Role of Lipids on Endurance Capacity in Man

Abstract

A man whose weight is near 70 kg has approximately 15 kg of fat as triglycerides in adipose tissue, representing about 140,000 kcal. With such a quantity of stored fat, the question is to know why triglycerides are not the only fuel for exercise. Probably because this fuel cannot sustain maximal rates of exercise. The ability to sustain maximal exercise is dependent on carbohydrate use. The reason for the limited rate at which energy can be derived from fat store is not clear. We can examine successively:

1. The rate of release from adipose tissue. Hydrolysis of the adipose tissue triglyceride is regulated by hormonal and nervous influence. It has recently been shown that 70% of fatty acids released from adipose tissue at rest are reesterified. This value decreases to 25% at the onset of submaximal exercise at 40% of V̇O₂max. One part of the increase in fat oxidation could therefore result from the reduced reesterification.

2. The capacity of transport and muscle extraction. A close correlation has been shown between the increase in FFA concentration and FFA uptake during increased energy expenditure under the effect of exercise. Exercise increases liprotein lipase (LPL) activity in muscle. This causes increase in muscle and cardiac FFA uptake and a decrease in LPL activity in adipose tissue. The control of this enzyme is coordinated by hormonal mechanisms resulting from the reduction of insulin and the increase in catecholamines induced by exercise.

3. The oxidative capacity of the muscle. During heavy work carbohydrate fuel contributes to 80-90% of energy expenditure when the participation of lipid fuel is reduced to 10%. The regulation of this fuel selection could result from several factors capable of inhibiting fatty acid oxidation when glycolysis is elevated and, conversely, inhibiting glycolysis when FFA oxidation is elevated. The more detailed biochemical pathway is the inhibition of glycolysis when FFA oxidation is high. It is sustained by the concept of FFA glucose cycle of Randle (1963). The biochemical basis of this concept is that oxidation of FFA increases acetyl COA/COA ratio which inhibits pyruvate dehydrogenase, phosphofructokinase, and thus glycolysis. Also, the inhibition of FFA oxidation when glycolysis is high is regulated by the process of reesterification in the muscle.

Enhanced lipid availability resulting from eating a fatty meal before exercise, or a chronic high fat diet, or fasting, is not capable of enhancing endurance capacity in humans. The glucose-fatty acid cycle which has previously been proposed to spare muscle glycogen stores is not operative in man.

Key words

Physical exercise - lipid metabolism - lipid diet - endurance capacity - glucose - fatty acid cycle