VasodilationNCT04271241
Vascular Function Improvements After Chronic Passive Stretching
A study testing Passive stretching (PS) training in people with Vasodilation and Vasoconstriction, run by University of Milan at 1 site in Italy.
Trial summary
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. Read more about this study
- Who is it for?
- Ages 18 years and olderHealthy volunteers can take part
- Conditions the study is for
- Vasodilation, Vasoconstriction, Stretch
- What is being tested?
- Passive stretching (PS) training
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 39 participants
- Where
- 1 siteItaly
- Study dates
- 7 Jan 2019to 7 Feb 2020
- Phase
- Interventional
- Are there results?
- None posted in the registry
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- None
Who cannot join
- presence of neurological, vascular and musculoskeletal impairments at the lower and upper limbs level;
- being on pharmacological therapy related to either neural and/or vascular response, including hormonal contraceptives and oral supplements;
- being a current or former smoker;
- having an irregular menstrual cycle (26 to 35 days) up to three months before the beginning of the study,
- presenting contraindication for joint mobilization;
- being regularly involved in PS program.
Trial locations and contacts
1 site in 1 country.
About this study
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.
Read the detailed description
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.
- Conditions
- Vasodilation, Vasoconstriction, Stretch, Sympathetic; Imbalance
- Being tested
- Passive stretching (PS) training
- Keywords
- Chronic passive stretching, Central and peripheral arterial stiffness, Blood pressure, Vasomotor response, Crossover effect
- Medical subject headings
- Aneurysm
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Passive stretching (PS) trainingOther
PSBil and PSMono underwent 12 weeks of PS training, 3 sessions per week (36 sessions in total). In PSBil, each session lasted 40 min and included two maneuvers for both the knee extensor and plantar flexor muscles with the following protocol: 45 s elongation and 15 s recovery in the resting position, all the cycle repeated for five times 7. In PSMono, exercises were performed only on the right limb and each session had a duration of 20 min. Ctrl did not underwent any PS exercise throughout the study. To promote participants' compliance, daily classes were held at different day time (morning and afternoon) at the University Sports Centre gym. Each class was supervised by an expert operator, which monitored the attendance, the correct exercise execution and the intensity exerted during the exercise (80% of the point of discomfort). The participants not attending at least the 80% of classes were excluded from the study, and a new participant was recruited to substitute the drop out.
| Study group | Role | What they receive |
|---|---|---|
| Control (Ctrl) | No intervention | Ctrl group di not undergo any training |
| PS bilateral limbs (PSBil) | Experimental | PSBil underwent 12 weeks of passive stretching on both the lower limbs Receives: Other: Passive stretching (PS) training |
| PS monolateral limb, stretched limb (PSMonoSL) | Experimental | PSMonoSL underwent 12 weeks of passive stretching on just one lower limb (SL). Outcomes form this group were obtained from the stretched Receives: Other: Passive stretching (PS) training |
| PS monolateral limb, contralateral limb PSMonoCL | Experimental | PSMonoCL involved the same participants as in PSMonoSL. Outcomes form this group were obtained from the contralateral not stretched limb (CL). Data from this limb helped in identify possible PS-induced crossover effects in the vasomotor response. Receives: Other: Passive stretching (PS) training |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change from baseline in augmentation Index
The radial artery pressure wave and amplitude were recorded non-invasively by means of applanation tonometry of the radial artery. Twenty sequential waveforms covering a complete respiratory cycle were acquired from the system and used by the software to generate an average peripheral and corresponding central waveform. The systolic part of the wave form was characterized by two pressure peaks of the central waveform. The first peak results from the left cardiac ventricle ejection while the second one results from the wave reflections from the periphery. The difference between these two peaks represents the degree of the central arterial pressure augmentation due to wave reflection (i.e., the augmentation index, mmHg)
Measured: Change from baseline in Augmentation Index at 12 weeks
Change from baseline in femoral artery delta blood flow
Femoral artery blood flow was calculated by Doppler ultrasound at baseline and at peak after single passive knee flexion and extension by using the femoral artery diameter and mean blood velocity. The difference between baseline and at peak blood flow identifies the Delta Blood Flow (ml/min).
Measured: Change from baseline in Delta Blood Flow at 12 weeks
Change from baseline in brachial artery flow mediated dilation
Flow mediated dilation was performed at brachial artery level. An arterial pressure cuff was placed around the forearm immediately distal to the olecranon process to provide an ischemic stimulus when inflated. Following baseline assessment, the blood pressure cuff was inflated to 250 mmHg. Artery diameter was and blood flow were resumed at baseline, 30 s prior to cuff deflation and continued for 2 min post-deflation by a linear array transducer attached to a high-resolution ultrasound machine. When an optimal image was obtained, the probe was held stable and longitudinal in B-mode, acquiring images of the lumen-arterial wall interface. Continuous Doppler velocity assessments were also obtained and collected using the lowest possible insonation angle (<60°). Data were exported and analyzed using commercially available software. Flow mediated dilation was quantified as the maximal change in artery diameter after cuff release, expressed as a percentage increase above baseline (%).
Measured: Change from baseline in brachial artery flow mediated dilation at 12 weeks
Secondary outcomes (2)
Change from baseline in knee range of motion
To monitor the changes in knee range of motion, a bi-axial electrogoniometer was utilized. For the knee joint, the electrogoniometer was placed with one axis on the external condyle of the knee and the other on the external face of the fibula. The knee range of motion was expressed in degrees (deg)
Measured: Change from baseline in in Knee Range of Motion at 12 weeks
Change in knee extensor muscles maximum isometric voluntary contraction
The maximum isometric voluntary contraction of the knee extensor muscles was measured with the participant laying supine on an ergometer with the knee flexed at 90° and firmly secured at the ankle level by a Velcro® strap to a load cell for the force signal detection. Hip and shoulders were also firmly secured to the ergometer. After a warm-up (10 x 2-s contractions at 50% maximum isometric voluntary contraction), three maximum isometric voluntary contraction attempts were performed, interspersed by at least 3 min of recovery. The participants were instructed to push as fast and hard as possible for 3 s. The maximum isometric voluntary contraction (N) was identified as the highest force produced during contraction.
Measured: Before, after 6 weeks, at the end (12th week), and after 6 weeks (Follow-up) of PS training
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted17 Feb 2020
- Study start7 Jan 2019
- Primary completion7 Jan 2020
- Study completion7 Feb 2020
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for VasodilationStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Model description
- Four groups in parallel (three intervention groups and one control) tested at the beginning, during, after and after six weeks (follow-up) from intervention
- Masking
- Single blind
- Who is masked
- Outcomes assessor
- Enrolment
- 39 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Milan
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Emilano Cè, University of Milan
- Investigators
- Emiliano Cè, PhD, Principal investigator, University of Milan
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT04271241
- Sponsor's protocol ID
- Stretching vasomotor response
- Status last verified
- Feb 2020
- First submitted
- 10 Feb 2020
- Last updated
- 17 Feb 2020
- Results posted
- No
- Data monitoring committee
- Yes
- FDA-regulated drug
- No
- FDA-regulated device
- No
Study at a glance
From the registry record, last updated by the sponsor on 17 Feb 2020. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Evidence of Central and Local Vascular Function Improvements After Chronic Passive Stretching
- ClinicalTrials.gov ID
- NCT04271241
- Acronym / sponsor ID
- Stretching vasomotor response
- Conditions
- Vasodilation, Vasoconstriction, Stretch, Sympathetic; Imbalance
- Keywords
- Chronic passive stretching, Central and peripheral arterial stiffness, Blood pressure, Vasomotor response, Crossover effect
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 39 participants (actual)
- Lead sponsor
- University of MilanUniversity, hospital or other
- Study start
- 7 Jan 2019 (actual)
- Primary completion
- 7 Jan 2020 (actual)
- Study completion
- 7 Feb 2020 (actual)
- First posted
- 17 Feb 2020 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Detailed description
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.
Study design
- Primary purpose
- Treatment
- Allocation
- Randomised
- Intervention model
- Parallel groups
- Masking
- Single blind (outcomes assessor)
- Number of arms
- 4
- Model description
- Four groups in parallel (three intervention groups and one control) tested at the beginning, during, after and after six weeks (follow-up) from intervention
| Arm | Type | Receives |
|---|---|---|
| Control (Ctrl) | No intervention | –Ctrl group di not undergo any training |
| PS bilateral limbs (PSBil) | Experimental | Other: Passive stretching (PS) trainingPSBil underwent 12 weeks of passive stretching on both the lower limbs |
| PS monolateral limb, stretched limb (PSMonoSL) | Experimental | Other: Passive stretching (PS) trainingPSMonoSL underwent 12 weeks of passive stretching on just one lower limb (SL). Outcomes form this group were obtained from the stretched |
| PS monolateral limb, contralateral limb PSMonoCL | Experimental | Other: Passive stretching (PS) trainingPSMonoCL involved the same participants as in PSMonoSL. Outcomes form this group were obtained from the contralateral not stretched limb (CL). Data from this limb helped in identify possible PS-induced crossover effects in the vasomotor response. |
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (1 listed)
- None
Key exclusion criteria (6 listed)
- presence of neurological, vascular and musculoskeletal impairments at the lower and upper limbs level;
- being on pharmacological therapy related to either neural and/or vascular response, including hormonal contraceptives and oral supplements;
- being a current or former smoker;
- having an irregular menstrual cycle (26 to 35 days) up to three months before the beginning of the study,
- presenting contraindication for joint mobilization;
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| Passive stretching (PS) trainingPSBil and PSMono underwent 12 weeks of PS training, 3 sessions per week (36 sessions in total). In PSBil, each session lasted 40 min and included two maneuvers for both the knee extensor and plantar flexor muscles with the following protocol: 45 s elongation and 15 s recovery in the resting position, all the cycle repeated for five times 7. In PSMono, exercises were performed only on the right limb and each session had a duration of 20 min. Ctrl did not underwent any PS exercise throughout the study. To promote participants' compliance, daily classes were held at different day time (morning and afternoon) at the University Sports Centre gym. Each class was supervised by an expert operator, which monitored the attendance, the correct exercise execution and the intensity exerted during the exercise (80% of the point of discomfort). The participants not attending at least the 80% of classes were excluded from the study, and a new participant was recruited to substitute the drop out. | Other | PS bilateral limbs (PSBil), PS monolateral limb, contralateral limb PSMonoCL, PS monolateral limb, stretched limb (PSMonoSL) |
Primary outcome
Change from baseline in augmentation Index
Time frame: Change from baseline in Augmentation Index at 12 weeks
The radial artery pressure wave and amplitude were recorded non-invasively by means of applanation tonometry of the radial artery. Twenty sequential waveforms covering a complete respiratory cycle were acquired from the system and used by the software to generate an average peripheral and corresponding central waveform. The systolic part of the wave form was characterized by two pressure peaks of the central waveform. The first peak results from the left cardiac ventricle ejection while the second one results from the wave reflections from the periphery. The difference between these two peaks represents the degree of the central arterial pressure augmentation due to wave reflection (i.e., the augmentation index, mmHg)
Change from baseline in femoral artery delta blood flow
Time frame: Change from baseline in Delta Blood Flow at 12 weeks
Femoral artery blood flow was calculated by Doppler ultrasound at baseline and at peak after single passive knee flexion and extension by using the femoral artery diameter and mean blood velocity. The difference between baseline and at peak blood flow identifies the Delta Blood Flow (ml/min).
Change from baseline in brachial artery flow mediated dilation
Time frame: Change from baseline in brachial artery flow mediated dilation at 12 weeks
Flow mediated dilation was performed at brachial artery level. An arterial pressure cuff was placed around the forearm immediately distal to the olecranon process to provide an ischemic stimulus when inflated. Following baseline assessment, the blood pressure cuff was inflated to 250 mmHg. Artery diameter was and blood flow were resumed at baseline, 30 s prior to cuff deflation and continued for 2 min post-deflation by a linear array transducer attached to a high-resolution ultrasound machine. When an optimal image was obtained, the probe was held stable and longitudinal in B-mode, acquiring images of the lumen-arterial wall interface. Continuous Doppler velocity assessments were also obtained and collected using the lowest possible insonation angle (<60°). Data were exported and analyzed using commercially available software. Flow mediated dilation was quantified as the maximal change in artery diameter after cuff release, expressed as a percentage increase above baseline (%).
2 secondary outcomes
Change from baseline in knee range of motion
Time frame: Change from baseline in in Knee Range of Motion at 12 weeks
Change in knee extensor muscles maximum isometric voluntary contraction
Time frame: Before, after 6 weeks, at the end (12th week), and after 6 weeks (Follow-up) of PS training
Results and safety
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 17 Feb 2020.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part. This study is not recruiting at the moment.
Emiliano Cè, PhD principal investigator
University of Milan
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Passive stretching (PS) training in people with Vasodilation and Vasoconstriction, run by University of Milan at 1 site in Italy.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 1 inclusion and 6 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: finished, as of the sponsor's last update on 17 Feb 2020. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in Italy. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
The study is completed, but results are not available in the source record. That does not mean the treatment did or did not work.
How can a doctor refer a patient or contact the research team?
The record lists no contact. The official record names the sponsor, who can be asked directly. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Change from baseline in augmentation Index (time frame: Change from baseline in Augmentation Index at 12 weeks). The study lists 3 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 17 Feb 2020.