Optimizing fat oxidation through exercise and diet.

Juul Achten; Asker E Jeukendrup

doi:10.1016/j.nut.2004.04.005

Home/Archive/PubMed

PubMed · 15212756

Optimizing fat oxidation through exercise and diet.

Juul Achten·Asker E Jeukendrup

View original source ↗Export metadata ↓

Abstract

Interventions aimed at increasing fat metabolism could potentially reduce the symptoms of metabolic diseases such as obesity and type 2 diabetes and may have tremendous clinical relevance. Hence, an understanding of the factors that increase or decrease fat oxidation is important. Exercise intensity and duration are important determinants of fat oxidation. Fat oxidation rates increase from low to moderate intensities and then decrease when the intensity becomes high. Maximal rates of fat oxidation have been shown to be reached at intensities between 59% and 64% of maximum oxygen consumption in trained individuals and between 47% and 52% of maximum oxygen consumption in a large sample of the general population. 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. Fat oxidation rates have been shown to decrease after ingestion of high-fat diets, partly as a result of decreased glycogen stores and partly because of adaptations at the muscle level.

Explore related subjects

Adipose Tissue Diet Dietary Carbohydrates Exercise Fatty Acids Humans Hydrolysis Lipid Metabolism Lipolysis Mitochondria Muscle, Skeletal Oxidation-Reduction Physical Endurance Triglycerides Journal Article Review

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

Juul Achten, Asker E Jeukendrup. Optimizing fat oxidation through exercise and diet.. https://doi.org/10.1016/j.nut.2004.04.005

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2025

Rapidly decellularized adipose tissue induces soft tissue vascularization in potential anatomical spaces.

Decellularized tissues provide biological cues owing to the wealth of structural and regulatory factors that promote angiogenesis, adipogenesis, and myogenesis and facilitate neurite outgrowth. Here, we demonstrated the advantages of decellularized adipose tissue (adipoECM) over defined collagen-based biomaterials for host tissue integration. Three batches of human adipose tissue were decellularized using a rapid decellularization protocol and analyzed using mass spectrometry. To assess the biological activity of the decellularized materials, adipoECM and a reference standard of care biomaterial (Integra®DRT, also containing collagen I and glycosaminoglycans) were implanted subcutaneously, but far from the wound bed (in anatomical potential spaces) of immunocompetent BALB/c mice. The mice were euthanized in the acute (1 day) and chronic (day 60) inflammatory reaction phases, followed by biomaterial excision and Masson’s trichrome immunohistofluorescence imaging of the paraffin-embedded specimens. Each batch of processed tissue passed a quality control check, showing a low level of donor genomic DNA, lack of nuclei, lipids, endotoxins, and bacterial contamination. Mass spectrometry revealed that all batches of decellularized tissue mainly contained collagen I and, to a lesser degree, collagen III, collagen IV, collagen V, laminin, fibrillin, fibronectin, tenascin, and elastin. No acute inflammatory reaction was observed in either material one day post-transplantation. At 60 days post-implantation, different cell types were detected in adipoECM specimens, whereas Integra®DRT remained acellular. Additional immunohistochemical staining of adipoECM revealed CD31-positive cells in the blood vessels. Mesenchymal (CD90 positive) and myeloid (CD14 positive) cells were also detected. Primary cell types involved in soft tissue healing and remodeling were found in the adipoECM-treated group. The ingrowth of blood vessels and mesenchymal cells confirmed the effective integration of adipoECM with host tissues. Our results demonstrate that decellularized adipose tissue implanted away from the wound bed possesses contextual biological activities that promote efficient integration with host tissues.

Adipose Tissue↗

PubMed2006

Interrelationships of serum estradiol, estrone, and estrone sulfate, adiposity, biochemical bone markers, and leptin in post-menopausal women.

OBJECTIVE: The aim of this study was to examine the relationships between endogenous estrogens and adiposity, bone markers, and leptin in post-menopausal (PM) women. DESIGN: Seventy-three post-menopausal (PM) women participated in a clinical correlational study. Weight, height, waist-hip ratio, fasted morning serum and first morning voided urine samples were obtained to compare body mass index (BMI), waist-hip ratio, endogenous estrogens, leptin, and bone markers. Serum estradiol, estrone (E1), estrone sulfate (E1S), leptin, osteocalcin, and urinary deoxypyridinoline (Dpd) were determined. RESULTS: Significant positive relationships were found between BMI and estradiol, E1, and E1S (r = 0.52, 0.38, and 0.29; P < or = 0.001, 0.001, and 0.013 respectively). Significant relationships between leptin and estrogens were revealed, but were not significant when BMI was used as a covariate. Although many subjects revealed elevated bone marker levels, no correlation between estrogens or BMI and bone markers (Dpd and osteocalcin) was found. CONCLUSIONS: There are significant positive correlations between estrogens and BMI in PM women. Increasing levels of estradiol, E1, and E1S with increasing BMI may be an indicator of adiposity, but are without effect as a stimulatory factor on leptin production. Waist-hip ratio did not significantly affect leptin concentrations when accounting for BMI. Due to assay sensitivity in the present study, data represent a more precise representation of these relationships. The lack of correlation between estrogens and bone marker levels may have been due to low estrogen levels in PM women.

Adipose Tissue↗

PubMed2006

Bone formation using human adipose tissue-derived stromal cells and a biodegradable scaffold.

Human adipose tissue, obtained by liposuction, was processed to obtain a fibroblast-like population of cells or adipose tissue-derived stromal cells (ATSCs). The ATSCs, as well as bone marrow-derived mesenchymal stem cells (BMSCs), have the capacity for renewal and the potential to differentiate into multiple lineages of mesenchymal tissues. These cells are capable of forming bone when implanted ectopically in an appropriate scaffold. The aim of this study was to evaluate a beta-tricalcium phosphate (beta-TCP) as a scaffold and to compare the potential of osteogenic differentiation of ATSCs with BMSCs. Both cell types were loaded into beta-TCP disk and cultured in an osteogenic induction medium. Optimal osteogenic differentiation in ATSCs in vitro, as determined by secretion of osteocalcin, scanning electron microscope, and histology, were obtained in the culturing with the beta-TCP disk. Furthermore, bone formation in vivo was examined by using the ATSC- or BMSC-loaded scaffolds in nude mice. The present results show that ATSCs have a similar ability to differentiate into osteoblasts and to synthesize bone in beta-TCP disk as have BMSCs.

Adipose Tissue↗