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1 McGill Nutrition and Food Science Centre, Royal Victoria Hospital, Montreal, Quebec, Canada H3A 1A1; 2 Departments of Physiology and Medicine, University of Toronto, Toronto, Ontario, Canada 5S 1A8; and 3 Department of Internal Medicine and Institute of Gerontology, University of Michigan, Veterans Affairs Medical Center, Ann Arbor, Michigan 48109
Glucose infusion
can prevent the increase in glucose production (Ra) and
increase glucose uptake (Rd) during exercise of moderate intensity. We postulated that 1)
because in postabsorptive intense exercise (>80% maximal
O2 uptake) the eightfold increase
in Ra may be mediated by catecholamines rather than by
glucagon and insulin, exogenous glucose infusion would not prevent the
Ra increment, and 2)
such infusion would cause greater Rd. Fit young men were exercised at >85% maximal O2
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 · min1),
and in seven subjects it was varied (VI) to mimic the exercise Ra response in Con. Although glucose suppressed
Ra to zero (with glycemia ~6 mM and insulin ~150 pM),
an endogenous Ra 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-to-insulin ratio
occurred in all three groups. Catecholamine responses were similar in
all three groups, and correlation coefficients of Ra with
plasma norepinephrine and epinephrine were significant in all. In all
CI and VI, Rd at rest was 2× Con, increased earlier
in exercise, and was higher for the 1 h of recovery with glucose
infusion. Thus the Ra response was only partly attenuated,
and the catecholamines are likely to be the regulators. This suggests
that an acute endogenous Ra rise is possible even in the
postprandial state. Furthermore, the fact that more circulating glucose
is used by muscle during exercise and early recovery suggests that
muscle glycogen is spared.
norepinephrine; epinephrine; glucose turnover; insulin; glucagon
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