title: Arterial stiffening following eccentric exercise-induced muscle damage.
abstract: 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.
authors.affiliation: Cardiovascular Aging Research Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin, Austin, Texas, USA. Barnes.Jill@mayo.edu
authors.forename: Jill N
authors.initials: JN
authors.lastname: Barnes
authors.forename: Justin R
authors.initials: JR
authors.lastname: Trombold
authors.forename: Mandeep
authors.initials: M
authors.lastname: Dhindsa
authors.forename: Hsin-Fu
authors.initials: HF
authors.lastname: Lin
authors.forename: Hirofumi
authors.initials: H
authors.lastname: Tanaka
mesh_terms: D000293:Adolescent; D000328:Adult; D001158:Arteries / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity; D002097:C-Reactive Protein / Q000378:metabolism; D002339:Carotid Arteries / Q000503:physiopathology; D003402:Creatine Kinase / Q000097:blood; D018592:Cross-Over Studies; D004548:Elasticity; D015444:Exercise; D005263:Femoral Artery / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007537:Isometric Contraction; D008297:Male; D053580:Muscle Strength; D018482:Muscle, Skeletal / Q000201:enzymology / Q000503:physiopathology*; D009135:Muscular Diseases / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D010146:Pain / Q000209:etiology / Q000503:physiopathology; D011673:Pulsatile Flow; D013997:Time Factors; D055815:Young Adult
chemical_list: D015415:Biomarkers; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D002097:C-Reactive Protein; D003402:Creatine Kinase