The Physiology of Fat Loss Part 2

From the fat cell to the furnace, find out exactly what causes the body to burn fat. 
By: Mike Deyhle, Christine Mermier, and Len Kravitz
Fitness Journal- January 14

Adaptations to Exercise That Improve Fat Usage 

Trained people can use more fat at both the same speed or power output and the same relation percentage of heart rate maximum than untrained people.  Lipolysis and fat release from adipocytes are identical in untrained and trained people.  This shows that trained people are better able to burn fat because of differences in the muscle’s ability to take up and use fatty acids, not because of the adipocytes’ ability to release fatty acids.  Adaptations that enhance fat usage in trained muscle can either improve fatty-acid availability to the muscle and mitochondria or improve the ability to oxidize fatty acids.

Fatty-Acid Availability

Exercise causes specific proteins to deliver more fatty acid to the muscle and mitochondria.  Exercise also increases the amount of FAT/CD 36 on the muscle membrane and mitochondrial membrane and boosts CPT1 on the mitochondrial membrane.  Together, these proteins improve fat transport into the muscle and mitochondria to be sued for energy.  Exercise may also cause changes in the intramuscular lipid droplets, which contain IMTAGs that usually reside near the mitochondria.  The close proximity allows an efficient release of fatty acids from the lipid droplets to the mitochondria.  Exercise also boosts IMTAG availability by causing lipid droplets to conform more closely to the mitochondria.  Exercise may increase total IMTAG stores.  Another training adaptation that may improve fatty-acid availability is an increase in the number of small blood vessels within the muscle.  Fatty acids can enter the muscle through small capillaries.  By increasing the number of capillaries around the muscle it enables increased fatty-acid delivery into the muscle. 

 

The Physiology of Fat Loss

From the fat cell to the fat furnace, find out exactly what causes the body to burn fat.
By: Mike Deyhle, Christine Mermier, and Len Kravitz
Fitness Journal- January 2014

Two Fates of Fate Inside Muscle

When fat gets inside the muscle, the molecule coenzyme A (CoA) is added to the fatty acids.  Coenzyme A is a transport protein that maintains the inward flow of fatty acids entering the muscle and prepares the fatty acid for one of two things.  The first being oxidation which electrons are removed from a molecule to produce energy.  The second being storage within the muscle.  80% of fatty acids entering the muscle during exercise are oxidized for energy.  Most fatty acids entering the muscle after a meal are repackaged into TAGs (triacylglycerol, a common molecular form of the fat inside adipocytes) and stored in the muscle in lipid droplets.  Fatty acids stored in muscle are called intramyocellular triacylglycerols (IMTAGs) or intramuscular fat.  IMTAGs are stored two to three times more in slow-twitch muscle fibers than in fast-twitch muscle fibers.  Even though IMTAG supply makes up 1-2% of the total fat stores within the body, it is of great interest to exercise physiologists because it is a metabolically active fatty-acid substrate used during periods of increased energy expenditure, like endurance exercise.

 

Fatty-Acids Burned for Energy

 

Fatty acids burned for energy (oxidized) in the muscle can come either from the blood or from IMTAG stores.  For fatty acids to be oxidized, they must be transported into the cells’ mitochondria.  A mitochondrion is an organelle that functions like a cellular power plant.  A mitochondrion produces fatty acids, and other fuels, to create a readily usable energy currency (ATP) in order to meet the energy needs of a muscle cell.  Most fatty acids are transported into the mitochondria via the carnitine shuttle.  The carnitine shuttle is a system for transporting fatty acids to the mitochondria.  The carnitine shuttle uses two enzymes and carnitine (an amino acid-like molecule) to do the transporting.  Once inside the mitochondria, fatty acids are broken down through several enzymatic pathways to produce ATP.

 

Fatty-Acid Oxidation During a Single Bout of Exercise

At the start of exercise, more blood flows to adipose tissue and muscle, releasing more fatty acids from adipose tissue and delivering more fatty acids to the muscle.  Exercise intensity has a big impact on fat oxidation.  We burn the most fat when exercising at low to moderate intensity.  Low to moderate intensity is defined as oxygen consumption between 25-60% of maximum.  At very low exercise intensities, 25% maximum, most of the fatty acids come from the blood.  Around 60% of maximum exercise intensity the fatty acids oxidized mostly come from IMTAG stores.  At high exercise intensity, any exercise greater than 70% of maximum, total fat oxidation falls below the levels observed at moderate intensity.  This reduction in fatty-acid oxidation is coupled with an increase in carbohydrate breakdown to meet the energy demands of the exercise.  Often the fatty-acid contribution to calories burned during exercise is overemphasized.  It’s important to consider recovery from exercise, as well as training adaptations to repeated exercise.

 

Energy and Fat Used During Recovery

After exercising, our body still needs to burn more energy, to help muscle cells recover and replace lost glycogen.  This elevated metabolic rate is called excess post exercise oxygen consumption (EPOC), this is the greatest after high-intensity exercise.  EPOC is higher after high-intensity interval training than after longer-duration, lower-intensity exercise.  EPOC is also in affect after resistance training which disturbs the working muscle cells’ homeostasis to a great degree, meaning that more energy is needed to restore the contracting muscle cells to pre exercise levels.  EPOC stays elevated for longer after eccentric exercise, because this activity creates a higher demand for cellular repair and protein synthesis.  Many studies show that fat-oxidation rates rise during EPOC.  Comparatively, fatty-acid use during high-intensity bouts of exercise, such as high-intensity interval training and resistance training, may be lower than in moderate-intensity endurance training however high-intensity exercise and weight training may make up for this deficit with increased fatty-acid oxidation through EPOC.