Continuous measurement of left ventricular performance during and after maximal isometric deadlift exercise.

Abstract

Isometric exercise produces a reflex increase in arterial blood pressure that is proportional to the intensity and mass of muscle used during contraction. Little is known about the transient effects of heavy weight lifting on left ventricular performance. In this study, we measured continuous changes in left ventricular performance during maximal large-muscle isometric exercise using the standing deadlift position. Ten healthy young men performed serial deadlifts at 50% of maximal voluntary effort for 90 seconds and 100% of maximal effort for 30 seconds. Echocardiographic imaging (apical four-chamber view), arterial blood pressure (brachial artery catheter), and electrocardiographic monitoring were recorded throughout the deadlift and for 30 seconds of recovery. Aortic flow velocity was also monitored during a separate series of deadlifts. During 100% maximal deadlift, mean arterial pressure increased from 108 +/- 4 to 164 +/- 6 mm Hg. Left ventricular ejection fraction declined initially (from 57 +/- 2% to 49 +/- 3%) at 15 seconds into the lift and recovered (56 +/- 1%) due to significant increases in end-diastolic volume (104 +/- 11 ml to 132 +/- 16 ml) by the end of the lift. The peak systolic pressure/end-systolic volume ratio did not change during the deadlift. After cessation of the deadlift, mean arterial pressure declined precipitously (to 88 +/- 4 mm Hg) within 5 seconds and gradually returned to baseline after 30 seconds. Left ventricular performance indexes all increased significantly during the recovery phase (ejection fraction to 68 +/- 3%, peak systolic pressure/end-systolic volume ratio to 5.9 +/- 0.9). Findings were qualitatively similar for the 50% deadlift. During an intense isometric deadlift, left ventricular performance declines initially but is restored by the Frank-Starling mechanism. Upon release of the deadlift, increased left ventricular performance develops in conjunction with a rapid decrease in arterial pressure. The combined effects of increased wall stress during the lift phase and enhanced contractility during the release phase probably contribute to left ventricular hypertrophy associated with repetitive weight training.