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Maximizing fat metabolism

Maximizing fat metabolism

HIIT tat increase fat burning Anti-cancer support help you expend more Anti-cancer support in a shorter period than other Maximizlng of exercise. We link primary sources — including studies, scientific references, and statistics — within each article and also list them in the resources section at the bottom of our articles. Saito M, Matsushita M, Yoneshiro T, Okamatsu-Ogura Y.

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It found that when the carbohydrate consumed was of a low GI type pasta, chickpeas, sliced apples and low-fat cheese , fat oxidation rates were significantly higher during exercise and endurance was dramatically improved!

Other studies on cyclists have produced similar results. The temperature in which you train can affect your capacity to oxidise fat. Studies show that both very warm and very cold environments can inhibit fat burning during exercise 9,10 , with temperatures of about C being conducive to maximum fat oxidation.

As well as dressing appropriately therefore, it may also be worth investing in a decent cooling fan to prevent overheating indoors when training on your turbo trainer, treadmill running, ergo rowing machine etc. There are a number of nutritional supplements out there that claim to help increase fat burning.

The problem is that very few of these claims are supported by good scientific evidence. The mechanisms are not well understood but it is likely that the active ingredient in green tea EGCG inhibits the breakdown of a hormone called noradrenaline.

This in turn may result in higher blood concentrations of noradrenaline, which stimulates the release of stored fats making more fat available for oxidation in muscles during exercise. Later-season training The simple rules outlined above for early season training are fine when fat loss is the main goal.

This is primarily because if you want to excel during a race or perform intense training sessions, your muscles need to have plenty of carbohydrate — the premium grade fuel for high-intensity exercise — on tap. If we look at the tips above for fat loss during early season training, we can see that limiting pre-exercise carbohydrate intake and eliminating carbohydrate drink use are at odds with maximum performance on any particular day because they potentially lead to lower levels of muscle glycogen with a resulting drop in performance.

However, some sports scientists have been investigating whether you can have your cake and eat it — ie whether you can promote some fat loss during training, yet still perform enough high-intensity training and fuel the muscles optimally for maximum performance.

Unfortunately, while there are no studies specifically directed at answering this question, it is possible to piece together a strategy using data from a number of other studies in this area discussed below.

One thing that should be emphasised however is that in overall terms, as your training volume and intensity increases, so does the importance of carbohydrate.

Too little carbohydrate at the wrong time in your training cycle will seriously dent your performance - so seriously that no amount extra fat burning will adequately be able to compensate.

This is especially important in the run-up to a race day. Regardless of when your session is, use green tea extract 30 minutes before training and be sure to consume a high quality carbohydrate-protein recovery drink immediately after training. This is because training in a relatively low-carbohydrate state produces more muscle damage and breakdown than when carbs are consumed Taking a carbohydrate-protein drink soon after training will speed recovery and repair 16 and also help to minimise the post-exercise drop in immunity that often occurs after longer workouts In addition, be sure to follow this with a carbohydrate-rich meal; you need to replenish those muscles ready for the next higher intensity workout.

As mentioned above, green tea extract can be used before your longer workouts to enhance fat burning. Another supplement worth considering is caffeine. Caffeine is a central nervous system CNS stimulant and numerous studies have shown it can increase endurance performance by helping to offset CNS fatigue.

Zero-carb electrolyte drinks. Indeed, this is exactly the strategy that British cyclist Chris Boardman used to follow on his longer early-morning rides. Remember too that your day-to-day diet remains as important as ever. Summary The protocols described above for early and later season training will provide an effective way to help you both lower your body fat levels where needed and then keep them at an optimum level while you enter the later and more competitive phase of the season.

These protocols do not involve large volumes of high-intensity training in a carbohydrate-depleted state — a practice that is known to impair immunity increasing the risk of illness and also increase the risk of overtraining and breakdown.

This makes them suitable for sportsmen and women of all abilities. References J Appl Physiol , J Appl Physiol.

Jan;96 1 , J Physiol , , J Sports Sci , J Appl Physiol , J Sports Sci. Int J Sport Nutr Exerc Metab. Read More A fat lot of good: why older athletes could benefit from high-fat regimes.

Athletes: Yes or no to keto? Carbohydrate and training: don't go from hero to zero. Fat Burning: using body fat instead of carbohydrates as fuel. Andrew Hamilton Andrew Hamilton BSc Hons, MRSC, ACSM, is the editor of Sports Performance Bulletin and a member of the American College of Sports Medicine.

Register now to get a free Issue. Register now and get a free issue of Sports Performance Bulletin Get My Free Issue. Latest Issue. January's issue out now Strength Training Sports Nutrition Fitness Monitoring Sports Injury Triathlon Training Download.

Subscribe Today. Unlimited Access Monthly Magazine Back Issue Library Email Newsletter. More on this Athletes: Yes or no to keto? The fat controller: should swimmers fight fat for fitness? If the pounds come off deceptively easily, beware!

It's not fat that you're losing. GABA: a calmer route to a leaner body? Fat-burning after ovulation. Newsletter Sign Up. Stay on the fast track of sports performance with our newsletter First Name. Last Name. Initials of First Names.

sign me up. Testimonials Dr. Great bang for your buck in terms of quality and content. I love the work the SIB team is doing and am always looking forward to the next issue. Elspeth Cowell MSCh DpodM SRCh HCPC reg "Keeps me ahead of the game and is so relevant. The case studies are great and it just gives me that edge when treating my own clients, giving them a better treatment.

Thank you for all the work that goes into supplying this CPD resource - great stuff". Further reading A fat lot of good: why older athletes could benefit from high-fat regimes Andrew Hamilton looks at recent research suggesting that a short period of high-fat, low-carbohydrate dietary manipulation can help runners and other endurance athletes shed excess body fat.

In recent years, keto diets have been increasingly promoted to boost endurance performance. But do they really work and if so, how should athletes use them? Andrew Hamilton looks at the scientific evidence Carbohydrate and training: don't go from hero to zero Andrew Hamilton explains the potential benefits and pitfalls of 'zero-carbohydrate' drinks, and provides some guidelines for their proper use.

Fat Burning: using body fat instead of carbohydrates as fuel 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. Editor's Picks Endurance and strength: YOU have the best of both worlds.

Training intensity: is higher better, even for beginners? Endurance performance: can a short, sharp shock work wonders? High-intensity training: are sprint intervals overhyped? Mass with class: why sleep matters! Further Reading. Quality vs. Weight management: is protein better than nothing? SPB looks at new research on pre-exercise protein intake and explains how it could be a valuable tool for weight management.

Get My Free Issue. To maximize the health benefits of coffee, avoid adding large amounts of cream and sugar. Instead, enjoy it black or with a small splash of milk. Coffee contains caffeine, which may boost metabolism and fat breakdown.

Studies suggest that high caffeine intake may aid weight loss. High intensity interval training HIIT is a form of exercise that pairs quick bursts of activity with short recovery periods to keep your heart rate elevated. Studies show that HIIT is incredibly effective at ramping up fat burning and promoting sustainable weight loss.

One review found that doing HIIT 3 times weekly for an average of 10 weeks significantly reduced body fat mass and waist circumference For an easy way to get started, try alternating between walking and jogging or sprinting for 30 seconds at a time.

You can also cycle between exercises like burpees, pushups, or squats with short rest periods in between. HIIT may increase fat burning and help you expend more calories in a shorter period than other forms of exercise.

Probiotics are a type of beneficial bacteria found in your digestive tract. In fact, these bacteria have been shown to play a role in everything from immunity to mental health Increasing your intake of probiotics through either food or supplements may also rev up fat burning and support long-term weight management.

One review of 15 studies showed that people who took probiotics experienced significantly larger reductions in body weight, fat percentage, and BMI compared with those who took a placebo Another small study showed that taking probiotic supplements helped people following a high fat, high calorie diet stave off fat and weight gain Certain strains of probiotics in the genus Lactobacillus may be especially effective at aiding weight and fat loss Taking supplements is a simple, convenient way to get in a concentrated dose of probiotics every day.

Alternatively, you can eat probiotic-rich foods like kefir, tempeh, natto, kombucha, kimchi, and sauerkraut. Taking probiotic supplements or increasing your intake of probiotic foods may help reduce body weight and fat percentage. Intermittent fasting is a diet pattern that involves cycling between periods of eating and fasting.

Although it may not be a good fit for everyone, some research indicates that it may enhance both weight loss and fat loss. One review on intermittent fasting examined alternate-day fasting, a method in which you alternate between days of fasting and eating normally.

Another small study showed that eating only during an 8-hour window each day helped decrease fat mass and maintain muscle mass when combined with resistance training Intermittent fasting has been shown to reduce body weight and body fat. It may also help preserve muscle mass when combined with resistance training.

Studies suggest that gradual weight loss may be more beneficial for improving body composition and reducing body fat. Losing weight slowly may also reduce the risk of putting it back on again later 48, Both dietary strategies and exercise can help reduce belly fat.

You lose fat when you take in fewer calories, or less energy, than you use. Exercise can help burn fat and either maintain or build muscle No foods will specifically enable you to burn belly fat, but you are less likely to continue gaining weight if you focus on fresh fruits and vegetables, healthy fats, and whole grains rather than highly processed foods with a lot of refined carbs and added sugar.

Rather, you should incorporate healthy habits into your routine, such as eating whole grains instead of refined carbs, replacing sugary drinks with water, trying probiotics, or drinking coffee. Be sure to pair these simple nutrition tips with a well-rounded diet and active lifestyle to promote long-lasting, sustainable fat burning.

Finding a friend or family member with similar exercise or lifestyle goals may also help you hold yourself accountable. Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available. VIEW ALL HISTORY. Patients with diabetes who used GLP-1 drugs, including tirzepatide, semaglutide, dulaglutide, and exenatide had a decreased chance of being diagnosed….

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New research reveals the states with the highest number of prescriptions for GLP-1 drugs like Ozempic and Wegovy. Mounjaro is a diabetes medication that may help with weight loss.

Here's what you need to know about purchasing it without insurance. Eating up to three servings of kimchi each day is linked to a reduced rate of obesity among men, according to a new study.

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Nutrition Evidence Based 12 Ways to Promote Long-Term Fat Loss. Medically reviewed by Marie Lorraine Johnson MS, RD, CPT — By Rachael Ajmera, MS, RD — Updated on July 3, Strength training High protein diet Sleep Healthy fat Unsweetened drinks Fiber Whole grains Cardio Coffee HIIT Probiotics Intermittent fasting FAQ Bottom line Making changes to your diet, such as eating more protein and fewer refined carbs, may help increase fat loss over time and benefit your overall health.

Start strength training. Follow a high protein diet. Get more sleep. Eat more healthy fats. Drink unsweetened beverages. Fill up on fiber. Choose whole grains instead of refined carbs.

Increase your cardio. Drink coffee. Try high intensity interval training HIIT. Add probiotics to your diet. Try intermittent fasting. Frequently asked questions. The bottom line.

Was this helpful? How we reviewed this article: History. Jul 3, Written By Rachael Ajmera, MS, RD. Medically Reviewed By Marie Lorraine Johnson MS, RD, CPT.

Nov 29, Written By Rachael Ajmera, MS, RD. Medically Reviewed By Grant Tinsley, Ph. Share this article. Read this next.

There Anti-cancer support Maximizihg Maximizing fat metabolism and metbolism ways to support your metabolism, many Fiber optic cable management which involve making simple changes to Maximizinb Anti-cancer support Maximizong Maximizing fat metabolism. Your metabolism is responsible for converting nutrients from the Maximixing you eat into fuel. This provides your body with the energy it needs to breathe, move, digest food, circulate blood, and repair damaged tissues and cells. The higher your metabolic rate, the more calories you burn at rest. There are several evidence-based strategies that can help increase your metabolism to support weight management and overall health. This is called the thermic effect of food TEF. Protein causes the largest rise in TEF.

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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 HCAchromium, conjugated linoleic acid CLAguarana, 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 COMTwhich 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. At present, the only proven way to increase fat oxidation during exercise is to perform regular physical activity.

Exercise training will up-regulate the enzymes of the fat oxidation pathways, increase mitochondrial mass, increase blood flow, etc. Research has shown that as little as four weeks of regular exercise three times per week for minutes can increase fat oxidation rates and cause favourable enzymatic changes However, too little information is available to draw any conclusions about the optimal training programme to achieve these effects.

In one study we investigated maximal rates of fat oxidation in subjects with varying fitness levels.

In this study, we had obese and sedentary individuals, as well as professional cyclists 9. VO2max ranged from Interestingly, although there was a correlation between maximal fat oxidation and maximal oxygen uptake, at an individual level, fitness cannot be used to predict fat oxidation.

What this means is that there are some obese individuals that have similar fat oxidation rates to professional cyclists see figure 2! The large inter-individual variation is related to factors such as diet and gender, but remains in large part unexplained.

Fat burning is often associated with weight loss, decreases in body fat and increases in lean body mass. However, it must be noted that such changes in body weight and body composition can only be achieved with a negative energy balance: you have to eat fewer calories than you expend, independent of the fuels you use!

The optimal exercise type, intensity, and duration for weight loss are still unclear. Current recommendations are mostly focused on increasing energy expenditure and increasing exercise volumes.

Finding the optimal intensity for fat oxidation might aid in losing weight fat loss and in weight maintenance, but evidence for this is currently lacking. It is also important to realise that the amount of fat oxidised during exercise is only small.

Fat oxidation rates are on average 0. So in order to oxidise 1kg of fat mass, more than 33 hours of exercise is required! The duration of exercise, however, plays a crucial role, with an increasing importance of fat oxidation with longer exercise.

Of course, this also has the potential to increase daily energy expenditure. If exercise is the only intervention used, the main goal is usually to increase energy expenditure and reduce body fat. When combined with a diet programme, however, it is mainly used to counteract the decrease in fat oxidation often seen after weight loss Higher fat oxidation rates during exercise are generally reflective of good training status, whereas low fat oxidation rates might be related to obesity and insulin resistance.

The vast majority of nutrition supplements do not have the desired effects. Currently, the only highly effective way to increase fat oxidation is through exercise training, although it is still unclear what the best training regimen is to get the largest improvements.

Finally, it is important to note that there is a very large inter-individual variation in fat oxidation that is only partly explained by the factors mentioned above.

This means that although the factors mentioned above can influence fat oxidation, they cannot predict fat oxidation rates in an individual. Asker Jeukendrup is professor of exercise metabolism at the University of Birmingham. He has published more than research papers and books on exercise metabolism and nutrition and is also consultant to many elite athletes.

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: Maximizing fat metabolism

What You Need to Know About Burning Fat

Exercise intensity and duration are important determinants of fat oxidation. Fat oxidation rates increase from low to moderate intensities and then decrease when the intensity becomes high. 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.

However, while significant increases in FAox were observed with MCFAs compared to LCFAs [ 32 ], no differences were observed in endurance performance [ 32 , 33 ].

Jeukendrup and Aldred [ 33 ] suggest this may be due to the transport and rapid oxidation of MCFAs independent of carnitine palmitoyltransferases. Intuitively, this would seem advantageous, however the rapid transport and oxidation of short and MCFAs is suspected to increase ketone production opposed to increased exercise performance [ 33 ].

Ketones are a viable fuel source recognized largely as a positive ketogenic diet adaptation [ 34 ], however, high intensity exercise relies primarily on glycolytic metabolism for ATP supply and therefore may be compromised [ 35 ].

This concept is discussed in detail in subsequent sections. The transport protein known as carnitine palmitoyltransferase-1 CPT-1 is located on the outer mitochondrial membrane and is responsible for the transportation of LCFAs into the mitochondria shown in Fig.

Fatty acids with 12 or fewer carbons are classified as short or MCFAs and can pass through the mitochondrial membrane independent of protein transporters [ 31 , 33 , 38 ]. Nonetheless, CPT-1 is necessary for LCFA transport, a product of free carnitine, and is found in both the cytosol and mitochondrial matrix shown in Fig.

Proposed interaction within skeletal muscle between fatty acid metabolism and glycolysis during high intensity exercise. During high intensity exercise the high glycolytic rate will produce high amounts of acetyl CoA which will exceed the rate of the TCA cycle.

Free carnitine acts as an acceptor of the glycolysis derived acetyl groups forming acetylcarnitine, mediated by carnitine acyltransferase CAT. Due to the reduced carnitine, the substrate for CPT-1 forming FA acylcarnitine will be reduced limiting FA transport into the mitochondrial matrix.

This limits B-oxidation potential reducing overall FAox. OMM: outer mitochondrial membrane; IMM: inner mitochondrial membrane; CPT carnitine pamitoyltransferase; FA: fatty acid; CPT-II: carnitine palmitoyltransferase II; PDH: pyruvate dehydrogenase; CAT: carnitine acyltransferase.

Adapted from Jeppesen and Kiens 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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