| Endogenous triglycerides represent the largest fuel reserve in the body. Most triglycerides (~17,500 mmol in a lean adult man) are compactly stored in adipose tissue as an oil. Triglycerides are also present in skeletal muscle (~300 mmol) and in plasma very low-density lipoproteins (~0.5 mmol). The total amount of energy stored as triglyceride (~ 135,000 kcal) is 65-fold greater than the amount of energy stored as glycogen (~ 2,000 kcal). Therefore, the use of fat as a fuel during endurance exercise permits sustained physical activity and delays the onset of hypoglycemia. The relative contribution of different endogenous fat depots for energy production Durham endurance exercise is not precisely known because of methodological limitations. The major source of fatty acids oxidized during prolonged exercise is derived from adipose tissue. It has been estimated that intramuscular triglycerides comprise 5-50 percent of the fat oxidized, whereas the contribution from circulating lipoproteins is minimal.1
The use of triglyceride as a fuel requires hydrolysis to free fatty acids (FFA) and glycerol and subsequent oxidation of FFA by working muscles. Therefore, the level of FFA and glycerol in plasma has been used as an index of lipolysis. However, plasma FFA and glycerol concentration represent a balance between FFA and glycerol release into plasma and their uptake by peripheral tissues. Therefore, plasma FFA and glycerol concentrations may not accurately reflect lipolytic activity. For example, we have found that the relationship between plasma FFA concentration and lipolysis can vary markedly during different physiological conditions.2 Plasma FFA concentrations during exercise correspond to a much greater rate of lipolysis than do the same plasma FFA concentrations during ephiephrine infusion. Therefore, the use of isotope tracer methodology to measure free fatty acid and glycerol rates of appearance (Ra) in plasma represents the best approach for studying lipid kinetics during exercise.
Glycerol Ra, an index of whole body lipolysis, and FFA Ra, an index of FFA
availability, increase progressively during endurance exercise,3
primarily because of an increase in catecholamine stimulation of beta-adrenergic
receptors. In fact, strenuous exercise is the most potent physiologic stimulus
for lipolysis. Glycerol Ra during high-intensity exercise4 represents the highest
values reported in humans and is threefold higher than those reported during
critical illness5 or after 84 hours of starvation.6 The increase in lipolysis
in conjunction with an increase in skeletal muscle energy requirements is
responsible for the marked increase in fatty acid oxidation observed during
exercise. The rate of triglyceride-fatty acid cycling changes dramatically
during exercise because of differences in the relative increase in fatty
acid oxidation and lipolysis. In one study, approximately two-thirds of FFA
released into plasma were reesterified during resting basal conditions,
whereas only one-fourth of FFA released was reesterified during prolonged
moderate intensity exercise.7
The rate of lipolysis depends on the intensity and duration of the exercise bout,
previous exercise training, and recent dietary intake. Modifications in dietary
intake before exercise can cause changes in lipid metabolism during exercise.
Plasma FFA and glycerol concentrations are higher at rest and increase more
rapidly during exercise following a low-carbohydrate diet or short-term
fasting.8,9 Endurance training has been reported to decrease
lipolystic rates during exercise but increase total fat oxidation, presumably
because of an increase in intramuscular triglyceride oxidations.10
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