Mechanisms of Exercise Intolerance in Chronic Obstructive Pulmonary Disease (COPD)

The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Listing a study does not mean it has been evaluated by the U.S. Federal Government. Read our disclaimer for details. Identifier: NCT02360865
Recruitment Status : Completed
First Posted : February 11, 2015
Last Update Posted : June 16, 2016
Information provided by (Responsible Party):
Anders Rasmussen Rinnov, Rigshospitalet, Denmark

Brief Summary:

1: Is endothelium function impaired in COPD? Other chronic cardiovascular diseases are associated with endothelial dysfunction, and the endothelium plays an important role in regulating vascular tone, tissue blood flow, coagulation and the inflammation process. Although the specific causes of endothelial dysfunction remain unclear, physical inactivity, chronic systemic inflammation and smoking are all known to be associated with endothelial abnormality.

2. Is Muscular Sympathetic Nerve Activity (MSNA) increased in COPD? A balanced regulation of blood flow to skeletal muscles may be disturbed by pathophysiology and may therefore contribute to the exercise intolerance and skeletal muscle depletion seen in patients with COPD.Skeletal muscle blood flow is tightly regulated to match tissue oxygen demands and is thus adapted to meet energy requirements. During physical activity, the sympathetic nervous system is activated ("exercise pressor reflex"), resulting in increased ventilation, heart rate and a redistribution of cardiac output from inactive to active tissues. The redistribution of cardiac output to the body organs is heterogeneous. Blood flow to skeletal, respiratory and cardiac muscle increases as exercise intensity increases, whereas blood flow to gastrointestinal, renal and reproductive tissues decreases. As blood pressure during exercise remains largely unchanged, the redistribution of blood flow is caused by changes in vascular conductance. These conductance changes are caused by an overall vasoconstriction induced by the increased sympathetic outflow of noradrenaline (NA), and a vasodilation of vascular beds supplying the working skeletal -, cardiac- and respiratory muscle.

Condition or disease Intervention/treatment Phase
COPD Other: Exercise Not Applicable

Study Type : Interventional  (Clinical Trial)
Actual Enrollment : 18 participants
Allocation: Non-Randomized
Intervention Model: Parallel Assignment
Masking: None (Open Label)
Primary Purpose: Basic Science
Official Title: Mechanisms of Exercise Intolerance in Chronic Obstructive Pulmonary Disease
Study Start Date : February 2015
Actual Primary Completion Date : May 2016
Actual Study Completion Date : May 2016

Resource links provided by the National Library of Medicine

Arm Intervention/treatment
Experimental: COPD
Acute exercise bouts
Other: Exercise
Active Comparator: Healthy
Acute exercise bouts
Other: Exercise

Primary Outcome Measures :
  1. Endothelium function during acute exercise (one legged kicking) by Flow doppler [ Time Frame: On one experimental day during acute exercise (one legged knicking) and change from baseline ]
    Flow doppler

  2. Muscular Sympathetic Nerve Activity During acute exercise (handgrip and leg isometric leg extension) by Peroneal microneurography [ Time Frame: On one experimental day during acute exercise (handgrib and leg isometric leg extension) and change from baseline ]

Information from the National Library of Medicine

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Ages Eligible for Study:   40 Years to 80 Years   (Adult, Older Adult)
Sexes Eligible for Study:   All
Accepts Healthy Volunteers:   Yes

Inclusion Criteria:

  • Forced Expiratory Volume at on second/ Forced Vital Capacity fixed ratio <0.70, - Forced Expiratory Volume at one second <60% of predicted and Medical
  • Research Council scale > or equal to 3
  • Arterial oxygen saturation at rest> 90%,
  • Body Mass Index >18,
  • Left Ventricle Ejection Fraction> 45.

Exclusion Criteria:

  • Unstable ischemic heart disease,
  • severe heart valve failure,
  • pulmonary emboli,
  • severe heart failure,
  • severe infections,
  • musculoskeletal disorders,
  • malignant disease,
  • contraindicated medicine as anticoagulants.

Information from the National Library of Medicine

To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.

Please refer to this study by its identifier (NCT number): NCT02360865

Centre of Physical Activity Research
Copenhagen, Capital Region, Denmark, 2100
Sponsors and Collaborators
Rigshospitalet, Denmark

Responsible Party: Anders Rasmussen Rinnov, MD, PhD, Rigshospitalet, Denmark Identifier: NCT02360865     History of Changes
Other Study ID Numbers: H-2-2013-150 - project 2
First Posted: February 11, 2015    Key Record Dates
Last Update Posted: June 16, 2016
Last Verified: June 2016

Additional relevant MeSH terms:
Lung Diseases
Lung Diseases, Obstructive
Pulmonary Disease, Chronic Obstructive
Respiratory Tract Diseases