Arterial stiffening following eccentric exercise-induced muscle damage

Barnes, Jill N.; Trombold, Justin R.; Dhindsa, Mandeep; Lin, Hsin-Fu; Tanaka, Hirofumi

doi:10.1152/japplphysiol.00548.2010

Cited by 77 publications

(78 citation statements)

References 59 publications

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“…38 The subacute effects may persist upward of 2 weeks following exercise, 36 and exercise-induced muscle damage/inflammation is associated with subacute increases in arterial stiffness. 39 In conclusion, akin to what has been postulated with cardiac maladaptation, it is proposed herein that repetitive, sustained elevations of cardiac output for several hours in predisposed individuals causes fatigue fracture of elastin fibers and stimulates resident macrophages, pericytes, and fibroblasts, resulting in the deposition of collagen and vascular fibrosis, and an increase in arterial stiffness. This, coupled with bradycardia-induced augmented pressure from wave reflections and load-dependent increases in forward wave pressure, will increase pressure pulsatility, contributing to downstream endothelial damage, target organ damage (ie, LV hypertrophy and atrial enlargement), coronary ischemia, atrial fibrillation, and possible SCD.…”

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confidence: 74%

How Healthy Were the Arteries of Phidippides?

Heffernan

2011

Clinical Cardiology

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Subacute and chronic cardiac adaptations to marathon running may increase risk for sudden death. Herein, it is proposed that cardiac arrhythmogenic remodeling resulting from prolonged strenuous exertion may also have a systemic vascular component. Marathon running reduces coronary perfusion pressure and causes acute endothelial damage, possibly via altering concentrations of circulating angiogenic growth factors with novel vasoregulatory properties. Marathon runners have increased arterial stiffness and augmented pressure from wave reflections contributing to a widening of pulse pressure. Pulsatile hemodynamics may contribute to target organ damage. Moreover, each of these vascular maladaptations (increased arterial stiffness, augmented pressure from wave reflections, and widened pulse pressure) has been associated with atrial fibrillation and may provide a substrate for lethal arrhythmogenesis in the marathon runner. Clin. Cardiol. 2012 DOI: 10.1002/clc.21009The author has no funding, financial relationships, or conflicts of interest to disclose.This article ﬁrst published online 28 November 2011. It has since changed. The term “coronary pulse pressure” has been changed to “coronary perfusion pressure.”

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confidence: 74%

How Healthy Were the Arteries of Phidippides?

Heffernan

2011

Clinical Cardiology

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“…Previous studies have documented changes in arterial stiffness following both acute and chronic interventions, and acute changes have been detected in response to many stimuli other than diving or immersion [57,58,59,60,61]. Acute aerobic exercise (rowing) caused stiffness to decrease [62], and acute sprint interval exercise caused increased compliance but no change in brachial artery stiffness [63].…”

Section: Discussionmentioning

confidence: 99%

The Impact of Repetitive Long-duration Water Immersion on Vascular Function

Simmons

Bergeron

Florian

2017

Medicine &Amp; Science in Sports &Amp; Exercise

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While physiological responses to water immersion (WI) are well-studied, the vascular responses after WI are less understood. Fifteen male subjects performed six-hour resting thermoneutral water immersions (WI) at 1.35 atmospheres absolute for four consecutive days, with follow-up on the fifth day. Measurements included peripheral endothelial function and augmentation index (PAT, peripheral arterial tonometry), beat-to-beat blood pressure (BP, photoplethysmography), heart rate (HR), and plasma volume (PV) calculated from changes in hemoglobin and hematocrit. The reactive hyperemia index (RHI), a marker of peripheral endothelial function, increased with repeated immersions (p = 0.008). By WI2 and WI3, RHI increased 12% and 16%, respectively, compared to WI1 values, but no significant differences were detected between WI4 and WI1 for either measure. Absolute augmentation index (AI) increased by an average of 33% (p<0.001) and AI normalized for HR (AI@75) by 11% (p = 0.12) following each WI. PV decreased significantly by 13.2% following WI and remained 6.8% lower at follow-up compared to pre-WI. Systolic blood pressure significantly decreased by an average of 2.5% following each WI (p = 0.012). Compared to pre-WI HR, average post-WI HR decreased 4.3% lower (p<0.001), but increased overall by 8.2% over the course of repeated WI (p<0.001). Total peripheral resistance increased by an average of 13.1% following WI (p = 0.003). Thus, peripheral endothelial function increases after two days of WI, and PAT-derived measures of arterial stiffness increase transiently post-WI. Additionally, BP and PAT-derived endothelial function diverge from their usual associations with arterial stiffness (i.e. augmentation index) in the context of WI.

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“…Hence, the observed differences in exercise-induced changes in CK activity and cytokine levels resulted from differences in absolute WL and the related mechanical stress/muscle damage. Other contributing factors might be the relative inefficiency of the muscle pump during ECC exercise as compared to that during CONC exercise [7], and ECC exercise-associated temporary impairment of local microvascular [18] and macrovascular function, in particular arterial stiffness [2], as well as reduced vasodilator response [15]. Hence, it is possible that, despite identical relative VO 2 values, oxygen delivery to the working muscles differed between the two types of exercise, which might have affected the extent of muscle damage and responses to the latter.…”

Section: Discussionmentioning

confidence: 99%

Effects of Downhill and Uphill Exercises of Equivalent Submaximal Intensities on Selected Blood Cytokine Levels and Blood Creatine Kinase Activity

Pokora¹,

Kempa²,

Chrapusta³

et al. 2014

Biol Sport

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The study was aimed at comparing the effects of concentric (CONC) and eccentric (ECC) exercises of equivalent (in terms of relative work load expressed as a percentage of VO2max) moderate intensity on selected blood cytokine levels and blood creatine kinase (CK) activity. Twenty recreationally active healthy young male volunteers were randomized between two groups that performed a single 1 h bout of CONC (uphill running) or ECC (downhill running) exercise at 60% of the respective individual VO2max. Venous blood taken 1 h before, at the end, and 24 h after the exercise was processed for plasma and analyzed for CK activity and IL-6, IL-1β and TNFα levels. There was no between-group difference in these cytokines prior to or just after the exercise, and in pre-exercise CK activity. The cytokines elevated significantly and similarly in both groups during the exercise, with no significant change in CK activity. Twenty-four hours later, CK activity and IL-6 were at pre-exercise levels in the CONC group, but showed further major increases in the ECC group, resulting in marked between-group differences in these indices. Changes in IL-1β and TNFα levels during the recovery period showed only minor differences between the study groups and produced no significant between-group difference in these cytokines. However, IL-1β level normalized in the ECC but not in the CONC group. The study suggests that moderate intensity ECC exercise compared to CONC exercise of equivalent relative work load results in considerably greater muscle damage and its related elevation in circulating IL-6, but it does not cause a major systemic inflammatory response.

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Arterial stiffening following eccentric exercise-induced muscle damage

Abstract: Arterial stiffening following eccentric exercise-induced muscle damage.

Cited by 77 publications

References 59 publications

How Healthy Were the Arteries of Phidippides?

How Healthy Were the Arteries of Phidippides?

The Impact of Repetitive Long-duration Water Immersion on Vascular Function

Effects of Downhill and Uphill Exercises of Equivalent Submaximal Intensities on Selected Blood Cytokine Levels and Blood Creatine Kinase Activity

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