Reynisdottir, S. Fox, C. Nutrition —

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Metabolism - Fatty Acid Oxidation: Part 1

Metabolic fat oxidation -

On average, the active co-twins tended to have higher PFO rates and lower FAT MAX when compared with the inactive co-twins, but the differences were not statistically significant.

Figures include group means and standard deviations. Colours represent the same twin pairs in both charts. Note the different scale in the y -axis. RFO or PFO were not correlated with fasting glucose, fasting insulin or the Matsuda index in the twin individual-based analysis Table 4.

For the first time, our study data showed that fat oxidation rates at rest and during exercise were similar between MZ co-twins, even though the study group was enriched with pairs who had discordant LTPA habits.

The co-twins also exhibited similar FAT MAX values and thus tended to reach PFO at the same absolute exercise intensities. The finding supports those of Toubro et al.

In a study involving male MZ twin pairs Bouchard et al. As the researchers also investigated the substrate use of dizygotic twins, they were able to control their analysis for the common environmental effect.

Their calculated heritability estimates ranged from 0. However, as RER only describes the relative use of energy substrates, this study broadens the concept by showing that absolute fat oxidation rates behave accordingly and supports the earlier suggestion that genes play a role in determining fat oxidation capacity during exercise Jeukendrup and Wallis ; Randell et al.

This assumption seems evident, as the large cross-sectional studies investigating fat oxidation during exercise have been able to describe only partly the observed inter-individual variability in PFO Venables et al.

We identified a subpopulation of MZ twin pairs, where the co-twins differed in their past 3-year LTPA. In this study, we found no differences between the co-twins in their systemic energy metabolism at rest or during exercise.

In previous observational studies, PFO was associated with self-reported physical activity Venables et al. However, it is highly likely that physical activity participation and fat oxidation capacity have shared genetic factors, and the relationship noted in observational studies is partly genetically mediated.

In experimental studies, endurance-training interventions commonly increased PFO, at least in untrained populations reviewed by Maunder et al. Earlier mechanistic evidence from our laboratory also supports the role of physical activity as a modulator of PFO.

In same-sex twin pairs, an over year long physical activity discordance led to significant differences in myocellular gene expression related to oxidative phosphorylation and lipid metabolism Leskinen et al. The effects of physical activity on RFO have been investigated less, with mixed results. A modest increase in fat oxidation rates at rest has been reported in some Barwell et al.

When the current scientific evidence is taken together with our results, physical activity seems to be able to influence PFO, while its effect on RFO is questionable. However, we found no association between PFO and the Matsuda index, our main surrogate of insulin sensitivity. As explained in the methods section, the Matsuda index is influenced by fasting values, which were not associated with PFO in our study.

Previously, Robinson et al. As Robinson et al. However, it should be mentioned that PFO does not always seem to be associated with a healthier metabolic phenotype because an obesity-related increase in fatty acid availability has also been linked to higher PFO Ara et al.

In contrary to PFO, RFO was not associated with a healthy metabolic response to the OGTT. Previous studies have noted mixed findings. Rosenkilde et al. However, there were no differences in fasting glucose or insulin levels between the groups.

Some case—control studies Perseghin et al. An elevated RFO could potentially function as a protective mechanism against insulin resistance Perseghing et al.

Overall, further research is needed to clarify the interaction between systemic fat oxidation and metabolic health. Our study has both strengths and limitations. A key strength was our ability to measure RFO and PFO in 21 and 19 MZ twin pairs, respectively. This enabled us to investigate the influence of hereditary factors on RFO and PFO in a reasonably sized study group.

The calculated ICCs represent the upper bound of heritability, as differences between MZ twins are due to non-genetic factors. However, as MZ twin pairs share also many aspects of their development and environment, the actual heritability of the trait may be lower.

A more precise estimation of heritability would require several kinds of relatives for quantitative trait modeling or very large study population for measurement of all genetic variation by whole genome sequencing. Additionally, since our study included only males, the results cannot be generalised to females.

This enabled us to conduct a more in-depth examination of the possible associations between fat oxidation and metabolic health. However, our study protocol was not optimal for PFO determination, which should be considered when interpreting the results. Nutrition intake the day before Støa et al. In this study, we did not control for the nutrition intake before the exercise test.

For example, this could partially explain why we did not find any association between RFO and PFO, as previously shown by Robinson et al. Moreover, we used 2-min exercise stages during PFO testing. The 2-min stages might be too short to reach a steady-state, especially for the subjects with lower cardiorespiratory fitness Dandanell et al.

To assess whether the stage duration excessively affected the results, we compared VO 2 and VCO 2 between intervals 90— s and — s of the PFO-stage.

There were no systematic differences in VO 2 or VCO 2 between the intervals. Removing these participants from the analyses did not materially change the results. Therefore, the influence of the stage duration was considered acceptable.

Thus, the measurements seemed to reflect the PFO of our study participants. In conclusion, we show that fat oxidation rates at rest and during exercise are similar between MZ co-twins.

Our results support the suggestion that hereditary factors influence fat oxidation capacity. The internal factors likely set the baseline for fat oxidation capacity that the external factors can modulate.

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Comparison with the euglycemic insulin clamp. Diabetes Care 22 9 — Maunder E, Plews DJ, Kilding AE Contextualising Maximal Fat Oxidation During Exercise: Determinants and Normative Values. The mode of exercise can also affect fat oxidation, with fat oxidation being higher during running than cycling.

Endurance training induces a multitude of adaptations that result in increased fat oxidation. The duration and intensity of exercise training required to induce changes in fat oxidation is currently unknown. Ingestion of carbohydrate in the hours before or on commencement of exercise reduces the rate of fat oxidation significantly compared with fasted conditions, whereas fasting longer than 6 h optimizes fat oxidation.

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? When does Fat Oxidation occur?

For more information about PLOS Metabolci Areas, oidation here. South Asians are more insulin resistant oxidatioh Wholesome recovery meals, which cannot be fully explained by differences in Metabolic fat oxidation. We investigated whether differences in oxidative capacity and capacity for fatty Metaboilc utilisation in South Asians might contribute, using a range of whole-body and skeletal muscle measures. Twenty men of South Asian ethnic origin and 20 age and BMI-matched men of white European descent underwent exercise and metabolic testing and provided a muscle biopsy to determine expression of oxidative and lipid metabolism genes and of insulin signalling proteins. South Asians exhibited significantly higher skeletal muscle gene expression of CPT1A and FASN and significantly lower skeletal muscle protein expression of PI3K and PKB Ser phosphorylation.