GENERAL OVERVIEW

Fat plays a number of significant roles in the human body. Besides being used as an insulator to preserve body heat, fat has a number of benefits when it comes to health. Its primary function is to provide an energy reserve for daily activities. Fat also plays an important role for cell membrane structure and flexibility which helps to regulate substance movement through the cell membranes. Eicosanoids (special type of fat) help with hormone signal transduction between cells and certain fats serve as precursors for many important compounds in the body.


FAT AS AN ENERGY RESERVE

As mentioned above, the primary role of fat in the body is to provide an energy reserve. The reason that fat serves an efficient energy store is that it holds a large amount of energy per gram. In fact, fat actually contains more than double the amount of calories per gram than carbohydrates.


  • Carbohydrates – 4 calories / gram
  • Fat – 9 calories / gram

This means that someone who weighs 70kgs and who has a body fat percentage of 20 will store about 14 kilograms of fat mass. This represents about 126 000 kcal. On an average calorie requirement of 2000 calories per day, this individual would theoretically have enough body fat to sustain life for approximately 63 days.



EXCESSIVE CALORIE CONSUMPTION

Fat is stored as a result of excessive calorie consumption. If you consume a larger amount of calories than the energy you expend, you will gain fat weight irrespective of which macronutrients (protein, fat and carbs) you opt for and in what ratio.


BODY FAT PERCENTAGES – WHAT IS HEALTHY

Deciding what body fat percentage you would like to achieve is dependent upon the individual. Some may be within the average range and be happy with that while others may prefer to get into the lean range. It all depends on your goals.

If you want to see defined muscle tone, where for example your six pack pops, you will need to get into the lean lower digit range. However, because every person is different, muscular definition may be seen to different extents even at the same body fat. For example, I may weigh the same, have the same amount of muscle mass and have the same body fat percentage as someone else, but I may not have the same muscular definition in certain areas. This is because people carry weight in different places. The main thing is that you find what works for you.

The charts below show what body fat percentages which constitute lean, ideal, average and above average. Body fat percentages are categorized according to age and gender.


EXCESSIVE FAT STORAGE

Having excessive fat storage is proven to be unhealthy and can have a number of health implications which include, but are not limited to:


  • Coronary heart disease
  • High blood pressure
  • Stroke
  • Type II diabetes
  • Metabolic syndrome
  • Osteoarthritis
  • Sleep apnea
  • Reproductive Problems

THE PROCESSES OF FAT BURNING


STEP 1. LYPOLISYS OF THE ADIPOCYTE

Adipocytes are cells which are designated for fat storage. These are mainly located just under the skin throughout the body and in regions which surround the vital organs (visceral fat) for protection purposes. The fats in the adipocytes are in the form of triacylglycerol (TAG). TAG is structure which is formed by glycerol with 3 fatty acid attached.

Contingent to energy supply and demand, the adipocytes can either absorb and store fat from the blood or they can release fat back into the blood. When insulin and energy levels are high after eating, the insulin retains the fatty acids inside the adipocyte. By fasting for a few hours or performing exercise, you are able to lower insulin levels and encourage the release of hormones like epinephrine (A.K.A – adrenalin). The released epinephrine which then binds to the adipocytes causes the lipolysis of the TAG stores inside the fat cell.

Lipolysis is basically a process whereby fatty acids are separated from the glycerol structure. Once this has occurred, the fatty acids and glycerol can leave the adipocyte and enter the bloodstream.


STEP 2. FATTY ACIDS IN THE BLOODSTREAM

Because fat is non water-soluble, it is not able to dissolve into the bloodstream. It needs to be suspended in the bloodstream in order to be transported to the muscle where it can be burnt for energy. For this process to occur, it is necessary to keep fat suspended evenly in the blood. The principal protein carrier which does this is albumin. A single albumin protein is able to carry numerous fatty acids through the bloodstream to the muscle cell.



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STEP 3. FATTY ACIDS FROM THE BLOODSTREAM INTO THE MUSCLE

Now that the fatty acids have been transported to the muscle cells, they need to filter through 2 barriers in order to pass into the muscle. The first barrier is the endothelium (cell lining which makes up the capillary) and the second is the sarcolemma (muscle cell membrane). The process to transport these fatty acids through the cell membranes requires special binding proteins which need to be present at these membranes. The two proteins which are responsible for this transport are FAT/CD36 and FABPpm.



STEP 4. UTILIZING FATTY ACIDS IN THE MUSCLE

Once the fatty acid has made its way into the muscle, it binds with a molecule called Coenzyme A (CoA) which is a transport protein that maintains the inward flow of fatty acids entering the muscle and prepares them for either oxidation (definition below) or storage within the muscle cells. Fat which is stored inside muscle is called intramuscular triacylglycerol, or IMTAG. In general, the amount of IMTAG stored in slow twitch muscle fibers is 2 to 3 times more than that of IMTAG stored in fast twitch muscle fibers.


However, the amount of fat stores only make up < 1% to 2% > of the total fat stores. These stores are therefore generally used in extended periods of energy expenditure (endurance exercise).


  • Oxidation – a process in which electrons are removed from a molecule to produce energy.

Roughly 80% of the fatty acids which enter the muscle during exercise are oxidized for energy. Before this can happen, the fatty acids need to be transported into the cell’s mitochondria. The mitochondria is responsible for energy production. In this case, it processes the fatty acids to create a readily available energy currency (ATP) to meet the energy requirements of the muscle cell. The transport of fatty acids into the mitochondria is undertaken via a shuttle system called the carnitine shuttle. The carnitine shuttle utilizes carnitine, carnitine palmitoyl tranferase (CPT1) and FAT/CD36 protein to transport the fatty acids. Once the fatty acid penetrates the mitochondria, they are broken down through a number of enzymatic pathways including beta-oxidation, tricarboxylic acid cycle (TCA), and the electron transport chain to produce ATP.



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FATTY ACID OXIDATION DURING LOW, MODERATE AND HIGH INTENSITY EXERCISE

As you start to exercise, blood flow increases to both adipose tissue and to muscle. This process allows for an increased fatty acid release and delivery to the muscle. The intensity with which you exercise has a great impact on fat oxidation.


LOW TO MODERATE INTENSITY:

At a low to moderate exercise intensity which is between 25 – 60% of VO2max (maximal oxygen consumption), fatty acid oxidation is optimised. At this intensity the fatty acids used during exercise come from the blood.


MODERATE INTENSITY:

At a moderate exercise intensity which is between 60-70% of VO2max, the fatty acids oxidized appear to come from IMTAG.


HIGH INTENSITY:

At a higher exercise intensity which is 70 % of VO2max or greater, total fatty acid oxidation is reduced to lower levels than with moderate intensity exercise. As you reach a higher intensity and fatty acid oxidation lowers, an increased carbohydrate (mainly glucose) breakdown occurs to meet the energy demands of the exercise.


  • There are a several factors which impact the decrease in fat utilization. These include:

1. DECREASED BLOOD FLOW TO ADIPOSE TISSUE

As you reach a high intensity of exercise, blood flow will redirect away from adipose tissue. This means that the fatty acids in the adipose tissue become trapped in the capillary beds as there is no blood to carry them to the muscle.


2. ACTIVITY REDUCTION OF CPT1

High intensity exercise can also inhibit the activity of CPT1. If this happens, fatty acids cannot be transported to the mitochondria. Remember, CPT1 is a necessary constituent of the carnitine shuttle which transports the fatty acids to the mitochondria. There are 2 mechanisms which impact CPT1 activity. These include:


  • Increases in Malonyl CoA

As fatty acid oxidation decreases with high intense exercise, carbohydrate oxidation increases (remember this from above?). Increased carbohydrate oxidation then leads to increased levels of a molecule called Malonyl CoA in the muscle cell. The problem with this is that Malonyl CoA can bind to and inhibit the activity of CPT1.


  • Changes in cellular pH

The cellular pH is the measure of acidity in the cell’s cytoplasm. With high intensity exercise, the muscle becomes more acidic and the pH level therefore becomes lower. This low pH can impede CPT1 activity and therefore the carnitine shuttle. The increase acidity is because acidosis increases due to the ATP usage of the contracting muscle fibers. This is not because of lactic acid build up as previously thought. The splitting of ATP releases hydrogen ions into the cellular field which leads to acidosis in the cell.


POST EXERCISE ENERGY CONSUMPTION AND FAT UTILIZATION

Post exercise energy consumption, or EPOC, is a measurably increased rate of oxygen intake following strenuous activity intended to erase the body’s “oxygen deficit.” In simple terms, after you have completed a workout, the body continues to burn energy. This is mainly used for muscle cell recovery and glycogen replenishment.

The elevated metabolic state which occurs due to EPOC is at its greatest after high intensity exercise. For example, the EPOC effect is greater after HIIT cardio than after longer duration, low intensity cardio. EPOC is also notably seen after a bout of resistance training. This is because it disrupts the working muscle cells’ homeostasis (the body’s physiological equilibrium) to the extent that it requires energy post-exercise to restore worked muscles to their pre-exercise state. The EPOC effect can be seen for 24-48 hours post-exercise. This extended period is due to the additional cellular repair and protein synthesis requirements of the muscle cells.

Numerous studies show that fax oxidation rates are also increased during the period of EPOC (Ormsbee et al., 2009, Jamurtas et al. 2004, Achten and Jeukendrup, 2012). So even though high intensity training does not burn near as much fatty acids during the exercise as low to medium intensity training, the effect of EPOC after high intensity training may compensate for this deficit as it increases fatty acid oxidation post-exercise.


CREATING AVAILABLE FATTY ACIDS THROUGH EXERCISE

By creating more available fatty acids in the muscle cell’s mitochondria, you will essentially be able to burn more for fat for energy, especially through exercise. So how do create more available fatty acids?

Well, this can be done through the same way we are able to burn it, and that is through exercise. Exercise improves fatty acid availability by increasing the transport said fatty acids through the blood to the muscle and then the mitochondria. But because this process needs to be facilitated by specific proteins, we also need to increase these. So how is this done? Well, once again, the answer is exercise. Exercise training has been shown to increase the amount of the protein FAT/CD36 on the muscle and mitochondrial membranes. It has also been shown to increase CPT1 on the mitochondrial membrane.

Not just that, exercise may also facilitate changes in the intramuscular lipid droplets which contain IMTAGs. The fact that these lipid droplets are found in close proximity to the mitochondria gives way to efficient IMTAG usage so that fatty acids which are released from the lipid droplet don’t have to travel very far to enter the mitochondria. Exercise can also increase IMTAG availability to the mitochondria by causing the lipid droplet to conform more closely to the mitochondria which increases the overall surface area so that the fatty acid transport from the lipid droplet to the mitochondria is more rapid.

Exercise can also help to increase the number of tiny blood vessels within the muscle. This means that more fatty can enter the muscle through these tiny vessels for delivery into the muscle.



APPLYING WHAT WE HAVE LEARNT

Now that you understand the science of fat loss, we can look at applying real-world applications of what we have learnt.


When it comes to training, you will need to formulate a training plan which is aimed at causing the muscle adaptions which are described above in order to promote fatty acid oxidation. This should include high intensity interval training and endurance training, as these have been shown to improve mitochondrial density (number of mitochondria) and fat oxidation, as well resistance training in order to enhance EPOC and post-workout fat oxidation. Because you simply can’t exercise with a moderate to high intensity 7 days a week, it is advised to include low intensity training on “rest days” as this will help to further boost your calorie deficit and support muscle adaptions between training days.


If you are unsure of how to formulate an effective training routine that will help to maximize fatty acid oxidation, choose one of our fat loss programs listed below which have been specifically designed to manipulate factors listed in this article which play a role in fatty oxidation.



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