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The Most EFFICIENT Way To LOSE FAT - Andrew HubermanNatural fat oxidation -
For unlimited access take a risk-free trial. Fat burning is a very popular and often-used term among endurance 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. It is known that well-trained endurance athletes have an increased capacity to oxidise fatty acids.
This enables them to use fat as a fuel when their carbohydrate stores become limited. In contrast, patients with obesity, insulin resistance and type II diabetes may have an impaired capacity to oxidise fat.
As a result, fatty acids may be stored in their muscles and in other tissues. This accumulation of lipid and its metabolites in the muscle may interfere with the insulin-signalling cascade and cause insulin resistance. It is therefore important to understand the factors that regulate fat metabolism, and the ways to increase fat oxidation in patients and athletes.
Fats are stored mostly in subcutaneous adipose tissue, but we also have small stores in the muscle itself intramuscular triglycerides. At the onset of exercise, neuronal beta-adrenergic stimulation will increase lipolysis the breakdown of fats into fatty acids and glycerol in adipose tissue and muscle.
Catecholamines such as adrenaline and noradrenaline may also rise and contribute to the stimulation of lipolysis. As soon as exercise begins, fatty acids are mobilised. Adipose tissue fatty acids have to be transported from the fat cell to the muscle, be transported across the muscle membrane and then be transported across the mitochondrial membrane for oxidation.
The triglycerides stored in muscle undergo similar lipolysis and these fatty acids can be transported into the mitochondria as well. During exercise, a mixture of fatty acids derived from adipocytes and intramuscular stores is used. There is evidence that shows that trained individuals store more intramuscular fat and use this more as a source of energy during exercise 1.
Fat oxidation is regulated at various steps of this process. Lipolysis is affected by many factors but is mostly regulated by hormones stimulated by catecholamines and inhibited by insulin.
The transport of fatty acids is also dependent on blood supply to the adipose and muscle tissues, as well as the uptake of fatty acids into the muscle and into the mitochondria. By inhibiting mobilisation of fatty acids or the transport of these fatty acids, we can reduce fat metabolism.
However, are there also ways in which we can stimulate these steps and promote fat metabolism? Exercise intensity — One of the most important factors that determines the rate of fat oxidation during exercise is the intensity. Although several studies have described the relationship between exercise intensity and fat oxidation, only recently was this relationship studied over a wide range of intensities 2.
In absolute terms, carbohydrate oxidation increases proportionally with exercise intensity, whereas the rate of fat oxidation initially increases, but decreases again at higher exercise intensities see figure 1.
So, although it is often claimed that you have to exercise at low intensities to oxidise fat, this is not necessarily true. However, the inter-individual variation is very large. However, very little research has been done.
Recently we used this intensity in a training study with obese individuals. Compared with interval training, their fat oxidation and insulin sensitivity improved more after four weeks steady-state exercise three times per week at an intensity that equalled their individual Fatmax 4.
Dietary effects — The other important factor is diet. A diet high in carbohydrate will suppress fat oxidation, and a diet low in carbohydrate will result in high fat oxidation rates. This effect of insulin on fat oxidation may last as long as six to eight hours after a meal, and this means that the highest fat oxidation rates can be achieved after an overnight fast.
Endurance athletes have often used exercise without breakfast as a way to increase the fat-oxidative capacity of the muscle. Recently, a study was performed at the University of Leuven in Belgium, in which scientists investigated the effect of a six-week endurance training programme carried out for three days per week, each session lasting one to two hours 6.
The participants trained in either the fasted or carbohydrate-fed state. When training was conducted in the fasted state, the researchers observed a decrease in muscle glycogen use, while the activity of various proteins involved in fat metabolism was increased.
However, fat oxidation during exercise was the same in the two groups. It is possible, though, that there are small but significant changes in fat metabolism after fasted training; but, in this study, changes in fat oxidation might have been masked by the fact that these subjects received carbohydrate during their experimental trials.
It must also be noted that training after an overnight fast may reduce your exercise capacity and may therefore only be suitable for low- to moderate- intensity exercise sessions. The efficacy of such training for weight reduction is also not known.
Duration of exercise — It has long been established that oxidation becomes increasingly important as exercise progresses. During ultra-endurance exercise, fat oxidation can reach peaks of 1 gram per minute, although as noted in Dietary effects fat oxidation may be reduced if carbohydrate is ingested before or during exercise.
In terms of weight loss, the duration of exercise may be one of the key factors as it is also the most effective way to increase energy expenditure. Mode of exercise — The exercise modality also has an effect on fat oxidation.
Fat oxidation has been shown to be higher for a given oxygen uptake during walking and running, compared with cycling 7. The reason for this is not known, but it has been suggested that it is related to the greater power output per muscle fibre in cycling compared to that in running.
Gender differences — Although some studies in the literature have found no gender differences in metabolism, the majority of studies now indicate higher rates of fat oxidation in women. In a study that compared men and women over a wide range of exercise intensities, it was shown that the women had higher rates of fat oxidation over the entire range of intensities, and that their fat oxidation peaked at a slightly higher intensity 8.
The differences, however, are small and may not be of any physiological significance. There are many nutrition supplements on the market that claim to increase fat oxidation. These supplements include caffeine, carnitine, hydroxycitric acid HCA , chromium, conjugated linoleic acid CLA , guarana, citrus aurantium, Asian ginseng, cayenne pepper, coleus forskholii, glucomannan, green tea, psyllium and pyruvate.
With few exceptions, there is little evidence that these supplements, which are marketed as fat burners, actually increase fat oxidation during exercise see table 1. One of the few exceptions however may be green tea extracts. The mechanisms of this are not well understood but it is likely that the active ingredient in green tea, called epigallocatechin gallate EGCG — a powerful polyphenol with antioxidant properties inhibits the enzyme catechol O-methyltransferase COMT , which is responsible for the breakdown of noradrenaline.
This in turn may result in higher concentrations of noradrenaline and stimulation of lipolysis, making more fatty acids available for oxidation. Environment — Environmental conditions can also influence the type of fuel used. It is known that exercise in a hot environment will increase glycogen use and reduce fat oxidation, and something similar can be observed at high altitude.
Similarly, when it is extremely cold, and especially when shivering, carbohydrate metabolism appears to be stimulated at the expense of fat metabolism. Panel c : Individual observations for each subject grey lines , and the mean for all subjects black line.
All the significant differences reported above persisted after adjusting for age, chronotype, lean mass and fat mass data not shown. The present results indicate that caffeine intake increases MFO and Fat max as well as VO 2max independent of the time of day. The highest values for these variables were all obtained in the afternoon after caffeine intake.
The results also show that, in the morning, the values of MFO after caffeine ingestion are nearly equivalent to those recorded in afternoon tests without caffeine supplementation. This suggests that caffeine increases whole-body fat oxidation during graded exercise in the morning to a value similar to that seen without caffeine in the afternoon.
Overall, these results suggest that a combination of acute caffeine intake and exercise at moderate intensity in the afternoon provides the best scenario for individuals seeking to increase whole-body fat oxidation during aerobic exercise.
The present findings provide further evidence regarding the diurnal variation of MFO and Fat max , which have been reported higher in the afternoon than in the morning [ 7 , 8 , 9 ]. It should be noted that these previous studies were conducted using a treadmill graded exercise test to measure these variables.
In the present work, a cycloergometer graded exercise test was used. Thus, together, these results suggest that the diurnal variations in MFO and Fat max are independent of subject characteristics and of the ergometer and protocol used to assess the whole-body fat oxidation rate during exercise.
A number of studies have reported athletes to show better endurance performance during the afternoon than the early morning and late evening [ 10 , 35 ], a finding with which the present results agree.
However, in one study conducted in trained male athletes, no differences in VO 2max were seen between the morning and the afternoon [ 9 ].
With respect to this particular variable, the discrepancy might be explained by the different ergometers used i. Endurance performance peaks in the afternoon usually coinciding with the highest core body temperature reached during the day [ 36 ]. This temperature increases energy metabolism, improves muscle compliance, and facilitates actin-myosin cross bridging [ 11 ].
Moreover, the exercise-induced catecholamine peak is higher in the afternoon than in the morning [ 10 , 11 ]. This catecholamine release promotes an increase in lipolysis in both skeletal muscle and adipose tissue [ 11 , 35 ], raising the plasma fatty acid content and explaining the higher fat oxidation rates observed in the afternoon.
Since the present work collected no data on body core temperature or catecholamine release during exercise, further studies will be needed if these variables are to be better linked to the physiological mechanisms behind the observed diurnal variation in VO 2max , MFO and Fat max.
The results of the current study support the use of caffeine as an ergogenic aid to raise fat oxidation during exercise, as well as to increase VO 2max , and agree with the findings of previous investigations showing that caffeine improves fuel oxidation during prolonged exercise [ 20 , 21 , 22 ] and enhances endurance performance [ 12 ].
The present results also agree with those obtained by Gutiérrez-Hellín et al. These findings suggest that caffeine ingestion in the morning could be used by athletes as an ergogenic aid to help them avoid morning-induced reduction in muscle performance.
In addition, Boyett et al. These findings are partially in line with those of the present study, suggesting that acute caffeine intake before exercise serves as an effective ergogenic aid for reversing morning-induced reductions in resistance exercise performance and endurance-like performance.
Moreover, we did not control the sleep quality and quantity of the participants. Further, the present study was performed in active men; the results cannot, therefore, be directly extrapolated to women or sedentary populations, etc.
Finally, the sample size was relatively small. Caffeine intake increases MFO and Fat max as well as VO 2 max independent of the time of day. Caffeine increases MFO in the morning to a value similar to that seen without caffeine in the afternoon.
A combination of acute caffeine intake and exercise at moderate intensity in the afternoon provides the best scenario for individuals seeking to increase MFO. Further, the existence of a diurnal variation in MFO, Fat max and VO 2max was confirmed, with values for all being higher in the afternoon than in the morning.
The present findings also support the notion that caffeine ingestion in the morning helps to increase MFO and Fat max levels during exercise in the afternoon. These results support the use of caffeine as an ergogenic aid during training or competition during the morning.
The combination of acute caffeine intake and exercise at moderate intensity in the afternoon seems to be the best scenario for individuals seeking to increase the amount of fat utilized during continuous aerobic exercise. Whether higher doses of caffeine induce greater effects on whole-body fat oxidation during graded exercise tests and further improves endurance performance remains to be investigated.
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Cruz R, de Aguiar R, Turnes T, Guglielmo L, Beneke R, Caputo F. Caffeine affects time to exhaustion and substrate oxidation during cycling at maximal lactate steady state. Boyett J, Giersch G, Womack C, Saunders M, Hughey C, Daley H, et al. Time of Day and training status both impact the efficacy of caffeine for short duration cycling performance.
Mora-Rodríguez R, Pallarés JG, López-Samanes Á, Ortega JF, Fernández-Elías VE. Caffeine ingestion reverses the circadian rhythm effects on neuromuscular performance in highly resistance-trained men. PLoS One. Souissi Y, Souissi M, Chtourou H. 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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Journal Reference : Jorge Gutiérrez-Hellín, Juan Del Coso. Acute p-synephrine ingestion increases fat oxidation rate during exercise.
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: Natural fat oxidation| 11 Healthy Foods That Help You Burn Fat | By keeping insulin production low, the body can access and utilize fat as a fuel source more effectively. Glucagon stimulates the liver breakdown of glycogen to glucose and stimulates the gluconeogenesis in the liver by increasing the uptake of amino acids. Protein stimulates growth hormone GH release from the anterior pituitary. GH may indirectly promote fat loss. It acts directly on the fat cells and stimulates the release of fatty acids and glycerol into the blood stream. A particular amino acid, glutamine, has been shown to dramatically boost growth hormone release in the body, which then may promote greater fat burning Guo et al. Protein provides the building blocks of body tissues and regular consumption of it, i. Not only does protein promote greater energy expenditure by maintaining an elevated metabolic rate but it also boosts the metabolism because it requires more energy to be digested compared to the other macronutrients, carbohydrate, and fat. As a result, the thermic effect of food TEF , which means the amount of energy expended through the process of digestion increases, which increases the overall amount of calories the body burns during the day Banni Protein has powerful appetite suppressing effects, especially compared to the other macronutrients. Its appetite-suppressing qualities come from the fact that protein stimulates the release of cholecystokinin CCK from the stomach cells. This hormone then travels through the bloodstream to the hypothalamus in the brain where it tells the brain that the stomach is full Whingham et al. From the aforementioned 5 mechanisms, it is easy to conclude why protein can help promote fat burning in the body. It can help in fat burning by simply making an effort to add a small portion of protein, from a variety of protein sources to each meal. Protein, foliate, and vitamin D are found in red meat beef, veal, pork , skinless turkey, and chicken. Proteins are not only more complex to digest and assimilate but they also require more energy to be stored as fats, so, they help to feel full and help the body in fat loss Coyle and Patrick Dairy products provide whey protein and casein that build muscle, control appetite, and aid in weight loss Boirie et al. They contain CLA that works to lower the triglycerides and cholesterol leading to upregulate the body metabolism Leonard ; Kim et al. The process of converting dairy down into lactic acid causes the body to utilize the energy stored in fat. Low-fat dairy products such as cheese, milk, and yogurt contain calcium and complex carbohydrates which work to kick metabolism into action and burn fat Villarroel et al. Peanut butter provides protein, vitamins B 3 and E, magnesium, cortisol, foliate, dietary fiber, and arginine all of which increase protein synthesis, boost metabolism, and help in fat burning Christensen et al. Eggs are rich in satiating protein. Eggs for breakfast can boost weight loss plan more than a carbohydrate-rich breakfast Soerensen et al. Several studies have correlated higher calcium intakes with lower body weight or less weight gain over time Parikh et al. Two explanations have been proposed. First, high-calcium intakes might reduce calcium concentrations in fat cells by decreasing the production of parathyroid hormone and the active form of vitamin D. Decreased intracellular calcium concentrations, in turn, might increase fat breakdown and discourage fat accumulation in these cells Earthman et al. Second, calcium from food or supplements might bind to small amounts of dietary fat in the digestive tract and prevent absorption of this fat Mallard et al. Observational studies indicate that greater body weights are associated with lower vitamin D status, and obese individuals frequently have marginal or deficient circulating levels of vitamin D Lim et al. Nevertheless, the association between vitamin D and obesity raises the question of whether increasing vitamin D concentrations might reduce body weight Gittleman ; Young et al. Fruits, although all fruits are strong healthy food, the fact is that only some have fat-burning properties. The best choices include citrus fruits; the low-glycemic fruits lemons, limes, oranges, tangerines, and grapefruits , grapes, cherries, and kiwi fruits. These fruits contain vitamin C, which not only works to dilute fat and cholesterol by its acidity but also helps release the fat cells. Apples and berries, especially raspberries, are the most pectin-rich fruit which limits the ability to absorb fat. Another choice is peaches, pears, plums, strawberries, and pomegranates. They are rich in vitamins and minerals, high in water content, and have low glycemic index. They found to improve body metabolism and reduce bad cholesterol Denker et al. Bananas and mangoes make for excellent snack foods as well as breakfast foods. Berries are extremely high in B vitamins that stimulate the thyroid hormone and boost metabolism. It is advised to eat the fruits whole for added fiber and increased the feeling of fullness Gittleman Grapefruit has been an integral part of many diets. Its fat-burning mechanism is due to the high-fiber content that is known to burn more calories during the digestive process than calories in the grapefruit itself. Grapefruit pills were found to improve insulin resistance compared to its juice Terry Vegetables have a low-calorie profile while containing essential minerals and vitamin that improve the metabolism of the body, except for certain calorie-rich vegetables like potatoes and sweet potatoes. Potatoes were preferred to be cooked with the outer skin because it is a good source of insoluble fibers Li Veggies like broccoli, spinach, artichoke, peas, cauliflower, cabbage, and carrots are excellent sources of minerals and have low calories that offer fat burning. They are rich in fiber, which delays hunger Biesiekierski Cucumbers are high in sulfur and silicone, both of which help the body rid itself of fat content. Beets are rich in iron, potassium, magnesium, and fiber. They enrich the blood and aid in liver function, thus helping to rid the body of fat through elimination Whitehead et al. Onions and garlic also make great fat burners. The best way to cook veggies would be to boil them or stir fry them with healthy oils like olive oil, sunflower oil, Soybean oil or sesame oil Julkunen et al. Grains and Seeds are rich in fibers which can control the blood sugar. Oats are rich in fiber, especially, insoluble β-glucan which is found in researches to stabilize the blood sugar of type II diabetics better than other types of fiber and improves metabolism Ramdath et al. Oats also are digested slowly, keeping insulin production down. It is advised to eat one bowl of oatmeal at breakfast Mudryj et al. They can balance copper and zinc which support thyroid function and boost metabolism Whiting et al. They are excellent sources of dietary fiber and are known to lower the bad cholesterol and thus contribute to heart health. The best way to eat legumes would be to eat the whole grains Earthman et al. Not only is flax oil rich in omega-3 but it also is found to lower cholesterol van Avesaat et al. Thermogenic foods, are foods that help burn fat by heating up the body Pathak et al. Capsaicin, a well-known thermogenic compound found in chili peppers, jalapenos, and ginger, works to heat up the body, speed up metabolism, and burn fats Rhoades and Tanner It would not count as food because it has no calories. Water helps improve the overall metabolism of the body and thus helps burn fat. And of course, water helps flush out toxins and thus improves the capacity of the body to stay healthy Gittleman Many studies have shown that extra water intake, especially up to ml at mealtime, was conducive to weight loss Stookey et al. Certain foods are rich in their water content and thus help in the process of fat reduction and feeling full quickly, for example are watermelons, cantaloupes, cucumbers, snake gourd, papaya, and chard Rosenberg et al. The ingested and the environmental toxins that were taken every day can be stored in fat cells. Toxins released during weight loss had the capacity to damage the fat-burning mitochondria and interfere with the thyroid hormones and their receptor sites, interfere with enzymes, and interfere with leptin signals to hunger reflex. A number of studies have been found that a decreased metabolic rate is in response to the presence of toxins affecting the thyroid hormones and the rate at which the liver excretes them Hsueh et al. Fat flush is a low-carbohydrate eating plan devised with a focus on weight loss while detoxing the liver and lymphatic systems to enhance overall health. In addition to limiting carbohydrates, it recommends eating fat-burning fats, high-fiber vegetables and fruit, clean protein, and thermogenic foods and supplements Gittleman Caloric intake on the fat flush plan ranges from to calories per day, which is in line with the nutrition recommendations for weight loss Klein and Kiat During this phase, margarine, sugar, oils except flaxseed oil , grains, bread, cereal, starchy vegetables, dairy products, and some spices are restricted. During the second phase, calories are increased from to calories daily. It includes the same food that is in the first but with the addition of butternut, sweet potato, fresh or frozen peas, brown rice, and carrots once weekly. This phase continues until reaching the needed weight. The last phase is to maintain weight loss and entail or more calories daily. Certain foods that were eliminated in phase 1 are reintroduced back such as some starchy carbohydrates, dairy, and gluten-free grains Gittleman It aims to cleanse the liver, improve wellness, and produce weight loss. An expert opinion is that the elimination of all margarine, fats, oil, sugar, bread, grains, high-carbohydrate vegetables, and dairy products can be difficult for some people because they found the remaining food list so restrictive. Fat flush plan is incompatible with vegetarian diet because of the importance of eating lean protein from animal sources, which they cannot do; so vegetarians face difficulty in following this diet. The plant-based protein could be a substitute animal-based protein for vegetarians. Protein found in soybean and legumes is considered as an acceptable protein substitute on the Fat flush plan. The lacto-ovo vegetarians consume eggs, light yogurt, and light cheeses as a source of protein Picco We can turn our body into fat-burning machine by including low-calorie foods instead of high-calorie foods in our diet. The fat burning supplements are not alone to burn fats alone. Without a proper diet and regular exercise, we cannot reach the needed goal. If we decide to start any fat flush dietary program, we should seek approval from the doctor prior to starting. To avoid toxins which delay the burning process, we should eat organic foods as much as we can, avoid processed foods, and use natural product to be away from chemicals, additives, or preservatives. Too much fats increase the risk of diabetes with the alarming complications of cardiovascular disorders. Modification of an unhealthy diet, bad eating habits, and lifestyle factors should remain the cornerstone in managing body fats. 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Lambert JD, Sang S, Yang CS Possible controversy over dietary polyphenols: benefits vs risks. Chem Res Toxicol 20 4 — Lardy H, Partridge B, Kneer N, Wei Y Ergosteroids: induction of thermogenic enzymes in liver of rats treated with steroids derived from dehydroepiandrosterone. Proc Natl Acad Sci 92 14 — Article ADS Google Scholar. Lenz TL, Hamilton WR, Ernst E Supplemental products used for weight loss. J Am Pharm Assoc — Leonard ST, Worrel ME, Gurkovskaya OV, Lewis PB, Winsauer PJ Effects of 7-keto dehydroepiandrosterone on voluntary ethanol intake in male rats. However, this assumption is unlikely valid since fat cells are continuously dying and regenerating throughout our life. Approximately 8. Abdominal fat mass is determined by the balance of fat cell death and regeneration of adipose tissue, which is influenced by exercise Allerton et al. Acute adrenergic stimulation has been reported to induce fat cell death Kim et al. The balance between fat cell death and regeneration is also strongly influenced by plasma insulin concentrations, which varies with exercise habit, meals, and sleeping fast. Lowering physical activity increases plasma insulin concentration and waist circumference without an observable change in body weight Chen et al. In a contrast, high-intensity exercise lowers fasting and post-meal insulin levels while increasing the insulin sensitivity of exercised muscle Ivy et al. The second basic assumption of the fat burning theory is that muscle and fat cells are not interconvertible in a human body. However, we could not preclude the possibility that the fat mass loss concurrent with muscle mass gain after exercise training is associated with conversion between muscle and fat progenitor cells, derived from circulating bone marrow stem cells. Conversion from muscle satellite cells to an adipogenic lineage contributes the development of obesity and muscle mass loss in animals Durschlag and Layman, ; Scarda et al. Glucose and reactive oxygen species ROS also stimulate the adipogenic conversion from muscle-derived stem cells Aguiari et al. Both plasma glucose and ROS elevate with age and weight growth Ho et al. However, exercise training lowers plasma glucose Colberg et al. Circulating myokines released from contracting muscle also suppress adipogenesis and stimulate myogenesis Barra et al. As a result, exercise appears to, at the very least, attenuate the conversion of muscle to fat and may instead activate the conversion of fat to muscle. Further evidence of this mechanism comes from the wide array of exosomes containing nucleic acids or peptide released from exercising skeletal muscle implicating the crosstalk between muscle and fat tissues. Adipose tissues are a major source of circulating exosomes containing a variety of mediators, which may influence muscle development Thomou et al. Some nucleic acid molecules encapsulated in the extracellular vesicles may play a role in the interconvertibility between fat and muscle progenitor cells. For example, muscle contraction induces acute increases of miR into circulation Xu et al. This molecule has been shown to inhibit proliferation of human adipose tissue-derived mesenchymal stem cells and high-fat diet-induced obesity Kim et al. In addition, circulating miR level has been found lowered in obese women and exercise stimulates release of miR from skeletal muscle into circulation which inhibits adipogenesis Lee et al. The third assumption of the fat burning theory is that the increased carbon and nitrogen demands for airway epithelial cells regeneration in lungs does not contribute to fat loss during and after exercise. However, the possibility that the fat loss effect of high-intensity aerobic training due to competition for carbon and nitrogen between lungs and adipose tissues cannot be excluded Leibacher and Henschler, ; Saat et al. The lungs are strong competitors for bone-marrow stem cells main source of muscle and adipose progenitor cells which is required for cell regeneration of peripheral tissues. This suggests a much higher demand of the lungs for carbon and nitrogen against other tissues. Acute airway epithelium damage induced by acute ventilations during aerobic exercise significantly increases phagocyte infiltration to the lungs Adams et al. This also induces cell regeneration following phagocytic clearance of unhealthy cells in airway epithelial lining in a way similar to muscle inflammation Su et al. Massive consumption of bone marrow immune cells and stem cells by the lungs may explain why high-intensity aerobic exercise has greater magnitude of fat loss effect compared with resistance exercise Willis et al. During unfed conditions, visceral adipose tissues continuously releases fatty acids into circulation Coppack et al. Therefore, post-meal carbon and nitrogen returning to fat cells determines the abdominal fat mass Coppack et al. Skeletal muscle is a competitor for the post-meal carbon and nitrogen Ivy et al. Increasing muscle demand at the time when post-meal nutrients are supplying into circulation can minimize the substrates returning to adipose tissue. This concept is supported by animal and human studies in which providing meal immediately after resistance training results in greater magnitude of muscle mass gain and fat mass loss compared with the condition of detaching mealtime away from the workout Suzuki et al. Studies employing dual energy X-ray absorptiometry have also provided solid support for the carbon and nitrogen redistribution effect of exercise training by the evidence of concurrent increases in lean body mass and decreases in fat mass Cribb and Hayes, ; Abbasi, ; Kemmler et al. This nutrient redistribution effect remains noticeable in sarcopenic elderly aged above 70 years and above Kemmler et al. It is likely that the decreased abdominal fat accumulation after exercise training is associated with increased muscle regeneration attracting more postprandial carbon and nitrogen to challenged muscle tissue against abdominal adipose tissues Huang et al. Interventions that promote muscle growth have been shown to decrease fat mass Mcpherron and Lee, ; Leong et al. Muscle regeneration during inflammation is known to contribute muscle mass gain St Pierre and Tidball, High-intensity exercise causes immune cell infiltration into challenged muscle to eliminate senescent cells Huang et al. The inflammation process includes stem cell homing, proliferation, and differentiation after phagocytosis by infiltrated immune cells in challenged muscle tissues Tidball, ; Wu et al. The increased reconstruction demand of exercised muscle may partly explain the disparity in the development of muscle and adipose tissues after exercise training. Lipoprotein lipase LPL attached on the surface of endothelial cells in capillary lumen determines relative partition of circulating triglycerides to muscle and adipose tissues after meals. The molecular size of triglyceride carried by chylomicron and VLDL is too large to transport across cell membrane of adipocytes from blood unless it is locally hydrolyzed by LPL in the adipose and muscle tissues. Relative LPL expression in adipose tissue and muscle tissues thus determines the daily distribution of circulating triglycerides chylomicron and VLDL partitioning into adipose tissues and skeletal muscle after meals. This suggests that exercise training favors postprandial triglyceride partitioning into skeletal muscle rather than adipose tissue. Fatty acids from lipolysis are continuously released from abdominal adipose tissue into the circulation and fat cells are continuously dying in normal human adults. The size of adipose tissue is determined by the magnitude of nutrient competition from muscle and lungs for cell regeneration and energy replenishment after exercise. This is varied by types of exercise aerobic or resistance exercise. Despite the fact that lower exercise intensity relies more on fatty acid oxidation, high-intensity exercise training anaerobic in nature provides a superior abdominal fat loss effect than low- and moderate-intensity exercise training. Given the fact that exercise does not increase h fatty acid oxidation during and after exercise training, the carbon and nitrogen redistribution theory is more suitable to explain the abdominal fat loss outcome of exercise training than fat burning theory. This reasonably explains why low- and moderate-intensity exercise often fail as strategies for fat loss despite the greater percentage of fatty acid oxidation compared with high intensity exercise. Studies on inter-tissue communication during exercise such as muscle-derived extracellular vesicles for post-meal carbon and nitrogen redistribution are promising and may provide useful application to normalize body composition and prevent obesity. Furthermore, the role of fatty acids on repairing post-exercise damage deserves further investigation. More data are needed to support the carbon and nitrogen redistribution theory on fat loss effect of exercise. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Abbasi, J. For fat burning, interval training beats continuous exercise. JAMA , — doi: PubMed Abstract CrossRef Full Text Google Scholar. Adams, G. Exercise and leukocyte interchange among central circulation, lung, spleen, and muscle. Brain Behav. Aggel-Leijssen, D. Effect of exercise training at different intensities on fat metabolism of obese men. Aguiari, P. High glucose induces adipogenic differentiation of muscle-derived stem cells. U S A , — Allerton, T. Exercise reduced the formation of new adipocytes in the adipose tissue of mice in vivo. PloS one e Barra, N. Interleukin treatment induces weight loss independent of lymphocytes. PloS One 7:e Chen, S. Effect of 2-month detraining on body composition and insulin sensitivity in young female dancers. Colberg, S. Exercise and type 2 diabetes. Diabetes Care 33, e—e Coll-Risco, I. Body composition changes following a concurrent exercise intervention in perimenopausal women: The FLAMENCO Project randomized controlled trial. Combes, A. Continuous exercise induces airway epithelium damage while a matched-intensity and volume intermittent exercise does not. Coppack, S. Postprandial substrate deposition in human forearm and adipose tissues in vivo. Cribb, P. Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. 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. Science has pretty clearly shown that during exercise, your muscles can use both dietary carbohydrate and fat operate as substrates used for energy. Your body has a finite amount of glycogen stored in the muscle. Once these stores are exhausted, the body will start pulling from your fat stores for energy. Low to moderate intensity forms of exercise primarily use fat as their source of energy. The higher you go with exercise intensity, the more you shift to burning glycogen and glucose. The longer you train, the more you deplete glycogen and once those stores are depleted, you will switch to burning fat for fuel. Additionally, the more fit you are, the lower your resting insulin levels will be, thus allowing you to burn more fat outside of your eating windows. Due to these factors, you can begin to understand why most fasted cardio sessions are performed at a relatively low intensity -- it maximizes fat burning in the body. The oxygen deficit created by high-intensity forms of training such as weight lifting or interval training leads to greater overall calorie burning as your body works to restore homeostasis. The point of this is to say that both steady-state and high-intensity interval training can be used to lose body fat. The mechanisms by which they work are different, but the end result is the same. Fat burning is a billion-dollar industry, yet very few people actually understand the theory and science of what it takes to burn fat, and even fewer know how to apply it to daily life. And, if you need some help burning extra calories and shifting your body towards a greater fat burning environment, check out Steel Sweat. Steel Sweat is the ideal pre-workout for fasted training. Not only does it include ingredients such as caffeine which help release fatty acids to be burned for energy it also includes several pro-fat burning compounds, such as L-Carnitine L-Tartrate and Paradoxine, which take those liberated fatty acids and burn them for energy. The Complete Guide to Thermogenesis. How Nutrients Get Absorbed into Muscles. Close 🍪 Cookie Policy We use cookies and similar technologies to provide the best experience on our website. Accept Decline. Your cart is empty Continue shopping. Clear Close. Ingredients The Complete Guide to Fat Oxidation. Educate them. Fat Burning vs. What does fat oxidation mean? What Happens during Fat Oxidation? Oxidation: Burning Fat for Fuel 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. How to Increase Fat Oxidation 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. Reduce Calories One of these ways is by reducing caloric expenditure, i. |
| Optimizing fat oxidation through exercise and diet | oxdation Arner, P. Determinants of fat oxidation during Nathral in Natural fat oxidation men Oxieation women: a cross-sectional study. Naturql FJ, Sanchez-Delgado G, Helge JW, Body composition and aging gracefully JR. Lipids are the substrate largely responsible for energy supply during submaximal exercise [ 123 ]. Circadian rhythms in sports performance—an update. J Sports Med Phys Fitness. Brenot F, Abenhaim L, Moride Y, Rich S, Benichou J, Kurz X et al Appetite-suppressant drugs and the risk of primary pulmonary hypertension. |
| Burning fat not so sweet | Nature Medicine | Nafural are Natural fat oxidation oxidaation fuel Natueal recognized largely as a positive Diuretic effect on liver diet adaptation [ 34 ], however, high intensity Natural fat oxidation relies primarily on glycolytic metabolism for ATP supply and therefore may be compromised [ 35 ]. Curr Opin Endocrinol Diabetes — Article CAS Google Scholar Carmen GY, Víctor SM. The result of increased beta-oxidative proteins is directly related to increased FAox potential [ 2954 ]. J Med Food 35 5 — With regard to human studies, Dulloo et al. |
| Physiological process of fat loss | Bulletin of the National Research Centre | Full Text | 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. Science has pretty clearly shown that during exercise, your muscles can use both dietary carbohydrate and fat operate as substrates used for energy. Your body has a finite amount of glycogen stored in the muscle. Once these stores are exhausted, the body will start pulling from your fat stores for energy. Low to moderate intensity forms of exercise primarily use fat as their source of energy. The higher you go with exercise intensity, the more you shift to burning glycogen and glucose. The longer you train, the more you deplete glycogen and once those stores are depleted, you will switch to burning fat for fuel. Additionally, the more fit you are, the lower your resting insulin levels will be, thus allowing you to burn more fat outside of your eating windows. Due to these factors, you can begin to understand why most fasted cardio sessions are performed at a relatively low intensity -- it maximizes fat burning in the body. The oxygen deficit created by high-intensity forms of training such as weight lifting or interval training leads to greater overall calorie burning as your body works to restore homeostasis. The point of this is to say that both steady-state and high-intensity interval training can be used to lose body fat. The mechanisms by which they work are different, but the end result is the same. Fat burning is a billion-dollar industry, yet very few people actually understand the theory and science of what it takes to burn fat, and even fewer know how to apply it to daily life. And, if you need some help burning extra calories and shifting your body towards a greater fat burning environment, check out Steel Sweat. The mode of exercise can also affect fat oxidation, with fat oxidation being higher during running than cycling. Endurance training induces a multitude of adaptations that result in increased fat oxidation. The duration and intensity of exercise training required to induce changes in fat oxidation is currently unknown. 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. Article ADS CAS Google Scholar. Canoy D Distribution of body fat and risk of metabolic disorders in man and woman. 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