Fat metabolism during exercise

Fats are oxidized together with carbohydrates in muscle to provide energy for working muscles. The extent to which they can compensate for energy expenditure depends on the duration and intensity of the exercise. Endurance (>90 min) athletes typically train at 65-75% V02max and are limited by the body's carbohydrate reserves. After 15-20 min of endurance exercise, oxidation of fat stores (lipolysis) is stimulated and glycerol and free fatty acids are released. In resting muscle, fatty acid oxidation provides a large amount of energy, but this contribution decreases during light aerobic exercise. During intense exercise, a switch in energy sources from fat to carbohydrates is observed, especially at intensities of 70-80% V02max. It is suggested that there may be limitations in the use of fatty acid oxidation as an energy source for working muscles. Abernethy et al. suggest the following mechanisms.

• Increased lactate production will reduce catecholamine-induced lipolysis, thereby reducing plasma fatty acid concentrations and muscle fatty acid supply. Lactate is thought to have an antilipolytic effect in adipose tissue. Increased lactate levels may result in decreased blood pH, which reduces the activity of various enzymes involved in energy production and leads to muscle fatigue.
• Lower ATP production per unit time during fat oxidation compared to carbohydrates and higher oxygen demand during fatty acid oxidation compared to carbohydrate oxidation.

For example, oxidation of one glucose molecule (6 carbon atoms) results in the formation of 38 ATP molecules, while oxidation of fatty acid molecules with 18 carbon atoms (stearic acid) yields 147 ATP molecules (the ATP yield from one fatty acid molecule is 3.9 times higher). In addition, complete oxidation of one glucose molecule requires six oxygen molecules, and complete oxidation of palmitic acid requires 26 oxygen molecules, which is 77% more than in the case of glucose, so during prolonged exercise, the increased oxygen demand for fatty acid oxidation can increase the stress on the cardiovascular system, which is a limiting factor in relation to the duration of the load.

The transport of long-chain fatty acids into the mitochondria depends on the capacity of the carnitine transport system. This transport mechanism may inhibit other metabolic processes. Increased glycogenolysis during exercise may increase acetyl concentrations, which will result in increased levels of malonyl-CoA, an important intermediate in fatty acid synthesis. This may inhibit the transport mechanism. Similarly, increased lactate formation may increase acetylated carnitine concentrations and decrease free carnitine concentrations, thereby impairing fatty acid transport and oxidation.

Although fatty acid oxidation during endurance exercise provides a greater energy output than carbohydrate, fatty acid oxidation requires more oxygen than carbohydrate (77% more O2), thus increasing cardiovascular strain. However, due to the limited storage capacity of carbohydrate, exercise intensity performance deteriorates as glycogen stores are depleted. Therefore, several strategies are considered to conserve muscle carbohydrate and enhance fatty acid oxidation during endurance exercise. They are as follows:

• training;
• medium chain triacylglycerol nutrition;
• oral fat emulsion and fat infusion;
• high fat diet;
• supplements in the form of L-carnitine and caffeine.

Training

Observations have shown that trained muscles have high activity of lipoprotein lipase, muscle lipase, acyl-CoA synthetase and fatty acid reductase, carnitine acetyltransferase. These enzymes enhance the oxidation of fatty acids in mitochondria [11]. In addition, trained muscles accumulate more intracellular fat, which also increases the intake and oxidation of fatty acids during exercise, thus preserving carbohydrate reserves during exercise.

Medium-chain triglyceride intake

Medium-chain triacylglycerides (MCTs) contain fatty acids with 6-10 carbon atoms. These Ts are thought to pass rapidly from the stomach to the intestine, are transported via the blood to the liver, and may increase plasma MCTs and Ts. In muscle, these Ts are rapidly taken up by the mitochondria because they do not require the carnitine transport system, and are oxidized more rapidly and to a greater extent than long-chain Ts. However, the effects of MCTs on exercise performance are equivocal. Evidence for glycogen preservation and/or endurance enhancement with MCTs is inconclusive.

Oral fat intake and infusion

Reduction of endogenous carbohydrate oxidation during exercise can be achieved by increasing plasma fatty acid concentrations using fatty acid infusions. However, fatty acid infusions are impractical during exercise and impossible during competitions, as they can be considered an artificial doping mechanism. In addition, oral consumption of fatty emulsions can inhibit gastric emptying and lead to gastric disorders.

High fat diets

High-fat diets may increase fatty acid oxidation and improve endurance performance in athletes. However, current evidence suggests that such diets may improve performance by regulating carbohydrate metabolism and maintaining muscle and liver glycogen stores. Long-term high-fat diets have been shown to have adverse effects on cardiovascular health, so athletes should be cautious when using high-fat diets to improve performance.

L-Carnitine Supplements

The main function of L-carnitine is to transport long-chain fatty acids across the mitochondrial membrane to be included in the oxidation process. Oral consumption of L-carnitine supplements is believed to enhance fatty acid oxidation. However, scientific evidence to support this claim is lacking.

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