rich diet is superior to that when a fat-rich diet
is consumed. Thus, in the classic study by
Christensen and Hansen from 1939, three trained
subjects consumed either a fat-rich diet (contain-
ing only 5 E% carbohydrates) or a carbohydrate-
rich diet (90 E% carbohydrates) for 3–5 days.
Exercise to exhaustion at approximately 65–70%
of maximal oxygen uptake revealed an average
endurance time on the carbohydrate diet of
210 min, which was markedly longer than when
on the fat diet (90 min). Also, when intermittent
exercise (30 min running followed by 10 min rest)
at 70% of maximal oxygen uptake was per-
formed in trained men, endurance performance
time to exhaustion was significantly impaired
after consuming a fat diet, consisting of 76 E%
fat, 13.5 E% protein, for 4 days (62±6 min) com-
pared with when a carbohydrate-rich diet (77 E%
carbohydrate, 13.5 E% protein) was consumed
for 4 days (106±5 min) (Galbo et al. 1979). Also,
the short-term studies by Bergström et al. (1967)
and Karlsson and Saltin (1971) suggested that
3–7 days of fat diet were detrimental to exercise
performance. Thus, it is evident from these brief
dietary manipulations that ‘fat-loading’ impairs
endurance performance. However, in these
short-term dietary studies, the primary goal was
to determine the extent to which muscle glyco-
gen content could be altered by varying the
dietary regimen after depletion of the glycogen
196 nutrition and exercise
stores and subsequently to ascertain the relation
between the individual muscle glycogen content
and the capacity for prolonged exercise. Thus,
these short-term carbohydrate-restricted diets
probably reflect rather acute responses to
changes in diet.
Longer-term adaptation to fat-rich diets may,
on the other hand, induce skeletal muscle adap-
tations, metabolic as well as morphological,
which in turn could influence exercise perfor-
mance. It has been known for a long time that
endurance training induces several adaptations
in skeletal muscle such as increased capillariza-
tion, increased mitochondrial density, increased
activity of several oxidative enzymes (Saltin &
Gollnick 1983) and, furthermore, as recently
shown, an increased content of fatty acid binding
protein in the sarcolemma (FABPpm) (Kiens et al.
1997), parameters that all are suggested to play a
significant role in enhancing lipid oxidation.
It might be speculated that a way to influence
the fat oxidative system further, is to increase the
substrate flux of fatty acids through the system
by increasing the fat content of the diet. This
might result in further adaptations in the fat
oxidative capacity, providing possibilities for an
increased fat oxidation, a sparing of carbohy-
drates and an increasing endurance perfor-
mance. Thus, in the study by Muoio et al. (1994),
five well-trained runners followed a dietary2.50.02.01.51.0Control0.5Plasma FFA concentration (mmol–1.l
)Lipid
heparin400302010ControlFat oxidation (μmol.kg–1.min–1)Lipid
heparin* *(a) (b)Fig. 14.2(a) Plasma free fatty acid
(FFA) concentrations, and (b) total
fat oxidation during a 20–30-min
exercise period for six subjects
during a control trial and during
intralipid infusion. Subjects
exercised for 30 min at 85% of
maximal oxygen uptake. *,
P<0.05 compared with control
trial. Adapted from Romijn et al.
(1995).