Limitations to FAox are due in part to a multi-faceted delivery system that has a series of regulatory events [ 18 ].

Once FAs leave the adipocyte they first bind to albumin, which can bind as many as 12 FA molecules [ 15 ]. Interestingly, due to poor circulation in peripheral adipose tissue and an increased ratio of FA:albumin after exercise, the albumin binding capacity may be surpassed and high levels of unbound serum free fatty acids can create a harmful condition [ 15 ].

Due to poor circulation in type II diabetics, a high percentage of liberated FAs as a result of exercise-induced, catecholamine-stimulated lipolysis are not released into the circulation during high intensity exercise [ 13 ]. However, endurance training has been shown to increase blood flow to subcutaneous adipose tissue by 2—3 fold [ 13 ], which can increase overall FA transport to working muscle.

Despite the positive circulatory effects of endurance training, limitations to the rate of FAox appear to be mediated by cellular transport rather than systematic transport of serum FAs from adipose tissue [ 24 ].

Fatty acid transport across the muscle cell membrane occurs via transport proteins, mainly CD36 [ 24 , 25 ]. CD36 appears within the plasma membrane in as little as 1 min after the initiation of muscle contraction [ 25 ].

Moreover, CD36 upregulation occurs rapidly and remains elevated for 3 days post exercise. In humans, sex differences have been shown to effect CD36 expression [ 27 , 28 ] due to circulating estrogen concentrations [ 29 ].

Additionally, Kiens et al. In summary, transport of FAs across the cell membrane positively affects FAox [ 13 , 26 , 30 ]. Endurance training increases CD36, thereby increasing intracellular transport for oxidation.

Increasing transport of FAs into the cell for oxidation spares CHO stores for both high intensity exercise and prolonged exercise [ 11 ]. Within the cell, FA chain type and length have been shown to determine oxidative rates within the mitochondrion largely due to transport specificity [ 31 ].

An inverse relationship of FA carbon chain length and oxidation exists where the longer the FA chain the slower the oxidation [ 31 ]. Interestingly, this relationship inspired the supplementation of short and medium chain fatty acids MCFA as an ergogenic aid.

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.

Achten J, Jeukendrup A. Optimizing fat oxidation through exercise and diet. Article CAS PubMed Google Scholar. Venables M, Achten J, Jeukendrup AE. Determinants of fat oxidation during exercise in healthy men and women: a cross-sectional study. J Appl Phys.

Google Scholar. Volek JS, Noakes T, Phinney SD. Rethinking fat as a fuel of endurance exercise. Eur J Sport Sci. Article PubMed Google Scholar. Brooks GA, Mercier J. Balance of carbohydrate and lipid utilization during exercise: the "crossover" concept.

CAS Google Scholar. Achten J, Gleeson M, Jeukendrup AE. In contrast to our findings, the LGI diet over 3 weeks resulted in a slight downregulation of fat oxidation during exercise However, in the study by Durkalec-Michalski et al.

Furthermore, the decrease in RER values was not statistically significant and did not reach the MID in the present study. The LGI intervention seemed to have a smaller impact on metabolic adaptations than the HFLC diet. The up-regulating signals of fat oxidation are low insulin concentration and increased concentrations in plasma free fatty acids 2 , 3.

A direct comparison between four meals, each different in the amount and GI of the ingested carbohydrates, has shown that both high fat groups were associated with the highest postprandial free fatty acid and lowest insulin concentrations.

The lowest free fatty acid concentrations were in the group consuming a low glycemic carbohydrate-rich meal. Furthermore, postprandial insulin response was lower in the high carbohydrate low GI group compared to the high carbohydrate high GI group Consequently, the abovementioned adaptation processes might be less in a high carbohydrate low glycemic diet compared to a HFLC diet due to the different impact on postprandial free fatty acid and insulin concentrations.

The nutritional impact on fat metabolism might also be reflected by the circulating glucose concentrations.

Fasting glucose plasma concentrations dropped in the LGI-G to a significant and MID relevant extent. Changes in the HFLC-G seemed to be less pronounced, potentially as a consequence of relatively low baseline values compared to the other groups.

During the post-intervention, incremental test glucose concentrations are lower at the same exercise intensity as in the unconditioned pre-values state in both LGI-G and HFLC-G.

This is probably related to a stimulation of fat oxidation under resting conditions and during exercise The results of the HGI-G seemed to be controversial. The increased RER at rest in the HGI-G indicates an elevated metabolization of carbohydrates under resting conditions.

In addition, the lactate concentration increase was clinically relevant under pre-exercise condition. Despite increased lactate concentrations during the incremental test, it seems that there is an improved fat metabolism -decreased glucose and lactate values- in the submaximal cycle test.

It had previously been described that carbohydrates prior to exercise appear to be beneficial to performance 1. Hence, the slightly decreased carbohydrate metabolism in the submaximal test might be partly explained by the increased lactate threshold over the time as a possible adaptation in response to enhanced performance.

As a result, at post-intervention, the participants performed the test closer to their lactate threshold compared to baseline.

The current investigation also observed an improvement in body composition due to a decrease in fat mass following the 4-week LGI or HFLC diet on the level of significance and MID. It is not assumed that the present results can be attributed to the differences in energy intake between groups.

Despite the significant difference in proportions of nutrients, the mean energy intake was equivalent between groups with an energy add-on of kcal in the HFLC-G. According to the findings of Hall et al.

There is evidence that athletes can improve their body composition by a high fat in particular ketogenic diet 42 — Low carbohydrate diets compared with control diets have been suggested to be relatively more effective in body weight management.

However, the benefits of a low carbohydrate diet can be rather attributed to the relatively high protein content, but not the relatively lower carbohydrate content 45 , In a recent study with athletes, different approaches high vs. low fat but similar protein intakes resulted in a similar change of body composition mean loss in body fat was 1.

These are in accordance with a meta-analysis examining the impact of different diet types in obese or overweight people Data from the meta-analyses of the Cochrane Database of Systematic Reviews suggest that a low glycemic diet without energy restriction results in a significantly greater decreased fat mass and an increased fat free mass compared with a high glycemic or even high fat and energy restricted diet Although low glycemic diets seem to promote weight loss and metabolic improvements in obese and overweight adults 48 , research about the impact of the GI on body composition in endurance athletes is limited.

A recent study by Durkalec-Michalski et al. has shown that consuming a low glycemic diet led to a change in body composition.

In particular, a statistically significant reduction in body mass Physiologically, the significant changes in body composition in the present investigation might be explained by changes in fat oxidation and a more balanced carbohydrate metabolism as a potential consequence of the altered amount and quality of ingested carbohydrates.

Despite an improvement in fat metabolism and body composition, there is a growing body of evidence that these changes induced by ketogenic or non-ketogenic HFLC diets are not in association with improved endurance performance, aerobic capacity and peak performance in particular 9 , 32 , 50 , 51 , due to an impaired carbohydrate provision during higher intensities 2.

This assumption is supported by the changes in time to exhaustion in the present investigation. Furthermore, HFLC diets seem to be impractical and accompanied by side effects that include fatigue, headaches, poor concentration, lethargy, gastrointestinal discomfort, nausea, and unintentional weight loss.

One reason might be an insufficient proliferation of essential micronutrients and fibers and glycogen depletion which might be a cause of impaired concentration and hence the neuromuscular connection 9 , The values of the VAS scores of all categories decreased in all groups, indicating that the participants got familiar with the respective dietary concepts.

In general, none of the groups experienced clinically relevant elevated VAS scores. Mild symptoms can be defined by a score of 5 to 45 mm on the VAS This might be explained by the fact that endurance subjects tolerate the effects of a high-fat diet better than untrained individuals during exercise In addition, according to the nutritional protocols, an impaired delivery of minerals in the HFLC group was not expected.

However, only the LGI-G and HGI-G have shown an improvement in VAS scores of the subscale activity and gastrointestinal comfort on a statistical or MID level with a superior effect in the LGI-G.

These results might be associated with impaired training sessions in the HFLC-G since higher intensity levels could not be reached without the provision of carbohydrates 2.

Furthermore, the advantage of LGI diet over HFLC and HGI diets might be in the choice of carbohydrates. A LGI diet is predominantly characterized by high-fiber and plant-based foods. This has shown to be associated with reduced fatigue, a strengthened immune system, and an improved ability to regenerate through the increased supply of micronutrients, essential fatty acids and amino acids, and low postprandial glucose concentrations Moreover, controlled clinical trials demonstrated that low glycemic foods have a positive impact on digestive conditions, such as gastroesophageal reflux disease or the irritable bowel syndrome, due to high fiber content 56 , It can be assumed that the present results can be attributed to the implementation of nutritional patterns.

According to the analysis of the nutritional protocols, the participants' dietary intake reflected the specified intake of carbohydrates and fats in the respective group. While the HGI-G had a higher percent and total carbohydrate intake, the LGI-G showed a higher carbohydrate intake on a g-per-kg-body-weight basis.

The current guidelines for endurance athletes during training on the competition level are 6—10 g carbohydrates per kg body weight and day.

These recommendations do not address the GI of the ingested carbohydrates The participants of the current investigation were non-elite athletes with a training workload of 3—5 sessions per week.

In both groups, the carbohydrate intake seems to be sufficient since recommendations are 5—7 g carbohydrates per kg bodyweight and day for general training needs Nevertheless, increasing the carbohydrate intake to 6—10 g carbohydrates per kg body weight and day would be an interesting approach in future studies with high trained endurance athletes.

The carbohydrate upper limit of 50 g per day in the HFLC-G was based on the current focus of carbohydrate-restricted diets 9. This trial has some limitations. It has to be mentioned that the changes in fat and carbohydrate oxidation were not measured directly but extrapolated from the lactate diagnostics.

However, it is reported that measuring blood lactate is an effective way to estimate the rates of fat and carbohydrate oxidation Furthermore, using the values of the spiroergometry to confirm the results from the lactate diagnostic during the incremental test has to be taken with caution since values for VO 2 are overestimated by a step compared to a ramp incremental test When taking the impact of the nutritional concepts into account, limitations of the self-reported protocols might entail an over or underreporting of the consumed foods Moreover, recommendations for the macronutrient intake based on the body weight seems to be more accurate than percentage values to determine nutritional guidelines for endurance athletes.

Future studies with a larger sample size should include different sex groups and pre-exercise nutritional conditions to state practical use of high fat vs. high carbohydrate diets. Furthermore, the analysis of the muscle glycogen would be helpful for a better interpretation of the energy supply 9.

Ultrasonic assessment can be used to quantify glycogen content in the skeletal muscle In conclusion, the effect of the LGI diet was a decrease in lactate concentrations under resting and submaximal exercise conditions, while HFLC diet resulted additionally in decreased RER values.

However, these lower adaptations in the LGI-G seem to be beneficial in terms of an enhanced metabolic flexibility, since an increased carbohydrate metabolism was unaffected during higher intensities, while the utilization of fats was facilitated during submaximal exercise due to decreased plasma lactate concentrations.

Despite the positive impact on the fat oxidation and body composition, following a HFLC diet might have a negative effect on exercise performance due to the lack of carbohydrate provision at higher intensity levels.

In addition, there might be negative long-term health consequences due to the high fat content and decreased intake of essential micronutrients. The HGI-G changes in metabolism might impair the ability to effectively use fats and carbohydrates during different exercise intensities.

Taking these findings together, the implementation of a LGI diet leads to a more flexible fat and carbohydrate metabolism after 4 weeks of intervention in contrast to a HFLC or HGI diet, which might be of advantage, particularly during strenuous endurance exercise.

After the study was finished, DZ started as a researcher in the Collagen Research Institute, Kiel. The raw data supporting the conclusions of this article will be made available by the authors, without undue reservation.

DZ, HF, AG, and DK designed the study. DZ, HF, and DK were responsible for data acquisition and performed the analysis. All authors read and approved the final version of the 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. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers.

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.

We would like to thank all the participants and the staff of the University of Freiburg who supported us with the examination. Ormsbee MJ, Bach CW, Baur DA. Pre-exercise nutrition: the role of macronutrients, modified starches and supplements on metabolism and endurance performance.

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

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

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

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

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

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

What is Fat Oxidation? When does Fat Oxidation occur? How can I measure Fat Oxidation? How can I Increase Fat Oxidation? Will Fat Oxidation help me lose Body Fat? Share This. Next Post High Lactate Levels During Exercise: What Causes Them? You May Also Like. Leave A Comment Cancel reply Your email address will not be published.

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On the basis that conventional competitive sports generally provide opportunities to achieve adequate carbohydrate availability, that fat-adaptation strategies reduce rather than enhance metabolic flexibility by reducing carbohydrate availability and the capacity to use it effectively as an exercise substrate, and that athletes would be unwise to sacrifice their ability to undertake high-quality training or high-intensity efforts during competition that could determine the outcome of even an ultra-endurance sport, this author decided to abandon a research and practical interest in fat-adaptation strategies.

Given the recent escalation in the promotion of LCHF diets for sports performance, it could be assumed that the last decade has seen the publication of a considerable number of studies with clear evidence of benefits to sports performance following the implementation of fat-adaptation strategies.

Yet, to the knowledge of this author, only two new investigations of LCHF diets in athletes have appeared in the peer-reviewed literature since [ 49 , 50 ].

These studies, summarized in Table 2 , fail to show performance benefits associated with a ketogenic LCHF diet, although there is evidence of a small but favorable reduction in body fat levels.

Nevertheless, there are some peculiarities with the design or methodologies of these studies, including the failure of one study to achieve the carbohydrate restriction typically associated with the ketogenic LCHF diet, and they have failed to become widely cited, even by supporters of the LCHF movement.

Rather, the current interest in chronic application of LCHF eating by athletes appears to be driven by enthusiastic discussion in lay and social media by mostly non-elite athletes of sporting success following experimentation with such diets as well as a range of outputs from several sports scientists who are researchers and advocates of this eating style [ 3 — 8 ].

It is uncertain whether there is a cause—effect relationship between these sources or the direction of any relationship , but the fervor merits attention. In the absence of compelling new data, the reader is alerted to several elements in the discussions that are positive and some that are concerning:.

Peer-reviewed publications from the key scientific protagonists of the LCHF movement [ 3 , 5 , 6 ] generally show measured and thoughtful insights, based on a re-examination of previously conducted studies, personal experiences, anecdotal observations from the sports world, and the general interest in tackling modern health problems with the LCHF approach [ 51 , 52 ].

In these forums, the discussion points include the lack of evidence and equivocal outcomes of research to support the performance benefits of LCHF but also theoretical constructs around potential benefits to metabolism, muscle, and brain function, inflammatory and oxidative status, and body composition management.

While there are some suggestions that a larger group of athletes might benefit from an LCHF approach, the general tone is that further investigation of these theories is required [ 3 — 6 ]. The apparent caution expressed in peer-reviewed publications is generally not present in other outputs from the same authors.

The differences between these viewpoints can be confusing, as is the misrepresentation of the physiological requirements of competitive sports see Sect. Many of the theorized benefits from the LCHF diet are claimed to come from the adaptation to high circulating levels of ketone bodies, which provide an additional fuel source for the brain and muscle as well as achieve other health and functional benefits [ 5 , 6 ].

The amount of energy that can be provided by ketones as an exercise substrate has been neither calculated nor measured, making it impossible to verify this claim. The time required to achieve optimal adaptation and, therefore, the period that requires investigation in new studies is claimed to be at least 2—3 weeks, with at least 1 week required before the feelings of lethargy and reduced exercise capacity abate [ 5 , 6 ].

With such chronic keto-adaptation, it is considered unnecessary to consume carbohydrate during exercise, or perhaps to consume it in small amounts [ 5 , 6 ]. As has been discussed in this review, the current evidence for these claims is equivocal and mostly anecdotal.

Until or unless further research is undertaken, we are unlikely to resolve any of the current questions and claims. The role of non-ketogenic LCHF diets is not clear. The current literature on LCHF diets is relentless in promoting misunderstanding or misinformation on the current guidelines for athletes in relation to carbohydrate intake in the training or competition diet.

It would benefit sports nutrition for researchers and practitioners to show mutual respect in recognizing the evolution of new ideas and the replacement of old guidelines with new recommendations [ 53 ]. Indeed, modern sports nutrition practitioners teach athletes to manipulate their eating practices to avoid unnecessary and excessive intakes of carbohydrates per se, to optimize training outcomes via modification of the timing, amount and type of carbohydrate-rich foods and drinks to balance periods of low- and high-carbohydrate availability and to adopt well-practiced competition strategies that provide appropriate carbohydrate availability according to the needs and opportunities provided by the event and individual experience [ 14 , 54 — 57 ].

This author and others continue to undertake research to evolve and refine the understanding of conditions in which low carbohydrate availability can be tolerated or actually beneficial [ 58 , 59 ].

However, we also recognize that the benefits of carbohydrate as a substrate for exercise across the full range of exercise intensities via separate pathways [ 16 ], the better economy of carbohydrate oxidation versus fat oxidation ATP produced per L of oxygen combusted [ 60 ], and the potential CNS benefits of mouth sensing of carbohydrate [ 61 ] can contribute to optimal sporting performance and should not be shunned simply because of the lure of the size of body fat stores.

Considering that athletes might best benefit from a range of options in the dietary tool box is likely to be a better model for optimal sports nutrition than insisting on a single, one-size-fits-all solution.

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Download references. This article was published in a supplement supported by the Gatorade Sports Science Institute GSSI. The supplement was guest edited by Lawrence L.

Spriet, who attended a meeting of the GSSI expert panel XP in March and received honoraria from the GSSI for his participation in the meeting.

He received no honoraria for guest editing the supplement. Spriet selected peer reviewers for each paper and managed the process.

Louise Burke attended a meeting of GSSI XP in February , and her workplace Australian Institute of Sport received an honorarium from the GSSI, a division of PepsiCo, Inc.

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Leckey J, Burke J, Morton J, Hawley J. Altering fatty acid availability does not impair prolonged, continuous running to fatigue: evidence for carbohydrate dependence. J of Appl Physiol. Download references. Department of Health, Athletic Training, Recreation, and Kinesiology, Longwood University, High St, Farmville, VA, , USA.

Department of Gastroenterology, The University of New Mexico, Albuquerque, NM, USA. You can also search for this author in PubMed Google Scholar. Correspondence to Troy Purdom. TP currently has accepted abstracts with ACSM, NSCA, and ISSN in the area of fat metabolism, athletic performance evaluation, energy expenditure, and body composition.

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Abstract Lipids as a fuel source for energy supply during submaximal exercise originate from subcutaneous adipose tissue derived fatty acids FA , intramuscular triacylglycerides IMTG , cholesterol and dietary fat. Background Lipids are the substrate largely responsible for energy supply during submaximal exercise [ 1 , 2 , 3 ].

Lipid oxidation Lipolysis Triacylglycerol TAG is the stored form of fat found in adipocytes and striated muscle, which consists of a glycerol molecule a three-carbon molecule that is bound to three fatty acid FA chains. Fatty acid transport Limitations to FAox are due in part to a multi-faceted delivery system that has a series of regulatory events [ 18 ].

Within-cell FA transport into mitochondrion Within the cell, FA chain type and length have been shown to determine oxidative rates within the mitochondrion largely due to transport specificity [ 31 ].

Full size image. Conclusion In summary, FAox is contingent on many factors which can modify cellular expression in a short amount of time.

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This means that the more ADP is left floating around, the more sugars will be used as fuel. 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. Due to their low energy flow rate, the percentage contribution of fat oxidation to total energy provision is low during short intensive exercises and increases with the duration of the exercise and the decrease in intensity 6.

The intake of high glycemic carbohydrates and the resulting high insulinemic response are one of the strongest inhibitors of fat oxidation 7. Therefore, several clinical studies focused on improving fat utilization during endurance exercise by high fat low carbohydrate diets 8.

The current state of evidence suggests a diet with less than 50 g of carbohydrates per day 9. A metabolic adaptation toward increased fat oxidation is usually achieved following a 2- to 4-week dietary intervention 9 , However, high fat diets are associated with an impaired carbohydrate utilization during higher intensities 11 — 14 and, consequently, with small positive effects on endurance performance even with a carbohydrate restoration phase prior to competitions 9.

This altered metabolic flexibility can be explained by a reduced enzyme activity in the carbohydrate metabolism due to a reduced training effect within the carbohydrate metabolism following reduced carbohydrate availability or reduced signaling at low glycogen concentrations 2 , 3.

In this context, a promising concept might be the consideration of the glycemic index GI in the diet. It was shown that the fat oxidation during exercise increased after the consumption of low GI carbohydrates compared to high GI carbohydrates 15 — This effect can be explained by a reduced postprandial insulin release which leads to an increased plasma concentration of free fatty acids and increased fat oxidation in the skeletal muscles 2 , 3.

In consequence, intramuscular and intrahepatic glycogen stores are spared and can be used during higher intensities of exercises. In addition to the GI, the glycemic load GL which considers the amount of carbohydrates in a given serving of a food also affects blood glucose concentrations and insulin responses To the best of our knowledge, studies comparing high fat with high carbohydrate diets have not considered the GI or GL of the carbohydrates.

In addition, long-term investigations examining the influence of the GI or GL are limited and without a high fat low carbohydrate control. Therefore, the aim of the current pilot study was to examine the impact of a high fat low carbohydrate HFLC-G vs.

high carbohydrate low glycemic LGI-G vs. high carbohydrate high glycemic HGI-G diet on metabolic parameters, body composition, and perceptual responses to the diets.

The study was designed as a monocentric, prospective, open pilot trial conducted at the University of Freiburg, Germany. In total, 30 healthy male endurance athletes as distance runners, cyclists, and athletes performing basic endurance training e.

The sample size was set on 10 participants per group to obtain information for a power analysis to specify meaningful group differences Professional-level athletes more than five training sessions per week were not eligible to participate.

Reported health problems during or after physical activity or unstable weight and eating behavior were also defined as exclusion criteria. In addition, contraindications to physical activity according to the American College of Sports Medicine guidelines, such as cardiovascular, metabolic, or renal diseases 22 diagnosed from anamnestic data, led to an exclusion of the screened participants.

The examination was approved by the Ethical Committee of the University of Freiburg ETK: and registered in the German Clinical Trials Register DRKS For all visits, the participants were advised to arrive at the University of Freiburg in the morning at the same time following a fasted period of 12 h.

In addition, general guidelines were to drink 1 L of water in the evening and another 0. In addition, the participants had to void bladder before the measurement. Alcoholic beverages had to be avoided 48 h prior to respective examination.

All experimental testing was supervised by a licensed physician and experienced researchers. After the start of the intervention, any concerns were clarified directly with the study physician or researcher via telephone call.

The study was completed within a timeframe of 4 weeks. The different phases of the study are summarized in Figure 1. Figure 1. Overview of the study schedule. BIA, bioelectric impedance analysis; VAS, visual analog scale. Following written informed consent, participants completed a screening with a medical history questionnaire to ensure that the inclusion criteria were met and that there were no risk factors that might be aggravated by the exercise protocols.

Furthermore, anthropometric data, including the body composition as described in the test block below , were measured. An incremental cycling test was performed cycling 3 min at W, then increasing 20 W per 3 min until exhaustion on a stationary cycloergometer Ergoline; ZAN Austria e.

For this purpose, a breath-by-breath gas analyzer Innocor ® Innovision, Odense, Denmark was used. Matching for the lactate threshold was used to assign participants to the study groups HGI-G, LGI-G, and HFLC-G to minimize baseline differences in the incremental test results.

As the first measurable increase in blood lactate concentration during physical activity, the lactate threshold was automatically evaluated by the computer software Ergonizer 4. In addition, participants were asked to complete a 3-day nutrition protocol which included 2 weekdays and 1 day of the weekend before the intervention.

The protocols were analyzed with Nutriguide Nutri-Science GmbH, Pohlheim, Germany. At baseline T0 and post-intervention T4 , body composition fat free mass and fat mass was estimated by using a bioelectric impedance analysis BIA with a high reliability for evaluating body composition in healthy adults 25 , Participants were assessed on the BIA scale OMRON BF Medizintechnik GmbH, Mannheim, Germany , which involved entry of the participant's age, height, and male gender.

Still wearing the skin-tight clothing, participants stood on the scale barefoot and grasped the handle electrodes for ~10 s until the process was completed. According to the manufacturers recommendation to use this unit in the same environment and daily circumstances, participants were measured in the morning at the same time following a fasted period of 12 h.

The resting energy expenditure REE was measured in a quiet, lying position. The actual REE measurement was preceded by a discarded 5-min measuring phase. The respiratory gases were measured for 10 min using the same device from the preliminary incremental cycle test The mean values of VO 2 and the RER were used in the following Equation 1 by Weir 28 to calculate the REE:.

To determine submaximal exercise metabolism, participants performed a min submaximal cycle test at 20 W above the lactate threshold, which was individually identified in the preliminary incremental cycle test. Blood samples were collected from the ear lobe at rest and at 5 and 10 min.

The lactate and glucose concentrations during exercise were determined as the mean value of 5 and 10 min. Values of gas analysis RER, VO 2 during exercise were calculated by the mean of each minute. Ten minutes after completing the submaximal cycle test, an incremental test followed under the same conditions: cycling 3 min at W, then increasing 20 W per 3 min until exhaustion, as described for the screening.

For RER, lactate, and glucose values, the area under curve AUC was calculated between the start of the test and the final increment completed by all participants before exhaustion t n to assess the concentrations during the incremental cycle test using the following Equation 2 :.

Participants were instructed to follow the dietary pattern according to their respective group over the time course of 4 weeks:.

Supplementary Tables S1—S4 summarizes the general nutritional guidelines and example meals for each group. The GI of the foods was based on Foster-Powell et al. All nutritional instructions, including the preparation of the meals, were given by a licensed dietarian who was contacted in case of any questions or concerns about the respective diet.

Participants were asked to complete a daily nutrition protocol during the intervention by quantifying the consumed food using household measurements. For self-monitoring the nutritional compliance, participants were instructed to use the diet tracking apps.

The ingestion of ergogenic supplements during or prior to the intervention was defined as exclusion criteria. Changes in physical activity behavior during the intervention led to exclusion of the participants. Since the present investigation was conducted as pilot trial, no hierarchy for the efficacy endpoints had been defined in the study protocol.

The statistical evaluation was performed to determine an adequate sample size and the primary outcome of a main RCT study which will be designed on the basis of the present study protocol.

All data are presented as mean ± standard deviation SD. Medians Md were additionally presented if outliers were identified by the interquartile range method.

SPSS statistics IBM SPSS Statistics for Windows, Version Armonk, NY: IBM Corp. was used for all statistical analyses. Data distribution was examined with a Shapiro—Wilk test.

If variable data of all groups were normally distributed, the homogeneity of the baseline values between the study groups was checked using one-way ANOVA. In addition, the mean differences obtained from all three groups were compared using one-way ANOVA. The Gabriel post-hoc test was performed to identify the groups that differed significantly.

The Kruskal—Wallis test was used when data cannot be assumed to be normally distributed. Following a significant Kruskal—Wallis test, pairwise comparisons using the Dunn-Bonferroni approach were automatically produced. The significance of changes from baseline to post-intervention in the respective endpoints within groups were analyzed with the paired sample t -test or Wilcoxon signed-rank test.

As a magnitude of the change in the respective outcomes, the minimally important difference MID was calculated. The value of 0. Furthermore, the effect sizes were calculated from differences in means between baseline and post-intervention and between groups at the end of the investigation Cohen's d.

A total of 30 men met the inclusion criteria and were allocated to the intervention groups Figure 2. Twenty-eight participants completed the trial and were included in the statistical analysis. In the HGI-G 9, the LGI-G 10, and the HFLC-G 9, participants were, respectively, analyzed.

The participants of the HGI-G were slightly older The mean height was 1. Drop outs were whose who had voluntarily withdrawn from participation after the initial examination. No adverse events were noted, and no pathological findings were observed in the routine anamnesis.

Endurance running, cycling, team sports, and cross-country skiing were the main reported activities in all groups. As shown in Table 1 , no significant baseline differences between the study groups were detected for the nutritional protocols. The baseline data of the study participants are summarized in Table 2.

No significant baseline differences between the study groups were detected in any outcome of the study. The current investigation identified a statistically significant decrease in weight, BMI, and fat mass in the LGI-G and HFLC-G.

As a consequence, the percentage of fat free mass increased statistically significantly in the LGI-G and HFLC-G Table 2. These results were confirmed by the MID and medium effect size in the LGI-G and HFLC-G.

Table 2. Body composition and metabolic outcomes at baseline and following the nutritional concepts. Due to favorable changes in body fat, the increase in percentage fat free mass was also statistically significantly higher LGI-G vs. No statistically significant differences were observed when comparing the changes in fat mass or fat free mass between LGI-G and HFLC-G.

The REE did not change to the level of statistical significance or the MID during the intervention period in any of the groups. In addition, there were no significant differences between the groups.

Under resting conditions, the RER increased in the HGI-G by 0. In contrast, the HGI-G and LGI-G had no statistically significant changes in the RER values Table 2.

As a consequence, the changes in the RER values in the HFLC-G differed statistically significantly from the HGI-G and LGI-G as confirmed by the post-hoc analysis HFLC-G vs. Differences between groups were not statistically significant.

In the HGI-G RER, values at maximum effort were similar at post-intervention compared to baseline. The same results could be observed in the LGI-G Table 2.

Figure 3. Column diagram for group differences in area under curve AUC. A Changes in respiratory exchange ratio RER values, B changes in lactate concentrations, and C changes in glucose concentrations during the first 21 min of the incremental cycle test. Data shown as mean ± SD. Lactate concentrations at exhaustion had not statistically significantly changed in any group.

However, lactate concentrations at exhaustion increased in the HGI-G 1. Nevertheless, the changes in lactate concentration at exhaustion did not differ significantly between groups in contrast to the time to exhaustion TTE Table 2. TTE increased in the LGI-G 1. Glucose concentrations at exhaustion did not change between baseline and post-intervention in any group.

Furthermore, no group differences could be detected for glucose concentrations during the incremental test or at exhaustion.

Changes in the VAS Score are shown in Figure 4. For all other analyses, no statistical or meaningful differences between week 1 and 4 could be detected in the respective group. Figure 4. Changes in visual analog scale VAS Scores. A General, B during physical activity, C gastrointestinal comfort.

Data shown as mean ± SD at week 1 and week 4. The main purpose of the present investigation was to examine the effect of nutrition strategies varying in amount and type of carbohydrates on metabolic processes under resting conditions and different exercise scenarios.

Compared to baseline levels, lactate concentrations under resting conditions and in submaximal test settings decreased in the group consuming low glycemic carbohydrates in a period of 4 weeks. During the incremental test, changes in lactate concentration were statistically significant and metabolically relevant.

Although the fat oxidation was not measured directly in the current investigation, evidence suggests that there is a strong inverse relationship between plasma concentrations of lactate, free fatty acids, and β-oxidation during exercise As a potential consequence, the alterations in lactate concentrations might be indicative for an influence of a LGI diet on fat metabolism.

These finding were supported by the changes in lactate concentrations during exercise. In the current investigation, lactate concentrations decreased in the HFLC-G during the submaximal and the incremental cycle test.

As a potential result of low baseline data, lactate concentrations under pre-exercise conditions remained unchanged in the HFLC-G. In contrast, the carbohydrate-rich control diets were associated with the opposite effect 32 , 33 , Furthermore, major carbohydrate metabolizing enzymes glycogen phosphorylase, phosphofructokinase, and pyruvate dehydrogenase are less activated, while the activity of hormone-sensitive lipase and adipose triacylglycerol lipase has been shown to be increased.

Carbohydrate-induced high plasma insulin concentrations caused the opposite effects 2 , 3. It has to be mentioned that in most studies, the carbohydrate-rich controls have been defined by the amount but not the GI of the ingested carbohydrates.

The consumption of low glycemic carbohydrates is characterized by reduced postprandial glucose concentrations, which stimulates less insulin release. Consequently, the associated effects in the carbohydrate and fat metabolism, such as reduced lactate concentrations, decreased RER values, and increased use of free fatty acids, could be identified despite a high amount of carbohydrates 15 — 17 , However, there are controversial results whether low glycemic vs.

high glycemic meals prior to exercise improved fat oxidation and performance during exercise To our best knowledge, there is little evidence coming from studies that have focused on longer-term low GI diets. In a study by Hamzah et al.

the effect of the GI of high carbohydrate diets on energy metabolism and running capacity have been investigated The authors concluded that the GI had no influence on rates of fat oxidation.

Taking metabolic adaptations to HFLC diets under consideration, 5 days might be insufficient for a LGI diet to have an impact on the metabolic response 9 , A long-term effect has only been investigated in a study by Durkalec-Michalski et al. In contrast to our findings, the LGI diet over 3 weeks resulted in a slight downregulation of fat oxidation during exercise However, in the study by Durkalec-Michalski et al.

Furthermore, the decrease in RER values was not statistically significant and did not reach the MID in the present study. The LGI intervention seemed to have a smaller impact on metabolic adaptations than the HFLC diet.

The up-regulating signals of fat oxidation are low insulin concentration and increased concentrations in plasma free fatty acids 2 , 3.

A direct comparison between four meals, each different in the amount and GI of the ingested carbohydrates, has shown that both high fat groups were associated with the highest postprandial free fatty acid and lowest insulin concentrations.

The lowest free fatty acid concentrations were in the group consuming a low glycemic carbohydrate-rich meal. Furthermore, postprandial insulin response was lower in the high carbohydrate low GI group compared to the high carbohydrate high GI group Consequently, the abovementioned adaptation processes might be less in a high carbohydrate low glycemic diet compared to a HFLC diet due to the different impact on postprandial free fatty acid and insulin concentrations.

The nutritional impact on fat metabolism might also be reflected by the circulating glucose concentrations. Fasting glucose plasma concentrations dropped in the LGI-G to a significant and MID relevant extent.

Changes in the HFLC-G seemed to be less pronounced, potentially as a consequence of relatively low baseline values compared to the other groups.

During the post-intervention, incremental test glucose concentrations are lower at the same exercise intensity as in the unconditioned pre-values state in both LGI-G and HFLC-G. This is probably related to a stimulation of fat oxidation under resting conditions and during exercise The results of the HGI-G seemed to be controversial.

The increased RER at rest in the HGI-G indicates an elevated metabolization of carbohydrates under resting conditions. In addition, the lactate concentration increase was clinically relevant under pre-exercise condition. Despite increased lactate concentrations during the incremental test, it seems that there is an improved fat metabolism -decreased glucose and lactate values- in the submaximal cycle test.

It had previously been described that carbohydrates prior to exercise appear to be beneficial to performance 1. Hence, the slightly decreased carbohydrate metabolism in the submaximal test might be partly explained by the increased lactate threshold over the time as a possible adaptation in response to enhanced performance.

As a result, at post-intervention, the participants performed the test closer to their lactate threshold compared to baseline. The current investigation also observed an improvement in body composition due to a decrease in fat mass following the 4-week LGI or HFLC diet on the level of significance and MID.

It is not assumed that the present results can be attributed to the differences in energy intake between groups. Despite the significant difference in proportions of nutrients, the mean energy intake was equivalent between groups with an energy add-on of kcal in the HFLC-G.

According to the findings of Hall et al. There is evidence that athletes can improve their body composition by a high fat in particular ketogenic diet 42 — Low carbohydrate diets compared with control diets have been suggested to be relatively more effective in body weight management.

However, the benefits of a low carbohydrate diet can be rather attributed to the relatively high protein content, but not the relatively lower carbohydrate content 45 , In a recent study with athletes, different approaches high vs.

low fat but similar protein intakes resulted in a similar change of body composition mean loss in body fat was 1. These are in accordance with a meta-analysis examining the impact of different diet types in obese or overweight people Data from the meta-analyses of the Cochrane Database of Systematic Reviews suggest that a low glycemic diet without energy restriction results in a significantly greater decreased fat mass and an increased fat free mass compared with a high glycemic or even high fat and energy restricted diet Although low glycemic diets seem to promote weight loss and metabolic improvements in obese and overweight adults 48 , research about the impact of the GI on body composition in endurance athletes is limited.

A recent study by Durkalec-Michalski et al. has shown that consuming a low glycemic diet led to a change in body composition. In particular, a statistically significant reduction in body mass Physiologically, the significant changes in body composition in the present investigation might be explained by changes in fat oxidation and a more balanced carbohydrate metabolism as a potential consequence of the altered amount and quality of ingested carbohydrates.

Despite an improvement in fat metabolism and body composition, there is a growing body of evidence that these changes induced by ketogenic or non-ketogenic HFLC diets are not in association with improved endurance performance, aerobic capacity and peak performance in particular 9 , 32 , 50 , 51 , due to an impaired carbohydrate provision during higher intensities 2.

This assumption is supported by the changes in time to exhaustion in the present investigation. Furthermore, HFLC diets seem to be impractical and accompanied by side effects that include fatigue, headaches, poor concentration, lethargy, gastrointestinal discomfort, nausea, and unintentional weight loss.

One reason might be an insufficient proliferation of essential micronutrients and fibers and glycogen depletion which might be a cause of impaired concentration and hence the neuromuscular connection 9 , The values of the VAS scores of all categories decreased in all groups, indicating that the participants got familiar with the respective dietary concepts.

In general, none of the groups experienced clinically relevant elevated VAS scores. Mild symptoms can be defined by a score of 5 to 45 mm on the VAS This might be explained by the fact that endurance subjects tolerate the effects of a high-fat diet better than untrained individuals during exercise In addition, according to the nutritional protocols, an impaired delivery of minerals in the HFLC group was not expected.

However, only the LGI-G and HGI-G have shown an improvement in VAS scores of the subscale activity and gastrointestinal comfort on a statistical or MID level with a superior effect in the LGI-G. These results might be associated with impaired training sessions in the HFLC-G since higher intensity levels could not be reached without the provision of carbohydrates 2.

Furthermore, the advantage of LGI diet over HFLC and HGI diets might be in the choice of carbohydrates. A LGI diet is predominantly characterized by high-fiber and plant-based foods.

This has shown to be associated with reduced fatigue, a strengthened immune system, and an improved ability to regenerate through the increased supply of micronutrients, essential fatty acids and amino acids, and low postprandial glucose concentrations Moreover, controlled clinical trials demonstrated that low glycemic foods have a positive impact on digestive conditions, such as gastroesophageal reflux disease or the irritable bowel syndrome, due to high fiber content 56 , It can be assumed that the present results can be attributed to the implementation of nutritional patterns.

According to the analysis of the nutritional protocols, the participants' dietary intake reflected the specified intake of carbohydrates and fats in the respective group. While the HGI-G had a higher percent and total carbohydrate intake, the LGI-G showed a higher carbohydrate intake on a g-per-kg-body-weight basis.

The current guidelines for endurance athletes during training on the competition level are 6—10 g carbohydrates per kg body weight and day. These recommendations do not address the GI of the ingested carbohydrates The participants of the current investigation were non-elite athletes with a training workload of 3—5 sessions per week.

In both groups, the carbohydrate intake seems to be sufficient since recommendations are 5—7 g carbohydrates per kg bodyweight and day for general training needs Nevertheless, increasing the carbohydrate intake to 6—10 g carbohydrates per kg body weight and day would be an interesting approach in future studies with high trained endurance athletes.

The carbohydrate upper limit of 50 g per day in the HFLC-G was based on the current focus of carbohydrate-restricted diets 9.

This trial has some limitations. It has to be mentioned that the changes in fat and carbohydrate oxidation were not measured directly but extrapolated from the lactate diagnostics. However, it is reported that measuring blood lactate is an effective way to estimate the rates of fat and carbohydrate oxidation Furthermore, using the values of the spiroergometry to confirm the results from the lactate diagnostic during the incremental test has to be taken with caution since values for VO 2 are overestimated by a step compared to a ramp incremental test When taking the impact of the nutritional concepts into account, limitations of the self-reported protocols might entail an over or underreporting of the consumed foods Moreover, recommendations for the macronutrient intake based on the body weight seems to be more accurate than percentage values to determine nutritional guidelines for endurance athletes.

Future studies with a larger sample size should include different sex groups and pre-exercise nutritional conditions to state practical use of high fat vs.