Evidence of Central and Local Vascular Function Improvements After Chronic Passive Stretching

Vasomotor response is an important marker of cardiovascular health and has been related to cardiovascular co-morbidity. An alteration of vasomotor response, indeed, often precedes an increase in arterial stiffness. By improving and/or maintaining this vascular function, therefore, plays a pivotal role in the prevention of cardiovascular disease. The overall control of the vasomotor response and, in turn, of blood flow distribution in the human body is regulated by two main mechanisms: a systemic control given by the sympathetic nervous system that acts on the arterial smooth muscle fibers causing vasoconstriction, and a local action of vasoactive molecules released by the endothelial cells, such as nitric oxide (NO), leading to vasodilation.

Recent studies report that acute passive stretching (PS), a well-established practice in rehabilitation and sport environments to increase range of motion, may influence the vasomotor response. Specifically, PS provokes two conflicting events: (i) a vasoconstriction with blood flow reduction in the feeding artery of the stretched muscle, triggered by the systemic increase in sympathetic neural tone due to the PS-induced stress on the muscle mechano- and metaboreceptors, and (ii) a vasodilation and subsequent increase in blood flow in the feeding artery due to the prevalence of local vasoactive factors release as a result of the stretch-induced stress applied to the vessel wall, which overwhelms the systemic sympathetic activation. Interestingly, throughout several stretch-shortening cycles, the first acute hyperemic response to stretch described above seems to progressively attenuate until its disappearance during the subsequent stretching cycles, possibly due to NO and other vasoactive molecules depletion.

The shortening phase in between two stretch bouts, instead, is always characterized by hyperemia due to a reduction in the peripheral vascular resistance after the stretch-induced vessels deformation. Possible explanation of these phenomena involves the shear rate, which is the frictional or drag force acting on the inner lumen of the vessels that can trigger a chain of reactions, possibly leading to higher endothelial NO-synthase activity. Continuous and repetitive increases in shear rate induced by PS have been observed to act as vascular training to modulate endothelium remodeling and to improve vasomotor response.

Interestingly, during an acute PS administration, a reduction in blood flow during stretching was described in the contralateral, no-stretched limb. Such a reduction was promptly recovered during the shortening phase. The authors suggested that this occurrence was induced by a systemic sympathetic-mediated vasoconstriction, which was activated by the stretch-induced mechanoreflex.

However, whether chronic PS administration may also affect the vasomotor response in the feeding artery of the contralateral muscle, which was not directly involved in the stretching maneuver, is still an open question.