Cardio or Weights

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Cardio or Weights – What gets you into Keto Faster?- Thomas DeLauer

Aerobic Activity to generate ketones via Beta Oxidation

Maximal fat oxidation occurs at low to moderate intensity (between 25% and 60% of maximal oxygen consumption (VO2max)

At lower exercise intensities, most of the fatty acids used during exercise come from the blood

As exercise increases to moderate intensity (around 60% of VO2max) the majority of fatty acids oxidized appear to come from IMTAG

At higher exercise intensities (greater than 70 % VO2max), total fat oxidation is reduced to levels lower than that of moderate intensity

This reduced rate of fatty acid oxidation is coupled with an increase in carbohydrate breakdown to meet the energy demands of the exercise

This counterintuitive drop in fat utilization during high intensity exercise is caused by several factors

One factor is related to blood flow to adipose tissue and thus reduced fatty acid supply to the muscle

At high exercise intensity, blood flow is shunted (or directed) away from adipose tissue so that fatty acids released from adipose tissue become “trapped” in the adipose capillary beds, and are not carried to the muscle to be used

Another reason for reduced fat usage at high exercise intensities is related to the enzyme CPT1

CPT1 is important in the carnitine shuttle that moves fatty acids into the mitochondria for oxidation – the activity of CPT1 can be reduced under conditions of high intensity exercise.

As mentioned, with increasing exercise intensity fatty acid oxidation drops while carbohydrate oxidation increases

The increased usage of carbohydrate leads to increased levels of a molecule called malonyl CoA inside the cell – Malonyl CoA can bind to and inhibit the activity of CPT1


An inverse relationship of FA carbon chain length and oxidation exists where the longer the FA chain the slower the oxidation

The slowed oxidation of long chain FAs (LCFAs) (more than 12 carbons) are due to the requirement of a mitochondrial transport protein for LCFA transport

The transport protein known as carnitine palmitoyltransferase-1 (CPT-1) is located on the outer mitochondrial membrane and is responsible for the transportation of LCFAs into the mitochondria

CPT-1 is necessary for LCFA transport, a product of free carnitine, and is found in both the cytosol and mitochondrial matrix

CPT-1 catalyzes the transfer of a FA acyl group from acyl-CoA and free carnitine across the outer mitochondrial membrane forming acyl-carnitine

Once in the intermembrane space, translocase facilitates the transport of acyl-carnitine via CPT-II across the inner mitochondrial membrane at which point carnitine is liberated

During high intensity exercise however, large quantities of acetyl-CoA are also produced via fast glycolysis which enter the mitochondrial matrix and supersede TCA cycle (tricarboxylic acid/citric acid) cycle utilization

The result of the abundant glycolytic derived acetyl-CoA forms acetyl-carnitine and monopolizes the available free carnitine limiting FA derived acyl-CoA transport.

Thus, free carnitine is used to buffer excess glycolytic derived acetyl-CoA by forming acetyl-carnitine, and therefore the limited concentration of free carnitine is a rate limiting step in FA transport/oxidation

**CPT-1 is a product of free carnitine, but during high intensities free carnitine is used to buffer excess glycolytic derived acetyl-CoA, therefore limiting CPT-1’s ability to transport fatty acids into the cell**


Study – Nutrition

“Maximal rates of fat oxidation have been shown to be reached at intensities between 59% and 64% of maximum oxygen consumption in trained individuals and between 47% and 52% of maximum oxygen consumption in a large sample of the general population.”



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