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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 (8a). 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: a) brief
overview of fatty acids; b) fat mobilization and oxidation during
exercise; c) factors that may limit fat oxidation; d) summary.
Most fatty acids are stored
in the body in the form of triglycerides. Fatty acids that are not
incorporated into a triacylglycerols 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 for instance protein: i.e., albumin.).
Further, 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 (4, 8a).
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 (1, 2, 3, 4, 5,
6, 8a, 8b, 9, 10, 12).
At the onset of exercise, the Sympathetic
Nervous System (SNS) releases two important Catecholamines (epinephrine
& 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) (4, 6, 8a, 8b).
Once the free fatty acids are released from
the adipose tissue, they will bind to the protein albumin. In fact,
over 99% 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-
(8A, 10).
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 (3, 5, and 12). For
instance, it has been suggested (3) 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 the fat cell 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
(3).
Horton and colleagues (1998) 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%) when compared to their male counterparts (44%) during 2 hours
of cycling (40% 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) (3).
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
to1) an increase in mitochondrial content and density; 2) an increase
in the number of oxidative enzymes; 3) increase in fatty acid uptake;
4) an increased lipolytic response to catecholamines (6, 8b). 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% up to around 70% of one’s maximal oxygen
uptake - MaxVo2- ( 1, 2, 7, 9, 11,12). Achten and co-workers (2002)
reported greater fat oxidation at exercise intensities of 51% to
76% (MaxVo2).
On the other hand, fat oxidation appears to be impaired at exercise
intensities of about 80 to 85% of one’s MaxVo2 and/or higher
(2, 7, 9, and 12). Thus, at higher exercise intensities (i.e, >
90%), the contribution of fat oxidation to energy becomes negligible
(1). Romijn and co-workers (1995), reported that plasma free fatty
acid mobilization did not increase above resting level during high-intensity
exercise (>85%). 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 (9, 12).
Sidossis and colleagues (1997), 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% of one’s MaxVo2. More research
needs to be done in regards to the mechanisms that enhances and/or
inhibits adipose tissue lipolysis; fatty acid transport and uptake
by the skeletal muscle tissue.
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