Fat oxidation diet -
Substrate oxidation rates. Post-diet CHO and FAT oxidation were significantly altered by diet. No Pre-Post substrate oxidation changes were detected for HCLF.
This increased relative oxygen consumption after LCHF is largely explained by weight-loss, and partly explained by the non-significant increase in heart rate i.
Prior to dietary intervention, capillary blood R -βHB was below the limit of nutritional ketosis pre-diet and pre-TT mean ± SD: 0. Post-LCHF treatment significantly increased R -βHB from baseline 0. Capillary blood glucose concentrations were similar Pre- and Post-diet between LCHF and HCLF treatments LCHF average: HCLF average: There was a main effect of time observed Post one-mile TT that raised blood glucose from baseline Capillary blood lactate before the one-mile TT was at the same concentration Pre- and Post-diet in both LCHF and HCLF treatments LCHF average: 1.
HCLF average: 1. There was a main effect of time induced by exercise that increased blood lactate significantly from baseline 1.
Figure 6. One-mile time-trial metabolite impact. Capillary ketones, glucose and lactate were measured immediately pre- and post-one mile time trial TT to evaluate the within- and between-diet effects in the context of exercise. There were no significant Pre-diet and Pre-TT differences.
A significant post-diet effect was detected in capillary ketones Pre-TT. Glucose and lactate were significantly elevated over time, independent of diet and dependent on TT.
Capillary blood R -βHB was below the limit of nutritional ketosis Pre-diet and Pre-RSP 0. LCHF significantly increased R -βHB into nutritional ketosis compared to pre-diet concentrations 0.
Over the course of the RSP, R -βHB decreased by approximately 0. Capillary blood glucose concentrations Pre-diet and Pre-RSP Capillary lactate concentrations Pre-diet and Pre-RSP 1. Peak lactate concentrations 6. Diet did not significantly influence the rate of lactate appearance in the blood nor peak lactate Figure 7 and Supplementary Table 3.
Figure 7. Repeated sprint performance metabolite impact. Capillary R-βHB, glucose, and lactate were measured in capillary blood immediately after each repeated sprint performance RSP set. There were no significant between-treatment differences pre-diet.
The significant time effects were detected in lower R-βHB values at set 1 and 2, higher glucose values at set 5 and post, and significantly higher lactate values from set 1 and thereafter. Post-diet ketones were significantly influenced by low carbohydrate high fat LCHF treatment, with 3-fold higher R-βeta-Hydroxybutyrate R-βHB concentrations throughout the sets compared to HCLF.
Lactate was not affected significantly by diet. There were no significant changes over time in any of the variables of interest Figure 8 and Supplementary Table 4. Between-condition effects reveal higher total cholesterol Δ: Interaction effects revealed total cholesterol Δ: Figure 8.
Cardiometabolic scores. Statistics were conducted on absolute values and are presented as mean change from Pre-diet. There were no cardiometabolic differences Pre-diet or significant time effects. Between-diet effects revealed greater total cholesterol and LDL-C concentrations during the LCHF versus HCLF treatment.
The significant interaction revealed greater total cholesterol and HDL-C concentrations Post-LCHF treatment. All glycemic parameters significantly improved on LCHF Figures 9 , Average glucose was significantly lower during LCHF treatment starting day 8, and remained lower on day 13, , and 22 Figure 9.
Additionally, this prediabetic phenotype was present in these subjects despite them losing weight on both nutritional strategies LCHF: —2. Figure 9. Continuous glucose monitoring. Average glucose was significantly lower on LCHF on day 8, 13, , and All glycemic parameters over the days dietary intervention were significantly improved during LCHF.
The day mean glucose predicted the percent change in mean glucose between LCHF and HCLF diets. These same subjects also reported the highest peak fat oxidation rate as the percent change in mean glucose between LCHF and HCLF diets predicted the peak oxidation rates across the entire cohort.
Peak fat oxidation rates on LCHF were also associated with higher cholesterol demonstrating a potential interaction between oxidation rates and global lipid metabolism. Figure Circadian glucose patterns.
Red, LCHF. Black, HCLF. Dashed line, individual pre-diabetic subject circadian glucose patterns. There are four key findings of this study Figure 1.
i Athletes achieved equivalent exercise performances during a 1, m time trial and a 6 × m interval session after a day habituation to LCHF or HCLF diets when controlling calories, training load, and body composition changes across groups. ii During the latter stages of the 6 × m interval session, athletes achieved the highest rates of fat oxidation yet reported.
According to current understanding, this is paradoxical since these high rates were measured in subjects exercising at an intensity iii days on each diet produced equivalent fasting insulin, hsCRP, and HbA 1c , with elevated total, low-density lipoprotein, and high-density cholesterol on LCHF.
iv LCHF consistently reduced glucose levels and variability with a large inverse relationship observed between mean glucose on HCLF and the percent change in mean glucose when switching to LCHF.
Additionally, relationships were observed between glycemic change, peak fat oxidation, and circulating lipids, as the larger the reduction in mean glucose on LCHF the larger the peak fat oxidation on LCHF, and the larger the peak fat oxidation on LCHF and the higher circulating lipids were.
These results challenge the existing paradigm that diets with higher carbohydrate intake are superior for athletic performance, even during shorter-duration, higher-intensity exercise. Critically, these results demonstrate that lower carbohydrate intake may be a therapeutic strategy, even in athletes, to improve glycemic control, particularly in those with, or at risk for diabetes, without requiring changes in body composition or physical activity.
Interestingly, these results also demonstrate a unique association between glycemic responsiveness to carbohydrate restriction, fat oxidation rates, and circulating lipids, suggesting an important relationship between continuous glycemic parameters and systemic metabolic responsiveness.
Performance during the 1, m time trials was the same when athletes ate HCLF or LCHF diets. This is in keeping with our previous study 31 in which the 5-km time trial performances of athletes, similar in ability to those studied here, were equivalent on either diet. It adds further weight to the conclusions from two recent meta-analyses 63 , 64 that that LCHF and HCLF diets produce equivalent performances across a wide range of athletic events.
Our reasoning was that if the pre-exercise muscle glycogen stores are a critical determinant of exercise performance and if the LCHF diet is associated with lower muscle glycogen concentrations in recreational athletes 28 but perhaps not in highly competitive athletes 65 , and since very high rates of muscle glycogen use are measured during m repetitions 66 so that, if significant muscle glycogen depletion can be produced by a high intensity interval session, then any impaired performance of athletes eating the LCHF diet should become apparent in the latter intervals of that session.
For example, Impey et al. reported rates of muscle glycogen use of Webster et al. In contrast to our expectation, based on this prediction that significant muscle glycogen depletion would occur in athletes following the LCHF diet and this would impair their performance, in fact exercise performance was identical across all the intervals on either diet Tables 4 , 5 ; Figure 4 and Supplementary Table 1.
These finding raise the important question of why our two studies have failed to detect diet-induced differences in performance whereas prior meticulously conducted studies 16 — 18 detected meaningful differences in their studies of Olympic standard race walkers.
Five key factors may have contributed to these differences: randomization, dietary controls during exercise, training load, body composition, and dietary habituation timeline. Prior studies with differing results allowed subjects to choose the diet they preferred 16 — As a result, blood glucose levels were lower in the LCHF group in the two trials 16 , 17 in which it was measured, with a trend toward a progressive hypoglycemia in one trial [figure 5A from 17 ].
As the authors of those studies appreciate, even in the absence of hypoglycemia, carbohydrate ingestion alone can have an ergogenic effect even if the carbohydrate is not ingested Thus, these trials did not control for the potential effects of carbohydrate ingestion during exercise.
The potential role of hypoglycemia in explaining differences in exercise performance has recently been revisited The intensified training load and across group differences in body composition in these trials 16 — 18 also illustrates key differences as increased physical activity levels 68 and body weight reductions 69 both illustrate biological stressors requiring adaptation and may independently impact performance.
The increased physical activity across groups and more significant reductions in bodyweight in LCHF arm 16 — 18 , on top of introducing a diet which requires systemic metabolic reprogramming 70 , illustrate three co-administered biological stressors all requiring adaptions and which may influence performance.
Thus, it is not surprising that when we controlled randomization within-subject , dietary controls during performance testing, calories, training load, and body compositional changes across groups to allow for the isolation of diet-induced changes across these key parameters, we observed different results from prior observations 16 — Of note, when Burke et al.
The described method for measuring maximal rates of fat oxidation during exercise is to have subjects exercise for short periods of approximately 3 minutes at exercise intensities that gradually increase 22 — Maximal rates of fat oxidation measured with this method are usually in the range of 0.
Higher rates of fat oxidation have been measured in athletes adapting to the LCHF diet. Volek et al. measured rates of 1. measured rates in excess of 1. In a case study of an elite Ironman triathlete, Webster et al. reported a peak fat oxidation rate of 1. Shaw et al. demonstrate fat oxidation ranging from 0.
Our data is in line with these prior studies showing elevated fat oxidation rates LCHF: 1. However, what is particularly unique in our findings is that we observed the peak fat oxidation rates LCHF: 1.
Three out of eight cardiometabolic markers were significantly modulated by diet, most notably post-diet LCHF vs. HCLF total cholesterol vs. The significant main effects in this study were directly attributable to the between-diet differences in dietary fat and fat composition, however, the fact that more than half of participants had borderline elevated total cholesterol, LDL-C, and HDL-C at baseline was somewhat unexpected.
While carryover effects were ruled out by identical concentrations at baseline i. Moreover, it is unclear if similar dietary interventions in mildly hypercholesterolemic athletes will exert any significant impact on cardiometabolic indices that are beyond the effects induced by their habitual diet.
Individual cardiometabolic responses are available for review in the supplement Supplementary Figure 1. We detected a small, but significant change in weight over time, primarily derived from fat mass. Based on prior evidence 73 , 76 the LCHF diet was projected to lower cardiometabolic markers beyond a HCLF diet, even in the absence of weight-loss 77 ; however, we did not observe these results with our between-diet isocaloric feeding design.
Additionally, it is important to acknowledge that HbA 1c is a 2—3-month biomarker that we quantified to predict directional trends rather than significant changes over four weeks. Based on our findings, we expect that these markers will continue decreasing after four-weeks of LCHF, similar to isocaloric HCLF feeding when duration, energy intake, and weight are controlled between conditions.
When measuring continuous glucose levels every 15 min over a day period, we observed improvements across all glycemic parameters in virtually all subjects on the LCHF diet, with initial significant differences in mean glucose observed on day 8 of dietary habituation.
Carbohydrate restriction is a known therapeutic strategy to help facilitate improvements in glycemic control and other key metabolic parameters in other clinical conditions such as obesity 82 , type-1 diabetes 36 , and type-2 diabetes 33 , These illustrate critical controls allowing us to extract diet-induced impact on glycemic parameters as prior observations have shown that caloric intake and changes in body weight both influence glucose levels regardless of diet 83 , Additionally, prior evaluations have found that intensified training programs can disrupt not only glycaemia and mitochondrial function, but also performance While there have been small short-term investigations exploring glycemic control during exercise in athletes 79 , 85 , very few studies have investigated the relationship between the long-term i.
Nolan et al. reported the impact of a ketogenic diet on an individual type-1 diabetic cyclist during a day, km race This case report demonstrated remarkable glycemic control for a Type-1 Diabetic compared to historical glycemic norms for Type-1 Diabetics during this 20d race window, but nature of the report did not allow for the comparison of performance on- and off-diet.
These subjects fitting the pre-diabetes glycemic phenotype in our study could not be explained by underlying demographics, body composition or physical activity differences as these pre-diabetic subjects had near equivalent age pre-diabetic: This is in line with the understanding that multiple factors contribute to diabetes onset 88 , 89 , some of which may go undetected until overt diagnosis.
Potential explanations for early pathogenic progression of diabetic dysglycemia include genetic predisposition, adiposity-induced insulin resistance, fasting insulin, and beta-cell dysfunction However, markers of elevated adiposity were not higher in the prediabetic group.
In fact, this sub-cohort lost weight on both dietary protocols. Additionally, circulating lipids tended to be lower on the HCLF diet suggesting lipids could not explain dysglycemia on HCLF. While intense exercise overtraining has also been demonstrated to acutely disrupt mitochondrial and glycemic function 68 , this dysfunction was reversed following reduction in activity and cannot explain our results as our subjects did not increase or decrease physical activity levels.
Importantly, Al-Ozairi et al. found that a 6-day LCHF diet in Type-2 Diabetic subjects who kept calories and bodyweight controlled were unable to find differences in mean and post-prandial glycaemia utilizing CGM devices This could be due to the short treatment duration as we observed significant differences on day 8 of the isocaloric HCLF and LCHF diets.
Alternatively, it may be explained by the influence of engaging in physical exercise regularly as Moholdt et al. Importantly, when looking to observe if the entire cohort also observed a relationship between day average mean glucose on HCLF diet and percentage change in mean glucose between LCHF and HCLF diet, we observed a large significant inverse relationship, indicating that those individuals with a higher mean glucose, are more responsive to carbohydrate restriction treatment, not just those with pre-diabetic glycemic phenotypes.
As our study and prior literature suggests this change is in response to diet and not other factors i. While multiple studies have shown reductions in glucose 35 , 80 , 83 and elevations in fat oxidation 16 — 18 , 28 , 31 , 91 on a LCHF diet, we are unaware of any data which has demonstrated that the magnitude of glycemic changes across diet predicted the magnitude of peak fat oxidation rates.
Interestingly, we also observed that higher peak fat oxidation levels on LCHF predicted higher total cholesterol on LCHF suggesting a potential interaction between higher rates of fat turnover and higher levels of circulating lipids while on a diet that restricts carbohydrates and increases fat intake.
While elevated fat oxidation rates have been observed on LCHF diet in the absence in changes of insulin or calories, explained by elevated fat intake, 91 , they did not see a change in glucose levels nor did they explore whether the magnitude of fat oxidation rate was associated with glucose or lipid parameters.
In line with our data, there has been a report demonstrating that individuals with healthy bodyweight undergoing a LCHF diet can have elevated circulating lipid i. While this prior observation did not look at either total cholesterol or fat oxidation rates, in light of our data, there remains a possibility that these individuals 92 , have elevated levels of systemic fat oxidation which requires further analyses.
The ability for i d mean glucose on HCLF to predict changes in mean glucose following carbohydrate restriction, ii changes in mean glucose with carbohydrate restriction to predict peak oxidation rates, and iii peak fat oxidation to predict total cholesterol suggests a unique predictable physiologic relationship between glycemia, substrate oxidation, and circulating lipids biomarkers which requires further validation.
This study had middle-aged competitive male athletes which may limit our understanding of the translatability of these findings to female athletes due to potential differences across sex on the magnitude of metabolic response 93 — 95 , particularly for those women in middle age during pre-menopause and post-menopause who may benefit most due to elevated risk for cardiovascular and metabolic disease 96 , While our short-duration high-intensity exercise 6 × m would be sufficient to reduce muscle glycogen content based on prior work, 28 , 65 , 66 we did not measure muscle glycogen content so we cannot say for certain what levels of muscle glycogen were achieved and if they were associate with elevated fat oxidation levels during exercise.
While HbA 1c is gold-standard for diagnosing diabetic phenotype due to its established role in diabetes, our dietary intervention was 4 weeks in length, an insufficient time to observe the full diet-induced impact on HbA 1c which requires a minimum of weeks 98 , We utilized CGM to capture the 4-week h glycemic control as i CGM tracks long-term to HbA 1c 54 — 56 , ii shorter term CGM readings d are good estimates of 3-month CGM averages 57 , and iii can also capture both fasting and post-prandial differences in glucose which is a validated diagnostic tool Figures 9 , Although limitation have been cited when looking different CGM technology and different insertion sites, both technology and insertion site were controlled in our analyses However, it is important to note the clear limitation of HbA 1c and oral glucose tolerance test OGTT in our present analyses and why CGM was the primary glycemic metric.
It is well-established that for a given HbA 1c value, there is a wide-range of mean glucose concentrations, and for any given mean glucose concentration, there is a wide-range of HbA 1c values, suggesting some limitation around this biomarker Thus, some expert consensus has argued for moving beyond just HbA 1c at the individual levels Additionally, it has been known for decades that OGTT is inappropriate for individuals not adhering to an HCLF diet as this test was only validated under high-carbohydrate consumption While we feel confident that our h 4-week glycemic values across subjects accurately capture the glycemic impact over our study duration, future studies with benefit from longer dietary interventions m in duration to capture changes in HbA 1c.
We observed record high peak oxidation rates with elevations in cholesterol in LCHF. All individuals experienced reductions in day average glucose means, median, and variability with carbohydrate restriction LCHF which resolved the pre-diabetic phenotype across all subjects without requiring caloric restriction, increased physical activity, or significant changes in body composition across groups.
Interestingly, the average glucose during high carbohydrate consumption predicted the degree of glycemic response to carbohydrate restriction suggesting that individuals with higher starting glucose may benefit most from carbohydrate restriction.
Surprisingly, we also found that the magnitude of glucose reduction during carbohydrate restriction predicted the elevation in fat oxidation rates during exercise suggesting that glucose response is linked to systemic fat oxidation. Taken together, LCHF may represent a therapeutic strategy to improve glucose levels, particularly in those at risk for diabetes, without compromising high intensity exercise performance in middle-aged athletes.
Future studies should evaluate the impact of these dietary strategies in middle-aged women who are at elevated risk for cardiovascular and metabolic disease. The studies involving human participants were reviewed and approved by Institutional Review Board of Grove City College IRB number PP and TN conceived the original study design.
KH designed the diets and provided the nutritional counseling. PP, AB, and AK conducted the data analysis. PP, TN, AK, and AB drafted the final manuscript. All authors have read and agreed to the published version of the manuscript.
We thank Levels, Inc. We also thank Azure D. Grant, Ph. for her assistance in organizing continuous glucose monitoring data and developing code for circadian glucose analyses and illustration. We also thank the participants for their vital contribution to this study. TN and JV were authors of low-carbohydrate nutrition books.
TN book royalties go to The Noakes Foundation which contributes to the Eat Better South Africa Campaign. JV receives royalties from book sale; is a founder, and has equity in, Virta Health; and is a science advisor for Simply Good Foods and Cook Keto.
AK was a patent inventor and has consulted for Simply Good Foods. The remaining 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.
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Department of Sport Performance, National Taiwan University of Sport, Taichung, , Taiwan. Senior Wellness and Sport Science, Tunghai University, Taichung, , Taiwan.
Clinical Trial Center, China Medical University Hospital, Taichung, , Taiwan. Graduate Program in Department of Exercise Health Science, National Taiwan University of Sport, Taichung, , Taiwan.
You can also search for this author in PubMed Google Scholar. Chih-Hui Chiu carried out the experiment, blood analysis and assisted the manuscript preparation.
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Abstract Studies have revealed that time-restricted feeding affects the fat oxidation rate; however, its effects on the fat oxidation rate and hyperlipidemia following high-fat meals are unclear. Introduction Consuming high-fat meals increases the triglyceride TG level in blood plasma.
Design This study used a crossover design for the experiment. Protocol Pretest The pretest was to assess the total daily energy expenditure by indirect calorimetry through a series of resting assessments and exercising assessments.
Formal experiment The experiment was conducted on a 6-day period. Table 1 The macronutrient consumption for TRF and CON. Full size table. Table 2 The participants physiological information and fasting plasma biochemistry. Figure 1. Full size image. Figure 2. Figure 3.
Discussion In this study, meals were provided that met the h energy requirement of each participant for 5 days. Conclusion This study discovered that consuming meals with the same amount of calories for 5 days and using time-restricted feeding as the intervention can effectively increase the fasting fat oxidation rate and the fat oxidation rate after the consumption of high-fat meals.
Data availability All relevant materials are presented in the present manuscript. References Liu, H. Article CAS Google Scholar Nordestgaard, B.
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Article CAS Google Scholar Download references. Acknowledgements Thanks for Sports Science Research Center of National Taiwan University of Sport to provide the equipment for this study. Funding This study was funded by Ministry of Science and Technology in Taiwan H Author information Authors and Affiliations Graduate Program in Department of Exercise Health Science, National Taiwan University of Sport, No.
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People who have fatty acid oxidation disorders FAODs struggle Fat oxidation diet oxidatioh fats. The Natural remedies for cold sores is that the body is unable to dieg create oxodation energy during times of doet, stress, or fasting. While some people with these disorders face serious health complications, others dief still able to lead mostly normal lives. Fat oxidation diet of the best ways for these people to manage their symptoms is to follow a strict diet. If you or a family member has a fatty oxidation disorderyou may already be familiar with the FAOD diet. While everyone is different, and your doctor may have specific requirements, generally a fatty acid oxidation disorder diet will focus on the following:. Because the body is unable to effectively and efficiently break down fat in the mitochondria, it is often recommended that a person with one of these disorders follows a low-fat diet, specifically those with a long-chain fatty acid oxidation disorder. You are pxidation 1 of Thermogenic fat loss supplements 1 free articles. For oxidatipn access take a risk-free trial. Fat didt is a oxdiation Fat oxidation diet and often-used term among endurance athletes. But is it Exercise and blood sugar monitoring 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 ooxidation advantageous for an athlete. It is known that well-trained endurance athletes have an increased capacity to oxidise fatty acids.
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