Acute Exercise and Microvascular Function

NCT ID: NCT02727439

Last Updated: 2016-04-04

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Clinical Phase

NA

Total Enrollment

30 participants

Study Classification

INTERVENTIONAL

Study Start Date

2016-02-29

Study Completion Date

2017-12-31

Brief Summary

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It is well recognized that chronic exercise protects against the development of cardiovascular diseases. However, the responses of vasculature to acute exercise (AE) are not well known and not consistent in literature. Acute exertional exercise can induce large, transient increases in arterial pressure and development of metabolic acidosis which can be associated with pro-inflammatory response involving oxidant stress and circulating cytokines known to impair endothelial function.

The aim of this study is to test the impact of a single exposure to exhausting training on microvascular reactivity in healthy sedentary subjects and athletes.

Detailed Description

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Conditions

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Physical Exertion

Study Design

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Allocation Method

NON_RANDOMIZED

Intervention Model

PARALLEL

Primary Study Purpose

BASIC_SCIENCE

Blinding Strategy

NONE

Study Groups

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Sedentary Subjects

Healthy lean sedentary subjects.

Group Type EXPERIMENTAL

Acute Exhausting Exercise (AE)

Intervention Type OTHER

A single progressive rowing training to maximal exhaustion (AE).

Athletes

Active athletes.

Group Type EXPERIMENTAL

Acute Exhausting Exercise (AE)

Intervention Type OTHER

A single progressive rowing training to maximal exhaustion (AE).

Interventions

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Acute Exhausting Exercise (AE)

A single progressive rowing training to maximal exhaustion (AE).

Intervention Type OTHER

Eligibility Criteria

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Inclusion Criteria

* healthy volunteers
* active athletes
* lean sedentary subjects

Exclusion Criteria

* drugs that could affect the endothelium
* overweight
* hypertension
* coronary artery disease
* diabetes
* hyperlipidaemia
* renal impairment
* cerebrovascular and peripheral artery disease
Minimum Eligible Age

18 Years

Maximum Eligible Age

30 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

Yes

Sponsors

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Josip Juraj Strossmayer University of Osijek

OTHER

Sponsor Role lead

Responsible Party

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Ines Drenjancevic

Vice Dean for Science, Faculty of Medicine Josip Juraj Strossmayer University of Osijek

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Ines Drenjancevic, MD, PhD

Role: PRINCIPAL_INVESTIGATOR

Faculty of Medicine, Josip Juraj Strossmayer University of Osijek

Locations

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Faculty of Medicine Osijek, Laboratory for Clinical and Sport Physiology

Osijek, , Croatia

Site Status RECRUITING

Countries

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Croatia

Central Contacts

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Ana Stupin, MD, PhD

Role: CONTACT

+385915134958

Ines Drenjancevic, MD, PhD

Role: CONTACT

+385912241406

Facility Contacts

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Ana Stupin, MD, PhD

Role: primary

'385915134598

Ines Drenjancevic, MD, PhD

Role: backup

'385912241406

References

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Cavka A, Cosic A, Jukic I, Jelakovic B, Lombard JH, Phillips SA, Seric V, Mihaljevic I, Drenjancevic I. The role of cyclo-oxygenase-1 in high-salt diet-induced microvascular dysfunction in humans. J Physiol. 2015 Dec 15;593(24):5313-24. doi: 10.1113/JP271631. Epub 2015 Dec 7.

Reference Type BACKGROUND
PMID: 26498129 (View on PubMed)

Cavka A, Jukic I, Ali M, Goslawski M, Bian JT, Wang E, Drenjancevic I, Phillips SA. Short-term high salt intake reduces brachial artery and microvascular function in the absence of changes in blood pressure. J Hypertens. 2016 Apr;34(4):676-84. doi: 10.1097/HJH.0000000000000852.

Reference Type BACKGROUND
PMID: 26848993 (View on PubMed)

Phillips SA, Das E, Wang J, Pritchard K, Gutterman DD. Resistance and aerobic exercise protects against acute endothelial impairment induced by a single exposure to hypertension during exertion. J Appl Physiol (1985). 2011 Apr;110(4):1013-20. doi: 10.1152/japplphysiol.00438.2010. Epub 2011 Jan 20.

Reference Type BACKGROUND
PMID: 21252216 (View on PubMed)

Other Identifiers

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215861071403

Identifier Type: -

Identifier Source: org_study_id

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