| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Dept of Critical Care and Pulmonary Services, University of Athens Medical School, Evangelismos Hospital, Athens, Greece
CORRESPONDENCE: T. Vassilakopoulos, Critical Care Dept, Evangelismos Hospital, 45–47 Ipsilandou Str, GR-10675 Athens, Greece. Fax: 30 17216503. E-mail: tvassil@med.uoa.gr
Keywords: Control of breathing, exercise immunology, interleukin-6, oxidants/antioxidants, respiratory immunology, respiratory muscle
Received: June 8, 2004
Accepted August 17, 2004
Abstract
Resistive breathing is an "immune challenge" for the body, initiating an inflammatory response consisting of an elevation of plasma cytokines, and the recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes, but are, instead, produced within the diaphragm, secondary to the increased muscle activation.
Oxidative stress is a major stimulus for the cytokine induction, secondary to resistive breathing. The production of cytokines within the diaphragm may be mediating the diaphragm muscle fibre injury that occurs with strenuous contractions, or contributing towards the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute towards the development of muscle cachexia. They may also have systemic effects, mobilising glucose from the liver and free fatty acid from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal axis, leading to production of adrenocorticotropin and ß-endorphins.
The adrenocorticotropin response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles via the production of glucocorticoids and the induction of the acute phase-response proteins. The ß-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing, which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles.
This article has been cited by other articles:
|
|
 |
|
  A. Agusti Systemic Effects of Chronic Obstructive Pulmonary Disease: What We Know and What We Don't Know (but Should) Proceedings of the ATS, October 1, 2007; 4(7): 522 - 525. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Degens, A. K. Swisher, Y. F. Heijdra, P. M. Siu, P. N. Richard Dekhuijzen, and S. E. Alway Apoptosis and Id2 expression in diaphragm and soleus muscle from the emphysematous hamster Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2007; 293(1): R135 - R144. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Zakynthinos, P. Katsaounou, M.-H. Karatza, C. Roussos, and T. Vassilakopoulos Antioxidants Increase the Ventilatory Response to Hyperoxic Hypercapnia Am. J. Respir. Crit. Care Med., January 1, 2007; 175(1): 62 - 68. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Agusti Thomas A. Neff Lecture. Chronic Obstructive Pulmonary Disease: A Systemic Disease Proceedings of the ATS, August 1, 2006; 3(6): 478 - 481. [Full Text] [PDF]
|
|
|
|
 |
|
 T. Vassilakopoulos, S. Zakynthinos, and C. Roussos From the authors Eur. Respir. J., June 1, 2005; 25(6): 1129 - 1130. [Full Text] [PDF]
|
|
|
|
|
|
N. M. Siafakas and I. Mitrouska The immune response to resistive breathing Eur. Respir. J., June 1, 2005; 25(6): 1128 - 1129. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
