Document Detail

Arterial stiffening following eccentric exercise-induced muscle damage.
MedLine Citation:
PMID:  20671032     Owner:  NLM     Status:  MEDLINE    
Acute inflammatory responses are linked to a transient increase in risk of a cardiovascular event, and this risk may be mediated by a concomitant reduction in vascular function. Humans experience an acute inflammatory response as a consequence of infection, injury, or muscle damage. We measured macrovascular function before and after eccentric exercise to determine whether muscle damage from unaccustomed exercise has an unfavorable effect on the large elastic arteries. A total of 27 healthy sedentary or recreationally active men (age 18-38 years) participated in either bilateral leg press eccentric exercise or unilateral elbow flexor eccentric exercise. Postexercise muscle damage was confirmed by significant reductions in isometric strength and increases in muscle soreness (P < 0.05). Carotid-femoral pulse-wave velocity was significantly elevated 48 h after leg exercise (808 ± 31 vs. 785 ± 30 cm/s; P < 0.05) and arm exercise (790 ± 28 vs. 755 ± 24 cm/s; P < 0.05). There were no changes in mean arterial pressure. C-reactive protein was elevated after leg exercise but not after arm exercise. The increase in carotid-femoral pulse wave velocity 48 h after arm exercise was associated with muscle strength (r = -0.47; P < 0.05) and creatine kinase concentrations (r = 0.70; P < 0.01). We concluded that eccentric exercise in both small and large muscle mass translates to transient, unfavorable changes in central macrovascular function and that the increase in central arterial stiffness after small muscle eccentric exercise is associated with indicators of muscle damage.
Jill N Barnes; Justin R Trombold; Mandeep Dhindsa; Hsin-Fu Lin; Hirofumi Tanaka
Publication Detail:
Type:  Journal Article; Randomized Controlled Trial     Date:  2010-07-29
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  109     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-13     Completed Date:  2011-05-23     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1102-8     Citation Subset:  IM    
Cardiovascular Aging Research Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Arteries / physiopathology*
Biological Markers / blood
Blood Flow Velocity
C-Reactive Protein / metabolism
Carotid Arteries / physiopathology
Creatine Kinase / blood
Cross-Over Studies
Femoral Artery / physiopathology
Inflammation Mediators / blood
Interleukin-6 / blood
Isometric Contraction*
Muscle Strength
Muscle, Skeletal / enzymology,  physiopathology*
Muscular Diseases / blood,  etiology,  physiopathology*
Pain / etiology,  physiopathology
Pulsatile Flow
Time Factors
Young Adult
Reg. No./Substance:
0/Biological Markers; 0/IL6 protein, human; 0/Inflammation Mediators; 0/Interleukin-6; 9007-41-4/C-Reactive Protein; EC Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  The phosphatase interactor NIPP1 regulates the occupancy of the histone methyltransferase EZH2 at Po...
Next Document:  Measuring FMD in the brachial artery: how important is QRS gating?