Quantitative analysis of exercise-induced enhancement of early- and late-systolic retrograde coronary blood flow

Bender SB, van Houwelingen MJ, Merkus D, Duncker DJ, Laughlin MH. Quantitative analysis of exercise-induced enhancement of early- and late-systolic retrograde coronary blood flow. J Appl Physiol 108: 507-514, 2010. First published December 10, 2009; doi:10.1152/japplphysiol.01096.2009.-Coronary blood flow (CBF) is reduced and transiently reversed during systole via cardiac contraction. Cardiac contractility, coronary tone, and arterial pressure each influence systolic CBF (CBFSYS), particularly by modulating the retrograde component of CBFSYS. The effect of concurrent changes in these factors on CBFSYS during dynamic exercise has not been examined. Using chronically instrumented swine, we hypothesized that dynamic exercise enhances retrograde CBFSYS. Phasic CBF was examined at rest and during treadmill exercise [2-5 miles/h (mph)]. Absolute values of mean CBF over the cardiac cycle (CBFCYCLE) as well as mean CBF in diastole (CBFDIAS) and mean CBFSYS were increased by exercise, while relative CBFDIAS and CBFSYS expressed as percentage of mean CBFCYCLE were principally unchanged. Early retrograde CBFSYS was present at rest and increased in magnitude (-33 +/- 4 ml/min) and as a percent of CBFCYCLE (-0.6 +/- 0.1%) at 5 mph. This reversal was transient, comprising 3.7 +/- 0.3% of cardiac cycle duration at 5 mph. Our results also reveal that moderately intense exercise (> 3 mph) induced a second CBF reversal in late systole before aortic valve closure. At 5 mph, late retrograde CBFSYS amounted to -53 +/- 11 ml/min (-3.1 +/- 0.7% of CBFCYCLE) while occupying 11.1 +/- 0.3% of cardiac cycle duration. Wave-intensity analysis revealed that the second flow reversal coincided with an enhanced aortic forward-going decompression wave (vs. rest). Therefore, our data demonstrate a predictable increase in early-systolic CBF reversal during exercise and additionally that exercise induces a late-systolic CBF reversal related to the hemodynamic effects of left ventricular relaxation that is not predictable using current models of phasic CBF.