Exercise and Fat Oxidation
By:
Derek Charlebois
A study done by Ronallo
and Rhodes (1998) showed that the highest rate of plasma FFA turnover
was seen at an exercise intensity of 35% VO2max. At this intensity,
plasma FFA turnover rate was 4-5 times the resting rate after 30
minutes of exercise. Interestingly, plasma catecholamine levels
increased by only 50-60% above resting levels, which would not explain
the 400-500% increase in plasma FFA turnover. At an exercise intensity
of 65%-85% VO2max, plasma FFA turnover was lower than that at 25%
VO2max, but catecholamine concentrations were 3-6 times higher at
65% VO2max and 17-19 times higher at 85% VO2max than at rest. While
catecholamines concentrations are directly related to the rate of
lipolysis at rest (Ronallo & Rhodes
1998), during exercise other factors clearly play a large role.
The increase in fat oxidation seen during exercise is due to an
increase in FFA availability and a decrease in the re-esterification
of FFA. Wolfe et al (1990) found that FFA re-esterfication dropped
from 70% at rest to 25% during low to moderate intensity exercise.
This decrease in the re-esterification of FFA means more FFA will
be available for oxidation.
High intensity exercise (>70% VO2max) causes a decrease in the
release of fatty acids from adipose tissue. Data suggest that this
decrease in circulating fatty acids is due to decreased blood flow
and removal of the fatty acids from adipose tissue to the circulation
(Horowitz and Klein 2000). An increase in muscle glycogen usage
is also believed to play a role in the decreased oxidation of fatty
acids during high-intensity exercise. Glycogenolysis elevates acetyl-CoA
(derived from glycogen) concentrations that in turn elevate malonyl-CoA
concentrations (Horowitz and Klein 2000). Malonyl-CoA inhibits CPT-I,
which is the rate-limiting step for fatty acid (specifically long-chain
fatty acids) entry in mitochondria. Interestingly, the skeletal
muscle of trained individuals is more sensitive to malonyl-CoA than
the skeletal muscle of untrained individuals (Starritt et al 2000).
It is believed that decreased CPT-I activity is the main cause of
decreased fat oxidation at high exercise intensities. During moderate
to high-intensity exercise, half of the total energy used is acquired
from fat sources and the other half from carbohydrate sources (Achten & Jeukendrup,
2004).
Endurance exercise training leads to an increase in FFA oxidation
during submaximal exercise, due to a decrease in CHO oxidation.
Achten and Jeukendrup (2003) found that at an exercise intensity
of 62% VO2max moderately trained cyclist oxidized fat at a rate
of 0.48 g/min while highly-trained cyclist oxidized fat at a rate
of 0.56 g/min. Endurance training causes an increase in mitochondria
density and CPT-I gene expression, which would create a greater
capacity to oxidize fat. Tunstall et al. (2002) found that nine
days of endurance training caused a 57% increase in CPT-I gene expression
at rest and after exercise. Endurance training as increases capillarization
of skeletal muscle. Because transport to FFA from adipose tissue
to skeletal muscle is a limited factor in fat oxidation, such adaptation
should increase the rate of fat oxidation during exercise.
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