Unveiling the principles of fat burning through exercise: Scientifically promoting fat breakdown for efficient weight loss.

Experimental reports indicate that physical exercise induces increased secretion of catecholamines and adrenocortical hormones, as well as decreased insulin secretion, which in turn promotes increased activity of triglyceride esterase (the rate-limiting enzyme in lipolysis), cytochrome C oxidase, and citrate synthase. Enzyme activity is related to fatty acid uptake, esterification, and mobilization; increased enzyme activity accelerates fat breakdown. Therefore, exercise can promote fat breakdown.

Exercise training significantly enhances the responsiveness of adipocytes to adrenocortical and medullary hormones and increases lipase levels by 3–4 times. While the hormonal and enzymatic responses induced by exercise generally inhibit fat synthesis, exercise does not comprehensively inhibit fat metabolism. Isotope-labeled incorporation techniques have shown that the fatty acid synthesis rate in exercised mice is several times higher than in sedentary mice, and the synthesis rate is directly proportional to the diameter of the mouse's adipocytes. Furthermore, reports indicate that during exercise, animals exhibit fatty acid carbon chain elongation, decreased saturation, and increased polyunsaturated fatty acids, suggesting that exercise can simultaneously enhance fatty acid breakdown and synthesis. Measuring respiratory quotient (RQ) during prolonged exercise at intensity below 55% of maximum oxygen uptake reveals the energy provided by fatty acid breakdown. The fatty acids broken down during exercise are primarily free fatty acids (triglycerides stored in adipose tissue, lipoproteins, triglycerides in chylomicrons, and triglycerides in muscles). During exercise, free fatty acids, after mobilization from adipose tissue, appear in the blood in three phases: circulation, metabolism, and recovery. Free fatty acids are released to the exercising muscles, where they can be oxidized and utilized, and are cleared. Increased metabolic activity and heightened sensitivity to hormones are accompanied by increased fat uptake, esterification, mobilization, metabolic conversion rate, and shortened half-life.

When glucose supply is insufficient, ketone bodies can also be oxidized by extrahepatic tissues (including muscles). Blood ketone body increases only slightly during exercise but significantly afterward; however, individuals with high levels of training have a strong ability to oxidize ketone bodies, resulting in fewer ketone bodies appearing after exercise. There is a lack of consensus on the significance of energy generated by ketone body oxidation; some believe that the energy from ketone body oxidation can meet the needs of exercise, while others believe that the energy generated by ketone body oxidation is only 100-200 kcal, which is quantitatively insignificant for skeletal muscle movement.

The utilization of fat during exercise is coordinated and controlled by the following three factors:

(1) Intensity and duration of exercise load: During high-intensity, short-duration exercise (exercise intensity > VO₂max 60%–70%), fat is generally not utilized, released, or oxidized; in the initial stage of exercise intensity < VO₂max 55%, fat is also not oxidized for energy, and there is a time lag in fat utilization and release, which is only utilized during low-intensity, long-duration exercise.

(2) Good individual training status and training adaptation can increase the ability to oxidize free fatty acids and ketone bodies.

(3) The sugar and fat content in the diet several days before exercise; if the sugar content in the diet before exercise is high, the proportion of energy supplied by liver glycogen and muscle glycogen during exercise will be relatively higher.

Athletes who undergo long-term systematic training have lower plasma triglyceride levels than those who work at rest. After a 1-hour exercise session, the serum triglyceride level does not change significantly within 4 hours after exercise, and only decreases significantly after 24 hours; therefore, some have proposed that the decrease in serum triglycerides caused by exercise is a delayed response with no obvious threshold. Using the C20-labeled diglyceride injection technique, the clearance constant of triglycerides at rest is observed to be (26.5±1.9)% per minute, while it can increase to (33.8±3.6)% during exercise, indicating that exercise can increase the clearance rate of triglycerides. The effect of exercise on plasma triglyceride concentration is related to the amount, intensity, and duration of exercise.