A. Manzon et al., GLUCOSE-INFUSION PARTIALLY ATTENUATES GLUCOSE-PRODUCTION AND INCREASES UPTAKE DURING INTENSE EXERCISE, Journal of applied physiology (1985), 85(2), 1998, pp. 511-524
Glucose infusion can prevent the increase in glucose production (R-a)
and increase glucose uptake (R-d) during exercise of moderate intensit
y. We postulated that 1) because in postabsorptive intense exercise (>
80% maximal O-2 uptake) the eightfold increase in R-a may be mediated
by catecholamines rather than by glucagon and insulin, exogenous gluco
se infusion would not prevent the R-a increment, and 2) such infusion
would cause greater R-d. Fit young men were exercised at >85% maximal
O-2 uptake for 14 min in the postabsorptive state [controls (Con), n =
12] or at minute 210 of a 285-min glucose infusion. In seven subjects
, the infusion was constant (CI; 4 mg.kg(-1).min(-1)), and in seven su
bjects it was varied (VI) to mimic the exercise R-a response in Con. A
lthough glucose suppressed R-a to zero (with glycemia similar to 6 mM
and insulin similar to 150 pM), an endogenous R-a response to exercise
occurred, to peak increments two-thirds those in Con, in both CI and
VI. Glucagon was unchanged, and very small increases in the glucagon-t
o-insulin ratio occurred in all three groups. Catecholamine responses
were similar in all three groups, and correlation coefficients of R-a
with plasma norepinephrine and epinephrine were significant in all. In
all CI and VI, R-d at rest was 2 x Con, increased earlier in exercise
, and was higher for the 1 h of recovery with glucose infusion. Thus t
he R-a response was only partly attenuated, and the catecholamines are
likely to be the regulators. This suggests that an acute endogenous R
-a rise is possible even in the postprandial state. Furthermore, the f
act that more circulating glucose is used by muscle during exercise an
d early recovery suggests that muscle glycogen is spared.