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Combined Effects of Phytochemicals and Exercise on Fatty Acid Oxidation.

ABSTRACT: The purpose of this review is to discuss current views regarding the acute effects of phytochemicals, exercise, and exercise plus phytochemicals on fatty acid oxidation.Data acquired from human and animal studies were comprehensively assessed to determine the single and combined effects of phytochemicals and exercise on fatty acid oxidation. In addition, underlying mechanisms associated with those conditions that may contribute to the regulation of fat metabolism are discussed.Although not all phytochemicals are effective at increasing fatty acid oxidation, some significantly improve the rate of fatty acid oxidation at rest. In addition, dietary supplementation of p-synephrine, catechins, or anthocyanins in combination with moderately intense exercise has the additive effect of increasing fatty acid oxidation, but not total energy expenditure during exercise.The data reported from current reviewed studies suggest positive outcomes regarding facilitation of fatty acid oxidation from the combined effects of certain phytochemicals with exercise. Those data provide new insight for developing a strategy to boost fat loss and control weight in obese patients.

SUBMITTER: Kim JH

PROVIDER: S-EPMC5545207 | biostudies-other | 2016 Dec

REPOSITORIES: biostudies-other

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Project description:BackgroundFree fatty acids (FFAs) are an important source of energy, and also serve as signaling molecules to regulate gene expression. Exercise performed in a post-absorptive state, in contrast to that performed in a postprandial state, increases 24-h fat oxidation under an energy-balanced condition. The primary aim of the present study was to clarify whether the effects of exercise on the concentration and composition of plasma FFAs, which may underlie distinct effects of exercise on 24-h fat oxidation, depend on the nutritional state of the individual when performing the exercise.MethodsTen healthy young men underwent 3 trials of indirect calorimetry in a metabolic chamber. The subjects performed exercise at 60% of VO2max for 60 min in either a post-absorptive or postprandial state, or remained sedentary without an exercise session (control). All trials were designed to be energy balanced over 24 h. Blood samples were collected immediately before and after exercise.ResultsFat oxidation over 24 h was increased only when exercise was performed in a post-absorptive state (control, 531 ± 60; post-absorptive, 779 ± 70; postprandial, 569 ± 37 kcal/24 h). The increase in the 24-h fat oxidation was related to the magnitude of the transient carbohydrate deficit after exercise. The plasma FFA concentration after exercise was higher in the post-absorptive trial (0.38 ± 0.04) than in the control (0.13 ± 0.01) and postprandial (0.15 ± 0.02 mM) trials. The ratio of unsaturated to saturated (U/S) fatty acids after exercise was higher in the post-absorptive trial (1.76 ± 0.06) than in the control (1.56 ± 0.07) and postprandial (1.53 ± 0.08) trials. On the other hand, the plasma FFA concentration after exercise in a postprandial state did not differ significantly from that in the control trial.ConclusionExercise performed in a post-absorptive state effectively increased the plasma FFA concentration and U/S ratio to a greater degree than exercise performed in a postprandial state, underlying the increase in the 24-h fat oxidation. The increase in the plasma FFA concentration was related to the transient carbohydrate deficit after exercise.

Project description:Carnitine is essential for the transfer of long-chain fatty acids across the inner mitochondrial membrane for subsequent β-oxidation. It can be synthesized by the body or assumed with the diet from meat and dairy products. Defects in carnitine biosynthesis do not routinely result in low plasma carnitine levels. Carnitine is accumulated by the cells and retained by kidneys using OCTN2, a high affinity organic cation transporter specific for carnitine. Defects in the OCTN2 carnitine transporter results in autosomal recessive primary carnitine deficiency characterized by decreased intracellular carnitine accumulation, increased losses of carnitine in the urine, and low serum carnitine levels. Patients can present early in life with hypoketotic hypoglycemia and hepatic encephalopathy, or later in life with skeletal and cardiac myopathy or sudden death from cardiac arrhythmia, usually triggered by fasting or catabolic state. This disease responds to oral carnitine that, in pharmacological doses, enters cells using the amino acid transporter B(0,+). Primary carnitine deficiency can be suspected from the clinical presentation or identified by low levels of free carnitine (C0) in the newborn screening. Some adult patients have been diagnosed following the birth of an unaffected child with very low carnitine levels in the newborn screening. The diagnosis is confirmed by measuring low carnitine uptake in the patients' fibroblasts or by DNA sequencing of the SLC22A5 gene encoding the OCTN2 carnitine transporter. Some mutations are specific for certain ethnic backgrounds, but the majority are private and identified only in individual families. Although the genotype usually does not correlate with metabolic or cardiac involvement in primary carnitine deficiency, patients presenting as adults tend to have at least one missense mutation retaining residual activity. This article is part of a Special Issue entitled: Mitochondrial Channels edited by Pierre Sonveaux, Pierre Maechler and Jean-Claude Martinou.

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Combined Effects of Phytochemicals and Exercise on Fatty Acid Oxidation.

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