Fat oxidation at rest predicts peak fat oxidation during exercise and metabolic phenotype in overweight men

Rosenkilde, Mads; Nordby, Pernille; Nielsen, Lars Bo; Stallknecht, Bente; Helge, Jørn Wulff

doi:10.1038/ijo.2010.11

Cited by 66 publications

(76 citation statements)

References 44 publications

(49 reference statements)

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“…Contrary to suggestions that a negative energy balance would increase FAT-OX (47), but consistent with the results of Rosenkilde et al (48), we showed no relation between energy balance and the MFO. The potential limitations of the estimation of EI and EI expenditure with the use of a self-report in free-living individuals have been well documented (49, 50).…”

Section: Discussionsupporting

confidence: 89%

Dietary intake is independently associated with the maximal capacity for fat oxidation during exercise,

Fletcher

Eves

Glover

et al. 2017

The American Journal of Clinical Nutrition

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Background: Substantial interindividual variability exists in the maximal rate of fat oxidation (MFO) during exercise with potential implications for metabolic health. Although the diet can affect the metabolic response to exercise, the contribution of a self-selected diet to the interindividual variability in the MFO requires further clarification.Objective: We sought to identify whether recent, self-selected dietary intake independently predicts the MFO in healthy men and women.Design: The MFO and maximal oxygen uptake (O2 max) were determined with the use of indirect calorimetry in 305 healthy volunteers [150 men and 155 women; mean ± SD age: 25 ± 6 y; body mass index (BMI; in kg/m2): 23 ± 2]. Dual-energy X-ray absorptiometry was used to assess body composition with the self-reported physical activity level (SRPAL) and dietary intake determined in the 4 d before exercise testing. To minimize potential confounding with typically observed sex-related differences (e.g., body composition), predictor variables were mean-centered by sex. In the analyses, hierarchical multiple linear regressions were used to quantify each variable’s influence on the MFO.Results: The mean absolute MFO was 0.55 ± 0.19 g/min (range: 0.19–1.13 g/min). A total of 44.4% of the interindividual variability in the MFO was explained by the O2 max, sex, and SRPAL with dietary carbohydrate (carbohydrate; negative association with the MFO) and fat intake (positive association) associated with an additional 3.2% of the variance. When expressed relative to fat-free mass (FFM), the MFO was 10.8 ± 3.2 mg · kg FFM−1 · min−1 (range: 3.5–20.7 mg · kg FFM−1 · min−1) with 16.6% of the variability explained by the O2 max, sex, and SRPAL; dietary carbohydrate and fat intakes together explained an additional 2.6% of the variability. Biological sex was an independent determinant of the MFO with women showing a higher MFO [men: 10.3 ± 3.1 mg · kg FFM−1 · min−1 (3.5–19.9 mg · kg FFM−1 · min−1); women: 11.2 ± 3.3 mg · kg FFM−1 · min−1 (4.6–20.7 mg · kg FFM−1 · min−1); P < 0.05].Conclusion: Considered alongside other robust determinants, dietary carbohydrate and fat intake make modest but independent contributions to the interindividual variability in the capacity to oxidize fat during exercise. This trial was registered at clinicaltrials.gov as NCT02070055.

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Section: Discussionsupporting

confidence: 89%

Dietary intake is independently associated with the maximal capacity for fat oxidation during exercise,

Fletcher

Eves

Glover

et al. 2017

The American Journal of Clinical Nutrition

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“…Workload was increased with 25-W increments every minute after warm-up until exhaustion, and attainment of V O2 max was accepted using previously defined criteria (46).…”

Section: Methodsmentioning

confidence: 99%

Body fat loss and compensatory mechanisms in response to different doses of aerobic exercise—a randomized controlled trial in overweight sedentary males

Rosenkilde

Auerbach

Reichkendler

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

104

185

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A diet-induced negative energy balance triggers compensatory mechanisms, e.g., lower metabolic rate and increased appetite. However, knowledge about potential compensatory mechanisms triggered by increased aerobic exercise is limited. A randomized controlled trial was performed in healthy, sedentary, moderately overweight young men to examine the effects of increasing doses of aerobic exercise on body composition, accumulated energy balance, and the degree of compensation. Eighteen participants were randomized to a continuous sedentary control group, 21 to a moderate-exercise (MOD; 300 kcal/day), and 22 to a high-exercise (HIGH; 600 kcal/day) group for 13 wk, corresponding to ϳ30 and 60 min of daily aerobic exercise, respectively. Body weight (MOD: Ϫ3.6 kg, P Ͻ 0.001; HIGH: Ϫ2.7 kg, P ϭ 0.01) and fat mass (MOD: Ϫ4.0 kg, P Ͻ 0.001 and HIGH: Ϫ3.8 kg, P Ͻ 0.001) decreased similarly in both exercise groups. Although the exercise-induced energy expenditure in HIGH was twice that of MOD, the resulting accumulated energy balance, calculated from changes in body composition, was not different (MOD: Ϫ39.6 Mcal, HIGH: Ϫ34.3 Mcal, not significant). Energy balance was 83% more negative than expected in MOD, while it was 20% less negative than expected in HIGH. No statistically significant changes were found in energy intake or nonexercise physical activity that could explain the different compensatory responses associated with 30 vs. 60 min of daily aerobic exercise. In conclusion, a similar body fat loss was obtained regardless of exercise dose. A moderate dose of exercise induced a markedly greater than expected negative energy balance, while a higher dose induced a small but quantifiable degree of compensation.exercise; body weight regulation; compensatory mechanisms; energy balance ALTHOUGH A MODERN SEDENTARY lifestyle along with overeating has been put forward as "Big Two" factors in the etiology of obesity (3,10,29), the outcomes of structured exercise programs designed to promote weight loss are often modest (42,58). This has led to the general (mis)conception that exercise, in itself, is a poor weight management strategy (20,42,49). Apart from a potential lack of compliance, the discrepancy between predicted and observed weight loss is likely due to a combination of physiological and behavioral compensatory changes affecting energy balance. These compensatory changes cause the accumulated energy balance during an exercise intervention to be less negative than would be theoretically predicted from the exercise-induced energy expenditure (ExEE), i.e., the total amount of energy expenditure that is caused by the exercise intervention (12,32,34).Body energy stores are protected against long-term negative energy balance resulting from caloric restriction by a greater than predicted reduction in resting energy expenditure (REE) (28), a decrease in nonexercise activity thermogenesis (NEAT) (40,45), an increase in the metabolic efficiency of physical activity (16,35), and an increase in hedonic (21) and hormonal mediators o...

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“…This trait was already present at young age and may explain reduced blood lipids and the leaner phenotype and better fat tolerance exhibited by Rb ϩ/Ϫ mice later in life. In humans, a low RER predicts a healthy metabolic phenotype in overweight, sedentary men (38), and a high RER (low fat oxidation) has been implicated as a risk factor for weight gain and obesity (3). Animal studies have specifically Fig .…”

Section: E179mentioning

confidence: 99%

Improved metabolic regulation is associated with retinoblastoma protein gene haploinsufficiency in mice

Petrov

Ribot

Palou

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

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Petrov PD, Ribot J, Palou A, Bonet ML. Improved metabolic regulation is associated with retinoblastoma protein gene haploinsufficiency in mice. Am J Physiol Endocrinol Metab 308: E172-E183, 2015. First published November 18, 2014 doi:10.1152/ajpendo.00308.2014 is involved in the control of energy metabolism, and its inactivation protects mice against high-fat diet-induced diabesity. Here, we tested the hypothesis that partial deficiency in the Rb gene could confer metabolic advantages in front of acute challenges to metabolism and as mice age on a regular diet. Rb haploinsufficient (Rb ϩ/Ϫ ) mice and wild-type (WT) littermates were studied from weaning and characterized at 1.5-2.5 mo of age (young adults) and 6 -7.5 mo of age (mature adults). Whereas no differences in body weight or composition were observed at young age, mature adult Rb ϩ/Ϫ mice were leaner than WT littermates, displaying 36% reduced body fat content. At both ages studied, Rb ϩ/Ϫ mice displayed improved blood lipids, enhanced sensitivity to the blood glucose-lowering effect of insulin and to the anorectic effect of leptin, and a reduced respiratory exchange ratio, indicative of an increased use of fatty acids as a fuel. Insulin sensitivity and oral fat tolerance were better maintained with age in the Rb ϩ/Ϫ than the WT mice. Mature adult Rb ϩ/Ϫ mice displayed gene expression changes consistent with increased fatty acid oxidation in white adipose tissue and skeletal muscle and paramount signs of browning in the inguinal white adipose tissue. In conclusion, Rb haploinsufficiency provides metabolic advantages in front of acute metabolic stressors and ameliorates body fat gain and metabolic impairments that normally accompany transition from young to mature adult age. retinoblastoma; insulin sensitivity; fat tolerance; browning THE CONCEPT THAT CELL CYCLE regulatory proteins modulate metabolism in addition to cell proliferation and survival is strengthened by recent research (14). One important protein in this context is the retinoblastoma protein (pRb), encoded by the Rb gene and best known for its role in the control of the cell's proliferation/differentiation switch (25). pRb is the archetypical member of the retinoblastoma protein family, which also includes p107 and p130. In its active hypophosphorylated form, pRb functions as a cofactor for many transcription factors, including E2Fs and cell differentiation-related factors. Interaction with pRb represses the transactivating activity of E2F1 on genes encoding proteins required for entry into the DNA replication phase of the cell cycle while it stimulates the activity of cell differentiation inducers, including master transcription factors required for the differentiation of skeletal myocytes, osteoblasts, and adipocytes (8, 47).Retinoblastoma protein family members have been shown to be involved in nonredundant complex ways in adipogenic commitment and terminal adipogenesis in different model systems of murine and human origin (9 -11, 34 -36). pRb is unique in this context in that its activit...

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Fat oxidation at rest predicts peak fat oxidation during exercise and metabolic phenotype in overweight men

Cited by 66 publications

References 44 publications

Dietary intake is independently associated with the maximal capacity for fat oxidation during exercise,

Dietary intake is independently associated with the maximal capacity for fat oxidation during exercise,

Body fat loss and compensatory mechanisms in response to different doses of aerobic exercise—a randomized controlled trial in overweight sedentary males

Improved metabolic regulation is associated with retinoblastoma protein gene haploinsufficiency in mice

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