Review articleOptimizing fat oxidation through exercise and diet
Introduction
An inability to oxidize lipids appears to be an important factor in the etiology of obesity and type 2 diabetes. An elevated 24-h respiratory quotient in Pima Indians has been associated with a high rate of weight gain.1 It has also been reported that individuals with obesity and non–insulin-dependent diabetes mellitus have a decreased capacity to oxidize fatty acids (FAs) and this is related to increased insulin resistance.2 Further, some of the benefits of performing regular exercise, such as decreased insulin resistance, reduced hypertension, and reduced plasma low-density lipoprotein (LDL) concentration, are likely to be related to enhanced fat oxidation. This effect could be direct by adaptations in the fat metabolism pathways or indirect by reducing fat mass.3, 4 Exercise training and regular physical activity have been shown to increase fat oxidation in healthy individuals5, 6 and in obese populations.7 Having a better understanding of the factors that influence the rate of fat oxidation at rest and during exercise is therefore important. Interventions aimed at increasing fat metabolism could potentially reduce the symptoms of the disease in these groups of patients and might have tremendous clinical relevance.
One of the main training adaptations observed in endurance athletes is increased fat oxidation, and it has been suggested that an increased capacity to oxidize fat is related to endurance capacity and exercise performance.8 Training or diet interventions that optimize fat metabolism could therefore, at least in theory, also benefit endurance athletes.
Understanding the mechanisms behind the changes in fat metabolism that might occur as a result of various interventions and knowledge of the different sources of fat that may be utilized is important. Long-chain fatty acids (LCFAs) are a major source of energy at rest and during low- to moderate-intensity exercise. The source of FA utilized during exercise (FA from adipose tissue, FA in circulating lipoproteins (plasma triacylglycerol [TAG]) or muscle TAG, may vary depending on the conditions. Several sites have been suggested at which FA oxidation can be regulated: 1) adipose tissue lipolysis and FA delivery to the muscle, 2) FA movement across the muscle membrane, 3) hydrolysis of intramuscular TAGs (IMTAG), and 4) FA movement across the mitochondrial membranes. In Figure 1 these sites have been graphically displayed.
This review focuses on several interventions that influence fat oxidation, including the selection of the exercise intensity or the type of exercise, exercise training, and the influence of diet. In addition, the mechanisms behind the effects of these interventions on fat metabolism are discussed. This discussion is structured around the sites, displayed in Figure 1, where regulation of FA metabolism is believed to take place. For a more detailed discussion of these mechanisms, the reader is referred to several recent reviews.9, 10, 11, 12, 13, 14 This review is based predominantly on human studies in healthy individuals.
Section snippets
Acute exercise and fat oxidation
An important question from a practical point of view is: At what exercise intensity can the highest rates of fat oxidation be found? In 1932, Christensen15 showed, using respiratory exchange ratios (RERs), that changes in exercise intensity induce changes in substrate utilization. It was also observed that, with increasing exercise duration, fat oxidation progressively increased.16 Later this was attributed to a reduction in muscle glycogen breakdown and total carbohydrate (CHO) oxidation.
The
Short-term CHO intake and fat oxidation
Fatty meals have been suggested as a way to increase fat oxidation and the ingestion of medium-chain triacylglycerols (MCTs). The effectiveness of these nutritional interventions have been discussed elsewhere in this issue.93 Here we discuss the effects of CHO intake before and during exercise.
It has been demonstrated that the ingestion of CHO before or during exercise can result in a marked reduction in FA oxidation. The magnitude of the effect that CHO intake has depends on several factors
Large variation in fat oxidation still unexplained
Although a number of important factors regulating fat oxidation have been identified, It is apparent from many studies that a considerable degree of intersubject variability in substrate utilization persists. This is especially apparent in a study by Venables et al.20 in which fat oxidation was measured in a large group of healthy individuals. Peak fat oxidation rates ranged from 0.18 to 1.01 g/min. This variation still exists (although to a lesser degree) when all factors such as training
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