overuse carbs, it is the contractile force needed that sets the recruitment path of muscle fibers, as has been established by neuroscience.

The elite walkers used in the study, and this really depends upon their nutrition and training used up to the study period, used their slow"er" (note: not "slow") fibers for the work, which would naturally use more fat and O2. The same elite who stuffed his face with carbs would, for the same work, use a higher percentage of faster fibers, using less fat and less O2. Arousal too would make a major difference in muscle fiber employment and substrate use.

The "bottleneck", in my opinion, is at least threefold:
1. the contractile force needed for motion; also implying the training state (re: strength) of the slower fibers
2. the dominant macronutrient fuel that the organism is adapted to; implying the metabolic flexibility of the system
3. the anxiety state of the organism

I don't know if I answered your question, or explained this in a digestible manner, but it makes sense in my head. @mprevost can probably elaborate more/better than I can.

 

[Wesker11]

Well, I honestly regret posting this. I will refrain from doing so in the future.

 

[Al Ciampa]

Well, I honestly regret posting this. I will refrain from doing so in the future.

Why? These are the type of questions that start useful discussions.

 

[Pavel Macek]

Excellent analysis @aciampa , thank you.

 

[North Coast Miller]

@ aciampa


Thanks. Your response makes sense. It also to some extent (maybe) answers my other thought re diet triggered adaptation to motor unit composition - in the absence of tailored training.

 

[mprevost]

Found this study really interesting, thought others might as well. With my current diet, slow carb/fasting, I sort of unintentionally cycle carbs. A couple weeks ago I tried testing S&S time with my 24KG. I've hit the time multiple times before. After I was a couple sets in I was gassed...and pissed that it was so hard. Now usually I test later in the week, this week I decided to test on a Monday after a fast day. I am now wondering if that is why it seemed so hard.

Low-carbing for endurance: the oxygen problem | Examine.com

This issue gets technical quickly. When burning carbohydrates, you get some ATP without oxidative phosphorylation (where oxygen is directly used). Specifically, you get 2 ATP per glucose by substrate level phosphorylation (no oxygen required), and the rest through oxidative physphorylation (using oxygen). When you burn fat, you don't get those two substrate level phosphorylation events, so you are relying more on oxidative phosphorylation (and oxygen) more than you are when you are burning carbohydrates. Basically, with carbohydrates, you get a couple of extra ATP without oxygen. So, you use more oxygen to get the same amount of ATP when burning fat. However, to call it less efficient when burning fat is not entirely correct. You are still using the same number of ATP whether burning fat or carbohydrates. You just use a little more oxygen to do it when burning fat.

This shows up in the respiratory quotient (RQ). RQ is carbon dioxide produced, divided by oxygen consumed (CO2/O2). For pure fat burning the RQ is 0.70. For pure carbohydrate burning it is 1.00. If you flip it, it makes more sense intuitively. So, for fat burning the inverse RQ (O2/CO2) is 1.43 (how much oxygen it costs per carbon "burned). For carbohydrates it is still 1.00.

This turns out not to be an issue because at higher intensities (where oxygen delivery may be limiting) you are burning primarily carbohydrates anyway (see below):

Most people are at about 50% fat in zone 2, or at a moderate-easy effort pace. Higher intensities would shift towards carbohydrates. Even a moderately hard effort is 90% or more carbohydrates.

The ketogenic diet shifts the whole curve to the right but the same general effect occurs.

 

[Anna C]

RQ.... makes more sense now. Thanks, @mprevost !

I'll contribute an example here, my last LT and VO2max laboratory test on the bike.

I have forgotten, though... what does it mean when RER goes above 1.0, as it does at 200 watts and above?

 

[North Coast Miller]

@ mprevost

Not to be overly simplistic, but would this imply a lower heart rate in the mid range for folks burning primarily carbohydrate? Eg if the same person were to jog at the upper limit of their MAF heart rate and record the distance/time on a higher carb diet, then repeat the same distance /time after becoming keto-adapted, would you expect to see higher heart rate due to higher amounts of CO2 in the blood during exertion?

 

[mprevost]

RQ.... makes more sense now. Thanks, @mprevost !

I'll contribute an example here, my last LT and VO2max laboratory test on the bike.

I have forgotten, though... what does it mean when RER goes above 1.0, as it does at 200 watts and above?

View attachment 2868

The reason RQ exceeds 1 is due to the buffering of acid by bicarbonate. When you start to experience a large acid load during higher intensity work, bicarbonate buffers the hydrogen ions and breaks into water and CO2. This CO2 adds to the metabolically produced CO2, driving the RQ (CO2/O2) up above 1.0. This typically occurs at about 10K race pace, zone 4, and around the point referred to as the Onset of Blood Lactate Accumulation (OBLA) and the maximum lactate steady state.

 

[mprevost]

@ mprevost

Not to be overly simplistic, but would this imply a lower heart rate in the mid range for folks burning primarily carbohydrate? Eg if the same person were to jog at the upper limit of their MAF heart rate and record the distance/time on a higher carb diet, then repeat the same distance /time after becoming keto-adapted, would you expect to see higher heart rate due to higher amounts of CO2 in the blood during exertion?

Possibly, but heart rate is an "integrator" that integrates several signals, including but not limited to CO2 levels.

 

[North Coast Miller]

The reason RQ exceeds 1 is due to the buffering of acid by bicarbonate. When you start to experience a large acid load during higher intensity work, bicarbonate buffers the hydrogen ions and breaks into water and CO2. This CO2 adds to the metabolically produced CO2, driving the RQ (CO2/O2) up above 1.0. This typically occurs at about 10K race pace, zone 4, and around the point referred to as the Onset of Blood Lactate Accumulation (OBLA) and the maximum lactate steady state.

Great discussion!

Next thought - I have seen recommendation to switch around higher intensity movement or muscle group activities to avoid or limit the local effects of acid and hydrogen ion accumulation, giving it a better chance to clear and reduce system wide effects.

In my own experience this generally doesn't work as a lot of the accumulation is rapidly cleared into the blood stream where it seems to have a system wide effect anyway that increases heart rate and perceived fatigue, even with a switch to a fresh muscle group. Real endurance seems to be compromised with the "new" group as well, leading me to believe this strategy is not effective or at least becomes increasingly ineffective as intensity increases.

What do folks think about this?

 

[mprevost]

Reduced power output, or fatigue, is biochemical and local (there is some debate here, see Noakes' central governor theory). But there is no doubt that fatigue in one area can increase perceived exertion while training another. I generally don't try too hard to sort out the physiology and focus on which methodology lets me do what I intend to do.