Glucose infusion partially attenuates glucose production and increases uptake during intense exercise

Glucose infusion can prevent the increase in glucose production (R(a)) and increase glucose uptake (R(d)) during exercise of moderate intensity. We postulated that 1) because in postabsorptive intense exercise (>80% maximal O₂ uptake) the eightfold increase in R(a) may be mediated by catecholamines rather than by glucagon and insulin, exogenous glucose 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 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^-1min^-1), and in seven subjects it was varied (VI) to mimic the exercise R(a) response in Con. Although glucose suppressed R(a) to zero (with glycemia ~6 mM and insulin ~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-to- 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 2x Con, increased earlier in exercise, and was higher for the I h of recovery with glucose infusion. Thus the 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 fact that more circulating glucose is used by muscle during exercise and early recovery suggests that muscle glycogen is spared.