Limiting factor in MFO: Oxidation NOT transportation 

Cell metabolism is the limiting factor of fatty acid oxidation NOT fat transportation. Trained and untrained males showed a similar rate of lipolysis and fatty free acid uptake from blood plasma. Yet trained individuals used more fat as a fuel in low intensity exercise. 

This leaves with two conclusions: 

1. Greater contribution of intramuscular fat (fat stored in the muscle) use in trained.

2. Greater percentage of fatty acid uptake is actually oxidized to make energy. (Mitochondria are better at making ATP from fat) 

As stated above,  trained and untrained individuals will have similar serum (blood) fatty acid levels during exercise. However the trained individuals are able to use the fatty acids for energy production better and therefore will have a higher MFO. Not only do trained individuals oxidize more fat at an absolute level but they do this at a higher workload/greater intensity. This = better performance with less discomfort.

How do I improve MFO? 

Training will have the largest effect on MFO. Training impacts fatty acid oxidation via:

1. Increased intramuscular triglycerides (IMTG)

2. Hormonal regulation

3. Cellular mitochondrial protein and enzyme changes

Endurance training enhances Type I fiber IMTG concentrations as much as 3 fold, compared to Type II fibers. The more type 1 fibers you have the more potential to a higher MFO. When training, the workload needs to be intense enough to stimulate the mitochondria but not too intense where lactate accumulates and inhibits lipolysis and fat oxidation. There is a positive relationship with lactate levels and fat oxidation inhibition. This is one example why at the highest intensities we don’t use fat as a fuel source. For more details keep reading below and check out our articles on Carnitine Palmitoyl transferase (CPT-1) or Lactate: Explained.

Fat oxidation is 90% of energy expenditure when exercise intensity is below 25% of vo2 max. So this is where we want to train, right? Nope! Even though 90% of the energy is from fat the absolute amount of fat is not high. Therefore the mitochondria are not being stressed or worked to the limit. 

An exercise intensity between 40-70% of Vo2 max (depends on individual) will use about 50% fuel from fat and muscle glycogen. Right below this level is where MFO lives and where we want to train, this is your zone 2. 

**When analyzing 300 healthy individuals in the general public, MFO in trained humans averaged between 59-64% of Vo2 Max. The untrained had an MFO between 47-52% of vo2 max. As a reference to what’s physically possible, endurance athletes have an MFO between 70-80% of Vo2 max.

Why is MFO important? 

The higher one’s MFO the greater ability they have to perform at submaximal levels for longer periods of time. For endurance athletes a high MFO is a necessity for success. Two athletes with the same Vo2 max but different fat oxidation levels will perform vastly differently over an extended period of time. 

MFO ranges between .10 and 1.27 grams per min or 6-76 grams an hour 

What controls this range? 

• Sex: On average women have a higher MFO % of Vo2 max than men

• Training status: Endurance trained individuals have higher MFO than untrained  

• Nutritional intake: If you eat a high fat diet (>60% calories from fat) you will burn more fat at submaximal levels

• Exercise intensity: The greater the intensity the less % of fuel derives from fat

• Duration: The longer you train the more glycogen is depleted and more fuel is oxidized from fat

• Type I fiber count: The more type 1 fibers you have, the greater MFO potential.

Examples Below: 

Professional athletes: 40g of lipids per hour at 250 watts with blood lactate around 1.0 mmols

Trained: 24g of lipids an hour at 130 watts, blood lactate around 1.2 mmols

Untrained: 12g of lipids an hour at 100 watts with blood lactate at 2 mmols

Lactate and MFO

As you can see below: San-Millián and Brooks found a near perfect (.97 and .98) inverse relationship between blood lactate levels and fat oxidation rates.

Above:

Using carbohydrates as fuel does not necessarily mean more blood lactate accumulation. Yes the bi-product of glycolysis may be lactate, and we use carbs to fuel glycolysis. But this only tells us 1/2 of the story. How well your body handles the lactate and re-uses for fuel will determine your blood lactate accumulation. Professional athletes are producing more lactate as they are burning more carbs for fuel but the lactate is not showing up in the blood because their mitochondria recycle the lactate and re-use as fuel.

These two graphs to show the difference between cells that recycle lactate very well (A) compared to cells that are average at re-using lactate and fat for fuel (B).

Professional athletes have an MFO of 40g an hour at 250 watts. This comes with 180g of CHO burning per hour. But only a blood lactate of 1 mmol.

Amature athletes at 1 mmol blood lactate have an MFO of 24g an hour at 130 watts, while burning only 120g of CHO.

Once the amature atheltes burns 180g of CHO per hour their blood lactate doubles to 2 mmols. Their fat burn is roughly 18-19g/h at this rate. If CHO utilization was the sole reason for lactate accumulation these results would not be possible.

How well you burn fat AND utilize lactate for fuel are the largest determinants for success at endurance events. The longer the event, the more important these two biomarkers are.

MFO and Diet 

Diet can influence what we burn for fuel, but by how much? What are the pros and cons? Let’s look at the contributors to fatty acid oxidation: 

• Subcutaneous adipose tissue 

• Intramuscular triglycerides (IMTG) 

• Cholesterol 

• Dietary fat

Seeing as we eat everyday, dietary fat would be low hanging fruit for an improvement in fat oxidation. But how much do we need to eat to see benefits?

In short, eating a higher fat diet (greater than 60% calories from fat) with carb restriction will elicit a higher fat oxidation at lower intensity exercise. This is through two main mechanisms, more fat available to use and glycogen sparing. When the body doesn’t receive glucose, its glycogen stores will decrease and the body will hold onto that glycogen more than if we ate a diet rich in CHO. However, this comes at a cost of peak performance. IMPORTANT: These changes occur over long periods of time, if you eat a high fat meal, it will not translate to using fat for fuel from that meal. On the contrary, if you starve yourself from CHO for a day and exercise, you will use more fat for fuel on a % base. This is from lack of carbs, not your body getting better at utilizing fat for fuel. Carb restricted training may be ok for training purposes at submax levels, but NOT ok for performance. Check out our article here on carb restricted training.

High fat diet (K/Cal > 68% from Fat)

Fat used for fuel is higher at low-moderate intensities (64-70% of vo2 max) and prolonged exercise (greater than 3 hours) on high fat diet. This is from an increase in IMTG storage, and increase in fat oxidation. However, exercise intensity >70% vo2 max, power output was decreased. High fat diets increase beta oxidation potential at rest and during exercise.

• HOWEVER high intensity exercise > 75% vo2 max eclipses fat oxidation potential relying on fast glycolysis. In other words, once intensity becomes to high, how well you burn fat doesn’t matter as much but how well you can use carbs for fuel does.

• Pyruvate dehydrogenase is the enzyme responsible for oxidizing pyruvate (pyruvate is an end product of using CHO for fuel)

  • High fat diets reduce PDH activity, this enzyme becomes a limiting factor.  

  • Despite your CHO storage, PDH is needed to get energy from the CHO. 

Lets recap: It’s nearly impossible to benefit from a high fat diet, without sacrificing your top end performance. Unfortunately this lack of performance starts around 75-80% of vo2max, which is where you would spend most of your time during an event. But what happens if we have a high fat diet then do a quick 36-72 hour CHO load??

Results: High fat diet + acute cho loading:

Long term high fat diet with acute CHO loading (36-72 hours prior to event) was shown to maintain IMTG stores while increasing glycogen stores + glycolytic enzymes. 

5 days of High fat diet (67% total K/cal) with 24 hour CHO loading  (70% total k/cal) Maintains IMTG concentration and partially restores PDH to 71% of PDH levels on a high CHO diet. While maintaining 80% HSL activity. 

No differences were noted in a 10 min TT bike sprint (90% Vo2) between high CHO diets and 5 days HFD with 24 hour high carb diet.

• This is only one study, but it is promising proof that if you choose to live a low carb, high fat diet lifestyle you can load with carbs 36-72 hours prior to an event and not suffer the performance loss of carb restricted dieting while increasing IMTG.

Training fasted:

Regardless of your diet ingestion of CHO before activity has been shown to decrease fat oxidation. At the same time fasting 6 hours before has been shown to increase fat oxidation. For more information on training with restricted carbs check out our article here!

To Summarize Diet:

It’s hard to improve in fat oxidation without stealing from your CHO performance, using diet alone. Unless you are only working sub maximally I wouldn’t recommend a high fat diet for someone who performans/competes in endurance sports. That said, scientists have shown that long term high fat diets (as short as 5 days) with acute CHO loading 36-72 hours prior to an event can improve fat oxidation at submaximal levels while maintaining high intensity CHO performance. There are minimal studies on long term HFD with acute CHO loading so more research is needed on these acute changes in dietary programs.

Final Thought: Sex Differences in Fat Oxidation

There are minor differences in fat oxidation between men and women. On average (excluding professional athletes) Women have a higher percentage of their Vo2 max at their MFO. 55% compared to 45% in men. This is due to a few factors listed below:

1. Higher % of estrogen which aids in regulatory proteins for fat oxidation

2. Higher proportion of type I fibers 

3. Lower maximal capacity of glycolytic enzymes (lowers vo2 max potential)

4. Greater reliance on IMTG. (more efficient fatty acid substrate during exercise)

5. Higher amounts of FFA transporter protein CD36 (due to more estrogen)

   1. In a study men were given estrogen and CD36 increased independent of other factors.

6. Produce 50% more CD36 proteins in response to training compared to the same relative stimuli for men.