Relationship between oxygen consumption kinetics and BODE Index in COPD patients.

Int J Chron Obstruct Pulmon Dis

Cardiopulmonary Physiotherapy Laboratory, Nucleus of Research in Physical Exercise, Federal University of São Carlos, São Carlos, SP, Brazil.

Published: April 2013

Background And Objective: Patients with chronic obstructive pulmonary disease (COPD) present with reduced exercise capacity due to impaired oxygen consumption (VO(2)), caused primarily by pulmonary dysfunction and deleterious peripheral adaptations. Assuming that COPD patients present with slower VO(2) and heart rate (HR) on-kinetics, we hypothesized that this finding is related to disease severity as measured by the BODE Index. In this context, the present study intends to evaluate the relationship between VO(2) uptake on-kinetics during high-intensity exercise and the BODE Index in patients with COPD.

Methods: Twenty males with moderate-to-severe stable COPD and 13 healthy control subjects matched by age and sex were evaluated. COPD patients were screened by the BODE Index and then underwent an incremental cardiopulmonary exercise test and a constant speed treadmill session at 70% of maximal intensity for 6 minutes. The onset of the exercise (first 360 seconds) response for O(2) uptake and HR was modeled according to a monoexponential fit.

Results: Oxygen consumption and HR on-kinetics were slower in the COPD group compared with controls. Additionally, VO(2) on-kinetic parameters revealed a strong positive correlation (r = 0.77, P < 0.05) with BODE scores and a moderate negative correlation with walking distance (r = -0.45, P < 0.05).

Conclusion: Our data show that moderate-to-severe COPD is related to impaired oxygen delivery and utilization during the onset of intense exercise.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484529PMC
http://dx.doi.org/10.2147/COPD.S35637DOI Listing

Publication Analysis

Top Keywords

oxygen consumption
12
copd patients
12
impaired oxygen
8
copd
7
bode
5
patients
5
exercise
5
relationship oxygen
4
consumption kinetics
4
kinetics bode
4

Similar Publications

Methodological developments in biomedical research are currently moving towards single-cell approaches. This allows for a much better spatial and functional characterization of, for example, the deterioration of cells within a tissue in response to noxae. However, subcellular resolution is also essential to elucidate whether observed impairments are driven by an explicit organelle.

View Article and Find Full Text PDF

Mitochondrial endonuclease G (EndoG) contributes to chromosomal degradation when it is released from mitochondria during apoptosis. It is presumed to also have a mitochondrial function because EndoG deficiency causes mitochondrial dysfunction. However, the mechanism by which EndoG regulates mitochondrial function is not known.

View Article and Find Full Text PDF

Background: Mitochondrial bioenergetics are essential for cellular function, specifically the intricacies of the electron transport chain (ETC), with Complex IV playing a crucial role in unraveling the mechanisms governing energy production. Mathematical models offer a valuable approach to simulate these complex processes, providing insights into normal mitochondrial function and aberrations associated with various diseases, including neurodegenerative disorders. Our research focuses on introducing and refining a mathematical model, emphasizing Complex IV in the ETC, with objectives including incorporating mitochondrial activity modulation using inhibiting and uncoupling reagents, akin to oxygen consumption experiments.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

University of Miami, Coral Gables, FL, USA.

Background: Cerebral blood flow is decreased in mouse models and patients of Alzheimer's disease (AD). We identified that about 2% of cortical capillaries in the APP/PS1 mouse model of AD had stalled blood flow due to neutrophils obstructing capillaries and contributing to vascular inflammation. Neutrophils are more reactive in AD.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Background: While disease-modifying treatments that reduce Aβ have been recently approved by the FDA, the identification of novel therapeutic targets and strategies that target underlying mechanisms to delay the AD development are still needed. Abnormal brain energy homeostasis and mitochondria dysfunction are observed early in AD. Therefore, the development of treatments to restore these defects could be beneficial.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!