Vasodilation Clinical Trial
Official title:
Evidence of Central and Local Vascular Function Improvements After Chronic Passive Stretching
Acutely, during different bouts of passive stretching (PS), blood flow (Q ̇) and shear rate ( ) in the feeding artery of the stretched muscles increases during the first two elongations and then it reduces during the following bouts. This hyperemic response during the first two elongations is mediated by the local release of vasoactive molecules (e.g. nitric oxide, NO). This phenomenon disappears during the following elongations due to the NO and other vasoactive molecule depletion. The relaxation phase between stretching bouts, instead, is always characterized by hyperemia as results of stretch-induced peripheral resistances decrease. Whether chronic PS administration may influence vascular function is still a matter of investigation. The hypothesis is that repetitive PS-induced Q ̇ and changes may be an enough stimulus to provoke increments in NO bioavailability, thus improving vasomotor response.
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.
Together with the changes in local control mechanisms, also possible PS-induced changes in
the systemic autonomic control of blood flow has been reported (i.e., reduction in blood
pressure and aortic wave reflection magnitude, although its effectiveness remains a matter of
debate With this in mind, this study aimed to investigate the effect of PS on the vasomotor
response and the stiffness of the arteries directly involved (i.e., femoral and popliteal
arteries) and not directly involved (i.e., contralateral femoral and popliteal arteries and
brachial artery) with the maneuver applied on the plantar flexors, knee extensor and hip
flexor muscles. To this purpose, vasomotor response and arterial stiffness were assessed by
Doppler ultrasounds and applanation tonometry, respectively, before and after 12 weeks of PS
administration. Hypothesis has been made that repetitive PS bouts, with consequent changes in
blood flow and shear rate, may be an effective stimulus to (i) enhance local vasoactive
molecules bioavailability in the arteries involved with PS; and (ii) induce a systemic
re-modulation of the sympathetic autonomic activity, thus improving arterial compliance and
vasomotor response even in those districts not directly involved with PS.
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