NDLI: Central command dysfunction in rats with heart failure is mediated by brain oxidative stress and normalized by exercise training

Content Provider	PubMed Central
Author	Koba, Satoshi Ichiro, Hisatome Watanabe, Tatsuo
Copyright Year	2014
Abstract	Sympathoexcitation elicited by central command, a parallel activation of the motor and autonomic neural circuits in the brain, has been shown to become exaggerated in chronic heart failure (CHF). The present study tested the hypotheses that oxidative stress in the medulla in CHF plays a role in exaggerating central command-elicited sympathoexcitation, and that exercise training in CHF suppresses central command-elicited sympathoexcitation through its antioxidant effects in the medulla. In decerebrate rats, central command was activated by electrically stimulating the mesencephalic locomotor region (MLR) after neuromuscular blockade. The MLR stimulation at a current intensity greater than locomotion threshold in rats with CHF after myocardial infarction (MI) evoked larger (P < 0.05) increases in renal sympathetic nerve activity and arterial pressure than in sham-operated healthy rats (Sham) and rats with CHF that had completed longterm (8–12 weeks) exercise training (MI + TR). In the Sham and MI + TR rats, bilateral microinjection of a superoxide dismutase (SOD) mimetic Tempol into the rostral ventrolateral medulla (RVLM) had no effects on MLR stimulation-elicited responses. By contrast, in MI rats, Tempol treatment significantly reduced MLR stimulation-elicited responses. In a subset of MI rats, treatment with Tiron, another SOD mimetic, within the RVLM also reduced responses. Superoxide generation in the RVLM, as evaluated by dihydroethidium staining, was enhanced in MI rats compared with that in Sham and MI + TR rats. Collectively, these results support the study hypotheses. We suggest that oxidative stress in the medulla in CHF mediates central command dysfunction, and that exercise training in CHF is capable of normalizing central command dysfunction through its antioxidant effects in the medulla.
Related Links	http://dx.doi.org/10.1113/jphysiol.2014.272377
Ending Page	3931
Page Count	15
Starting Page	3917
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 17
Volume Number	592
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2014-09-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Exercise training prevents the exaggerated exercise pressor reflex in rats with chronic heart failure

Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats

Exercise training normalizes ACE and ACE2 in the brain of rabbits with pacing-induced heart failure

ß-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger.

Beneficial effects of exercise training in heart failure are lost in male diabetic rats

Improved insulin sensitivity after weight loss and exercise training is mediated by a reduction in plasma fatty acid mobilization, not enhanced oxidative capacity

Exercise training normalizes the blunted central component of the baroreflex in rats with heart failure: role of the PVN

Oxidative stress and the muscle reflex in heart failure

Central command and the onset of exercise

Central command dysfunction in rats with heart failure is mediated by brain oxidative stress and normalized by exercise training

Similar Documents

Exercise training prevents the exaggerated exercise pressor reflex in rats with chronic heart failure

Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise in rats

Exercise training normalizes ACE and ACE2 in the brain of rabbits with pacing-induced heart failure

ß-Adrenergic receptors desensitization is not involved in exercise-induced cardiac fatigue: NADPH oxidase-induced oxidative stress as a new trigger.

Beneficial effects of exercise training in heart failure are lost in male diabetic rats

Improved insulin sensitivity after weight loss and exercise training is mediated by a reduction in plasma fatty acid mobilization, not enhanced oxidative capacity

Exercise training normalizes the blunted central component of the baroreflex in rats with heart failure: role of the PVN

Oxidative stress and the muscle reflex in heart failure

Central command and the onset of exercise

Central command dysfunction in rats with heart failure is mediated by brain oxidative stress and normalized by exercise training