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
Performance during exercise depends, in part, on the provision of adequate
fuel to working muscles. Therefore, athletes often ingest carbohydrate during
intense endurance exercise to support plasma glucose concentrations and spare
muscle glycogen oxidation. Ingestion of typical dietary fat is not a useful
approach for providing fuel during exercise because it may take several hours
for the long-chain fatty acids to be oxidized. Long-chain triglycerides are
emptied slowly from the stomach, packaged into chylomicrons in the small
intestine, and secreted into the lymphatic system before entering the
bloodstream. Only a portion of triglycerides present in circulating
chylomicrons ultimately provide fatty acids to muscle. In contrast,
medium chain triglycerides (MCTs) have been proposed as a potential
ergogenic fuel during exercise and are currently present in several
commercially prepared sport bars. Medium-chain triglycerides are emptied
rapidly from the stomach,11 rapidly absorbed and hydrolyzed by the small
intestine, and secreted directly into the systemic circulation.
Furthermore, medium-chain fatty acids do not require the acylcarnitine
transferase system to cross the inner mitochondrial membrane in liver
and muscle for oxidation. However, several studies have demonstrated
that oral supplementation with MCTs is unlikely to improve performance
during endurance exercise. The amount of MCTs that can be given orally
is limited to approximately 25-30 grams because diarrhea and other
gastrointestinal side effects are common with higher doses.
Furthermore, although orally administered medium-chain triglycerides
are readily oxidized,12-14 they do not spare muscle glycogen during
either moderate or high-intensity exercise.12-16
1. Hurley BF, Nemeth PM, Martin WH, Hagberg JM, Dalsky GP, Holloszy JO. Muscle triglyceride utilization during exercise: effect of training. J Appl Physiol 1986;60:562-7.
2. Klein S. Coyle EF, Wolfe RR. Effect of exercise on lipolytic sensitivity in endurance-trained athletes. J Appl Physiol 1995;78:2201-6.
3. Klein S. Coyle EF, Wolfe RR. Fat metabolism during low-intensity exercise in endurance- trained and untrained men. AM J Physiol 1994;267:E934-40
4.Klein S, Weber J-M, Coyle EF, Wolfe RR. Effect of endurance training on glycerol kinetics during strenuous exercise in humans. Metabolism 1996;45:357-61
5.. Klein S. Peters EJ, Shangraw RE, Wolfe RR. Lipolytic response to metabolic stress in patients with critical illness. Crit Care Med 1991;19:776-9.
6. Klein S. Young VR, Blackburn GL, Bistrian BR, Wolfe RR. Palmitate and glycerol kinetics during brief starvation in young adult and elderly subjects. J Clin Invest 1986;78:928-33.
7. Wolfe RR, Klein S. Carraro F. Weber J-M. Role of triglyceride-fatty acid cycle in controlling fat metabolism in humans during and after exercise. Am J Physiol 1990;258:E382-9.
8. Dohm GL, Beeker RT, Israel RG, Tapscott EB. Metabolic responses to exercise after fasting. J Appl Physiol 1986;61:1363-8.
9. Conlee RK, Hammer RL, Winder WW, Bracken ML, Nelson AG, Barnett DW. Glycogen repletion and exercise endurance in rats adapted to a high fat diet. Metabolism 1990;39:289-94.
10. Martin B. Robinson S. Robertshaw D. Influence on diet on leg uptake of glucose during heavy exercise. Am J Clin Nutr 1978;31:62-7.
11. Beckers EJ, Jeukendrup AK, Brouns F. Wagenmakers AJM, Saris WHM. Gastric emptying oc carbohydratemedium chain triglyceride suspensions at rest. Int J Sports Med 1992;13:581-4.
12. Jeukendrup AK, Saris WHM, Van Diesen R. Brouns F. Wagenmakers AJM. Effect of endogenous carbohydrate availability on oral medium chain triglyceride oxidation during prolonged exercise. J Appl Physiol 1996;80:949-54.
13. Massicotte D, Peronnet F. Brisson GR, Hillarie-Marcel C. Oxidation of exogenous medium-chain free fatty acids during prolonged exercise: comparison with glucose. J Appl Physiol 1992;73:1334-9.
14. Decombaz J. Arnaud M-J, Milon H. Moesch H. Philippossian G. Thelin A-L, Howald H. Energy metabolism of medium-chain triglycerides versus carbohydrates during exercise. Eur J Appl Physiol 1980;52:9-14.
15. Jeukendrup AK, Saris WHM, Schrauwen P. Brouns F. Wagenmakers AJM. Metabolic availability of medium-chain triglycerides coingested with carbohydrates during prolonged exercise. J Appl Physiol 1995;79:756~2.
16. Ivy JL, Costill DL, Fink WJ, Maglischo E. Contribution of medium and long chain triglyceride intake to energy metabolism during prolonged exercise. Int J Sports Med 1980;1:15-20.
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