Coronary hemodynamics and myocardial metabolism during and after pacing stress in normal humans

We investigated coronary hemodynamics, myocardial utilization of circulating substrates (by coronary sinus catheterization), and overall use of oxidative fuels (by regional indirect calorimetry) in healthy adults during incremental atrial pacing (up to 159 ± 9 beats/min), and during 25 min of recovery. Great cardiac vein flow (thermodilution) increased from 52 ± 9 to 115 ± 15 ml/min (P < 0.001) with pacing; myocardial O₂ uptake (301 ± 53 to 593 ± 71 μmol/min, P < 0.001) and CO₂ production (225 ± 37 to 518 ± 66 μmol/min, P < 0.005) paralleled the pacing-induced rise in rate-pressure product (9.4 ± 0.9 to 21.1 ± 1.1 mmHg·beat·min^-1·10^-3, P < 0.001). During recovery, all the above variables returned to base line within 5 min, but myocardial O₂ extraction remained depressed (67 ± 2 vs. 71 ± 3%, P < 0.05). Circulating glucose uptake rose linearly with pacing (P < 0.05) and remained above base line throughout recovery. By contrast, free fatty acid (FFA) uptake (10 μmol/min) did not increase with pacing and fell during recovery (P < 0.01). Calorimetry, however, showed that net lipid oxidation exceeded FFA uptake throughout the study, whereas net carbohydrate oxidation was small at base line, rose significantly at maximal pacing (62% of myocardial energy output), and remained above base line during recovery (32% of energy output). In the basal state as well as during recovery, myocardial uptake of glucose equivalents (lactate plus glucose plus pyruvate) was in excess of carbohydrate oxidation, indicating nonoxidative disposal of these substrates. In concusion: 1) at rest or with submaximal pacing, heart metabolism relies predominantly on oxidation of lipids, both circulating FFA and triglycerides, 2) during maximal pacing stress, carbohydrate oxidation is substantial and exceeds uptake of circulating glucose equivalents, and 3) recovery from maximal pacing stress is characterized by impaired efficiency of O₂ utilization, protracted stimuation of circulating glucose uptake and storage of glucose equivalents.