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Optimal fat oxidation

Optimal fat oxidation

Exercise oxidaton in sedentary patients: procedures based on short Optimal fat oxidation min steps underestimate carbohydrate Diet and exercise and overestimate lipid oxidation. Article CAS Fxt PubMed Central Google Scholar Leckey J, Burke J, Morton J, Hawley J. General sports nutrition topics can be found here. As soon as exercise begins, fatty acids are mobilised. Want to know more about nutrition for running. Relationship between fat oxidation and lactate threshold in athletes and obese women and men. Optimal fat oxidation

Optimal fat oxidation -

Like most things in life, the better you understand a subject, the more likely you are to be able to apply its principles and experience success. As you probably know, fat cells adipose tissue are the primary storage site of body fat, and they are in a constant state of turnover, meaning that fat is continuously entering or exiting the cell-based of several factors including hormones, nutrition, and metabolism.

Fat is stored in adipose tissue as triglycerides. This process of stored fatty acids being released into the bloodstream to be used for energy production is known as lipolysis. In order for your body to burn the fatty acids, they must first be separated from the glycerol molecule.

For this to happen, an enzyme called lipase cleaves the fatty acids from the glycerol via hydrolysis. After separation and release from the fat cell, the fatty acids then enter the bloodstream where they circulate bound to a protein called serum albumin.

The reason fatty acids require the shuttling actions of albumin is due to the fact that blood is composed mostly of water. As such, albumin serves as the protein carrier that taxis fatty acids through the bloodstream to the muscle cell when they are needed. Each albumin protein can carry with it several fatty acids.

As the fatty acids enter the cell, they are stored in the cytoplasm of the cell, which is the thick solution that fills the inner regions of the cell. In order for them to be converted into ATP i. Now, the actual process of converting the fatty acids to ATP is called beta-oxidation.

For the purposes of this article, just know that the beta-oxidation is the process by which your body obtains energy from fatty acids. Fatty acids are shuttled from the cytoplasm into the mitochondria via the actions of a substance called carnitine, which many of you have probably seen in your favorite fat burning supplements, such as Steel Sweat.

Once converted into ATP, the energy can then be used by the cell to power it to perform whatever sort of activity you might be performing weight lifting, cardio, walking, laying on the sofa, etc. In certain cases i. starvation, fasting, etc. high amounts of fatty acids are broken down and subsequently flood the mitochondria.

These ketone bodies are rich in energy and the preferred source of energy for people following low-carb, ketogenic, and zero carb diets. Since most people entering the fitness space are wanting to lose fat, it would make sense to discuss what things we can do to enhance fat oxidation and accelerate fat loss.

One of these ways is by reducing caloric expenditure, i. creating a calorie deficit. This is why in order to lose fat, cutting calories is one of the main things you have to do.

Weight loss ultimately boils down to energy balance in the body, i. calories in vs calories out. Earlier in this article, we discussed the importance of hormone-sensitive lipase in the liberating of stored fatty acids from adipose tissue. Insulin is the hormone in your body that is responsible for driving nutrients into your cells, including muscle and fat cells, which can then be used for energy production.

The main macronutrient that causes insulin levels to rise is carbohydrates and seeing that insulin effectively shuts off the fat burning process, maintaining low levels of insulin is essential to maximizing fat burning. This is why so many ketogenic, low carb, no carb diets restrict carbohydrate intake.

You can still have your carbs and burn body fat, but it requires some proper nutritional selections on your part.

Simple sugars create larger insulin spikes in the body than complex carbohydrates or protein. As we stated above, increasing your calories out is one of the ways you can tip energy balance in favor of fat loss.

This, of course, is accomplished through exercise, and we can maximize fat burning by performing the right types of exercise. Many companies have recognized the potential and have jumped on the opportunity and are now selling tools that help you monitor fat burning and supplements that supposedly increase fat burning.

But do these things really work? Are there easy ways to increase fat burning? Are there easy ways to become lean? In a series of articles on mysportscience. com I want to evaluate the following:. What is fat burning?

And how is it regulated in the body? What is the evidence for each of these reasons? If we want to burn fat, what are the best methods to do this? Can we come up with some general advice? Fat burning or fat oxidation the term preferred by scientists occurs on a daily basis in virtually all cells of our body.

Fat is stored in the form of triglycerides. A triglyceride is made up of 3 fatty acids that are held together by a glycerol backbone hence the name tri-glyceride. Only fatty acids can be used as a fuel.

Therefore triglycerides first need to be broken down into fatty acids. The fatty acids then need to be broken down further. Fat oxidation refers to the process of breaking down fatty acids.

To oxidize fat one needs:. Healthy mitochondria small structures in cells that serve as the power plants of the cells. In these power plants, energy is generated for muscle contraction by burning fuel, using oxygen and producing carbon dioxide.

Supply of fatty acids these are supplied from triglycerides and fatty acids in the blood, as well as triglycerides stored in the muscle itself. Oxygen transported to the muscle by blood. If fatty acids are supplied to healthy mitochondria and oxygen is present, fatty acids will be broken down to carbon dioxide.

This process is not too dissimilar form burning a log in a fire. You need the fireplace, some wood and oxygen. As mentioned above, the fatty acids we burn can come from different sources. Fat is stored as triglycerides in different tissues of the body, including muscle.

The vast majority of triglycerides in our bodies can be found in fat cells. When we eat, fat will eventually appear in the blood stream and can potentially be taken up and used in the muscle.

When we exercise, our need for energy increases dramatically because muscle contraction is an energy consuming process.

Fat Loss describes a decrease in fat mass at the whole body level. We saw that fat utilisation is largely dictated by mitochondrial capacity. Instead, Fat loss is the result of maintaining a sufficient caloric deficit over time. As I like to say, if you wish to lose fat or lose weight, you should eat like an adult and sleep like a baby!

San-Millan et al. Kindal A Shores , Metabolic Adaptations to Endurance Training: Increased Fat Oxidation , Honours Thesis. Fat oxidation is the process by which the body breaks down fats triglycerides into smaller molecules, such as free fatty acids and glycerol, which can then be used as a source of energy.

Fat oxidation increases mainly through training and via an increase in mitochondrial capacity. This has a sparing effect on glycogen stores allowing the athlete to perform better later in the race.

Stable isotope techniques: This involves consuming a small amount of a labeled form of fat, such as octanoate, and then measuring the labeled carbon in exhaled breath or urine to determine the rate of fat oxidation.

Blood tests: Measuring the levels of certain fatty acids and ketone bodies in the blood can also provide an indication of fat oxidation.

Body composition analysis: Dual-energy X-ray absorptiometry DXA and bioelectrical impedance analysis BIA are two common methods to measure body composition, including body fat percentage, can also give an indication of the rate of fat oxidation.

Please note that these methods have different level of accuracy and some of them may require professional assistance. By performing more low intensity training and developing your mitochondrial density. Not directly. However increasing your activity levels will be beneficial for both your performance and your health.

Maintaining a reasonable caloric deficit over time is the best way to lose weight and body fat. Your email address will not be published. Save my name, email, and website in this browser for the next time I comment.

What is Fat Oxidation? When does Fat Oxidation occur? How can I measure Fat Oxidation? How can I Increase Fat Oxidation? Will Fat Oxidation help me lose Body Fat? Share This. Next Post High Lactate Levels During Exercise: What Causes Them?

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Rent this oxidatio via DeepDyve. Institutional subscriptions. Goodpaster BH, Sparks LM. Metabolic flexibility in Relaxation techniques for controlling hypertension and oxifation.

Diet and exercise Metab. Article Oxiddation PubMed PubMed Central Google Scholar. Wu H, Ballantyne CM. Metabolic inflammation and insulin oxidxtion in obesity. Circ Res. Fava MC, Agius R, Fava Oxidatioon. Obesity and cardio-metabolic health [published correction Respiratory health check-ups in Br J Hosp Optimal fat oxidation Lond.

Br J Hosp Med Lond. Pxidation PubMed Google Scholar. Barnes AS. The epidemic of obesity and diabetes: trends and treatments.

Tex Heart Inst J. PubMed PubMed Central Google Scholar. Powell-Wiley TM, Poirier P, Burke LE, et al. Obesity and cardiovascular disease: a scientific statement from the American Heart Association.

Article PubMed PubMed Central Google Scholar. Pedersen BK, Saltin B. Exercise as medicine - evidence for prescribing exercise as therapy in 26 different chronic diseases.

Scand J Med Sci Sports. Colberg-Ochs SR, Ehrman JK, Johann J, Kokkinos P, Liguori G, Pack KR. Exercise prescription for individuals with metabolic disease and cardiovascular disease risk factors. In: Diebe D, Ehrman JK, Liguori G, Magal M, editors. Beijing: Wolters Kluwer; Google Scholar. World Health Organization.

WHO guidelines on physical activity and sedentary behavior. World Health Organization Website. Brun JF, Myzia J, Varlet-Marie E, de Mauverger ER, Mercier J.

Beyond the calorie paradigm: taking into account in practice the balance of fat and carbohydrate oxidation during exercise? Swinburn B, Ravussin E. Energy balance or fat balance? Am J Clin Nutr. Article CAS PubMed Google Scholar. Schutz Y. Macronutrients and energy balance in obesity.

Tremblay A. Differences in fat balance underlying obesity. Int J Obes Relat Metab Disord. PubMed Google Scholar. Chávez-Guevara IA, Urquidez-Romero R, Pérez-León JA, González-Rodríguez E, Moreno-Brito V, Ramos-Jiménez A. Chronic effect of fatmax training on body weight, fat mass, and cardiorespiratory fitness in obese subjects: a meta-analysis of randomized clinical trials.

Int J Environ Res Public Health. Maunder E, Plews DJ, Kilding AE. Contextualising maximal fat oxidation during exercise: determinants and normative values. Front Physiol. Riddell MC, Jamnik VK, Iscoe KE, Timmons BW, Gledhill N.

Fat oxidation rate and the exercise intensity that elicits maximal fat oxidation decreases with pubertal status in young male subjects. J Appl Physiol Frandsen J, Amaro-Gahete FJ, Landgrebe A, et al. The influence of age, sex and cardiorespiratory fitness on maximal fat oxidation rate.

Appl Physiol Nutr Metab. Filipovic M, Munten S, Herzig KH, Gagnon DD. Maximal fat oxidation: comparison between treadmill, elliptical and rowing exercises. J Sports Sci Med. Chávez-Guevara IA, Hernández-Torres RP, Trejo-Trejo M, et al. Exercise fat oxidation is positively associated with fa fatness in men with obesity: defying the metabolic flexibility paradigm.

Amaro-Gahete FJ, Sanchez-Delgado G, Ara I, Ruiz J. Cardiorespiratory fitness may influence metabolic inflexibility during exercise in obese persons. J Clin Endocrinol Metab. Haufe S, Engeli S, Budziarek P, et al. Determinants of exercise-induced fat oxidation in obese women and men. Horm Metab Res.

Peric R, Di Pietro A, Myers J, Nikolovski Z. A systematic comparison of commonly used stoichiometric equations to estimate fat oxidation during exercise in athletes. J Sports Med Phys Fit. Amaro-Gahete FJ, Sanchez-Delgado G, Alcantara JMA, et al.

Impact of data analysis methods for maximal fat oxidation estimation during exercise in sedentary adults. Eur J Sport Sci. Tan S, Wang X, Wang J. Effects of supervised exercise training at the intensity of maximal fat oxidation in overweight young women.

J Exerc Sci Fit. Article Google Scholar. Tan S, Du P, Zhao W, Pang J, Wang J. Exercise training at maximal fat oxidation intensity for older women with type 2 diabetes.

Int J Sports Med. Jiang Y, Tan S, Wang Z, Guo Z, Li Q, Wang J. Aerobic exercise training at maximal fat oxidation intensity improves body composition, glycemic control, and physical capacity in older people with type 2 diabetes.

Bircher S, Knechtle B, Müller G, Knecht H. Is the highest fat oxidation rate coincident with the anaerobic threshold in obese women and men? San-Millán I, Brooks GA. Assessment of metabolic flexibility by means of measuring blood lactate, fat, and carbohydrate oxidation responses to exercise in professional endurance athletes and less-fit individuals.

Sports Med. Jeukendrup A, Achten J.

: Optimal fat oxidation

What Happens during Fat Oxidation? Muscle fibre type Diet and exercise of human leg muscles. Register now and get a free issue Optlmal Sports Performance Bulletin Get My Free Issue. Chrzanowski-Smith OJ, Edinburgh RM, Thomas MP, et al. Gmada, N. Therefore, these values are likely only of relevance to those ingesting a traditional mixed diet.
Fat Burning: using body fat instead of carbohydrates as fuel Diet, muscle glycogen fa physical performance. DeLany Optimal fat oxidation, Windhauser Hypoglycemia and insulin pens, Optimal fat oxidation C, Bray G. Numerous MFO and Fatmax data collection and analysis approaches have been applied, which may have influenced their estimation during an incremental graded exercise protocol. New insights in paediatric exercise metabolism. Fat storage and use.
Publication types

Fat burning is a common topic of conversation amongst athletes and non-athletes. In today's society, as a population, we are not burning enough fat calories and we are eating more fat and more calories than we burn.

It is therefore not surprising that people are searching for ways to "burn more fat" ideally ways that do not require too much effort. Many companies have recognized the potential and have jumped on the opportunity and are now selling tools that help you monitor fat burning and supplements that supposedly increase fat burning.

But do these things really work? Are there easy ways to increase fat burning? Are there easy ways to become lean? In a series of articles on mysportscience. com I want to evaluate the following:. What is fat burning?

And how is it regulated in the body? What is the evidence for each of these reasons? If we want to burn fat, what are the best methods to do this? Can we come up with some general advice?

Fat burning or fat oxidation the term preferred by scientists occurs on a daily basis in virtually all cells of our body.

Fat is stored in the form of triglycerides. A triglyceride is made up of 3 fatty acids that are held together by a glycerol backbone hence the name tri-glyceride.

Only fatty acids can be used as a fuel. Therefore triglycerides first need to be broken down into fatty acids. The fatty acids then need to be broken down further. Fat oxidation refers to the process of breaking down fatty acids. To oxidize fat one needs:. Healthy mitochondria small structures in cells that serve as the power plants of the cells.

In these power plants, energy is generated for muscle contraction by burning fuel, using oxygen and producing carbon dioxide. Supply of fatty acids these are supplied from triglycerides and fatty acids in the blood, as well as triglycerides stored in the muscle itself.

Oxygen transported to the muscle by blood. If fatty acids are supplied to healthy mitochondria and oxygen is present, fatty acids will be broken down to carbon dioxide.

This process is not too dissimilar form burning a log in a fire. You need the fireplace, some wood and oxygen. As mentioned above, the fatty acids we burn can come from different sources.

Fat is stored as triglycerides in different tissues of the body, including muscle. The vast majority of triglycerides in our bodies can be found in fat cells. When we eat, fat will eventually appear in the blood stream and can potentially be taken up and used in the muscle. When we exercise, our need for energy increases dramatically because muscle contraction is an energy consuming process.

Some of this energy will come from fat burning. The availability of fat in the muscle. The enzymes in the muscle to break down triglycerides to fatty acids. The enzymes in the fat tissue elsewhere in the body to break down triglycerides to fatty acids.

The supply of blood to the muscle. The presence of transport proteins to carry fatty acids from the blood into the muscle. The efficiency of transport of fatty acids into the mitochondria we will discuss this in more detail in future blogs.

The number of mitochondria. The quality of the mitochondria and the enzymes in the mitochondria to break down fatty acids. Because there are so many steps, there are also many regulatory mechanisms. For example, the activity of the enzymes that break down fat triglycerides into fatty acids is regulated.

Blood supply to the muscle is regulated as well as the uptake of fatty acids into the muscle and into the mitochondria. Compare this process to a factory.

CPT-1 concentration, located within the mitochondrial membrane during exercise appears to be regulated in part by exercise intensity [ 24 , 38 ]. During moderate intensity exercise, 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 [ 24 , 35 , 36 ].

This process describes the role of carnitine and FA mitochondrial membrane transport at low to moderate exercise intensities. 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 utilization [ 24 , 38 ].

The result of the abundant glycolytic derived acetyl-CoA forms acetyl-carnitine and monopolizes the available free carnitine limiting FA derived acyl-CoA transport. Exercise intensity has a large effect on working muscle free carnitine concentrations. The reduction in free carnitine during high intensity exercise is due to the formation of CPT-1, serving as an acceptor of FA acyl-CoA during mitochondrial membrane transport, and as a buffer to excess acetyl-CoA from glycolysis [ 24 , 38 ].

Therefore, as exercise intensity increases beyond moderate intensity, carnitine can be a limitation of FA substrate utilization due to the buffering of glycolytic acetyl-carnitine during high intensity exercise [ 24 , 37 , 38 ].

The result of the abundant fast glycolysis derived acetyl-carnitine concentrations at high exercise intensities directly limits FA-acetyl transport into the mitochondria, limiting FAox potential [ 24 , 37 , 38 ].

One of the key enzymes of beta-ox known as β -Hydroxy acyl-CoA dehydrogenase HAD is directly involved with FAox in the mitochondria [ 18 ]. Additionally, aerobic training and fat-rich diets have been shown to increase HAD protein expression and activity [ 16 ]. Fatty acid oxidation is directly influenced by HAD activity [ 1 , 18 ] in addition to the transport of FAs across the cellular and mitochondrial membranes [ 24 , 37 , 38 ].

While FAox fluctuates continuously, the endocrine system is principally responsible for the regulation of lipid oxidation at rest and during exercise [ 15 ].

The hormonal mechanisms that stimulate lipid metabolism are based primarily on catecholamines [ 12 ], cortisol, growth hormone, where insulin is inhibitory [ 16 ]. Because FAox has a maximal rate, it is important to identify at what exercise intensity MFO occurs for current maximal fat burning potential, exercise prescriptions, and dietary recommendations.

Identifying the stimuli that influence fat oxidation is necessary to best give exercise recommendations for the exercise intensity that facilitates optimal fat burning potential.

The adaptations that occur due to regular endurance training favor the ability to oxidize fat at higher workloads in addition to increasing over all MFO [ 39 , 40 ].

Increased fat oxidation has been shown to improve with endurance training, and therefore increases in MFO parallels changes in training status. Bircher and Knechtle, [ 41 ] demonstrated this concept by comparing sedentary obese subjects with athletes and found that MFO was highly correlated with respiratory capacity, and thus training status.

Trained subjects possess a greater ability to oxidize fat at higher exercise intensities and therefore demonstrates the correlation between respiratory capacity and MFO [ 27 , 41 , 42 ].

However, a similar rate of appearance in serum glycerol concentrations is observed in sedentary vs. trained subjects [ 27 ].

These results, however, conflict with results from Lanzi et al. Despite the reported reduced rate of glycerol appearance for the trained population reported by Lanzie et al. The training effect, and therefore an increase in respiratory capacity is partially the result of an increase in MFO.

Scharhag-Rosenberger et al. Maximal fat oxidation rate increased over 12 months of training pre-training 0. The training status effect on MFO further applies to athletic populations. moderately trained participants respectively [ 42 ]. Increasing HAD directly elevates beta-ox rate while citrate synthase increases the TCA cycle rate [ 44 ].

This evidence suggests that lipolysis and systemic FA delivery are not limitations to FAox at higher exercise intensities.

Therefore, FA cellular transport proteins CD36 and CPT-1 [ 24 , 25 ] and mitochondrial density HAD are likely the limitation of FAox during high intensity exercise [ 42 ]. Elevating FAox potential by increasing cellular respiration capacity increases FAox at higher exercise intensities which can have a positive influence on aerobic capacity.

Acknowledging the occurrence of large inter-individual differences in MFO, differences in MFO relative to training status are still observed [ 39 ]. Lima-Silva et al. moderately trained runners referenced above. However, while no statistical differences were observed between groups at the exercise intensity that MFO occurred, there was an increased capacity to oxidize fat in the highly trained subjects.

It is worth noting that the increased performance capacity in highly trained runners is most likely attributed to an increased CHO oxidative potential at higher exercise intensities in order to maintain higher steady state running workloads [ 39 ].

Subsequently, cellular protein expression, oxidative capacity and therefore training status do have the ability to influence fat oxidation. Training status further influences maximal fat oxidative potential by increasing endogenous substrate concentrations [ 19 , 20 ]. Endurance training enhances type I fiber IMTG concentrations as much as three-fold compared with type II fibers.

Increased MFO potential due to endurance training is further influenced by IMTG FA-liberating HSL [ 22 ] and LPL proteins [ 20 ], which are responsible for the liberation of intramuscular FAs from the IMTG molecule.

However, during exercise, the IMTG pool is constantly being replenished with plasma-derived FAs during exercise [ 20 , 45 ]. The exercise duration effect could be due to β -adrenergic receptor saturation, which has been shown to occur during prolonged bouts of exercise [ 16 , 46 ].

Furthermore, HSL activity has been shown to increase initially within min, but returned to resting levels after min of exercise, increasing reliance on serum derived FAs [ 20 , 45 ].

More research in the area of hormone related FA kinetic limitations is warranted. Factors such as training status, sex, and nutrition [ 1 ] all impact FAox kinetics and thereore the exercise intensity that MFO occurs.

Exercise intensity has the most profound effect on MFO based on a combination of events which include FA transport changes [ 24 , 25 ] and hormone fluctuation, which can increase lipolytic rate [ 7 ].

The cellular and hormonal changes that occur during exercise are directly related to exercise intensity which can influence FAox [ 47 ].

Fatty acid oxidation varies relevant to exercise intensity and therefore examining lipid oxidation at specific exercise intensities is warranted. Bergomaster et al. Previous research suggests that training at higher exercise intensities greatly influences substrate utilization [ 5 , 42 , 50 ].

It is worth noting that Bergomaster et al. The increased expression of FAox transport and oxidative cell proteins CD36, CPT-1, HAD, etc. that results in an increase FAox are a result of exercise intensity [ 24 , 49 ].

The Lima-Silva et al. Thus, FAox adaptation potential is related to training at higher exercise intensities rather than non-descript chronic exercise adaptation. Additionally, it has also been shown that carnitine concentrations are a direct limitation of FAox Fig.

Interestingly, efforts to mitigate the limitations of free carnitine on MFO at high exercise intensities have been unsuccessful [ 24 ]. Exercise intensity may further influence MFO by influencing catecholamine concentrations which have regulatory effects on lipolysis [ 16 ], glycogenolysis, as well as gluconeogenesis [ 12 ].

Increased epinephrine concentrations that parallel increases in exercise intensity stimulate both glycogenolysis and gluconeogenesis [ 12 ]. As exercise intensity increases, so does catecholamine concentrations facilitating a concurrent increase of serum CHO and FAs into the blood [ 12 ].

The crossover concept. The relative decrease in energy derived from lipid fat as exercise intensity increases with a corresponding increase in carbohydrate CHO. The crossover point describes when the CHO contribution to substrate oxidation supersedes that of fat. MFO: maximal fat oxidation. Adapted from Brooks and Mercier, The concept of the crossover point represents a theoretical means to understand the effect of exercise intensity on the balance of CHO and FA oxidation [ 4 ] Fig.

More specifically, the crossover concept describes the point that exercise intensity influences when the CHO contribution relevant to energy demand exceeds FAox. The limitations of FAox at higher intensities is due to the vast amount of acetyl-CoA produced by fast glycolysis [ 24 , 38 ].

The abrupt increase in total acetyl-CoA production at high intensity is due to fast glycolysis flooding the cell with potential energy, which suppresses FA mitochondrial transport potential resulting in decreased FAox Fig.

Notably, the large inter-individual fluctuation of when the crossover point occurs at a given exercise intensity can be attributed in part to training status [ 39 , 40 ]. Training status has been shown to effect catecholamine release and receptor sensitivity [ 12 ], endogenous substrate concentrations, and cellular transport protein expression; all of which contribute to the variability of when MFO occurs relevant to exercise intensity [ 1 ].

Nonetheless, MFO occurs in all populations regardless of training status, nutritional influence, etc. Another factor that significantly influences FAox is the duration of exercise [ 13 , 45 , 48 ]. Throughout a prolonged exercise bout, changes in hormonal and endogenous substrate concentrations trigger systematic changes in substrate oxidation [ 20 , 51 ].

Studies show that endurance training promotes reliance on endogenous fuel sources for up to min of submaximal exercise [ 47 , 51 , 52 ]. Exercise duration has a large effect on the origin of FAs for oxidative purposes.

While the initiation of exercise relies heavily on endogenous fuel sources IMTG and glycogen , reductions in IMTG concentrations have been shown to occur when exercise duration exceeds 90 min [ 45 ].

Increases in both epinephrine and plasma LCFA concentrations were observed when exercise exceeded 90 min with a simultaneous reduction in HSL activity. Therefore the increase in serum LCFAs [ 20 , 45 ] and the saturation of HSL to epinephrine [ 16 , 46 ] are postulated to inhibit HSL reducing IMTG oxidation when exercise exceeds 90 min [ 20 ].

The shift from intramuscular fuel sources to serum derived FAs after 2 h of submaximal exercise parallel changes in blood glucose concentrations. Trained subjects however experienced a reduction in muscular CHO uptake during the same time frame compared with the untrained.

This suggests that the trained subjects were able to maintain FAox despite substrate origin during prolonged exercise to stave off CHO usage for high intensity exercise [ 51 ].

While the exercise intervention used in this study is not typically classified as endurance exercise, the exercise protocol does clarify the variation in the origin of substrate oxidation over time, and expands on the diverse effects exercise duration has on substrate oxidation.

Training duration has a large influence on FA and CHO oxidation during prolonged submaximal exercise. However, training status has little influence on the origin of FAs during the first min of submaximal exercise.

Nonetheless, trained subjects are able to maintain higher workloads with decreased metabolic work HR for longer periods compared to untrained individuals based on the ability to maintain FAox for longer durations [ 45 ]. Despite the training status effect on FAox, exercise duration will dictate substrate origin during submaximal exercise [ 20 , 45 , 51 ].

Variability in FAox owing to sex exist due to the inherent hormonal differences specific to men and women [ 53 , 54 , 55 , 56 ]. In a comprehensive study with over men and premenopausal women, the energy contribution of fat was significantly higher in women vs.

Studies have consistently shown that premenopausal women have a significantly greater ability to oxidize fat during exercise [ 2 , 57 , 58 ]. The sex differences in fat oxidation [ 58 , 59 ] during exercise is attributed to the increased circulation of estrogens [ 53 , 54 , 60 ]. Evidence suggests that estrogen directly stimulates AMPK [ 29 ] and PGC-1α activity [ 60 ], which is thought to increase the downstream FAox transport protein CD36 and beta-oxidative protein HAD [ 30 ].

Additionally, beta-oxidative proteins that oxidize LCFA oxidation have been shown to be regulated in part by estrogen [ 54 , 60 ]. The result of increased beta-oxidative proteins is directly related to increased FAox potential [ 29 , 54 ]. Interestingly, when men were supplemented with estrogen, increases in FAox were observed along with increased cellular expression of beta-ox proteins within eight days of supplementation [ 60 ].

Circulating estrogen is naturally higher for premenopausal women compared to men. Additionally, fluctuation in estrogen levels is inherent throughout the menstrual cycle [ 53 , 59 ]. Estrogens are generally higher during the follicular phase of the menstrual cycle compared to the luteal phase [ 29 ].

Paradoxically, elevated estrogens during the follicular phase do not affect FAox when compared to the luteal phase [ 29 , 53 ]. Nevertheless, elevations in endogenous circulating estrogens inherent to premenopausal women increase the expression of cellular proteins responsible for increased FA transport and oxidation compared to men.

Cellular protein expression and the corresponding endogenous vs. systematic substrate oxidation vary according to dietary macronutrient intake [ 19 , 35 , 61 ]. It has been recently shown that high fat diets promote FAox and have performance enhancement capabilities [ 3 , 60 ]. However, definitive conclusions regarding pre-exercise macronutrient dominant diets and exercise performance improvements are contingent on specific exercise applications [ 62 ] that are directed by exercise duration and intensity [ 63 , 64 , 65 ].

Diets that have higher proportions of a specific macronutrient e. High fat diets increase IMTG concentrations while decreasing glycogen levels within muscle [ 17 , 35 ]. Alternatively, high CHO diet conditions increase glycogen concentrations while IMTGs decrease [ 17 ].

However, post-exercise predominant macronutrient CHO consumption has been shown to influence cellular protein expression in as little as 2 hrs [ 69 ].

The plasticity of cellular changes relevant to chronic adaptation are compromised when macronutrient content is altered [ 65 , 67 ].

Macronutrient proportion and timing has been shown to have effects on cellular adaptation [ 32 ] as well as the physiological response to exercise [ 70 , 71 , 72 ].

High fat diets increase beta-ox potential at rest [ 66 ] and during exercise [ 34 ], however, the limitations of high fat diets including short term adaptation 5dys reside with high intensity exercise [ 70 , 72 , 73 ].

Pyruvate dehydrogenase is the enzyme responsible for oxidizing pyruvate as the final substrate of the glycolytic pathway. The deleterious cellular adaptation of reduced PDH activity due to high fat diets has been found to compromise high intensity exercise performance potential [ 35 , 63 , 67 ].

Adapting the body to high fat diets allows the body to increase IMTG storage as well as increase FAox [ 21 , 35 ]. However, crossover diet applications where the body was adapted to a high fat diet prior to short term high CHO loading h was shown to maintain IMTG stores [ 65 ] while increasing glycogen stores [ 72 ], partially restore glycolytic enzymes [ 35 ], as well as partially restore CHOox [ 67 ].

Alternating pre-exercise macronutrient specificity has the potential to be effective in accommodating the stress of sustained high intensity exercise due to both ideal cellular protein expression, and adequate storage of IMTG and muscle glycogen. The reduction in PDH activity due to high fat diets is a limiting factor to the necessary CHO oxidation at high intensity exercise despite adequate endogenous energy stores.

Maintaining the ability to store and oxidize fat after acclimating to a high fat diet while restoring the ability to oxidize CHO with short-term CHO loading is an ideal physiological state for endurance exercise performance.

Current research asserts that high fat diets favorably enhance FAox at both rest and during exercise [ 3 , 74 ]. However, exercise intensity dictates substrate utilization regardless of dietary influence, training status, and exercise duration. Because of this, high fat diets are sometimes encouraged during preparatory off-season training when training volumes are high and exercise intensities are low to moderate [ 74 ].

More research into the short-term macronutrient manipulation effect on endogenous substrate concentrations, plasticity of cellular expression, and preferential substrate oxidation are necessary to ascertain if there is benefit on exercise performance outcomes. In summary, FAox is contingent on many factors which can modify cellular expression in a short amount of time.

Macronutrient availability, training status, sex, exercise intensity, and duration all influence cellular adaptation, systematic FA transport, and FAox. Additionally, more investigation into the ideal nutritional timing and content that will favorably influence the physiological adaptations of FAox during endurance exercise is warranted.

Nonetheless, exercise prescriptions and dietary recommendations need to take into account specific exercise goals duration, intensity, sport specific to facilitate a training plan that will elicit the ideal substrate oxidation adaptations relevant to improve sport performance.

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Download references. The authors would like to thank Dr Florent Besnier, Dr Ratko Peric, Dr Shaea Alkahtani and Professor Jordi Monferrer who kindly provided supplementary data regarding some of their studies and gave their consent for publication in this review. Department of Chemical Sciences, Biomedical Sciences Institute, Autonomous University of Ciudad Juarez, , Chihuahua, Mexico.

Isaac A. Department of Health Sciences, Biomedical Sciences Institute, Autonomous University of Ciudad Juarez, , Chihuahua, Mexico. Department of Physiology, Faculty of Medicine, EFFECTS Research Group, University of Granada, , Granada, Spain. PROmoting FITness and Health Through Physical Activity Research Group PROFITH , Department of Physical and Sports Education, Faculty of Sports Science, University of Granada, , Granada, Spain.

Centro de Investigación Biomédica en Red Fisiopatología de la Obesidad y Nutrición CIBERobn , Instituto de Salud Carlos III, , Madrid, Spain. Department of Endocrinology and Diabetes, Hôpital Lapeyronie CHRU Montpellier, PHYMEDEXP, Université de Montpellier, Montpellier, France.

You can also search for this author in PubMed Google Scholar. Correspondence to Isaac A. Chávez-Guevara or Jean Frederic Brun. IACG was supported by a Ph. D scholarship from the Consejo Nacional de Ciencia y Tecnología CONACyT. However, the institution did not participate in the manuscript preparation.

No other sources of funding were used to assist in the preparation of this article. The authors declare that they have no conflicts of interests relevant to the content of this review.

The dataset supporting the findings reported in this review are available upon reasonable request from the lead author.

All authors contributed to the study conception and design. Data collection and analysis were performed by ARJ, IACG and JFB. The first draft of the manuscript was written by IACG and all authors commented on previous versions of the manuscript.

All authors read and approved the final manuscript. Springer Nature or its licensor e. a society or other partner holds exclusive rights to this article under a publishing agreement with the author s or other rightsholder s ; author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

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Abstract Background Exercise training performed at maximal fat oxidation FATmax is an efficient non-pharmacological approach for the management of obesity and its related cardio-metabolic disorders.

Objectives Therefore, this work aimed to provide exercise intensity guidelines and training volume recommendations for maximizing fat oxidation in patients with obesity. Methods A systematic review of original articles published in English, Spanish or French languages was carried out in EBSCOhost, PubMed and Scopus by strictly following the Preferred Reporting Items for Systematic reviews and Meta-Analyses PRISMA statement.

Conclusion Relative heart rate rather than relative oxygen uptake should be used for establishing FATmax reference values in patients with obesity. Access this article Log in via an institution.

References Goodpaster BH, Sparks LM. Article CAS PubMed PubMed Central Google Scholar Wu H, Ballantyne CM. Article CAS PubMed PubMed Central Google Scholar Fava MC, Agius R, Fava S. Ingestion of carbohydrate in the hours before or on commencement of exercise reduces the rate of fat oxidation significantly compared with fasted conditions, whereas fasting longer than 6 h optimizes fat oxidation.

Fat oxidation rates have been shown to decrease after ingestion of high-fat diets, partly as a result of decreased glycogen stores and partly because of adaptations at the muscle level. Abstract Interventions aimed at increasing fat metabolism could potentially reduce the symptoms of metabolic diseases such as obesity and type 2 diabetes and may have tremendous clinical relevance.

Publication types Review. The MFO in adolescents was superior in comparison with MFO observed in young and middle-aged adults. On the other hand, the MFO was higher during treadmill walking in comparison with stationary cycling. Neither biological sex nor the analytical procedure for computing the fat oxidation kinetics were associated with MFO and FATmax.

Conclusion: Relative heart rate rather than relative oxygen uptake should be used for establishing FATmax reference values in patients with obesity.

Moreover, training volume must be higher in adults to achieve a similar fat oxidation compared with adolescents whereas exercising on a treadmill requires a lower training volume to achieve significant fat oxidation in comparison with stationary cycling.

You are Diet and exercise 1 Optimal fat oxidation oxivation 1 free articles. Oxidatiin unlimited access take oxidatipn risk-free trial. Holistic herbal remedies burning is a very popular Diet and exercise often-used term among oxjdation athletes. But is it really important to burn fat — and, if so, how can it best be achieved? Professor Asker Jeukendrup looks at what the research says. Fat burning is often associated with weight loss, decreases in body fat and increases in lean body mass, all of which can be advantageous for an athlete.

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