A widely cited figure is a pound of fat contains 3500 calories of energy in fatty acids.
However, a pound of fat also contains adipose cells, arranged in adipose tissue, connective tissue etc.
When a human breaks down fat to use as energy, from what I understand it doesn't break down the fat cells, just liberates the triglycerides stored inside those cells.
Those fat cells, and connective tissue took energy to assemble as well.
How much energy is used to create a pound of fat tissue?
Let's assume that all the cells and the triglyceride stored inside them are created from scratch.
A rough answer to a rough question
According to a study conducted in the 1960s, human adipose tissue, on average, contained (per 100g wet weight) 87g fat, 2g protein, 2g sodium and potassium and 10g water. (Nothing else was measured.) This suggests that approx. 3% of adipose tissue is solids other than triglyceride.
The figure quoted is presumably the energy yield for the complete oxidation of triglyceride. The energy yield for the complete oxidation of the non-triglyceride solids in adipose tissue - the appropriate, if hypothetical, comparison would be less than that for triglyceride, which is much more chemically reduced, so the yield for the oxidation of non-triglyceride might be approx. 1-2% that of triglyceride.
The energy needed to bio-synthesize any organic compound (triglyceride, carboyhdrate or protein) is more than is obtained from it by oxidation because a negative free energy change is needed to drive reactions. Hence, as regards the relatively constant (slowly turning-over) portion of the adipose tissue, the cost would be higher - perhaps 2-3% of that quoted produced by oxidizing the triglyceride.
The problem with this question
Some people say that there is no such thing as a stupid question. Nevertheless, there are questions that are formulated as if their answer will establish solve some problem, when in fact it will not because the premise on which it is based is false.
In this case a comparison is made between the triglyceride and non-triglyceride content of adipose tissue with the implication being that the latter should be assessed in the creation of the former:
“Those fat cells, and connective tissue took energy to assemble as well. How much energy is used to create a pound of fat tissue?”
As already mentioned, it is invalid to make a numerical comparison between the energy required to synthesize one compound with that released by the oxidation of another compound, as it costs more to synthesize a compound than is released by its oxidation.
However, quantitatively more fundamentally wrong is the implication that the one-time synthesis of the structural components of the cell should be costed into the repeated oxidation of triglyceride in that cell. How many grams of triglyceride are synthesised per gram of cell structural material during the lifetime of a cell? Very many, I should imagine if the cells turn over much more slowly than the lipid they contain.
It would be more pertinent (assuming that you are interested in such things) to ask what the cost is in terms of the energy used by whatever muscles are used by the lungs to breath in the oxygen needed to oxidize the fat, and the energy used by the heart muscle to pump the blood containing the oxygen to the fat cells so that it can be oxidized.
Finally, it is naïve to think of the energy cost of maintaining a fat cell in terms of the synthesis of its structural components. Other metabolic processes are continually occurring that require energy even in fat cells.
No doubt it would be possible to perform a calculation that took all these things into account (although what would you start with “from scratch” - ingested carbohydrate or carbon dioxide and water?). Personally, I am happy to accept that the system makes a profit and interest myself with the details of how it operates and adjusts to different circumstances.
Fat Respiration and Protein Respiration | Plants
Fats are stored as triglycerides in cells, primarily of adipose tissue. They have a high energy content, and form a better fuel than the carbohydrates. They break up into fatty acids and glycerol in the cytoplasm before use in respiration.
Fatty acids are broken by a series of reactions into 2-carbon acetyl coenzyme A. The latter enters the Krebs cycle.
Glycerol combines with a phosphate group, forming phosphoglyceraldehyde. The latter enters glycolysis.
A molecule of 18-carbon stearic acid on complete oxidation produces 147 high-energy phosphates. A 6-carbon glucose molecule yields 36 or 38 ATP. With this rate, an 18-carbon molecule is expected to give 3 times more energy (36 or 38 x 3 = 108 or 114 ATP) but it provides about 4 times more energy (36 or 38 x 4 = 144 or 152 ATP) than 6-carbon glucose produces.
(ii) Protein Respiration:
The proteins split into amino acids in the cytoplasm for use in respiration. The amino acids enter respiratory routes in two ways: deamination and transamination.
In deamination, an amino acid loses its amino group (- NH2) and changes into a keto acid. The latter may further change into pyruvic acid or acetyl coenzyme A. Pyruvic acid is oxidized to acetyl coezyme A. The latter enters the Krebs cycle.
In transamination, an amino group of an amino acid is transferred to an appropriate keto acid, forming a new amino acid and a new keto acid. The keto acids so formed are normal participants of glycolysis or Krebs cycle.
The trouble with visceral fat
Body fat, or adipose tissue, was once regarded as little more than a storage depot for fat blobs waiting passively to be used for energy. But research has shown that fat cells — particularly visceral fat cells — are biologically active. One of the most important developments [since the mid-1990s] is the realization that the fat cell is an endocrine organ, secreting hormones and other molecules that have far-reaching effects on other tissues.
Before researchers recognized that fat acts as an endocrine gland, they thought that the main risk of visceral fat was influencing the production of cholesterol by releasing free fatty acids into the bloodstream and liver. We now know that there's far more to the story. Researchers have identified a host of chemicals that link visceral fat to a surprisingly wide variety of diseases.
Subcutaneous fat produces a higher proportion of beneficial molecules, and visceral fat a higher proportion of molecules with potentially deleterious health effects. Visceral fat makes more of the proteins called cytokines, which can trigger low-level inflammation, a risk factor for heart disease and other chronic conditions. It also produces a precursor to angiotensin, a protein that causes blood vessels to constrict and blood pressure to rise.
A tape measure is your best home option for keeping tabs on visceral fat. Measure your waistline at the level of the navel — not at the narrowest part of the torso — and always measure in the same place. (According to official guidelines, the bottom of the tape measure should be level with the top of the right hip bone, or ilium — see the illustration — at the point where the ilium intersects a line dropped vertically from the center of the armpit.) Don't suck in your gut or pull the tape tight enough to compress the area. In women, a waist circumference of 35 inches or larger is generally considered a sign of excess visceral fat, but that may not apply if your overall body size is large. Rather than focus on a single reading or absolute cut-off, keep an eye on whether your waist is growing (are your pants getting snug at the waist?). That should give you a good idea of whether you're gaining unhealthy visceral fat.
What to know about calories and body fat
In relation to food and the body, calories are units of energy that allow the body to work. Food provides this energy, some of which the body stores and some of which it uses. As the body breaks down food, it releases calories as energy.
Max Wishnofsky first propagated the concept that there are approximately 3,500 calories in a pound (lb) of body fat.
Put simply, to lose 1 lb of body fat per week, people will need to have a deficit of around 500 calories per day. They can achieve this by consuming roughly 500 calories fewer than they are currently, by burning an extra 500 calories per day with exercise, or a combination of the two.
If the body takes in too many calories or burns too few, weight gain occurs. This is because the body stores calories it does not use as body fat. Organs including the brain, heart, lungs, liver, and kidneys account for roughly 80% of total daily energy use.
Recent research calls this rule into question, concluding that it overestimates someone’s weight loss potential. The rule does not take into account dynamic changes in metabolism, hunger, and satiety levels as weight loss occurs.
The National Institutes of Health (NIH) have developed a new, more accurate rule-of-thumb: Every 10 calorie decrease per day leads to an eventual 1 lb loss. Only time will tell how long that weight loss takes, so patience and consistency is key.
Share on Pinterest Having too much or too little body fat can cause health problems.
Body fat, or adipose tissue, consists of adipocytes.
These are fat cells, and they occur alongside other types of cells and proteins. Fat cells contain lipids, including cholesterol and triglycerides.
Adipose tissue stores energy for the body to use and protects the organs. It also releases hormones that control many functions in the body, such as insulin sensitivity and appetite.
People with more body fat may experience something called leptin resistance, in which the body is less sensitive to the satiety hormone leptin. This, in turn, drives up hunger and food intake, making weight maintenance harder over time.
There are two types of adipose tissue: white and brown. Brown adipose tissue is more metabolically active. It burns more calories and helps manage weight, insulin sensitivity, and overall health to a greater extent than white adipose tissue.
If people have excess body fat, it is most often due to the fact that their white adipose tissue has expanded.
Having too much body fat can cause obesity and result in many health problems, including diabetes, high blood pressure, and heart disease. Having too little body fat can also be harmful and lead to health concerns such as malnutrition and fertility issues.
Research estimates that muscle burns calories at a rate of 10–15 calories per kilogram (kcal/kg) per day. This amounts to 4.5–7 kcal/lb per day.
Muscle accounts for roughly 20% of total energy expenditure each day. For people with 20% body fat, body fat accounts for 5% energy expenditure.
So, people with more muscle tissue have a higher metabolic rate. This means that they burn more calories and are able to maintain their body weight more easily.
How do we calculate calories?
Calories in food do not amount to precisely the same measurement inside the body as outside the body.
That said, scientists measure the amount of caloric energy food contains by using a device called a bomb calorimeter.
By burning the food in this device, scientists can measure the heat released to find out the number of calories in the food.
This provides a figure for the total potential energy of food. However, this is not a true reflection of how the body will use the energy from food. The body cannot always use all of the calories that people consume.
Calorie losses can happen due to:
How people burn calories will depend on their metabolism, digestion, and overall health and fitness levels.
A calorimetry machine can show how many calories people burn when resting. This is called their basal metabolic rate. The machine measures carbon dioxide, which is the waste product from food the body burns as energy. Other accurate methods of estimating calorie expenditure use air or water displacement technology.
Using these tools, people can work out an accurate number for the calories they burn during rest and activity or exercise. It is important recheck this figure every 3–6 months to understand how the body composition and calorie needs change over time.
People can use calorie-counting tools and fitness trackers to build a rough idea of how many calories they are consuming and how many they are burning. However, this will not always be completely accurate.
Are different types of fat higher or lower in calories?
A gram (g) of fat contains 9 calories , which is over twice the number of calories in carbohydrates and proteins, both of which contain 4 kcal/g .
These are rough estimates, however, since specific foods affect insulin demands, gut bacteria, and digestion and absorption differently. All of these factors affect the calories per gram of food and an individual’s metabolic rate.
Certain fats are more healthful than others. Consuming too many trans and saturated fats can raise the levels of harmful cholesterol in the body and increase the risk of heart disease.
Monounsaturated and polyunsaturated fats are good for the body. Some good sources of these fats include oily fish, nuts, seeds, and vegetables.
The body needs a certain amount of healthful fat to function properly. Research suggests that although there is no single dietary macronutrient plan that will work for everybody due to individual needs, most health experts recommend the following amount of carbohydrates, proteins, and fats for a balanced diet:
How much energy is used to construct a pound of fat tissue? - Biology
Depending on energy supply and demand, adipocytes can take up and store fat from the blood or release fat back to the blood. After eating, when energy supply is high, the hormone insulin keeps the fatty acids inside the adipocyte (Duncan et al., 2007). After a few hours of fasting, or especially during exercise, insulin levels tend to drop while other hormones such as epinephrine (otherwise called adrenaline) increase. When epinephrine binds to the adipocyte it causes lipolysis of the TAG stores in the adipocyte (Duncan et al., 2007). Lipolysis is the separation of the fatty acids from the glycerol backbone. After lipolysis, the fatty acids and glycerol can leave the adipocyte and enter the blood.
Fatty Acids In the Blood
The blood is an aqueous (water based) environment. Because fat is not water-soluble (i.e., it does not dissolve or mix well in water), a carrier protein is required to keep it evenly suspended in the blood. The primary protein carrier for fat in the blood is albumin (Holloway et. al. 2008). One albumin protein can carry multiple fatty acids through the blood to the muscle cell (Horowitz and Klein, 2000). In the very small blood vessels (capillaries) surrounding the muscle, fatty acids can be removed from albumin and taken into the muscle (Holloway et al., 2008).
Fatty Acids From the Blood into the Muscle
In order for fatty acids to get from the blood into the muscle they must cross two barriers. The first is the cell lining that makes up the capillary (called the endothelium) and the second is the muscle cell membrane (known as the sarcolemma). Fatty acid movement across these barriers was once thought to be extremely rapid and unregulated (Holloway et al., 2008). More recent research shows that this process is not nearly as rapid as once thought and that it requires special binding proteins present at the endothelium and sarcolemma to take in fatty acids (Holloway et al. 2008). Two proteins that are important for fatty acid transport into the muscle cell are FAT/CD36 and FABPpm.
The Two Fates of Fat Inside the Muscle
Once inside the muscle, a molecule called Coenzyme A (CoA) is added to the fatty acid (Holloway et al., 2008). CoA is a transport protein which maintains the inward flow of fatty acids entering into the muscle and prepares the fatty acid for two fates: 1) oxidation (a process in which electrons are removed from a molecule) to produce energy or, 2) storage within the muscle (Holloway et al. 2008, Shaw, Clark & Wagenmakers 2010). The majority (80%) of fatty acids entering the muscle during exercise are oxidized for energy while most fatty acids entering the muscle after a meal are repackaged into TAGs and stored in the muscle in a lipid droplet (Shaw, Clark & Wagenmakers, 2010). Fat that is stored inside the muscle is called intramyocellular triacylglycerol (IMTAG or intramuscular fat). The amount of IMTAG in slow twitch muscles (the slow oxidative fibers) is two to three times greater than the IMTAG stored in fast twitch muscles fibers (Shaw, Clark and Wagenmakers). Shaw and colleagues continue that even though this IMTAG content makes up only a fraction (<1% to 2%) of the total fat stores within the body, it is of great interest to exercise physiologists. This is because it is a metabolically active fatty acid substrate especially used during periods of increased energy expenditure, such as endurance exercise.
Fatty Acids Burned for Energy
Fatty acids burned for energy (oxidized) in the muscle can either come directly from the blood or from the IMTAG stores. In order for fatty acids to be oxidized, they must be transported into the cell's mitochondria. The mitochondrion is an organelle that functions like a cellular power plant. The mitochondrion processes fatty acids (and other fuels) to create a readily usable energy currency (ATP) to meet the energy needs of the muscle cell. Most fatty acids are transported into the mitochondria using a shuttle system called the carnitine shuttle (Holloway et al. 2008). The carnitine shuttle works by using two enzymes and carnitine (an amino acid-like molecule) to bring the fatty acids into the mitochondria. One of these enzymes is called carnitine palmitoyl transferase I (CPTI). CPT1 may work with one of the same proteins (FAT/CD36) used to bring fatty acids into the muscle cell from the blood (Holloway et al. 2008). Once inside the mitochondria, fatty acids are broken down through several enzymatic pathways including beta-oxidation, tricarboxylic acid cycle (TCA), and the electron transport chain to produce ATP.
Focus Paragraph: An Overview of Fat Metabolism in the Mitochondrion
Fatty acids are transported into the muscle where they are either stored (as IMTAG) or transported into the mitochondrion, which can be referred to as the fat-burning furnace in a person's body cells (as this is the only place TAG are completely broken down). As the chemical bonds in TAG molecules are broken up in metabolism they begin to lose electrons (a process called oxidation) and are picked up (a process called reduction) by electron transporters (NADH+H+ and FADH2). The electron transporters take the electrons to the electron transport chain for further oxidation, which leads to a liberation of energy that is used to produce adenosine triphosphate (ATP). Unused energy becomes heat energy to sustain the body's core temperature. This ATP synthesizing process depends upon a steady supply of oxygen, which is why this process is aptly nicknamed aerobic metabolism or aerobic respiration.
Adapted from Achten, J., and Jeukendrup, A.E. 2012.
Fatty Aid Oxidation During a Single Bout of Exercise
At the start of exercise blood flow increases to adipose tissue and muscle (Horowitz and Klein, 2000). This allows for increased fatty acid release from adipose tissue and fatty acid delivery to the muscle. Exercise intensity has a great impact on fat oxidation. Maximal fat oxidation occurs at low to moderate intensity (between 25% and 60% of maximal oxygen consumption (VO2max) (Horowitz & Klein 2000). At lower exercise intensities, most of the fatty acids used during exercise come from the blood (Horowitz & Klein 2000). As exercise increases to moderate intensity (around 60% of VO2max) the majority of fatty acids oxidized appear to come from IMTAG (Horowitz and Klein, 2000). At higher exercise intensities (>70 % VO2max), total fat oxidation is reduced to levels lower than that of moderate intensity (Horowitz and Klein, 2000). This reduced rate of fatty acid oxidation is coupled with an increase in carbohydrate breakdown to meet the energy demands of the exercise (Horowitz & Klein, 2000).
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 (Horowitz and Klein, 2000). 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. Two mechanisms are thought to reduce CPT1 activity during intense exercise. As stated above, 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 (Horowitz and Klein, 2000). Malonyl CoA can bind to and inhibit the activity of CPT1 (Achten and Jeukendrup, 2012).
Another way intense exercise may reduce CPT1 activity is by changes in cellular pH. The cellular pH is the measure of the acidity in the cell's cytoplasm (fluid) in terms of the activity of hydrogen ions. As exercise intensity increases the muscle becomes more acidic. Increased acidity (which means the pH is lowering) can also inhibit CPT1 (Achten and Jeukendrup, 2012). The reason for the increased acidity during high intensity exercise is not because of lactic acid formation as once thought. Instead, acidosis increases because the muscle is using more ATP at the contracting muscle fibers (just outside of the mitochondria), and the splitting of ATP releases many hydrogen ions into the cellular fluid (sarcoplasm) leading to the acidosis in the cell (Robergs, Ghiasvand and Parker, 2004).
Too much emphasis is often placed on percent of fatty acid contribution of Calories burned during a single bout of exercise. Recovery from a bout of exercise as well as training adaptations to repeated bouts are important to consider when working with clients with fat loss goals.
Focus Paragraph. The Splitting of Adenosine Triphosphate (ATP)
ATP is split by water (called hydrolysis) with the aid of the ATPase enzyme. During intense exercise there is a high level of hydrolysis of ATP by the muscles fibers. Each ATP molecule that is split releases a hydrogen ion, which is the cause of acidosis in the cell (Robergs, Ghiasvand and Parker, 2004). This acidosis can slow the carnitine shuttle that moves fatty acids into the mitochondria for oxidation.
Energy/Fat Used During Recovery
After exercise an individual burns more energy, which is primarily used for muscle cell recovery and glycogen replacement with the muscle. This elevated metabolic rate is termed excess post exercise oxygen consumption (EPOC). EPOC appears to be greatest when exercise intensity is high (Sedlock, Fissinger and Melby, 1989). For example, EPOC is higher after high intensity interval training (HIIT) compared to exercise for a longer duration at lower intensity (Zuhl and Kravitz, 2012). EPOC is also notably observed after resistance training (Ormsbee et al. 2009), because it disturbs the working muscle cells' homeostasis to a great degree resulting in a larger energy requirement after exercise to restore the contracting muscle cells to pre-exercise levels. EPOC is particularly elevated for a longer period of time after eccentric exercise due to additional cellular repair and protein synthesis needs of the muscle cells (Hackney, Engels, and Gretebeck, 2008). Many studies also show that during the period of EPOC, fat oxidation rates are increased (Achten and Jeukendrup, 2012, Jamurtas et al. 2004, and Ormsbee et al., 2009). Comparatively, fatty acid use during high intensity bouts of exercise such as HIIT and resistance training may be lower as compared to moderate intensity endurance training however, high intensity exercise and weight training may make up for this deficit with the increased fatty acid oxidation through EPOC.
Focus Paragraph. Comparison of Effect of Light Exercise versus Heavy Exercise on EPOC
Some key factors that contribute to the elevated post-exercise oxygen consumption during high intensity exercise include the replenishment of creatine phosphate, the metabolism of lactate, temperature recovery, heart rate recovery, ventilation recovery, and hormones recovery (Sedlock, Fissinger and Melby, 1989).
Adaptations to Exercise that Improve Fat Usage
Trained people are able to use more fat at both the same absolute (speed or power output) and relative (% of VO2 Max) exercise intensity than untrained people (Achten and Jeukendrup, 2012). Interestingly, lipolysis (breakdown of fats to release fatty acids) and fat release from adipocytes is not different between untrained and trained people (Horowitz and Klein, 2000). This suggests that the improved ability to burn fat in trained people is attributed to differences in the muscle's ability to take up and use fatty acids and not the adipocyte's ability to release fatty acids. The adaptations that enhance fat usage in trained muscle can be divided into two categories: 1) those that improve fatty acid availability to the muscle and mitochondria and 2) those that improve the ability to oxidize fatty acids.
Fatty acid availability
One way exercise can improve fatty acid availability is by increasing fatty acid transport into the muscle and mitochondria. As mentioned above, specific proteins mediate transport of fatty acids into the muscle and mitochondria. Exercise training has been shown to increase the amount of FAT/CD36 on the muscle membrane and mitochondrial membrane (Holloway et al. 2008) and has been shown to increase CPT1 on the mitochondrial membrane (Horowitz and Klein 2000). Together these proteins will improve fat transport into the muscle and mitochondria to be used for energy.
Exercise may also cause changes in the intramuscular lipid droplet (that contains IMTAGs). The intramuscular lipid droplet is mostly found in close proximity to the mitochondria (Shaw, Clark and Wagenmakers, 2010). Having IMTAGs close to the mitochondria makes sense for efficient IMTAG usage so that fatty acids released from the lipid droplet do not have to travel far to reach the mitochondria. Exercise training can further increase IMTAG availability to the mitochondria by causing the lipid droplet to conform more closely to the mitochondria. This increases surface area for more rapid fatty acid transport from the lipid droplet into the mitochondria (Shaw, Clark and Wagenmakers, 2010). Exercise training may also increase the total IMTAG stores (Shaw, Clark and Wagenmakers, 2010).
Another training adaptation that may improve fatty acid availability is increased number of small blood vessels within the muscle (Horowitz and Klein, 2000). Remember, fatty acids can enter the muscle through the very small blood vessels. Increasing the number of capillaries around the muscle will allow for increased fatty acid delivery into the muscle.
Fatty acid breakdown
IMTAGs are a readily available substrate for energy during exercise because they are already located in the muscle. Trained athletes have an increased ability to use IMTAG efficiently during exercise (Shaw, Clark and Wagenmakers, 2010). Athletes also tend to have larger IMTAG stores than lean sedentary individuals. Overweight and obese individuals, interestingly, also have high levels of IMTAG but are not able to use IMTAGs during exercise like athletic individuals can (Shaw, Clark and Wagenmakers, 2010).
So what causes the reduced ability to use IMTAGs in obese individuals? A logical guess would be that they have dysfunctional mitochondria that cannot use fatty acid properly. Research has shown however, that the mitochondria from muscles of obese individuals are not dysfunctional (Holloway et al. 2008). Instead, the number of mitochondria per unit of muscle (mitochondrial density) is reduced in an obese population (Holloway et al. 2008). Reduced mitochondrial density is a more likely explanation for reduced ability to use fat for energy in obese individuals. An important adaptation to exercise training is increased mitochondrial density (Horowitz and Klein 2000 Zuhl and Kravitz, 2012). Increasing mitochondrial density would improve the ability to use fat and benefit individuals with fat loss goals.
Endurance exercise training is an effective way to improve the body's fatty acid usage abilities by improving the availability of fatty acids to the muscle and mitochondria and by increasing fatty acid oxidation (Horowitz and Klein, 2000). HIIT training has also been shown to result in similar fat burning adaptations while requiring fewer workouts and less total time commitment (Zuhl and Kravitz, 2012)
Rather than trying to maximize fat oxidation in a single bout of exercise, it is recommended that the personal trainer design a workout program aimed at causing muscle adaptations described above to improve fatty acid oxidation ability. The exercise professional should include interval and endurance training programs as these have been shown to improve mitochondrial density and fat oxidation (Zuhl and Kravitz, 2012). In addition, regular progressively increasing programs of resistance training are encouraged as this training will enhance EPOC and post-workout fat oxidation. Also, the personal trainer should encourage the client to engage in low to moderate intensity exercise (such as walking and cycling) on off hard workout days in order to enhance caloric deficit and support muscle adaptions between training days.
High intensity interval training (HIT) with variable recovery (modified from Seiler and Hetlelid, 2005)
High intensity interval training uses exercise intensity that corresponds to the individual's VO2max. Seiler and Hetlelid (2005) exercised subjects at their highest running speeds for 4 minutes with 1, 2 or 4 minutes of recovery and repeated this interval 6 times. The trainer can do HIT with clients with many different modes of exercise, simply having the client maintain his/her maximal sustained exercise effort for the 4 minutes. The idea of a systematic variation of the recovery is a very novel approach to interval training and certainly warrants more research.
Have the client complete up to 6 sets of 4-minute bouts at a maximal sustained workout effort and vary each recovery period to be 1 min, 2 min or 4 minutes at a light intensity (client's self-selected intensity).
Sprint interval training (SIT) (Modified from Burgomaster et al. 2008)
Sprint interval training is repeated all-out (maximum effort) bouts of exercise. The maximal effort generated in SIT necessitates a small work to larger rest ratio. That is, SIT is often done with a 30-second all-out effort followed by a 4.5-minute rest period. The trainer can do SIT with clients using a variety of different modes of exercise including the stationary bike, elliptical cross-trainer and rowing machine. The resistance on the chosen mode of exercise should be relatively challenging during the work bout. During the sprint interval the trainer should verbally encourage the client to maintain maximal effort throughout the bout. During the recovery phase between bouts the client is encouraged to continue moving on the exercise machine at a very low self-selected light effort.
Have the client complete 3 to 4 bouts of 30-second all-out bouts bout with 4.5 minutes of active recovery between bouts.
This is a very challenging workout. Modifications may be required to match the individual's fitness level needs.
Resistance Training (RT) (modified form Melby et al. 1993)
This workout is a slight modification of others that have been shown to cause EPOC (Melby et al. 1993) and increased fat usage (Jamurtas et al. 1993) in time period after the exercise. This is total body weight lifting workout that uses 10 exercises. The exercises are arranged in 5 pairs so that each pair of exercise is completed before resting and moving on to the next pair. The whole circuit of exercise should be completed up to 6 times. The rest interval between pairs should be no longer than 2 minutes. The resistance used on each exercise should allow the client to lift 8 to 12 repetitions.
o Pair 1
o Bench press
o Bent over row
o Pair 2
o Split squat (Right leg forward)
o Split squat (Left leg forward)
o Pair 3
o Military press
o Pair 4
o Biceps curls
o Triceps extensions
o Pair 5
o Half squat
o Lateral raises
As with any workout, exercise modifications or substitutions may be necessary to fit individual's fitness needs and abilities.
Tabata-inspired interval training (modified form Tabata et al., 2006)
Tabata-style intervals use 20 seconds of high-intensity work followed by 10 seconds of rest, repeated up to eight times. Tabata-style training can use cardiovascular equipment such as the treadmill, rowing machine or stationary bike, or in calisthenics such as burpees, mountain climbers or body-weight squats. During the rest interval, keep the client moving to avoid blood pooling in the lower extremities. This will also help prevent the client from feeling queasy or faint.
Have the client perform complete three sets of Tabata intervals, resting 3 minutes between sets. Use burpees for the first set, the stationary bike for the second and the rowing machine for the third. Workout should last about 21 minutes.
This type of exercise has been shown to be effective at improving VO2max. Encourage the client maintain a challenging effort during this workout. The personal trainer should provide verbal encouragement to help the client do this.
Moderate intensity steady-state exercise (MIR)
Light-to-moderate exercise should be encouraged on days when the client is recovering from one of the more intense condition workouts provided here. This exercise should be restorative, allowing for the client's body to promote new muscle adaptations they have gaining from the more intense training.
Walking is a great way to implement this workout. Encourage the client to walk around their neighborhood or local park for 30 minutes to 1 hour. The walking pace should be that which the client can sustain a conversation.
Mike Deyhle, B.S, CSCS, is an Exercise Science masters student at the University of New Mexico, Albuquerque. He is interested in neural and skeletal muscular physiology especially with respect to skeletal muscular damage, metabolism, fatigue, and exercise training/detraining.
Christine Mermier, Ph.D. is an assistant professor and exercise physiology laboratory director in the exercise science Program at UNM. Her research interests include the effect of exercise in clinical patients, women, and aging populations, and high altitude physiology.
Len Kravitz, PhD, is the program coordinator of exercise science and a researcher at the University of New Mexico, Albuquerque, where he won the Outstanding Teacher of the Year award. He has received the prestigious Can-Fit-Pro Lifetime Achievement Award and American Council on Exercise Fitness Educator of the Year.
Achten, J., & Jeukendrup, A.E. (2012). Optimizing fat oxidation through exercise. Nutrition. 20, 7-8.
Burgomaster, K.A., Howarth, K.R., Phillips, S.M., Rakobowchuk, M., et al. (2008). Similar metabolic adaptations during exercise after low volume sprint interval and traditional endurance training in humans. Journal of Applied Physiology, 1, 151-160.
Duncan, R.E, Ahmadian, M., Jaworski, K., Sarkadi-Nagy, E., & Sul, H.S. (2007). Regulation of lipolysis in adipocytes. Annual Review of Nutrition. 27, 79-101.
Hackney, K.J., Engels, H.J., and Gretebeck, R.J. (2008). Resting energy expenditure and delayed-onset muscle soreness after full-body resistance training with an eccentric concentration. Journal of Strength and Conditioning Research. 22(5):1602-1609.
Holloway, G.P., Luiken, J.J.F.P., Glatz, J.F.C., Spriet, L.L., & Bonen, A. (2008). Contribution of FAT/CD36 to the regulation of skeletal muscle Fatty acid oxidation: an overview. Acta Physiologica, 192, 293-309.
Horowitz, J.F, and Klein, S. (2000.) Lipid metabolism and endurance exercise. American Journal of Clinical Nutrition. 72 (suppl), 558S-563S.
Jamurtas, A.Z, Koutedkis, Y., Paschalis, V., Tafa, T, Yfanti, C., Tsiokanos, A, Koukoulis, G., et al. (2004). The effect of a single bout of exercise on resting energy expenditure and respiratory exchange ratio. European Journal of Applied Physiology. 92: 393-398.
Melby, C., Scholl, C., Edwards, G., and Bullough, R. (1993). Effect of acute resistance exercise on post-exercise energy expenditure and resting metabolic rate. Journal of Applied Physiology, 75, 1847-1853.
Ormsbee, M.J, Choi, M.D, Medlin, J.K, Geyer, G.H, Trantham, L.H. Dubis, G.S, and Hickner, R.C. (2009). Regulaton of Fat metabolism during resistance exercise in sedentary lean and obese men. Journal of Applied Physiology, 106, 1529-1537.
Robergs RA, Ghiasvand F, and Parker D. (2004). Biochemisty of exercise-induced metabolic acidosis. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology. 287 (3), 502-516.
Sedlock, D.A., Fissinger, J.A., and Melby, C.L. (1989). Effect of exercise intensity and duration on postexercise energy expenditure. Medicine and Science in Sports and Exercise, 21(6), 662-666.
Seiler, S., and Hetlelid, K.J. (2005). The impact of rest duration on work intensity and RPE during interval training. Medicine & Science in Sports & Exercise, 37(9), 1601-1607.
Shaw, C.S, Clark, J., Wagenmakers A.J.M. (2010). The effect of exercise and nutrition on intramuscular fat metabolism and insulin sensitivity. Annual Review for Nutrition. 30, 13-34.
Tabata, I., Nishimura, K., Kouzaki, M., Yuusuke, H., Ogita, F., Miyachi, M., & Yamamoto, K. (1996). Effects of Moderate-intensity endurance and High-intermittent Training on Anaerobic Capacity and VO2max. Medicine and Science in Sports and Exercise, 28(10), 1327-1330.
How Fat Cells Work
When you are not eating, your body is not absorbing food. If your body is not absorbing food, there is little insulin in the blood. However, your body is always using energy and if you're not absorbing food, this energy must come from internal stores of complex carbohydrates, fats and proteins. Under these conditions, various organs in your body secrete hormones:
- pancreas - glucagon
- pituitary gland - growth hormone
- pituitary gland - ACTH (adrenocorticotropic hormone)
- adrenal gland - epinephrine (adrenaline)
- thyroid gland - thyroid hormone
These hormones act on cells of the liver, muscle and fat tissue, and have the opposite effects of insulin.
When you are not eating, or you are exercising, your body must draw on its internal energy stores. Your body's prime source of energy is glucose. In fact, some cells in your body, such as brain cells, can get energy only from glucose.
The first line of defense in maintaining energy is to break down carbohydrates, or glycogen, into simple glucose molecules -- this process is called glycogenolysis. Next, your body breaks down fats into glycerol and fatty acids in the process of lipolysis. The fatty acids can then be broken down directly to get energy, or can be used to make glucose through a multi-step process called gluconeogenesis. In gluconeogenesis, amino acids can also be used to make glucose.
In the fat cell, other types of lipases work to break down fats into fatty acids and glycerol. These lipases are activated by various hormones, such as glucagon, epinephrine and growth hormone. The resulting glycerol and fatty acids are released into the blood, and travel to the liver through the bloodstream. Once in the liver, the glycerol and fatty acids can be either further broken down or used to make glucose.
Losing Weight and Losing Fat
Your weight is determined by the rate at which you store energy from the food that you eat, and the rate at which you use that energy. Remember that as your body breaks down fat, the number of fat cells remains the same each fat cell simply gets smaller.
Risk Factors - Overweight and Obesity
There are many risk factors for overweight and obesity. Some risk factors can be changed, such as unhealthy lifestyle habits and environments. Other risk factors, such as age, family history and genetics, race and ethnicity, and sex, cannot be changed. Heathy lifestyle changes can decrease your risk for developing overweight and obesity.
Lack of physical activity, unhealthy eating patterns, not enough sleep, and high amounts of stress can increase your risk for overweight and obesity.
Lack of physical activity
Lack of physical activity due to high amounts of TV, computer, videogame or other screen usage has been associated with a high body mass index . Healthy lifestyle changes, such as being physically active and reducing screen time, can help you aim for a healthy weight.
Unhealthy eating behaviors
Some unhealthy eating behaviors can increase your risk for overweight and obesity.
- Eating more calories than you use. The amount of calories you need will vary based on your sex, age, and physical activity level. Find out your daily calorie needs or goals with the Body Weight Planner.
- Eating too much saturated and trans fats
- Eating foods high in added sugars
Visit Heart-healthy eating for more information about healthy eating patterns.
Not enough sleep
Many studies have seen a high BMI in people who do not get enough sleep. Some studies have seen a relationship between sleep and the way our bodies use nutrients for energy and how lack of sleep can affect hormones that control hunger urges. Visit our Sleep Deprivation and Deficiency Health Topic for more information about lack of sleep.
High amounts of stress
Acute stress and chronic stress affect the brain and trigger the production of hormones, such as cortisol, that control our energy balances and hunger urges. Acute stress can trigger hormone changes that make you not want to eat. If the stress becomes chronic, hormone changes can make you eat more and store more fat.
Childhood obesity remains a serious problem in the United States, and some populations are more at risk for childhood obesity than others. The risk of unhealthy weight gain increases as you age. Adults who have a healthy BMI often start to gain weight in young adulthood and continue to gain weight until 60 to 65 years old, when they tend to start losing weight.
Many environmental factors can increase your risk for overweight and obesity:
- social factors such as having a low socioeconomic status or an unhealthy social or unsafe environment in the neighborhood
- built environment factors such as easy access to unhealthy fast foods, limited access to recreational facilities or parks, and few safe or easy ways to walk in your neighborhood
- exposure to chemicals known as obesogens that can change hormones and increase fatty tissue in our bodies
Genetic studies have found that overweight and obesity can run in families, so it is possible that our genes or DNA can cause these conditions. Research studies have found that certain DNA elements are associated with obesity.
Did you know obesity can change your DNA and the DNA you pass on to your children? Learn more about these DNA changes.
Eating too much or eating too little during your pregnancy can change your baby’s DNA and can affect how your child stores and uses fat later in life. Also, studies have shown that obese fathers have DNA changes in their sperm that can be passed on to their children.
Overweight and obesity is highly prevalent in some racial and ethnic minority groups. Rates of obesity in American adults are highest in blacks, followed by Hispanics, then whites. This is true for men or women. While Asian men and women have the lowest rates of unhealthy BMIs, they may have high amounts of unhealthy fat in the abdomen. Samoans may be at risk for overweight and obesity because they may carry a DNA variant that is associated with increased BMI but not with common obesity-related complications.
In the United States, obesity is more common in black or Hispanic women than in black or Hispanic men. A person’s sex may also affect the way the body stores fat. For example, women tend to store less unhealthy fat in the abdomen than men do.
Overweight and obesity is also common in women with polycystic ovary syndrome (PCOS). This is an endocrine condition that causes large ovaries and prevents proper ovulation, which can reduce fertility.
References: BCAA catabolism in brown fat controls energy homeostasis through SLC25A44. Yoneshiro T, Wang Q, Tajima K, Matsushita M, Maki H, Igarashi K, Dai Z, White PJ, McGarrah RW, Ilkayeva OR, Deleye Y, Oguri Y, Kuroda M, Ikeda K, Li H, Ueno A, Ohishi M, Ishikawa T, Kim K, Chen Y, Sponton CH, Pradhan RN, Majd H, Greiner VJ, Yoneshiro M, Brown Z, Chondronikola M, Takahashi H, Goto T, Kawada T, Sidossis L, Szoka FC, McManus MT, Saito M, Soga T, Kajimura S. Nature. 2019 Aug 21. doi: 10.1038/s41586-019-1503-x. [Epub ahead of print]. PMID: 31435015.
Funding: NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and National Cancer Institute (NCI) Edward Mallinckrodt Jr. Foundation American Diabetes Association Japan Agency for Medical Research and Development Japan Society for the Promotion of Science.
The 3,500 Calorie Rule
Most people have heard the notion that 3,500 calories is equivalent to one pound of fat. That being said, the caloric deficit or surplus of 3,500 doesn’t necessarily equate to a one pound weight loss or gain.
The 3,500-calorie rule only pertains to the gain or loss of one pound of body fat, which unfortunately does not apply to other aspects of body weight. In other words, losing one pound of body fat does not mean you are going to lose one pound of all-around weight. This is largely because other systems are affected by changes in calories consumed. If you drop calories mostly from carbohydrates, you may be losing more total "weight" than one pound of fat, simply because the drop in carbohydrates also creates some water loss.
People often experience the "woosh" phenomenon of weight loss. This is the scenario where you are in a calorie deficit but see no changes in weight for days or weeks at a time. Then suddenly, one morning you wake up a few pounds lighter. This can be attributed to the fact that with a calorie deficit you ARE losing fat. However, as the fat cells release triglycerides for energy use, they can take up water in it's place. So even though fat is being burned, weight stays the same becuse temporarily the fat cells hold onto water.
This is why expecting one pound loss for every 3.500 calories burned can create issues. Even if a pound of fat is lost we see wild fluctuations from fat cells holding water, changes in carb and sodium intake, how much food is in your stomach or bowels and so forth. "Weight" takes more forms than just fat!
So. in order to change actual body composition you need to see changes in actual tissue, body fat levels and skeletal muscle/lean body mass (LBM).
These aspects vary, however, from person to person depending on gender, diet, and starting body fat percentage.
For instance, women use more fat for fuel than men and lose less LBM. Diets with sufficient protein and exercise regimens with adequate resistance training spare LBM and therefore shed more fat. And finally, people with higher levels of body fat use more fat for fuel, and less LBM.
How much energy is used to construct a pound of fat tissue? - Biology
Sugar metabolism is the process by which energy contained in the foods that we eat is made available as fuel for the body. The body&rsquos cells can use glucose directly for energy, and most cells can also use fatty acids for energy. Glucose and fructose are metabolised differently, and when they are consumed in excess they may have different implications for health.
Looking at glucose first &ndash when food is consumed, there is a corresponding rise and subsequent fall in blood glucose level, as glucose is absorbed from the gastrointestinal tract into the blood and then taken up into the cells in the body.
Glucose in the blood stimulates the pancreas to release insulin, which then triggers uptake of glucose by cells in the body (e.g. muscle cells) causing blood glucose to return to base levels. Insulin will turn off fat burning and promote glucose burning as the body&rsquos primary fuel source. Any excess glucose ends up being stored as glycogen in the muscles, and it can also be stored as lipid in the fat tissue.
Fructose is also taken up into the blood from the gut, but in this case, the liver serves as a pre-processing organ that can convert fructose to glucose or fat. The liver can release the glucose and fat into the blood or store it as glycogen or fat depots, which, if sugars are consumed in excess, may lead to fatty liver disease and also increase risk for diabetes and cardiovascular disease.
There are also some noted interaction effects between glucose and fructose, in that glucose enables fructose absorption from the gut, while fructose can accelerate glucose uptake and storage in the liver.
If the sugar comes with its inherent fibre (as with whole fruit) then up to 30% of this sugar will not be absorbed. Instead, it will be metabolised by the microbes in the gut, which may improve microbial diversity and help prevent disease. The fibre will also mean a slower rise in blood glucose, which has shown to have positive health effects.
It is easy to over-consume sugar
It is easy to over-consume sugar in juice and sweet drinks, as they contain mostly water and sugar. One glass of orange juice can contain concentrated sugar from five or six whole oranges. And while it is easy to drink that much sugar, you would be less likely to eat that many oranges in one go.
Fizzy drinks do not make you feel full as quickly as foods do. This makes them easy to over-consume. And a small fizzy drink contains nine teaspoons of added sugar, so drinking just one can means that you have almost reached your recommended maximum intake for that whole day.
A broad term meaning any bodily process in which the liver is injured or does not work as it is supposed to. In this website we focus on liver diseases in which the diet hurts the liver
Any sugar added in preparation of foods, either at the table, in the kitchen or in the processing plant. This may include sucrose, high fructose corn syrup and others.
Usually shortened to just diabetes. Sometimes called sugar diabetes. Look at Type 1 Diabetes and Type 2 Diabetes for more information
A type of fat in our body and our food. Three fatty acids are combined with another chemical called glycerol to form a triglyceride.
Sugars are chemicals made of carbon, hydrogen, and oxygen found which taste sweet and are found in food. They are an important part of what we eat and drink and of our bodies. On this site, sugar is used to mean simple sugars (monosaccharides) like fructose or glucose, and disaccharides like table sugar (sucrose). Sucrose is two simple sugars stuck together for example (see Table sugar). Sugars are a type of carbohydrate. Carbohydrates are energy sources for our bodies Sugars enter the blood stream very quickly after being eaten.
Glucose is a sugar we eat. It is found in starch. It is the main fuel for our bodies. It is the sugar measured when we have a blood test to measure the blood sugar.
The pancreas is an internal organ that helps us digest our food by making insulin and other chemicals.
One of the three major groups of nutrients we eat. Much of this website is related to problems associated with too much fat storage in the body. Each gram of fat produces 9 calories of energy if burned by the body as fuel. Fat can be stored in many places in the body. We generally think of fat as under the skin (subcutaneous), but the fat that may be most damaging to us is the fat stored in the liver and around the organs of the abdomen (intrahepatic and visceral or abdominal or intra-abdominal)
A sugar that we eat. Also called fruit sugar. Most fructose comes in sucrose (table sugar, cane sugar, beet sugar), or from high-fructose corn syrup.
The largest internal organ. It weighs about three to four pounds and is located under the lower edge of the ribs on the right side. It helps us digest our food and remove toxins from our blood. "Hepat" in a word means liver, so an "hepato-toxin" is a liver poison or something that can cause damage to the liver
Insulin is a messenger released from the pancreas after eating, which shunts energy (glucose or triglycerides) from the blood into fat cells for storage. Insulin is given to some people with diabetes to lower the blood glucose it leaves the blood and enters the fat cell for storage.
SugarScience is the authoritative source for evidence-based, scientific information about sugar and its impact on health.