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Fat Metabolism at Rest and During Exercise

The two main energy fuel sources during aerobic exercise are carbohydrates and fat. In the past decade, extensive research has been done with regard to the role of carbohydrates during exercise. However, less research has been done on the role of fat metabolism during muscle contraction. For the purpose of this article, the following topics will be discussed:


Most fatty acids are stored in the body in the form of triglycerides. Fatty acids that are not incorporated into a tricylglycerols molecule are known as “free fatty acids” (although just a very small percentage of fatty acids are really “free.” Most fatty acids are bound to another compound such as protein: i.e., albumin.). Furthermore, most of the body fat in humans is stored in subcutaneous and deep visceral adipose tissue. In addition, a small percentage of body fat is stored in the skeletal muscle cells (approximately 300 grams).

Fat contains more energy when compared to carbohydrates (9 kcal x 4 kcal per gram). In fact, body fat stores are very large when compared to carbohydrate stores. Thus, theoretically, one would have enough energy from fats to last for days of activity. On the other hand, carbohydrate stores (from exercising muscles) may be depleted in 60 to 90 minutes of activity.


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 – ATP.



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.

Horton and colleagues suggested that women may be more sensitive to the effects of catecholamines on liposysis. Also, women may have a higher intramuscular free fatty acid oxidation capacity when compared to men. In this study, the female subjects had a higher fat oxidation (51 percent) when compared to their male counterparts (44 percent) during two hours of cycling (40 percent of maximal oxygen uptake).

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 (i.e., Max VO2). Achten and co-workers reported greater fat oxidation at exercise intensities of 51 to 76 percent (Max VO2).

On the other hand, fat oxidation appears to be impaired at exercise intensities of about 80 to 85 percent of one’s Max VO2 and/or higher. Thus, at higher exercise intensities (i.e, > 90 percent), the contribution of fat oxidation to energy becomes negligible. Romijn and co-workers reported that plasma free fatty acid mobilization did not increase above resting level during high-intensity exercise (>85 percent). In turn, there was a decrease in plasma free fatty acid concentration, which may have impaired fat oxidation in their subjects. It is important to note that there is a minimal concentration level of plasma free fatty acids where oxidation will take place (i.e., 1.0 mM). When plasma levels of free fatty acids decrease drastically (i.e., 0.2 – 0.3 mM), fat oxidation will be impaired. In addition, even if the normal plasma level of free-fatty acids are maintained during high intensity exercise (i.e., by lipid infusion), fat oxidation is only slightly increased when compared to lower exercise intensities.

Sidossis and colleagues suggested that 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 (CPT-I – carnitine palmitoyl-transferase) responsible to transport the fatty acid into the mitochondria.


In summary, there are several factors that may affect fat oxidation. It appears that women have a greater rate of fat oxidation when compared to men during sub maximal exercise. Also, individuals with greater aerobic capacity have a greater ability to oxidize more fatty acids when compared to an unfit individual. Finally, fat oxidation is most apparent at exercise intensities varying anywhere from 50 to 75 percent of one’s Max VO2. More research needs to be done in regards to the mechanisms that enhance and/or inhibit adipose tissue lipolysis, fatty acid transport and uptake by the skeletal muscle tissue.


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