traditionally provided the theoretical framework
for understanding of the nature of energy
balance in humans. More recently, alternative
approaches have been proposed which take
account of how different fuels are partitioned
among metabolic pathways. The body responds
differently to overfeeding with different nutri-
ents, suggesting that balance equations for sepa-
rate nutrients might be more informative.
Protein balance is achieved on a day-to-day
basis, with oxidation of intake in excess of needs;
and carbohydrate intake stimulates both glyco-
gen storage and glucose oxidation, with negligi-
ble conversion to TAG under dietary conditions
of industrialized countries. In marked contrast,
fat intake has little influence on fat oxidation so
that energy balance is virtually equivalent to
fat balance and there is a strong relationship
between fat balance and energy balance even
over a period as short as 24 h. Chronic imbalance
between fat intake and fat oxidation may there-
fore predispose to increased fat storage.
This line of thinking leads to the conclusion
that physical activity has greater potential to
influence body energy stores than would be
deduced on the basis of the tradtional energy
balance equation. Fat oxidation is of course
enhanced during submaximal exercise, and more
so in people who are well trained. It is also
enhanced for some hours afterwards, even when
the postexercise elevation of metabolic rate has
disappeared (Calles-Escandon et al. 1996). The
response to a fatty meal is changed, with greater
postprandial fat oxidation (Tsetsonis et al. 1997).
There might be synergistic benefits of increased
exercise if, as discussed above, there is an
increased appetite for high carbohydrate foods.
Conclusion
Substantial elevations in mortality are seen in
sedentary and unfit men and women. With
regard to CHD, a biological gradient has been
documented convincingly, although its exact
pattern remains unclear; high levels of rather
vigorous endurance exercise may be necessary
for optimal benefit but some studies show that
risk decreases steeply at the lower end of the
physical activity (or fitness) continuum, reaching
an asymptote in the mid-range. Detailed infor-
mation about the influence of either the amount
of exercise or the independent effect of intensity
is not available for the relation of physical activ-
ity with the development of either hypertension
or NIDDM.
Information on the mechanisms by which
activity decreases the risk of these diseases is
incomplete, but adaptive changes in the metabo-
lism of fat and carbohydrate, giving rise to ‘meta-
bolic fitness’, are undoubtedly involved. Many of
the health gains associated with high levels of
physical activity can be explained through the
consequences of increased exercise for the intake
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