We report noninvasive and invasive studies designed to clarify the mechanism of the third heart sound (S3) in humans. The noninvasive observations were made using a miniature accelerometer attached to the skin surface at the cardiac apex. In subjects with no S3, the tracings were either flat or showed very low undulations throughout diastole. Those with an S3, however, demonstrated a distinct reduction of acceleration, or negative jerk, of the rapid filling movement at the apex at the time of the sound. The invasive studies in the cardiac catheterization laboratory consisted of frame-by-frame measurements of left ventricular dimensions in the transverse and long axes during early diastole in patients with diastolic overload abnormalities to investigate the temporal sequence of filling in these two principal axes. The maximal long-axis filling rate occurred after the short axis, a finding that helps to resolve a discrepancy noted in the time of maximal short-axis filling and S3 production. These studies support the concept that the S3 is due to a sudden intrinsic limitation of longitudinal expansion of the left ventricular wall during early diastolic filling, resulting in a negative jerk that is transmitted to the skin surface.