Finally, the Top Antioxidant Sources of FAox in the ffat of performance during endurance oxodation is discussed. Maximal fat oxidation rates in an athletic population. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

Optimal fat oxidation -

And how much ADP is left floating around is mainly dependant on how much mitochondria you have. As muscular contractions occur, more ATP gets broken down.

Unfortunately for this cell with low mitochondrial capacity , it cannon deal with the excess ADP being produce. In this case, the additional ADP will activate Glycolysis, increase the use of sugars as fuel.

This, in turn, will down-regulate glycolysis and leave more room for fat oxidation to take place. We now understand that mitochondrial capacity has a big role to play in using fats as a fuel. Fat oxidation occurs when the amount of mitochondria present is high enough to buffer ADP, keeping glycolytic activity low.

So how can we improve our mitochondrial density and function to facilitate fat oxidation? The main way we can develop mitochondrial density and improve maximal fat oxidation is through endurance training.

But not all training intensities are the same! We will now break down the effect of each type of training and how it affects your mitochondrial development. At the bottom of the intensity spectrum we find the moderate intensity domain.

This domain sits below the first threshold and usually corresponds to Zone 1 and Zone 2. This type of training is really easy and can be done for many hours.

Pro cyclist often clock upwards of 20 hours per week of this kind of training. The advantage of this low intensity training is that is generates very little fatigue on the body. So you can do A LOT of it without burning out. Make sure you know what your physiological zones are to optimise your training.

Once we pass the first threshold we get to the heavy intensity domain. At those intensities, lactate levels will rise above baseline yet remain stable.

This type of training is obviously necessary for endurance performance. But performing too much of it without adequate recovery and without a strong low intensity foundation can have a negative impact on your mitochondrial development.

Once we move beyond this grey zone , we transition from the heavy to the severe intensity domain. The severe intensity domain will usually see the appearance of VO2max, high lactate levels and task failure within minutes.

However, we do see the development of both mitochondrial capacity AND function with those types of training sessions. The downside if this type of training if that it is very taxing both metabolically and mentally.

So accumulating large amounts of this type of work is not recommended. It should however be used as part of a structured training program with a sound intensity distribution. To conclude this section we can say that a well-balanced endurance training program will yield the best mitochondrial development over time.

This in turn will improve our fat oxidation ability and our performance. Now what is the link between fat oxidation and fat loss? Fat Oxidation describes the utilisation of fatty acid molecules by the mitochondria to recycle ATP.

Fat Loss describes a decrease in fat mass at the whole body level. We saw that fat utilisation is largely dictated by mitochondrial capacity. Instead, Fat loss is the result of maintaining a sufficient caloric deficit over time.

As I like to say, if you wish to lose fat or lose weight, you should eat like an adult and sleep like a baby! San-Millan et al.

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

Fat oxidation increases mainly through training and via an increase in mitochondrial capacity. This has a sparing effect on glycogen stores allowing the athlete to perform better later in the race. Stable isotope techniques: This involves consuming a small amount of a labeled form of fat, such as octanoate, and then measuring the labeled carbon in exhaled breath or urine to determine the rate of fat oxidation.

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

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

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

Maintaining a reasonable caloric deficit over time is the best way to lose weight and body fat. Your email address will not be published.

Save my name, email, and website in this browser for the next time I comment. What is Fat Oxidation? Therefore, the development of strategies aiming to decrease the total duration of a graded exercise protocol, while using long enough stage durations and relatively small workload increments, is of clinical relevance.

Of note is that despite the heterogeneity of protocols used, all studies consistently stopped the MFO and Fatmax test when the respiratory exchange ratio RER was 1.

This criterion was first applied by Achten et al. It remains unknown however whether reaching a RER of 1 is required to have an accurate, reliable, and valid measure of MFO and Fatmax in both sedentary and trained individuals.

This is a retrospective study of young sedentary adults age: Both cohorts completed two different exercise-based interventions 24 and 12 weeks, respectively and a total of 52 young trained adults age: Before participating in this study, the participants signed an informed consent form.

The investigations were approved by the Human Research Ethics Committee of the University of Granada no. We assessed MFO and Fatmax through a walking graded exercise protocol Amaro-Gahete et al. Participants were instructed to avoid any vigorous or moderate physical activity 48 and 24 h, respectively before the testing day.

They were asked not to consume stimulant beverages or dietary supplements during the 24 h before to test. Participants came to the research center in a fasting state of 6—7 h ~6. The graded exercise protocol began with a 3-min warm-up at 3.

Gas exchange parameters in the submaximal test were averaged every 10 s with the Breeze Suite software version 8. We considered the last 1 min of each 3-min stage Amaro-Gahete et al. We determined MFO and Fatmax using the measured-values data analysis approach i.

Figure 1. Case study example of a single participant. A It shows maximal fat oxidation during exercise MFO and the intensity that elicit MFO Fatmax using the measured-values data analysis approach i.

B It shows MFO and Fatmax building a 3rd polynomial curve with intersection at 0,0 from a graphical depiction of fat oxidation data as a function of exercise intensity expressed as percentage of the maximal oxygen uptake. We observed a RER at MFO of 0.

Interestingly, the RER at MFO were between 0. To note is that the graded exercise protocol total duration was Figure 2. The RER at MFO was 0. As in the sedentary group, we observed no sex 0.

The RER at MFO was between 0. Whereas these figures should be confirmed in other studies, we suggest reducing the RER from 1. More sophisticated data analysis approaches, such as 2nd or 3rd polynomial curve with intersection in 0,0 have been applied to accurately estimate MFO and Fatmax Stisen et al.

These methodologies require at least four fat oxidation values preferably six or more to determine MFO and Fatmax.

Reducing the maximum RER from 1. No meaningful differences in MFO were observed between both methodologies 0.

Similarly, there were no differences in MFO calculated with the measured-values data analysis approach 0.

These findings suggest that reducing maximum RER to 0. Reducing maximum RER until 0. Our data should however be taken with caution since we conducted a treadmill test, and we do not know whether these findings can be extended to cycle ergometer test.

Of note is also that our participants were healthy adults, thus future studies are needed to elucidate if these results can be applied to younger people or to patients. Future studies should confirm these findings in other populations of elite athletes or very well-trained individuals.

Moreover, future studies are needed to describe the slow component effect on VO2 kinetics in graded exercise protocols aiming to determine MFO and Fatmax. Finally, the work rates of our graded exercise protocol were based on absolute increments of the treadmill grade, instead of a personalized workload increase i.

In summary, our results have important implications, and may allow to substantially reduce the graded exercise protocol duration to assess MFO and Fatmax. Further studies are needed to investigate the impact of reducing the RER criteria on the MFO and Fatmax accuracy, by means of increasing the stage duration to attain the steady state and decreasing the workload increments magnitude.

The raw data supporting the conclusions of this manuscript will be made available by the authors, without undue reservation, to any qualified researcher. The investigations were approved by the Human Research Ethics Committee of the University of Granada No.

FA-G drafted the article. FA-G, GS-D, JH, and JR fully reviewed and criticized the original article. FA-G, GS-D, JH, and JR reviewed and approved the final manuscript.

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. We are grateful to Prof. Manuel Castillo and Ángel Gutiérrez for their scientific advices.

This study is part of a Ph. thesis conducted in the Biomedicine Doctoral Studies of the University of Granada, Spain. Achten, J.

Determination of the exercise intensity that elicits maximal fat oxidation. Sports Exerc. doi: CrossRef Full Text Google Scholar. Amaro-Gahete, F. Exercise training as S-Klotho protein stimulator in sedentary healthy adults: rationale, design, and methodology. Trials Commun.

Diurnal variation of maximal fat oxidation rate in trained male athletes. Sports Physiol. Impact of data analysis methods for maximal fat oxidation estimation during exercise in sedentary adults. Sport Sci. Assessment of maximal fat oxidation during exercise: a systematic review.

Sports 29, — Google Scholar. Commentary: contextualising maximal fat oxidation during exercise: determinants and normative values.

Bordenave, S. Exercise calorimetry in sedentary patients: procedures based on short 3 min steps underestimate carbohydrate oxidation and overestimate lipid oxidation. Diabetes Metab.

Journal oxidaion Top Antioxidant Sources International Society of Sports Nutrition Optiml 15 Wholesome nutrient sources, Optimal fat oxidation number: 3 Cite dat article. Metrics details. Lipids as a fuel source for energy supply during submaximal exercise originate from subcutaneous adipose tissue derived fatty acids FAintramuscular triacylglycerides IMTGcholesterol and dietary fat. These sources of fat contribute to fatty acid oxidation FAox in various ways. Fatty acid oxidation occurs during submaximal exercise intensities, but is also complimentary to carbohydrate oxidation CHOox. You are Top Antioxidant Sources 1 of Gluten-free diet for energy 1 free articles. Dat unlimited access take a risk-free oxidaton. Fat burning is a Top Antioxidant Sources popular and often-used Opfimal 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.

Optimal fat oxidation -

When we eat, fat will eventually appear in the blood stream and can potentially be taken up and used in the muscle. When we exercise, our need for energy increases dramatically because muscle contraction is an energy consuming process. Some of this energy will come from fat burning.

The availability of fat in the muscle. The enzymes in the muscle to break down triglycerides to fatty acids. The enzymes in the fat tissue elsewhere in the body to break down triglycerides to fatty acids. The supply of blood to the muscle. The presence of transport proteins to carry fatty acids from the blood into the muscle.

The efficiency of transport of fatty acids into the mitochondria we will discuss this in more detail in future blogs. The number of mitochondria. The quality of the mitochondria and the enzymes in the mitochondria to break down fatty acids. Because there are so many steps, there are also many regulatory mechanisms.

For example, the activity of the enzymes that break down fat triglycerides into fatty acids is regulated. Blood supply to the muscle is regulated as well as the uptake of fatty acids into the muscle and into the mitochondria.

Compare this process to a factory. The factory produces goods energy. For these goods to be produced we need raw materials fatty acids and oxygen. We also need machinery mitochondria and personnel enzymes.

There also needs to be a steady supply chain trucks that bring in the raw materials and it is important to remove any waste products CO2 or use them for recycling purposes.

With this analogy it is easier to understand that simply giving one of the workers in the factory more tools, will not automatically mean that the factory can produce more goods and will not mean that is uses more raw materials.

What will really improve productivity is if you could build more factories, with more machines, more personnel and improved delivery of raw materials. This is what training does.

By training you generate more mitochondria, more enzymes, more transport proteins, better blood supply to the muscle and faster breakdown of triglycerides into fatty acids. The end result is a greater capacity to burn fat. Fat oxidation is regulated at many levels and by many processes. It is therefore unlikely that a single intervention will significantly increase fat oxidation in a healthy person it may be different if there is something broken in the factory.

Training is a very effective way to increase the capacity of fat oxidation although this of course does not happen overnight. So now the basics are covered in future articles we can dive a little deeper and discuss the remaining questions about fat metabolism on mysportscience.

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Asker Jeukendrup 4 min read. Fat burning: how does it work? Why fat burning? People are searching for ways to "burn more fat". Back to basics. Fat storage and use. Perhaps the most fundamental determinant of whole-body fat oxidation rate is exercise intensity.

The relationship between exercise intensity and fat oxidation is generally parabolic; with fat oxidation initially increasing with exercise intensity before declining at high work rates Romijn et al.

Reductions in whole-body fat oxidation at high intensities are likely largely mediated by a reduction in delivery of fatty acids to skeletal muscle. Plasma non-esterified fatty acid NEFA rate of appearance is reduced at high exercise intensities despite unchanged rates of peripheral lipolysis Romijn et al.

The reduction in plasma NEFA availability and delivery to skeletal muscle is likely mediated by exercise intensity-induced reductions in adipose tissue blood flow Spriet, , which might itself be mediated by exercise intensity-induced increases in plasma catecholamine concentrations Romijn et al.

However, impaired mitochondrial fatty acid uptake might also contribute to the reduction in whole-body fat oxidation observed at high exercise intensities, given the observed reduction in mitochondrial uptake and oxidation of long-chain fatty acids with increasing exercise intensity Sidossis et al.

This may be explained by exercise intensity-induced reductions in free carnitine availability van Loon et al. Carnitine is a substrate in the CPT-I-catalyzed reaction resulting in mitochondrial fatty acid uptake Fritz and Yue, , and the reduced pH 7.

Therefore, the reduction in whole-body fat oxidation seen at high exercise intensities may be governed by reduced fatty acid delivery to and uptake in skeletal muscle. This graded exercise test elucidates whole-body fat oxidation rates across a range of exercise intensities, the maximal rate of fat oxidation MFO , and the intensity at which the MFO occurs Fat max using indirect calorimetry Figure 1.

This test advances on previous protocols using four incremental submaximal workloads Pérez-Martin et al. Importantly, this study found no significant difference in Fat max in a sub-set of well-trained participants asked to perform an additional 3-min step test, although it should be acknowledged that step durations of 6 min may be required for sedentary individuals to reach steady-state Bordenave et al.

Thus, the authors concluded two key theoretical limitations of step-test determination of substrate metabolism, namely shifts in substrate utilization over time and effects of prior steps, were not influential Achten et al.

The 3-min step protocol described here is indicative of those used in the literature subsequently Achten and Jeukendrup, a , b , , while the starting workload and work increment magnitude is adjusted in accordance with participant training status Rosenkilde et al.

Conceptually identical treadmill protocols have been used Achten et al. This relatively short protocol duration makes Fat max testing a viable monitoring tool for endurance athletes concerned with substrate metabolism during competition. Lastly, the practicality of this protocol is particularly important given attempts to predict MFO and Fat max based on heart rate, power, and estimated maximum oxygen uptake VO 2max have not been successful Brun et al.

Figure 1. Representative illustration of fat oxidation g. The reliability of Fat max assessments has been examined. The first reliability study of the Fat max protocol described above reported a coefficient of variation CV of 9. These CVs are similar to those for MFO measured in sedentary cohorts using 4—5 pre-defined submaximal workloads based on prior assessment of maximal aerobic power Gmada et al.

In contrast, a 6-min step test used to determine Fat max in a heterogeneous cohort of healthy males and females demonstrated wide limits of agreement and therefore considerable intra-individual variability Meyer et al. However, and critically, pre-trial diet and menstrual cycle was not controlled in this study, likely contributing to intra-individual variability given the reported influence of these variables on substrate oxidation during exercise Arkinstall et al.

The reason for this disparity in reliability is unclear, but may be related to the effectiveness of the pre-exercise dietary and exercise control measures Astorino and Schubert, Failing to adequately match pre-exercise muscle glycogen content is likely to impact MFO given muscle glycogen availability is an independent regulator of substrate metabolism during exercise Hargreaves et al.

As described above, the validity of the original Fat max protocol was examined against prolonged exercise bouts at intensities equivalent to those in the step test, with results from the step test demonstrated to be reflective of those over longer duration Achten et al.

Interestingly, Schwindling et al. No significant differences in absolute fat oxidation rates were observed between-intensities in the 1-h bouts, suggesting that results from short-duration Fat max tests may not be reflective prolonged exercise.

Therefore, Fat max testing might be used to quickly and non-invasively monitor metabolic adaptations to training, rather than to elucidate the metabolic consequences of given exercise bouts, which might require prolonged, steady-state assessments.

Regarding the use of Fat max assessments for deriving training prescriptions, statistical similarity has been observed between Fat max and the intensity at which the first increase of plasma lactate concentration LIAB occurs Achten and Jeukendrup, ; Tolfrey et al.

Agreement between Fat max and the lactate threshold has not always been observed, although it should be acknowledged that the dietary controls employed in this study were unclear González-Haro, This link might be explained by mitochondrial function, given β-oxidation of fatty acids to acetyl CoA, oxidation of fatty acid or non-fatty acid-derived acetyl CoA in the citric acid cycle, and oxidative phosphorylation along the electron transport chain all occur in the mitochondria McBride et al.

Indeed, mitochondrial fat oxidation capacity has been negatively correlated with whole-body respiratory exchange ratio during exercise Sahlin et al.

Given the already well-established relationship between cardiorespiratory fitness and a range of metabolic and cardiovascular disease outcomes Harber et al. However, this would require longitudinal studies investigating associations between changes in MFO and metabolic risk factors such as insulin sensitivity.

Therefore, Fat max tests appear a practical monitoring tool in performance settings where the capacity to utilize fat as a metabolic substrate is of concern, and might also be useful in clinical exercise physiology as an indicator of metabolic health.

The purpose of the present review is to extend previous summaries Jeukendrup and Wallis, ; Purdom et al. Normative values could be used to define the fat oxidation capacity of given research cohorts in exercise-metabolic studies in a manner analogous to VO 2max -based definitions of aerobic capacity.

Key directions for future research will be discussed. In order to explore the determinants of MFO and Fat max , a systematic literature search was performed to identify all studies using Fat max protocols in adult populations.

Hand searches of reference lists and key journals were also conducted. This search approach yielded 53 studies for inclusion in the review. In comparisons of trained endurance athletes with different levels of VO 2max , the better-trained group has greater MFO, with no difference in Fat max Lima-Silva et al.

Those studies comparing active with untrained individuals have observed significantly greater MFO Nordby et al. Alternatively, five large cohort studies with heterogeneous subject populations have all reported a significant small-to-moderate influence of VO 2max on MFO Venables et al.

A moderating effect of training status on MFO is not surprising given the previously observed significantly higher whole-body fat oxidation rates in trained compared to untrained males exercising at the same absolute workload van Loon et al.

Indeed, as a result of exercise training, skeletal muscle adaptations occur that augment fat oxidation during exercise Egan and Zierath, These include mitochondrial biogenesis Howald et al. An interesting direction for future research might be to compare MFO and Fat max between trained endurance athletes competing in events with different requirements for fat oxidation, e.

traditional endurance events such as half-marathon and marathon running and ultra-endurance events such as Ironman triathlons, and also to derive data from elite-level endurance populations. In order to quantitatively elucidate sex-mediated effects on these variables, sample size-weighted means and standard deviations SD for males and females were calculated.

Standard error was converted to SD through multiplication by the square root of the sample size Altman and Bland, SD for each study was collapsed by first squaring and then multiplying by the degrees of freedom.

A sample size-weighted overall SD was calculated as the square root of the sum of collapsed SDs divided by total degrees of freedom. However, some studies making comparisons between-sexes have reported MFO relative to fat-free mass FFM.

When expressed in these terms mg. This effect has been observed in moderately trained individuals Chenevière et al. In accordance with these findings, it has been observed that females have greater relative whole-body fat oxidation i.

The ovarian hormone estrogen may explain this sex difference Oosthuyse and Bosch, ; Devries, , as estrogen appears to stimulate lipolysis and NEFA availability D'Eon et al. The existing literature therefore suggests that whilst absolute MFO is generally greater in males compared to females, MFO relative to FFM is likely greater in non-obese females compared to non-obese males.

There also appears a minor tendency toward greater Fat max in females compared to males. Given sex-related differences in body mass and composition, MFO relative to FFM might be more descriptive when comparing between sexes. Whether these effects are observed in endurance-trained cohorts is unknown.

Similarly, effects of the menstrual cycle on MFO and Fat max have not been studied, but warrant consideration in the context of serial inter-individual measurement. Only one study has directly examined the effect of acute feeding status on MFO and Fat max Achten and Jeukendrup, b.

Trained males performed Fat max assessments on a cycle ergometer after an overnight fast, with 75 g of glucose or placebo ingested 45 min pre-exercise. MFO 0. This is likely explained by carbohydrate-induced insulinaemia, suppression of lipolysis, and suppression of fatty acid availability, which in turn might be expected to suppress whole-body fat oxidation in a manner similar to that seen at high exercise intensities Romijn et al.

Indeed, triglyceride and heparin infusion has been shown to increase plasma NEFA concentration, whole-body lipolysis, and fat oxidation rate during exercise with pre-exercise glucose feeding toward values observed during exercise after an overnight fast, suggesting that part of the suppressive effect of pre-exercise carbohydrate feeding on whole-body fat oxidation is explained by reduced fatty acid availability Horowitz et al.

Acute nutritional status is therefore a clear determinant of MFO and Fat max , and should be considered when comparing results between-studies as well as in serial intra-individual assessment.

However, further examination of this effect in untrained populations is warranted, as is the time-course and macronutrient content of pre-exercise feeding on measures of MFO and Fat max. Such data might provide exercise physiologists with guidelines when using Fat max tests for athlete monitoring and in health assessments, as conducting assessments at the exact same time of day is not always possible.

From a chronic dietary perspective, a recent large study of male and female subjects used hierarchical regression to elucidate the influence of a 4-day dietary record on MFO, and reported absolute carbohydrate and fat intakes accounted for 3. Whilst the degree of variance explained by diet was small in this mixed-cohort study, this contribution might be greater in homogenous cohorts.

Nevertheless, an independent effect of chronic macronutrient intake was observed, making it therefore a critical variable to control in repeat testing.

In a cross-sectional study involving a homogenous cohort of male ultra-endurance runners, MFO 1. high carbohydrate diet Volek et al. Interestingly, however, muscle glycogen utilization during prolonged steady-state exercise was not significantly different between-groups, suggesting habitual consumption of a ketogenic diet did not spare glycogen in working skeletal muscle Volek et al.

This might be particularly useful in a military context when long-duration tasks are performed McCaig and Gooderson, It is also possible that protein intake exerts an effect on MFO. During 3-month consumption of a weight-maintenance diet, increasing protein intake by ~10 g.

These results implicate modifying protein consumption as a potential strategy to alter MFO, although the contribution of the inevitably reduced daily carbohydrate consumption on MFO in this study was not quantified.

A further consideration is exercise modality. In general, studies comparing running and cycling at given exercise intensities have reported greater fat and reduced carbohydrate oxidation rates during running Snyder et al. However, comparisons of MFO and Fat max between-modalities have not been as conclusive.

The original study reported significantly greater MFO 0. A further study in a similar subject population failed to observe a significant difference in MFO, but did observe a greater Fat max during running Chenevière et al.

The reason for this disparate result in terms of MFO is not easily discernible, but could be related to between-study differences indirect calorimetry analysis of 1 vs. It is therefore recommended that the exercise modality in which Fat max tests are performed be considered when between-study and intra-individual comparisons are made, and by those preparing for multi-modal endurance competitions such as triathlons.

It has been demonstrated that the training status, sex, and acute and chronic nutritional status of the subject population or individual under study are clear determinants of MFO and Fat max , with a possible effect of exercise modality.

These determining factors must be considered when interpreting results between-studies and in serial intra-individual measurement. Given the interest in measurement of MFO and Fat max in research and non-research settings, it would be prudent to generate normative values from existing data in order to contextualize individually measured values and define the fat oxidation capacity of given research cohorts.

However, in order to do this, the aforementioned determinants of MFO and Fat max need to be considered. Accordingly, published MFO and Fat max values were synthesized from studies with homogeneous cohorts performing assessments after an overnight fast on a cycle ergometer. These criteria were applied in order to generate sufficient data to produce meaningful normative values.

Studies were subsequently partitioned into five populations: endurance-trained, lean males Achten et al. Baseline values were used for intervention studies. For synthesis, a sample size-weighted mean and SD for MFO was calculated for each population as described above for sex-mediated comparisons see section Sex.

Subsequently, normative percentile values were generated for each population assuming a within-population normal distribution Tables 1 , 2. Table 1. Normative percentile values for MFO g. Table 2. A trend toward greater MFO with increasing training status was observed Table 1 , and in males compared to females, which supports the evidence from individual studies presented above.

These normative percentile values might therefore be used by exercise physiologists to contextualize individual measurements and define the fat oxidation capacity of given research cohorts, whilst acknowledging the aforementioned determinants of MFO when making inferences.

It is worth noting that no data was available for endurance-trained female populations, which is a pertinent area for future research. It should also be noted that none of this data was derived from studies in which participants ingested a high-fat or ketogenic diet, which is known to increase fat oxidation during exercise Phinney et al.

Indeed, in many of the studies in endurance-trained males participants were specifically instructed to ingest a high-carbohydrate meal the evening before testing Achten et al. Therefore, these values are likely only of relevance to those ingesting a traditional mixed diet.

Many determinants of MFO and Fat max have been identified in the ~16 years since the original protocol was developed Achten et al.

However, given the practical utility of this protocol as a training monitoring tool in elite sport and as an indication of health status, further research is warranted to better understand what factors must be considered when measuring MFO and Fat max , as is research concerned with training effects on these variables and their relevance to endurance performance Figure 2.

Figure 2. Schematic illustration of the identified determinants of maximal fat oxidation during graded protocols black and key identified unknown factors gray. An unexplored parameter likely to alter MFO and Fat max is environmental temperature.

Environmental heat stress increases muscle glycogenolysis, hepatic glucose output, and whole-body carbohydrate oxidation rates, whilst reducing fat oxidation rates at given intensities Febbraio et al. This is attributed to independent effects of rising core temperature, enhanced muscle temperature, greater plasma catecholamine concentrations, and progressive dehydration Febbraio et al.

Given these effects, it might be hypothesized that MFO decreases in the heat compared to temperate conditions, although it is also possible that MFO is shifted to a lower Fat max. Elucidating this effect is a relevant consideration for endurance sport and military contexts given the likely negative effects of environmental heat on self-selected work intensity.

The effect of cold environments on substrate metabolism during prolonged exercise is less certain. Some investigations have reported augmented carbohydrate utilization in cold vs. temperate conditions Galloway and Maughan, ; Layden et al. Interestingly, Galloway and Maughan Galloway and Maughan, reported greater fat oxidation rates during moderate intensity cycling at 11 vs.

These disparities are not easily reconciled, and may be a result of interactions between the specific environmental conditions and exercise modality cycling vs. running Gagnon et al. Direct investigation of the impact of environmental temperature on laboratory measures of MFO and Fat max , and the environmental thresholds at which they occur, is therefore warranted.

This data would have strong applied relevance given the diverse environmental conditions in which endurance competitions take place Racinais et al. MFO is generally upregulated in response to exercise training Mogensen et al.

Training-induced increases in MFO have been consistently observed in sedentary populations Mogensen et al. Therefore, the existing literature suggests MFO is a malleable parameter that can be increased by both aerobic or interval training, particularly in sedentary populations.

Indeed, alongside long-standing observations of adaptations to fat metabolism in response to moderate-intensity training Howald et al. The most favorable training regimen for increasing MFO cannot presently be discerned. Training studies have generally utilized either prolonged moderate-intensity aerobic exercise Mogensen et al.

Interestingly, differences in the magnitude of training-induced increases in MFO were not observed for moderate and high-intensity interval training in these studies Venables and Jeukendrup, ; Alkahtani et al. Furthermore, whilst promising effects of training with low-glycogen availability on whole-body fat oxidation rates during prolonged exercise have been observed Yeo et al.

There is also a notable absence of data concerning the responsiveness of MFO and Fat max to training in endurance-trained cohorts. As endurance-trained individuals already have elevated MFO compared to lesser-trained populations, it remains to be determined if these individuals can accrue further advances in MFO through optimized training practices.

It would also be useful to discern if training-induced changes in MFO reflect alterations in substrate metabolism during prolonged exercise, as the relatively short-duration of this protocol makes it a viable monitoring tool in elite sport. Therefore, whilst it has been demonstrated that exercise training per se improves MFO in untrained populations, this effect remains to be elucidated in trained populations, and the most appropriate training regimen for increasing MFO is unknown.

These are worthy directions for future research given the likely importance of fat oxidation capacity in endurance sport and military settings, and the apparent relationship between MFO and insulin sensitivity Robinson et al.

If an individual makes extensive use of fat oxidation to support metabolism during prolonged exercise at their competitive or operational intensity, this should reduce the requirement for endogenous carbohydrate oxidation, and therefore muscle glycogen depletion, which is linked to fatigue Bergström et al.

Indeed, at a given absolute workload, significantly higher whole-body fat oxidation and lower muscle glycogenolysis have been observed in trained compared to untrained males van Loon et al. A link between MFO, Fat max , and endurance exercise performance is further supported by cross-sectional evidence demonstrating enhanced MFO in trained compared to untrained cohorts Nordby et al.

However, the importance of MFO and Fat max for exercise performance has not yet been comprehensively studied, and such research is warranted. Metabolically, a cross-sectional study of elite ultra-distance runners demonstrated greater MFO and Fat max in those adapted to ketogenic diets, but the rate of glycogenolysis in working skeletal muscle during prolonged exercise was not significantly different compared to those ingesting a high-carbohydrate diet, despite higher whole-body fat oxidation rates Volek et al.

Therefore, MFO, Fat max , and whole-body fat oxidation rates were dissociated from skeletal muscle glycogenolysis during prolonged endurance exercise between these groups, which might question the hypothesis linking MFO and Fat max to endurance exercise performance via muscle glycogen sparing.

However, it is possible this dissociation was an artifact of the measurement site, and that a carbohydrate sparing effect in the ketogenic group was observed in the liver, as observed previously Webster et al. An interesting avenue for future research might therefore be to determine if MFO and Fat max are indicators of the degree of endogenous carbohydrate utilization and skeletal muscle glycogenolysis during prolonged exercise within a homogenous group of endurance-trained athletes, and consequently if such an effect has implications for endurance exercise performance.

Such data would provide indication of the functional relevance of monitoring MFO and Fat max in endurance-trained athletes, and could serve to build on existing models of endurance exercise performance McLaughlin et al.

This review has systematically identified several key determinants of MFO and Fat max. These include training status, sex, acute nutritional status, and chronic nutritional status, with the possibility of an effect of exercise modality.

Accordingly, normative percentile values for MFO and Fat max in different subject populations are provided to contextualize individually measured values and define the fat oxidation capacity of given research cohorts.

However, the effect of environmental conditions on MFO and Fat max remain to be established, as does the most appropriate means of training MFO and Fat max , particularly in endurance-trained cohorts.

Furthermore, direct links between MFO, Fat max , and rates of muscle glycogenolysis during prolonged exercise remain to be established, as do relationships between MFO, Fat max , and exercise performance. This information might add to existing models of endurance exercise performance, and indicate how useful MFO and Fat max monitoring might be in endurance sport.

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. EM is funded by an Education New Zealand scholarship no role in preparation of the manuscript.

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