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Contents lists available at ScienceDirect

Journal of Science and Medicine in Sport

journa l h om epage: www.elsev ier .com/ locate / j sams

riginal research

rterial stiffness results from eccentrically biased downhill runningxercise

.F. Burr ∗, M. Boulter, K. Beckpplied Human Science, Human Performance and Health Research Laboratory, University of PEI, Canada

a r t i c l e i n f o

rticle history:eceived 18 January 2014eceived in revised form 18 February 2014ccepted 1 March 2014vailable online xxx

eywords:rterial complianceulse wave velocityarathon

ndurancenflammation

a b s t r a c t

There is increasing evidence that select forms of exercise are associated with vascular changes that arein opposition to the well-accepted beneficial effects of moderate intensity aerobic exercise.Objectives: To determine if alterations in arterial stiffness occur following eccentrically accentuated aer-obic exercise, and if changes are associated with measures of muscle soreness.Design: Repeated measures experimental cohort.Methods: Twelve (m = 8/f = 4) moderately trained (VO2max = 52.2 ± 7.4 ml kg−1 min−1) participants per-formed a downhill run at −12◦ grade using a speed that elicited 60% VO2max for 40 min. Cardiovascularand muscle soreness measures were collected at baseline and up to 72 h post-running.Results: Muscle soreness peaked at 48 h (p = <0.001). Arterial stiffness similarly peaked at 48 h (p = 0.04)and remained significantly elevated above baseline through 72 h.Conclusions: Eccentrically accentuated downhill running is associated with arterial stiffening in the

OMS absence of an extremely prolonged duration or fast pace. The timing of alterations coincides with thewell-documented inflammatory response that occurs from the muscular insult of downhill running, butwhether the observed changes are a result of either systemic or local inflammation is yet unclear. Thesefindings may help to explain evidence of arterial stiffening in long-term runners and following prolongedduration races wherein cumulative eccentric loading is high.

© 2014 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.

. Introduction

The health benefits of participation in regular aerobic exercisere well established.1 Amongst the cardiovascular benefits ofegular moderate intensity exercise is the reduction of arterialtiffness, which is associated with a reduced risk for cardiovascularisease and ischaemic events owing to decreased atherosclerosis,n improvement of coronary artery perfusion,2 and a lowering ofoth pulse pressure and wall stress.2,3 Given the clear relationshipo future morbidity and mortality, arterial stiffness is now rec-gnized as an important independent predictor of cardiovascularisk.4 Despite the known beneficial cardiovascular effects of habit-al moderate intensity aerobic exercise, high-volume resistanceraining has been shown to elicit transient arterial stiffening5 andong-term participants manifest these changes persistently such

Please cite this article in press as: Burr JF, et al. Arterial stiffness resulSport (2014), http://dx.doi.org/10.1016/j.jsams.2014.03.003

hat their resting levels substantially differ from controls who arenly recreationally active;6 however, this area remains a contro-ersial area and results are mixed.7,8 Counter intuitively, recent

∗ Corresponding author.E-mail address: jburr@upei.ca (J.F. Burr).

ttp://dx.doi.org/10.1016/j.jsams.2014.03.003440-2440/© 2014 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserve

evidence examining the arterial properties and cardiovascularhealth of long distance runners has similarly demonstrated higherthan expected baseline arterial stiffness compared to recreationallyactive controls9,10 and there is conflicting evidence as to whetheror not participation in a long-distance race itself causes arterialstiffness.9,11,12 From our own published and unpublished observa-tions, our laboratory has noted that substantial post-race arterialstiffening occurred only in races that were of prolonged duration(>24 h baseline to follow-up) and which involved heightenedphysical stresses including a higher exercise intensity or substan-tial terrain challenges, such as the traversing of mountains.11,12 Assuch, we posit that the observed effect on arterial stiffening maybe related to exercise induced muscle damage and inflammation,which typically requires 24–48 h to manifest13 and is enhancedby eccentric muscle contractions, which occur repeatedly duringrunning – particularly while descending hills. This theory fitswith existing evidence showing that long distance running causeshigh levels of oxidative stress and inflammation.13 In fact, recent

ts from eccentrically biased downhill running exercise. J Sci Med

strength training literature shows that eccentric training resultsin notable arterial stiffening from baseline and is associated withmeasures of muscle damage and inflammation whether usingsmall or large muscle mass.14 Using experimentally induced

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nflammation Vlachopoulos et al.15 have convincingly demon-trated a cause-and-effect relationship of systemic inflammationith arterial stiffening, however, some difference in the progress

f the inflammatory cascade may occur depending on whethernflammation is systemically induced or stimulated by exercise.16

Treadmill-based downhill running has long been establisheds a valid and reliable method to induce delayed onset muscleoreness and inflammation,17,18 particularly when the exposurexceeds an amount normally encountered by the participants. Aownhill running exercise model allows investigation of the effectsf the eccentric muscle contractions associated with running in thebsence of extreme aerobic exercise intensity or duration. The pur-ose of the present investigation was thus to determine the rolef eccentric muscle contractions during aerobically based exerciseor affecting changes in arterial stiffness. Furthermore, we soughto investigate the temporal course of alterations from baseline toetermine the time of onset, duration of the effect, and the asso-iation of changes in arterial stiffness with measures of muscleoreness. We hypothesized that even moderate intensity eccen-rically biased running would result in significant muscle soreness,nd associated arterial stiffening within twenty-four to forty-eightours.

. Methods

A mixed sex population of recreationally active subjects (n = 13, = 9, f = 4) were recruited from the university community. Inclu-

ion criteria indicated good general health, free from injury orregnancy, not currently or previously engaging in eccentric exer-ise training, and no history of smoking, alcohol dependence,iagnosed heart disease, peripheral vascular disease, diabetes,ancer, pulmonary disease, orthopaedic conditions or use of med-cation. Participants were 25 ± 6 years of age, had a mean systolicressure of 115 ± 9, diastolic pressure of 75 ± 5, were 175 ± 8 cmall, and weighed 74.6 ± 16 kg. VO2max was 52.2 ± 7.4 ml kg min−1

male 55.6, female 45.4). All participants provided written informedonsent and this study was approved by the institutional Researchthics Board for investigations involving human participants.

Participants visited the laboratory for baseline testing either 3r 4 days prior to the downhill running test. All baseline testingommenced on either Thursday or Friday morning, with exper-mental procedures taking place the following week. During thetudy period, participants were requested to abstain from exer-ise, and NSAID use was prohibited. Baseline measures includinglood pressure, carotid-femoral pulse wave velocity (PWV), radialrtery augmentation index (AIx), and both subjective and objectiveuscle pain were recorded at each time point. Participants were

iven a period of no less than 2 full days recovery following theO2max test, prior to the commencement of the downhill running

ntervention. Fig. 1 graphically illustrates the procedural timingf all measurements. With the exception of the 6 h follow-up, alleasures were taken at the same time each morning to control for

iurnal variation. Participants were instructed to eat a light break-ast 2 h prior to arrival, and to standardize their morning meal fromaseline through the last day of follow-up.

Following the assessment of baseline muscle pain and the car-iovascular measures described to follow, aerobic fitness testingas performed using a mechanically driven treadmill with analy-

is of expired gases. The fitness test commenced at a fast walkingpeed (4 mph) and progressed 0.45 ms−1 (1 mph) and 2% grade untilhe participant reached his or her maximal safe running speed, after

Please cite this article in press as: Burr JF, et al. Arterial stiffness resulSport (2014), http://dx.doi.org/10.1016/j.jsams.2014.03.003

hich only the incline was progressed. Breath-by-breath metaboliceasurements were performed using a Cosmed Quark CPET system

Cosmed, Rome, Italy) and were averaged over 30 s for analy-is. Metabolic testing required an average of 11.7 ± 1.2 min. The

PRESSdicine in Sport xxx (2014) xxx–xxx

test was terminated when participants reached volitional fatigue(RPE = 19 or 20) and had an RER greater than 1.15. Attainment ofa true VO2max was verified by a plateau in oxygen consumption(increase < 150 ml min−1) with an increase in workload. All partic-ipants reached a true max according to these criteria.

Blood pressure was measured using a standard sphygmo-manometer at the brachial artery of the left arm while theparticipant was seated with his or her arm supported on a table atthe level of the heart. Prior to the measurement of blood pressure,participants sat quietly for a period of 10 min to ensure accurateresting values. All measurements were taken in a quiet temperatureand humidity controlled laboratory.

Subjective muscle pain was recorded using a 10 cm visual ana-logue scale wherein the participant marked the line correspondingto their rating of leg pain in daily life since the last assessment.Participants were instructed to make a mark on the line with thefar left indicating “no discomfort at all” and the far right being “themost extreme muscular pain you have experienced”. This scale wasquantified by measuring the distance to the nearest 0.1 cm fromthe left edge of the scale to the participant’s mark. These meth-ods have been previously used and validated.19 Objective leg painwas quantified using a push-pressure strain gauge dynamometer(Fabrication Enterprises, White Plains, NY) with a cylindrical 1 cm2

flat contact head applied to the mid muscle belly (measured fromthe superior patella to the anterior inferior iliac crest) of the vastuslateralis, immediately anterior to the iliotibial band. Participantswere instructed to look away from the dynamometer and ver-bally indicate when the progressively applied pressure first becameuncomfortable. Push-pressure muscle pain measures have beenshown to be highly reproducible, and have been recommended forexperimentally induced alterations in muscle pain sensitivity.20

Carotid to femoral PWV was measured with participants in thesupine position. Using an electrocardiogram, pressure waves weregated to systolic contraction and were collected consecutively fromthe carotid then femoral artery. Signal capture at each site wasperformed manually once a sufficient quality signal was obtained.Pulse wave arrival was determined using the intersecting tangentmethod to detect the foot of each wave. For velocity calculations,distance was measured with a standard anthropometric tape usinga straight line above the body from the carotid to femoral sites,with an adjustment for the distance from the carotid site to thesuprasternal notch. Pulse wave velocity of the descending aorta wasour primary outcome variable to estimate arterial stiffness as PWVis recognized as the gold standard measure and is less affected bythe physiological alterations known to occur in conjunction with about of exercise compared to other common estimation methods.25

Resting AIx was calculated from pulse waves collected at theright radial artery using a high fidelity Millar strain gauge trans-ducer (Millar instruments, Houston, TX). Participants sat quietlywith the right forearm resting on a table and the wrist supported inslight hyperextension. Signal quality was controlled using the auto-capture feature of the Sphygmocor CPVH software (Atcor Medical,Sydney, Australia) and the operator index was recorded at 93 ± 5%for all captures. AIx measures standardized to a heart rate of 75 bpmwere employed for analysis to reduce the tachycardic effect of thedownhill run on post-run measures. Augmentation index is a mea-sure of the reflected waves within the arterial tree extending downto the radial artery level, and although this can offer some insightinto stiffness properties and the work of the myocardium, reflectedwaves can be affected by changes in other exercise related cardio-vascular factors, such as cardiac time intervals. As such, AIx wasincluded only as a secondary measure.

ts from eccentrically biased downhill running exercise. J Sci Med

The downhill run was performed using the same treadmill as theVO2max test set to a decline of −12◦ with a specifically constructedelevation device placed under the rear of the belt platform. Partici-pants ran at a speed eliciting 60% VO2max (pace range 1.9–3.2 m/s)

ARTICLE IN PRESSG ModelJSAMS-1008; No. of Pages 6

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ig. 1. Procedural timing of baseline testing, preparation, intervention and follow-uerobic power test, PWV = carotid to femoral pulse wave velocity, AIx = augmentatio

or 40 min while exercise intensity was monitored continuouslyith heart rate telemetry and periodic (approx. every 5 min) meas-res of expired gases. Participants were instructed against using theandrails of the treadmill while running so as not to affect the workequired of the legs. All follow-up measures succeeding the runnd at each follow-up visit were repeated using the methodologyeported above.

Temporal changes in muscle soreness, arterial stiffness (AIx,WV) and related cardiovascular indices were analyzed usingepeated measures 1 × 5 (baseline, post-run, 24 h, 48 h, 72 h)NOVA. To maintain adequate statistical power (>80%) no fur-

her division by age or gender was attempted. Both deviation andimple contrasts were used post hoc to compare to the immedi-tely preceding measure and the baseline, respectively. Possiblessociations between arterial stiffness and muscle soreness werexamined using Pearson correlation of both raw measures andhange scores from baseline. Analyses were performed using SPSSVersion 20.0), with significance for all tests set a priori at P ≤ 0.05.esults are reported as mean ± SD.

. Results

One participant was unable to complete the full 40 min durationf the run due to leg fatigue and was excluded from follow-upeasures. No other participants dropped-out nor did any adverse

vents occur during the intervention or follow-up. Included par-icipants reported regular participation in physical activity andemonstrated moderate to high levels of aerobic fitness (range1.3–66.1 ml kg−1 min−1). Table 1 presents cardiovascular, arterial,nd muscle soreness data at each measurement point. Baselineeasures of PWV and AIx confirmed that participants had mean

rterial stiffness measures that were comparable to expectedge and sex matched norms.21 Both systolic and diastolic bloodressure were within a normal range at baseline and revealedo significant deviation at any measurement point. Mean heartate remained elevated 15 min following the run (13 ± 12 bpm),

Please cite this article in press as: Burr JF, et al. Arterial stiffness resulSport (2014), http://dx.doi.org/10.1016/j.jsams.2014.03.003

ut heart rate was not different from baseline at any othereasurement. Muscle soreness varied throughout the trial for

oth the analogue and tolerable pressure measures (p = <0.001).ig. 2a presents delayed tolerable pressure muscle soreness, with

ccentrically biased downhill running study. BP = blood pressure, VO2max = maximalex of radial artery normalized to a pulse of 75 beats per minute.

the analogue scale measurements imposed on a secondary axis.Graphical presentation of this data illustrates the similarity of theshape of these curves, and it is noted that the two measures hadstatistically consistent changes in the reported muscle soreness atsuccessive time points.

Pulse wave velocity revealed a significant increase in arterialstiffness following the downhill running intervention (p = 0.04)which was first evident at 48 h post-run and remained elevated atthe final measurement 72 h later (Fig. 2b). A significant relationshipbetween the level of muscle soreness, or a change in muscle sore-ness, and changes in arterial stiffness was not evident at any timepoint; however, after removal of one significant non-respondingoutlier (circled in Fig. 2c) changes in PWV and changes in perceivedmuscle soreness were correlated r = 0.65, p = 0.03. No changes frombaseline were observed in AIx at any time point.

4. Discussion

The major novel finding of the present investigation was thatarterial stiffening, evidenced by an increase in carotid-femoralPWV, occurred approximately 48 h following a bout of downhillrunning. This is the first study to show this effect using an eccentri-cally biased aerobic exercise stimulus and we are unaware of otherinvestigations which have considered the temporal effect of an aer-obic exercise bout over a similar period of follow-up. Despite themodest duration and moderate aerobic intensity employed (com-pared to the typical intensity/duration of a typical running race),the work of downhill running represents a formidable muscularchallenge, and this stimulus is well known to cause significant mus-cular insult.17,18 Our hypothesis that eccentrically biased downhillrunning would precede arterial stiffening was supported, whichraises interesting questions about the potential long-term role ofrepeated or unaccustomed eccentric muscle loading for affectingarterial stiffness and health.

As expected, downhill running led to substantial increases inparticipant’s perception of muscle soreness, with a slight increase

ts from eccentrically biased downhill running exercise. J Sci Med

in pain immediately subsequent to the downhill run, followed bya more pronounced change at 24 h and peaking at 48 h of recov-ery. Changes in PWV similarly occurred between the 24 and 48 hmeasurements suggesting a possible relationship between these

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Table 1Cardiovascular indices, arterial stiffness measures, and muscle soreness associated with eccentrically biased aerobic exercise. Measures are reported at baseline, 15 min aftera 40 min downhill run and six, twenty-four, forty-eight and seventy-two hours post-run.

Measure Time point

Rest Post-run 6 h 24 h 48 h 72 h

Heart rate (bpm) 61 ± 7 77 ± 8 **,b 68 ± 12 63 ± 8 * 63 ± 8 63 ± 9Brachial systolic pressure (mmHg) 118 ± 10 114 ± 9 117 ± 8 118 ± 8 116 ± 10 117 ± 10Brachial diastolic pressure (mmHg) 76 ± 4 77 ± 3 77 ± 5 75 ± 4 74 ± 3 74 ± 4Mean arterial pressure (mmHg) 87.9 ± 4.8 88.3 ± 3.3 89.2 ± 3.5 88.1 ± 3.2 86.6 ± 3.9 86.4 ± 3.4Soreness pressure (kg) 3.8 ± 0.6 3.3 ± 0.7*,a 3.3 ± 0.9a 2.8 ± 1 *,b 2.6 ± 1 *,b 2.9 ± 1.2a

Soreness analogue scale (cm) 0.5 ± 0.6 2.9 ± 2.7 * 3.4 ± 2 **,b 6.1 ± 2.3 **,b 7.2 ± 2.4 **,b 4.5 ± 2.3b

Augmentation index @75 bpm −2 ± 3.2 −0.7 ± 2.6 −1.1 ± 3 −1.5 ± 2.9 −0.8 ± 3.2 −1.8 ± 3.1Pulse wave velocity (m/s) 5.1 ± 0.6 5.3 ± 0.6 5.3 ± 0.6 5.4 ± 0.7 5.6 ± 0.9 *,b 5.5 ± 0.5 b

* Different from previous, p < 0.05.** Different from previous, p < 0.001.a Different from baseline, p < 0.05.b Different from baseline, p < 0.001.

Fig. 2. (a, top left) Muscle soreness resulting from eccentrically biased downhill running. The primary axis (left-solid line) displays the pressure (kg) participants couldwithstand being pressed against the muscle belly of the vastus lateralis before notable discomfort. The secondary axis (right-dashed line) displays the participant’s subjectiverating of discomfort using a 10 cm visual analogue scale. Variability data and p values are only presented for the primary axis for clarity, but both revealed similar patterns. (b,top right) Carotid to femoral pulse wave velocity (PWV) at baseline, 15 min following a 40 min downhill run, and after six, twenty four, forty-eight and seventy-two hours ofr post rS nges

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ecovery. It can be seen that PWV was significantly increased at twenty-four hours

D. (c, bottom) Scatterplot of changes in muscle soreness (analogue scale) and chahen circled non-responder outlier data point is removed (r = 0.65, p = 0.03).

hysiological processes; however, this association was only sup-orted after removal of one apparent outlying response.

It has previously been shown that both inflammation andrterial stiffening independently occur in runners followingigh-intensity prolonged exercise, such as the marathon,9,22

nd moderate-intensity extreme duration, such as the ultra-arathon.11,23 In the present investigation, using a downhill

unning exercise model that promotes muscular insult withoutreat emphasis on the aerobic intensity or duration of exercise,

Please cite this article in press as: Burr JF, et al. Arterial stiffness resulSport (2014), http://dx.doi.org/10.1016/j.jsams.2014.03.003

hanges in arterial stiffness occurred in line with the expected tim-ng of a systemic inflammatory response. We did not specificallyrack plasma markers of oxidative stress and inflammation, how-ver, this well-accepted association offers a potential mechanism

un and did not return to baseline levels by seventy-two hours. Error bars representin PWV from baseline to 48 h peak. Non-significant relationship (r = 0.52, p = 0.08),

for the observed response. An alternative hypothesis to a systemicalteration is that localized inflammation led to swelling in the legsand associated alterations in the transmural pressure and perfusionof resistance vessels. With a decreased peripheral flow, upstreamflow could also be affected, thus decreasing shear stress and flowmediated dilatation in the proximal vascular tree. If such is thecase, it would be likely that changes in vascular resistance wouldbe associated with alterations in the arterial muscle tone of con-ductance vessels. Such a change in the lower extremities affecting

ts from eccentrically biased downhill running exercise. J Sci Med

upstream flow could also help to partially explain the differen-tial effect of PWV collected using carotid-femoral arteries versusAIx, which estimates purely from the radial artery and would beless affected by localized changes in the legs. These physiological

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athways offer possible explanations for the observed effect, butemain speculative at present.

Irrespective of the underlying mechanistic causes of arterialtiffening, the finding that an increased emphasis on the eccentricomponent of running preceded delayed onset arterial stiffenings noteworthy and contributes to our understanding of the humanascular response to exercise. The magnitude of arterial stiffen-ng in the present investigation was of modest clinical significance0.5 m/s), but must be interpreted in context. An increase in PWV of

m/s has been demonstrated to increase the risk of a cardiovascu-ar event by 15%.4 The observed increase of 0.5 m/s, although onlyalf of this value, notably occurred after only a 40 min runs thatas moderately taxing to the cardiovascular system, yet imposedigh muscular stress. This exercise duration and intensity wereelected because they offered a reasonable (but not overly intimi-ating) eccentric exercise challenge and approximated establishedrotocols known to be effective for producing DOMS. Although theurrent work was undeniably challenging, it is very possible thathe eccentric loading during a prolonged running event such ashe marathon or ultra-marathon (lasting >2–40 h) could still beignificantly higher, and post-race muscle soreness is a commonymptom for participants.

Recent reports have demonstrated additional cardiac specificffects of running including a strong association between the num-er of marathons or ultra-marathons completed and myocardialbrosis24 in long-term runners, which may also be related to arte-ial stiffness. With a better understanding of the interplay of thearious facets of exercise (frequency, intensity, duration, type) it isossible that potential cardiovascular risk could thus be better con-rolled through appropriate training cycles, particularly in light ofvidence showing that the negative effects of high volume resis-ance training on arterial stiffening can be negated through these of moderate intensity aerobic exercise before (but not after)eightlifting.25 Consideration of the timing between workouts and

he specific use (or avoidance) and timing of hill-workouts may alsorove important, but at present there is insufficient evidence onhich to base recommendations for athletes to alter their trainingractices.

There are some limitations to this study, which should be rec-gnized and significant areas for future direction. It is important toote that the downhill running stimulus was intentionally unfa-iliar to the participants, who were not specifically endurance

thletes and did not regularly run downhill. As such, the noveltyf the exercise stimulus itself may have contributed to the physio-ogical response and thus the dose–response remains uncertain. Atresent, it is unknown if this effect would occur to a similar extentnce participants were habituated to downhill running workouts,r if a period of adaptation would blunt this effect, but this is aorthy area of future investigation. It is also unknown if succes-

ive bout of moderate intensity exercise (downhill or otherwise)ould diminish this effect, or add to it in a stepwise cumulative

ashion, as has been shown for repeated bouts of sprint exercise.26

t this preliminary stage of investigation we are unable to deter-ine a precise mechanistic cause to explains why downhill running

s associated with changes in arterial stiffness (i.e. local or systemicactors), and thus extrapolation and generalization of these findings

ust be done with caution. Furthermore, the specific persistencef this effect still remains somewhat unclear, as the 72 h measure-ent remained significantly above baseline following the increase

t 48 h, despite indications that it was starting to decrease. In theresent investigation, changes were only observed in measures ofWV but not augmentation index, which matches previously pub-

Please cite this article in press as: Burr JF, et al. Arterial stiffness resulSport (2014), http://dx.doi.org/10.1016/j.jsams.2014.03.003

ished data following marathon participation9 and may well beelated to measurement methodology.27 In both of these investi-ations carotid-femoral PWV (i.e. the descending aorta) has beenmployed for central measures of arterial stiffness, but further

PRESSdicine in Sport xxx (2014) xxx–xxx 5

insight into vascular changes might be gained by including meas-ures of peripheral vasculature (i.e. femoral to dorsal pedis andcarotid to radial) and endothelial function in future work.

5. Conclusion

When exposed to an eccentrically accentuated aerobic exercisestimulus for 40 min, moderately trained participants demonstratedsignificant increases in arterial stiffness following 48 h of rest.Although a similar temporal pattern of increases were observedin measures of muscle soreness, a direct relationship betweenarterial stiffening and delayed onset muscle soreness was notapparent. Given the temporal relationship of changes, the knowneffect of downhill running to elicit an inflammatory response, andthe demonstrated relationship between inflammation and arterialstiffening it seems likely that inflammation (or inflammatory medi-ated alterations) plays a mechanistic role in the observed changes,whether systemically or locally.

It is essential to note that the present results should not beinterpreted to suggest that aerobic exercise is necessarily bad forcardiovascular health. In fact, there is a considerable body of per-suasive evidence that suggests otherwise. In the present study theexercise stimulus employed was considerably beyond that whichwould normally be encountered during health-related physicalactivity or without purposeful effort and design, and as such repre-sents the more extreme end of the exercise spectrum. The authorssuggest that the results of this study should be interpreted as moreevidence of an inverted U shaped hypothesis of physical activity,with overextending exercise leading to cardiovascular responsesthat are in opposition to the generally accepted beneficial effectsof the more moderate exercise that is recommended in most phys-ical activity guidelines. Although the present data demonstratesacute changes in arterial compliance, which may possibly con-tribute to more long-term alterations in vascular stiffness, the fullimplications of this finding for health or performance remain to beelucidated, and it is possible that the observed effects are withinthe natural process of adaptation.

Practical implications

• Eccentrically biased aerobic exercise is associated with a delayedarterial stiffness similar to eccentric strength training

• Muscle soreness and arterial stiffening peak at approximately48 h post-exercise

• It is premature to suggest that training practices be altered ashealth/performance implications are yet unclear

Acknowledgements

The authors have no financial support or competing interests todeclare.

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