intensity of exercise is moderate, resulting in a
relatively low rate of endogenous heat produc-
tion, or the exercise is intermittent in nature
allowing for effective heat dissipation, carbohy-
drate may be limiting. Accordingly, carbohy-
drate ingestion may (Murray et al. 1987; Davis et
al.1988b; Millard-Stafford et al. 1992) or may not
(Daviset al. 1988a; Millard-Stafford et al. 1990;
Febbraioet al. 1996a) increase exercise perfor-
mance in the heat. The benefit of carbohydrate
ingestion during and following exercise in the
heat may, however, be related to factors other
than exercise performance. Immune function has
been demonstrated to be depressed by increases
in stress hormones such as catecholamines, corti-
costeroids and growth hormone (Keast et al.
1988). These hormones are elevated when com-
paring exercise in the heat with that in a cooler
environment (Febbraio et al. 1994a; Hargreaves
et al. 1996a). There may be, therefore, a possible
relationship between exercise in a hot environ-
ment and immune suppression. Indeed, it has
been demonstrated that exercise and heat stress
results in a decrease in lymphocyte production
(Cross et al. 1996). Carbohydrate feeding during
exercise in comfortable ambient conditions
results in a decrease in circulating adrenaline
502 practical issues
(McConellet al. 1994), cortisol (Mitchell et al.
1990) and growth hormone (Smith et al. 1996). In
addition, plasma elastase, a marker of in vivo
neutrophil activation, is reduced during exercise
with carbohydrate feedings (Smith et al. 1996). It
is possible, therefore, that carbohydrate inges-
tion during and following exercise in the heat
may attenuate the rise in the counterregulatory
hormones which depress immune function, and
we are currently undertaking experiments to
examine this hypothesis.
As mentioned previously, glycogen content
within human skeletal muscle at the point of
fatigue during exercise in the heat is often ade-
quate to maintain energy turnover via oxidative
phosphorylation. It is somewhat surprising,
therefore, that a marked increase in IMP accumu-
lation at fatigue during exercise and heat stress is
observed despite glycogen concentration being
adequate to maintain the oxidative potential
of the contracting skeletal muscle (Fig. 38.2)
(Parkinet al. 1999).
These data suggest a disruption to mitochon-
drial function during exercise and heat stress and
support recent findings by Mills et al. (1996), who
observed an increase in plasma concentrations
of lipid hydroperoxides, a marker of oxidativeGlycogen (mmol.kg–1)5000400300200Rest Fatigue100IMP (mmol.kg–1
)1.2501.00.750.5Rest Fatigue0.25**(a) (b)Fig. 38.2(a) Glycogen content and (b) inosine 5¢-monophosphate (IMP) concentration before (rest) and after
(fatigue) submaximal exercise to exhaustion in different ambient temperatures: , 40 °C; , 20 °C; , 3 °C. Data
expressed as mean ±SE (n=8). From Parkin et al. (1999), with permission.