Question

Describe why fat metabolism declines as excerise intensity even through fat provides such a good source of energy?

Answer 1

The two main sources of energy during muscular exercise are fat (triglyceride) and carbohydrate (glycogen and glucose) stored within the body. The primary reason that glycogen reserves are essential is that athletes can only slowly convert their body fat stores into energy during exercise. Therefore, when muscle glycogen and blood glucose concentrations are low, the intensity of exercise must be reduced to a level that can be supported by the body's limited ability to convert body fat into energy. With endurance training, athletes can markedly increase the rate at which body fat can be oxidized, thus allowing them to exercise longer before becoming exhausted due to glycogen depletion. Of course, exercise training also increases an individual's ability to exercise more intensely, so trained athletes must continue to derive most of their energy from carbohydrate during intense training and competition because their increased ability to oxidize fat cannot meet their increased energy demands.

Exercise acutely increases fat oxidation, and endurance training increases the capacity to oxidize fat suggesting that regular exercise could induce loss of fat mass by increasing fat oxidation. Although endurance training increases the capacity of skeletal muscle to oxidize all substrates, including fatty acids, carbohydrate is still the predominant energy source in exercising skeletal muscle. It has been suggested that the major effect of exercise on fat metabolism may occur after exercise, although this has never clearly been demonstrated. To reduce fat mass, a state of negative fat balance must be achieved. To achieve negative fat balance, one must alter intake or expenditure such that fat oxidation exceeds fat intake. Since fat oxidation is increased during exercise, and since endurance exercise training increases the capacity to oxidize fat, by extension, it is assumed that 1) more fat is oxidized on a day that exercise is performed; and 2) trained individuals will oxidize more fat over 24 compared to sedentary individuals.

At rest and during exercise, most of the fat used for fuel comes from the adipose tissue triglycerides. Thus, fatty acids are released from the adipose tissue (i.e, Lipolysis - breakdown of triglycerides)) and hence delivered to the skeletal muscles for further oxidation (i.e., energy production). The activity of lipolysis is mediated by several hormones including glucagon, epinephrine, norepinephrine, growth hormone, cortisol and two main enzymes (hormone-sensitive lipase – HSL & Lipoprotein lipase – LPL). Other factors that may affect lipolysis may include but are are not limited to gender, fitness level and exercise intensity.

At the onset of exercise, the sympathetic nervous system (SNS) releases two important catecholamines (epinephrine and norepinephrine). These hormones bind to and stimulate key receptors located on the fat cell surface (Beta-Adrenergic receptors) which in turn activate the HSL enzyme, thus, initiating the breakdown of triglycerides in the adipose tissue (lipolysis).

Once the free fatty acids are released from the adipose tissue, they will bind to the protein albumin. In fact, over 99 percent of the free fatty acids in the plasma are carried bound to albumin. Eventually, fatty acids will be transported to the skeletal muscle bound to fatty-acid-binding proteins located both in the outer and inner portions of the skeletal muscle cell. Once inside the cell, fatty acids will undergo a series of metabolic reactions, and eventually be fully oxidized for the production of energy.

FACTORS THAT MAY LIMIT FAT OXIDATION
Gender
The rate of fat oxidation during aerobic activity appears to be different between the sexes. There is agreement among several researchers to the fact that the rate of fat oxidation is greater in women when compared to men during sub maximal exercise. For instance, it has been suggested that estrogen and progesterone may play an important role in lipolysis. Estrogen has been shown to increase the rate of adipose tissue lipolysis (either by inhibiting LPL enzyme and/or by activating the beta-adrenergetic receptors in fat cells which are lipolytic). In addition, progesterone has been associated with a decrease in the rate of glucose production, which in turn may enhance the effects of estrogen on fat mobilization.

Other factors that could promote a higher fat utilization in women may include a greater uptake of free fatty acids by the skeletal muscles, greater enzymatic activity for fat oxidation in the mitochondria and a greater mitochondrial beta oxidation (a process which “prepares” the fatty acids to enter the Kreb Cycle - aerobic metabolism - and thus for further oxidation to produce ATP).

Fitness Level
It is well known that one of the adaptations of an increased aerobic fitness capacity is the ability of the skeletal muscles to oxidize more fat for energy. This increase in fat oxidation is largely related to the following: 1) an increase in mitochondrial content and density; 2) an increase in the number of oxidative enzymes; 3) increase in fatty acid uptake; and 4) an increased lipolytic response to catecholamines. Regardless of gender, a more aerobically fit individual will have a higher fat oxidation (during exercise) when compared to an unfit individual.

Exercise Intensity
As exercise intensity increases, there is a shift in energy substrate mobilization and utilization. In general, most studies have shown that fat oxidation occurs in exercise intensities anywhere from 30 percent up to around 70 percent of one’s maximal oxygen uptake. Thus, at higher exercise intensities (i.e, > 90 percent), the contribution of fat oxidation to energy becomes negligible.

Fatty acid oxidation at higher intensity was limited due to a direct inhibition of long-chain fatty acid entry into mitochondria. Thus, at higher intensities, the breakdown of glucose for energy is greatly stimulated, which in turn may inhibit one of the enzymes responsible to transport the fatty acid into the mitochondria.