Intermittent HypoxiaNCT05423470
Effect of Intermittent Hypoxia on Ischemia-reperfusion Injury in Healthy Individuals
A study testing Intermittent hypoxia and Intermittent normoxia in people with Intermittent Hypoxia, run by University of Texas at Austin at 1 site in United States.
Trial summary
The objective of the present study is to determine whether intermittent hypoxia protects against ischemia-reperfusion injury in young and older healthy individuals. The investigators hypothesize that intermittent hypoxia will attenuate the reduction in flow-mediated dilation following ischemia-reperfusion injury. Read more about this study
- Who is it for?
- Ages 18 to 80 yearsHealthy volunteers can take part
- Conditions the study is for
- Intermittent Hypoxia
- What is being tested?
- Intermittent hypoxia and Intermittent normoxia
- Type of treatment
- Lifestyle or therapy programme
- Could I receive a placebo?
- Yes, some participants may receive a placebo
- How many people
- 41 participants
- Where
- 1 siteUnited States
- Study dates
- 30 May 2019to 1 Jul 2022
- 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 to 80 years
- All sexes
- Healthy volunteers accepted
- Adult, Older adult
Who may be able to join
- Men and women aged 18 to 80 years old
Who cannot join
- Have high blood pressure (above 130/80 mmHg)
- Are smokers
- Are pregnant
- Have a history of cardiovascular disease, diabetes or lung disease
- Are taking medication affecting the cardiovascular system
- Carpal tunnel syndrome
Trial locations and contacts
1 site in 1 country.
United States1 site
The Unviersity of Texas at Austin
Austin, Texas, 78712
About this study
The objective of the present study is to determine whether intermittent hypoxia protects against ischemia-reperfusion injury in young and older healthy individuals. The investigators hypothesize that intermittent hypoxia will attenuate the reduction in flow-mediated dilation following ischemia-reperfusion injury.
Read the detailed description
Ischemic heart disease represents the most common form of cardiovascular disease and the main cause of mortality in the United States. Ischemic heart disease originates from an inadequate blood supply to the coronary arteries. While immediate reperfusion of the tissues represents the first-line treatment for ischemia, restoration of blood flow causes further damage to the endothelial cells lining the blood vessels. Indeed, severe endothelial dysfunction occurs paradoxically during the initial period of reperfusion, partly due to oxidative stress caused by a burst of reactive oxygen species formation and a reduction in nitric oxide bioavailability. Ischemia-reperfusion injury represents the endothelial damage caused by the combined effects of ischemia and reperfusion. Myocardial ischemia-reperfusion injury induces coronary endothelial dysfunction, which in turn promotes myocardial infarction. Thus, interventions designed to attenuate the effect of ischemia-reperfusion injury are urgently needed to prevent myocardial injury in patients with ischemic heart disease.
The endothelial function of the brachial artery strongly correlates with coronary artery endothelial function. Accordingly, measures of brachial artery function such as flow-mediated dilation can act as a surrogate of coronary artery endothelial function. Flow-mediated dilation, an indicator of nitric oxide-dependent endothelial function, represents the dilation of the brachial artery following increases in blood flow and shear stress induced by a transient period of ischemia. A standard model of ischemia-reperfusion injury consists of occluding blood flow to the arm for a period of 20 minutes. This prolonged forearm occlusion causes a reduction in flow-mediated dilation ranging from 30 to 50% for at least 30 minutes after reperfusion in young individuals.
Local ischemic preconditioning offers protection against ischemia-reperfusion injury. Ischemic preconditioning consists of exposing an individual to repeated brief periods of ischemia, induced by inflating a cuff on the upper arm, before an ischemia-reperfusion injury. Ischemic preconditioning (3 cycles of 5-minute ischemia followed by 5 minutes of reperfusion) applied immediately before ischemia-reperfusion injury prevents the reduction in flow-mediated dilation in healthy individuals, suggesting that ischemic preconditioning could be protective in patients with acute ischemia about to undergo therapeutic reperfusion. The protection provided by ischemic preconditioning appears to depend on the activation of adenosine triphosphate-sensitive potassium channel. Therefore, ischemic preconditioning attenuates the impaired endothelial-dependent dilation from subsequent, prolonged ischemia-reperfusion injury in humans.
Intermittent hypoxia represents a potential systemic strategy to prevent the reduction in flow-mediated dilation following ischemia-reperfusion injury. Intermittently breathing mildly hypoxic air stimulates an endothelium-dependent dilation and prevents endothelial dysfunction through the production of reactive oxygen species and an increase in nitric oxide bioavailability. Short periods of intermittent hypoxia in animal models induces ischemic preconditioning and protect the heart from subsequent infarction. Indeed, intermittent hypoxia conditioning consisting of 5-8 cycles/day for 5-10 min/cycle at a fraction of inspired oxygen of 9.5-10% interspersed with 4 min normoxia over a period of 20 days protected the endothelium-dependent dilation of coronary and systemic arteries in rats through activation of free-radical processes. Moreover, intermittent hypoxia consisting of 5 cycles of 6-minutes of hypoxia at an oxygen concentration of 6% interspersed with 6 minutes of exposure to room air over 1 hour significantly reduced infarct size in hearts from mice when performed 24 hours before ischemia-reperfusion injury, in association with hypoxia-inducible factor expression. Intermittent hypoxia may therefore induce protection via a systemic response representing a distinct mechanism from the local protective response induced by brief ischemic preconditioning.
Healthy aging results in a greater decrease in flow-mediated dilation following blood flow occlusion. Indeed, decreases in flow-mediated dilation ranging from 50 to 68% were observed in middle-aged men, due to further oxidative stress and reduced nitric oxide bioavailability. While ischemic preconditioning prevented the decrease in flow-mediated dilation in young healthy individuals, the preventive effect of ischemic preconditioning against ischemia-reperfusion injury was abolished in older individuals. However, ischemic preconditioning significantly attenuated the decrease in flow-mediated dilation in older patients with atherosclerosis.
- Conditions
- Intermittent Hypoxia
- Being tested
- Intermittent hypoxia, Intermittent normoxia
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
Intermittent hypoxiaBehavioural
The intermittent hypoxia protocol will consist of three 4-minute hypoxic cycles (arterial oxygen saturation of 80%) interspersed with 4-minute normoxic cycles.
Intermittent normoxiaBehavioural
The intermittent normoxia protocol will consist of three 4-minute normoxic cycles (compressed air) interspersed with 4-minute normoxic cycles (room air).
| Study group | Role | What they receive |
|---|---|---|
| Intermittent hypoxia | Experimental | The intermittent hypoxia protocol will consist of three 4-minute hypoxic cycles (arterial oxygen saturation of 80%) interspersed with 4-minute normoxic cycles. Receives: Behavioral: Intermittent hypoxia |
| Intermittent normoxia | Sham comparator | The intermittent normoxia protocol will consist of three 4-minute normoxic cycles (compressed air) interspersed with 4-minute normoxic cycles (room air). Receives: Behavioral: Intermittent normoxia |
What is being measured
The primary outcome is the main question the study is designed to answer.
Change in endothelial-dependent vasodilation of the brachial artery will be assessed by flow-mediated dilation using an ultrasound machine
Indicator of nitric oxide-dependent endothelial function
Measured: Measured before and 15 minutes after an ischemia-reperfusion injury.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted21 Jun 2022
- Study start30 May 2019
- Primary completion30 Dec 2021
- Study completion1 Jul 2022
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Publications (25)Papers the sponsor has linked to this study.
- Other trials for Intermittent HypoxiaStudies of the same condition, open and under way.
- More trials run by University of Texas at AustinThe sponsor's other registered studies.
- 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
- Prevention
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Single blind
- Who is masked
- Participant
- Enrolment
- 41 participants (actual)
Sponsor and investigators
- Lead sponsor
- University of Texas at Austin
- Sponsor type
- University, hospital or other
- Responsible party
- Principal investigator, Sophie Lalande, University of Texas at Austin
- Investigators
- Sophie Lalande, Principal investigator, UT Austin
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT05423470
- Sponsor's protocol ID
- 2018110129
- Status last verified
- Dec 2022
- First submitted
- 9 Jun 2022
- Last updated
- 7 Dec 2022
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Publications
Kvietys PR, Granger DN. Endothelial cell monolayers as a tool for studying microvascular pathophysiology. Am J Physiol. 1997 Dec;273(6):G1189-99. doi: 10.1152/ajpgi.1997.273.6.G1189.
PubMed 9435543Csiszar A, Wang M, Lakatta EG, Ungvari Z. Inflammation and endothelial dysfunction during aging: role of NF-kappaB. J Appl Physiol (1985). 2008 Oct;105(4):1333-41. doi: 10.1152/japplphysiol.90470.2008. Epub 2008 Jul 3.
PubMed 18599677Grisham MB, Granger DN, Lefer DJ. Modulation of leukocyte-endothelial interactions by reactive metabolites of oxygen and nitrogen: relevance to ischemic heart disease. Free Radic Biol Med. 1998 Sep;25(4-5):404-33. doi: 10.1016/s0891-5849(98)00094-x.
PubMed 9741579Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci. 2005 Jun;1047:248-58. doi: 10.1196/annals.1341.022.
PubMed 16093501Powers SK, Murlasits Z, Wu M, Kavazis AN. Ischemia-reperfusion-induced cardiac injury: a brief review. Med Sci Sports Exerc. 2007 Sep;39(9):1529-36. doi: 10.1249/mss.0b013e3180d099c1.
PubMed 17805085Rodriguez-Manas L, El-Assar M, Vallejo S, Lopez-Doriga P, Solis J, Petidier R, Montes M, Nevado J, Castro M, Gomez-Guerrero C, Peiro C, Sanchez-Ferrer CF. Endothelial dysfunction in aged humans is related with oxidative stress and vascular inflammation. Aging Cell. 2009 Jun;8(3):226-38. doi: 10.1111/j.1474-9726.2009.00466.x. Epub 2009 Feb 26.
PubMed 19245678Anderson TJ, Uehata A, Gerhard MD, Meredith IT, Knab S, Delagrange D, Lieberman EH, Ganz P, Creager MA, Yeung AC, et al. Close relation of endothelial function in the human coronary and peripheral circulations. J Am Coll Cardiol. 1995 Nov 1;26(5):1235-41. doi: 10.1016/0735-1097(95)00327-4.
PubMed 7594037Harris RA, Nishiyama SK, Wray DW, Richardson RS. Ultrasound assessment of flow-mediated dilation. Hypertension. 2010 May;55(5):1075-85. doi: 10.1161/HYPERTENSIONAHA.110.150821. Epub 2010 Mar 29.
PubMed 20351340Aboo Bakkar Z, Fulford J, Gates PE, Jackman SR, Jones AM, Bond B, Bowtell JL. Prolonged forearm ischemia attenuates endothelium-dependent vasodilatation and plasma nitric oxide metabolites in overweight middle-aged men. Eur J Appl Physiol. 2018 Aug;118(8):1565-1572. doi: 10.1007/s00421-018-3886-z. Epub 2018 May 21.
PubMed 29785503Brunt VE, Jeckell AT, Ely BR, Howard MJ, Thijssen DH, Minson CT. Acute hot water immersion is protective against impaired vascular function following forearm ischemia-reperfusion in young healthy humans. Am J Physiol Regul Integr Comp Physiol. 2016 Dec 1;311(6):R1060-R1067. doi: 10.1152/ajpregu.00301.2016. Epub 2016 Oct 5.
PubMed 27707723Devan AE, Umpierre D, Harrison ML, Lin HF, Tarumi T, Renzi CP, Dhindsa M, Hunter SD, Tanaka H. Endothelial ischemia-reperfusion injury in humans: association with age and habitual exercise. Am J Physiol Heart Circ Physiol. 2011 Mar;300(3):H813-9. doi: 10.1152/ajpheart.00845.2010. Epub 2011 Jan 14.
PubMed 21239631DeVan AE, Umpierre D, Lin HF, Harrison ML, Tarumi T, Dhindsa M, Hunter SD, Sommerlad SM, Tanaka H. Habitual resistance exercise and endothelial ischemia-reperfusion injury in young adults. Atherosclerosis. 2011 Nov;219(1):191-3. doi: 10.1016/j.atherosclerosis.2011.07.099. Epub 2011 Jul 26.
PubMed 21840524Loukogeorgakis SP, Williams R, Panagiotidou AT, Kolvekar SK, Donald A, Cole TJ, Yellon DM, Deanfield JE, MacAllister RJ. Transient limb ischemia induces remote preconditioning and remote postconditioning in humans by a K(ATP)-channel dependent mechanism. Circulation. 2007 Sep 18;116(12):1386-95. doi: 10.1161/CIRCULATIONAHA.106.653782. Epub 2007 Aug 27.
PubMed 17724264Carden DL, Granger DN. Pathophysiology of ischaemia-reperfusion injury. J Pathol. 2000 Feb;190(3):255-66. doi: 10.1002/(SICI)1096-9896(200002)190:33.0.CO;2-6.
PubMed 10685060Gross GJ, Auchampach JA. Blockade of ATP-sensitive potassium channels prevents myocardial preconditioning in dogs. Circ Res. 1992 Feb;70(2):223-33. doi: 10.1161/01.res.70.2.223.
PubMed 1310443
Study at a glance
From the registry record, last updated by the sponsor on 7 Dec 2022. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effect of Intermittent Hypoxia on Ischemia-reperfusion Injury in Healthy Individuals
- ClinicalTrials.gov ID
- NCT05423470
- Acronym / sponsor ID
- 2018110129
- Conditions
- Intermittent Hypoxia
- Study type
- Interventional
- Recruitment status
- Completed
- Enrolment
- 41 participants (actual)
- Lead sponsor
- University of Texas at AustinUniversity, hospital or other
- Study start
- 30 May 2019 (actual)
- Primary completion
- 30 Dec 2021 (actual)
- Study completion
- 1 Jul 2022 (actual)
- First posted
- 21 Jun 2022 (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.
The objective of the present study is to determine whether intermittent hypoxia protects against ischemia-reperfusion injury in young and older healthy individuals. The investigators hypothesize that intermittent hypoxia will attenuate the reduction in flow-mediated dilation following ischemia-reperfusion injury.
Detailed description
Ischemic heart disease represents the most common form of cardiovascular disease and the main cause of mortality in the United States. Ischemic heart disease originates from an inadequate blood supply to the coronary arteries. While immediate reperfusion of the tissues represents the first-line treatment for ischemia, restoration of blood flow causes further damage to the endothelial cells lining the blood vessels. Indeed, severe endothelial dysfunction occurs paradoxically during the initial period of reperfusion, partly due to oxidative stress caused by a burst of reactive oxygen species formation and a reduction in nitric oxide bioavailability. Ischemia-reperfusion injury represents the endothelial damage caused by the combined effects of ischemia and reperfusion. Myocardial ischemia-reperfusion injury induces coronary endothelial dysfunction, which in turn promotes myocardial infarction. Thus, interventions designed to attenuate the effect of ischemia-reperfusion injury are urgently needed to prevent myocardial injury in patients with ischemic heart disease.
The endothelial function of the brachial artery strongly correlates with coronary artery endothelial function. Accordingly, measures of brachial artery function such as flow-mediated dilation can act as a surrogate of coronary artery endothelial function. Flow-mediated dilation, an indicator of nitric oxide-dependent endothelial function, represents the dilation of the brachial artery following increases in blood flow and shear stress induced by a transient period of ischemia. A standard model of ischemia-reperfusion injury consists of occluding blood flow to the arm for a period of 20 minutes. This prolonged forearm occlusion causes a reduction in flow-mediated dilation ranging from 30 to 50% for at least 30 minutes after reperfusion in young individuals.
Local ischemic preconditioning offers protection against ischemia-reperfusion injury. Ischemic preconditioning consists of exposing an individual to repeated brief periods of ischemia, induced by inflating a cuff on the upper arm, before an ischemia-reperfusion injury. Ischemic preconditioning (3 cycles of 5-minute ischemia followed by 5 minutes of reperfusion) applied immediately before ischemia-reperfusion injury prevents the reduction in flow-mediated dilation in healthy individuals, suggesting that ischemic preconditioning could be protective in patients with acute ischemia about to undergo therapeutic reperfusion. The protection provided by ischemic preconditioning appears to depend on the activation of adenosine triphosphate-sensitive potassium channel. Therefore, ischemic preconditioning attenuates the impaired endothelial-dependent dilation from subsequent, prolonged ischemia-reperfusion injury in humans.
Intermittent hypoxia represents a potential systemic strategy to prevent the reduction in flow-mediated dilation following ischemia-reperfusion injury. Intermittently breathing mildly hypoxic air stimulates an endothelium-dependent dilation and prevents endothelial dysfunction through the production of reactive oxygen species and an increase in nitric oxide bioavailability. Short periods of intermittent hypoxia in animal models induces ischemic preconditioning and protect the heart from subsequent infarction. Indeed, intermittent hypoxia conditioning consisting of 5-8 cycles/day for 5-10 min/cycle at a fraction of inspired oxygen of 9.5-10% interspersed with 4 min normoxia over a period of 20 days protected the endothelium-dependent dilation of coronary and systemic arteries in rats through activation of free-radical processes. Moreover, intermittent hypoxia consisting of 5 cycles of 6-minutes of hypoxia at an oxygen concentration of 6% interspersed with 6 minutes of exposure to room air over 1 hour significantly reduced infarct size in hearts from mice when performed 24 hours before ischemia-reperfusion injury, in association with hypoxia-inducible factor expression. Intermittent hypoxia may therefore induce protection via a systemic response representing a distinct mechanism from the local protective response induced by brief ischemic preconditioning.
Healthy aging results in a greater decrease in flow-mediated dilation following blood flow occlusion. Indeed, decreases in flow-mediated dilation ranging from 50 to 68% were observed in middle-aged men, due to further oxidative stress and reduced nitric oxide bioavailability. While ischemic preconditioning prevented the decrease in flow-mediated dilation in young healthy individuals, the preventive effect of ischemic preconditioning against ischemia-reperfusion injury was abolished in older individuals. However, ischemic preconditioning significantly attenuated the decrease in flow-mediated dilation in older patients with atherosclerosis.
Study design
- Primary purpose
- Prevention
- Allocation
- Randomised
- Intervention model
- Crossover
- Masking
- Single blind (participant)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Intermittent hypoxia | Experimental | Behavioral: Intermittent hypoxiaThe intermittent hypoxia protocol will consist of three 4-minute hypoxic cycles (arterial oxygen saturation of 80%) interspersed with 4-minute normoxic cycles. |
| Intermittent normoxia | Sham comparator | Behavioral: Intermittent normoxiaThe intermittent normoxia protocol will consist of three 4-minute normoxic cycles (compressed air) interspersed with 4-minute normoxic cycles (room air). |
Who may qualify
- Ages
- 18 to 80 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult, Older adult
Key inclusion criteria (1 listed)
- Men and women aged 18 to 80 years old
Key exclusion criteria (6 listed)
- Have high blood pressure (above 130/80 mmHg)
- Are smokers
- Are pregnant
- Have a history of cardiovascular disease, diabetes or lung disease
- Are taking medication affecting the cardiovascular system
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 |
|---|---|---|
| Intermittent hypoxiaThe intermittent hypoxia protocol will consist of three 4-minute hypoxic cycles (arterial oxygen saturation of 80%) interspersed with 4-minute normoxic cycles. | Behavioural | Intermittent hypoxia |
| Intermittent normoxiaThe intermittent normoxia protocol will consist of three 4-minute normoxic cycles (compressed air) interspersed with 4-minute normoxic cycles (room air). | Behavioural | Intermittent normoxia |
Primary outcome
Change in endothelial-dependent vasodilation of the brachial artery will be assessed by flow-mediated dilation using an ultrasound machine
Time frame: Measured before and 15 minutes after an ischemia-reperfusion injury.
Indicator of nitric oxide-dependent endothelial function
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 7 Dec 2022.
- Background: PubMed 9435543Kvietys PR, Granger DN. Endothelial cell monolayers as a tool for studying microvascular pathophysiology. Am J Physiol. 1997 Dec;273(6):G1189-99. doi: 10.1152/ajpgi.1997.273.6.G1189.
- Background: PubMed 18599677Csiszar A, Wang M, Lakatta EG, Ungvari Z. Inflammation and endothelial dysfunction during aging: role of NF-kappaB. J Appl Physiol (1985). 2008 Oct;105(4):1333-41. doi: 10.1152/japplphysiol.90470.2008. Epub 2008 Jul 3.
- Background: PubMed 9741579Grisham MB, Granger DN, Lefer DJ. Modulation of leukocyte-endothelial interactions by reactive metabolites of oxygen and nitrogen: relevance to ischemic heart disease. Free Radic Biol Med. 1998 Sep;25(4-5):404-33. doi: 10.1016/s0891-5849(98)00094-x.
- Background: PubMed 16093501Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci. 2005 Jun;1047:248-58. doi: 10.1196/annals.1341.022.
- Background: PubMed 17805085Powers SK, Murlasits Z, Wu M, Kavazis AN. Ischemia-reperfusion-induced cardiac injury: a brief review. Med Sci Sports Exerc. 2007 Sep;39(9):1529-36. doi: 10.1249/mss.0b013e3180d099c1.
- Background: PubMed 19245678Rodriguez-Manas L, El-Assar M, Vallejo S, Lopez-Doriga P, Solis J, Petidier R, Montes M, Nevado J, Castro M, Gomez-Guerrero C, Peiro C, Sanchez-Ferrer CF. Endothelial dysfunction in aged humans is related with oxidative stress and vascular inflammation. Aging Cell. 2009 Jun;8(3):226-38. doi: 10.1111/j.1474-9726.2009.00466.x. Epub 2009 Feb 26.
- Background: PubMed 7594037Anderson TJ, Uehata A, Gerhard MD, Meredith IT, Knab S, Delagrange D, Lieberman EH, Ganz P, Creager MA, Yeung AC, et al. Close relation of endothelial function in the human coronary and peripheral circulations. J Am Coll Cardiol. 1995 Nov 1;26(5):1235-41. doi: 10.1016/0735-1097(95)00327-4.
- Background: PubMed 20351340Harris RA, Nishiyama SK, Wray DW, Richardson RS. Ultrasound assessment of flow-mediated dilation. Hypertension. 2010 May;55(5):1075-85. doi: 10.1161/HYPERTENSIONAHA.110.150821. Epub 2010 Mar 29.
- Background: PubMed 29785503Aboo Bakkar Z, Fulford J, Gates PE, Jackman SR, Jones AM, Bond B, Bowtell JL. Prolonged forearm ischemia attenuates endothelium-dependent vasodilatation and plasma nitric oxide metabolites in overweight middle-aged men. Eur J Appl Physiol. 2018 Aug;118(8):1565-1572. doi: 10.1007/s00421-018-3886-z. Epub 2018 May 21.
- Background: PubMed 27707723Brunt VE, Jeckell AT, Ely BR, Howard MJ, Thijssen DH, Minson CT. Acute hot water immersion is protective against impaired vascular function following forearm ischemia-reperfusion in young healthy humans. Am J Physiol Regul Integr Comp Physiol. 2016 Dec 1;311(6):R1060-R1067. doi: 10.1152/ajpregu.00301.2016. Epub 2016 Oct 5.
- Background: PubMed 21239631Devan AE, Umpierre D, Harrison ML, Lin HF, Tarumi T, Renzi CP, Dhindsa M, Hunter SD, Tanaka H. Endothelial ischemia-reperfusion injury in humans: association with age and habitual exercise. Am J Physiol Heart Circ Physiol. 2011 Mar;300(3):H813-9. doi: 10.1152/ajpheart.00845.2010. Epub 2011 Jan 14.
- Background: PubMed 21840524DeVan AE, Umpierre D, Lin HF, Harrison ML, Tarumi T, Dhindsa M, Hunter SD, Sommerlad SM, Tanaka H. Habitual resistance exercise and endothelial ischemia-reperfusion injury in young adults. Atherosclerosis. 2011 Nov;219(1):191-3. doi: 10.1016/j.atherosclerosis.2011.07.099. Epub 2011 Jul 26.
- Individual participant dataSharing planned: No
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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.
Sophie Lalande principal investigator
UT Austin
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Intermittent hypoxia and Intermittent normoxia in people with Intermittent Hypoxia, run by University of Texas at Austin at 1 site in United States.
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 7 Dec 2022. 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 United States. 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. Some participants in this study may receive a placebo. 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 in endothelial-dependent vasodilation of the brachial artery will be assessed by flow-mediated dilation using an ultrasound machine (time frame: Measured before and 15 minutes after an ischemia-reperfusion injury.). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
On the ClinicalTrials.gov record for NCT05423470, which also lists 25 linked publications.
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 7 Dec 2022.