Effect of Acute Resistance Exercise and Resistance Exercise Training on Central Pulsatile Hemodynamics and Large Artery Stiffness: Part I

Background: Engaging in habitual resistance exercise training (RET; also known as strength training) causes systemic health effects beyond those caused by aerobic/endurance exercise training alone. Despite the resoundingly favorable effect of habitual RET on measures of cardiovascular disease risk, controversy still exists regarding the vascular health effects of this exercise modality largely because some studies find increases in large artery stiffness and central pulsatile hemodynamics with RET. In this two-part series, we examine the effect of acute resistance exercise (RE) and RET on large artery stiffness and pulsatile hemodynamics. We perform a historical overview of seminal/classic studies and report on key findings that have shaped the field. We provide personal commentary on the studies and potential implications of findings related to the acute effects of RE on large artery stiffness and central pulsatile hemodynamics. For part one of this two-part series, we perform a detailed analysis of the hemodynamic signature produced during RE and discuss the sub-acute effects on short-term modulation of large artery stiffness and central pulsatile hemodynamics. Summary: Acute RE elicits marked ("extreme") elevations in arterial pressure, mediated primarily by increases in vascular resistance and intrathoracic pressure (ITP). Vascular compression from muscular contraction contributes to increases in afterload via increased vascular resistance and pressure from wave reflections. However, as a result of the higher ITP associated with breath holds (Valsalva maneuver) during high relative efforts (>80%), the change in pressure across the aortic wall (transmural pressure) is less than the change in intra-arterial pressure. Key Messages: The high arterial pressures during some heavy weight lifting exercises are associated with positive swings with ITP related to the Valsalva maneuver and elevations in vascular resistance. The pressure oscillations lead to marked stress within the vascular wall and likely contribute to elevations in large artery stiffness over the subsequent hour.