Wingate test (WT) training programmes lasting 2-3weeks lead to improved peak oxygen consumption. If a single 30s WT was capable of significantly increasing stroke volume and cardiac output, the increase in peak oxygen consumption could possibly be explained by improved oxygen delivery. Thus, we investigated whether a single WT increases stroke volume and cardiac output to similar levels than those obtained at peak exercise during a graded cycling exercise test (GXT) to exhaustion. Fifteen healthy young men (peak oxygen consumption 45.0±5.3mlkg−1min−1) performed one WT and one GXT on separate days in randomised order. During the tests, we estimated cardiac output using inert gas rebreathing (nitrous oxide and sulphur hexafluoride) and subsequently calculated stroke volume. We found that cardiac output was similar (18.2±3.3 vs. 17.9±2.6lmin−1; P=0.744), stroke volume was higher (127±37 vs. 94±15ml; P<0.001), and heart rate was lower (149±26 vs. 190±12 beatsmin−1; P<0.001) at the end (27±2s) of a WT as compared to peak exercise during a GXT. Our results suggest that a single WT produces a haemodynamic response which is characterised by similar cardiac output, higher stroke volume and lower heart rate as compared to peak exercise during a GX

Betschon, Katharina

Boutellier, Urs

Fontana, Piero

Toigo, Marco

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SHORT COMMUNICATIONCardiac output but not stroke volume is similar in a Wingateand _VO2peak test in young menPiero Fontana • Katharina Betschon •Urs Boutellier • Marco ToigoAccepted: 31 August 2010 / Published online: 17 September 2010 Springer-Verlag 2010Abstract Wingate test (WT) training programmes lasting2–3 weeks lead to improved peak oxygen consumption. If asingle 30 s WT was capable of significantly increasingstroke volume and cardiac output, the increase in peakoxygen consumption could possibly be explained byimproved oxygen delivery. Thus, we investigated whether asingle WT increases stroke volume and cardiac output tosimilar levels than those obtained at peak exercise during agraded cycling exercise test (GXT) to exhaustion. Fifteenhealthy young men (peak oxygen consumption 45.0 ±5.3 ml kg-1 min-1) performed one WT and one GXT onseparate days in randomised order. During the tests, weestimated cardiac output using inert gas rebreathing (nitrousoxide and sulphur hexafluoride) and subsequently calcu-lated stroke volume. We found that cardiac output wassimilar (18.2 ± 3.3 vs. 17.9 ± 2.6 l min-1; P = 0.744),stroke volume was higher (127 ± 37 vs. 94 ± 15 ml;P \ 0.001), and heart rate was lower (149 ± 26 vs.190 ± 12 beats min-1; P \ 0.001) at the end (27 ± 2 s) ofa WT as compared to peak exercise during a GXT. Ourresults suggest that a single WT produces a haemodynamicresponse which is characterised by similar cardiac output,higher stroke volume and lower heart rate as compared topeak exercise during a GXT.Keywords Cardiac output  Stroke volume  Wingatetest  Sprint interval training  High-intensity intervaltrainingIntroductionSprint interval training (SIT) is a novel type of high-intensity interval training consisting of 4–6 repeated all-out30 s Wingate tests (WTs) separated by 4 min recovery. Ithas been demonstrated that 2–3 weeks (3 training sessionsper week) of SIT increases peak oxygen consumption(Burgomaster et al. 2008; Hazell et al. 2010). However, theunderlying adaptations in oxygen delivery and extractionpossibly mediating the increase in peak oxygen consump-tion following SIT are not yet clear.Peak oxygen consumption is bounded by the parametriclimits of the Fick equation (oxygen consumption = cardiacoutput 9 arterio-venous oxygen difference) (Fick 1870). Ifthe increase in peak oxygen consumption after SIT wasmediated by an increase in peak cardiac output, it should beexpected that a single WT is capable of increasing cardiacoutput to near-maximal values. In fact, high-intensity aer-obic training (HIT) is more effective in mediating increasesin cardiac output and stroke volume than continuoustraining at a power corresponding to lactate threshold(Daussin et al. 2007; Helgerud et al. 2007). HIT is char-acterised by 4–5 blocks of short (1–4 min) training inter-vals at a power output corresponding to, e.g. 90–100%peak power attained during a GXT, separated by 3–4 minCommunicated by Keith George.P. Fontana  K. Betschon  U. Boutellier  M. Toigo (&)Exercise Physiology,Institute of Human Movement Sciences,ETH Zurich, Winterthurerstrasse 190,8057 Zurich, Switzerlande-mail: marco.toigo@biol.ethz.chP. Fontana  M. Toigoexersciences gmbh, Zurich, SwitzerlandU. Boutellier  M. ToigoInstitute of Physiology and Zurich Centerfor Integrative Human Physiology (ZIHP),University of Zurich, Zurich, Switzerland123Eur J Appl Physiol (2011) 111:155–158DOI 10.1007/s00421-010-1645-xat a power corresponding to 50–60% peak GXT power.Daussin et al. (2007) concluded that the near-maximalcardiac output attained during HIT mediates the observedlong-term adaptations in peak cardiac output and strokevolume which, in turn, underlay the observed increase inpeak oxygen consumption after several weeks of HIT.One study compared cardiac output and stroke volumebetween a GXT and a WT by means of echocardiographicmeasurements (Sagiv et al. 2000). It was concluded thatstroke volume is increased only with GXT, and that theincrease of cardiac output is significantly less for WT thanfor GXT. This conclusion implies that a WT cannot pro-vide a sufficiently high stimulus for triggering cardio-circulatory adaptation, and consequently that the observedincrease in peak oxygen consumption after a WT trainingprogramme (Burgomaster et al. 2008; Hazell et al. 2010)cannot originate from an increase in peak stroke volumeand cardiac output. As echocardiographic measurementsare not feasible when the upper body is moving, the par-ticipants’ backs had to be strapped to the wall in the studyof Sagiv et al. (2000). As an obvious consequence, theparticipants could not generate as much power as during areal WT with freely moving upper body. In this study, wethus wanted to re-investigate the cardiac output responseduring WT using an inert gas (nitrous oxide and sulphurhexafluoride) rebreathing technique, which does notrestrict the participants’ position (and thus exercisecapacity).MethodsParticipantsFifteen male participants of age 26.7 ± 5.6 years, height1.81 ± 0.05 m, body mass 73.6 ± 7.0 kg and peak oxygenconsumption 45.0 ± 5.3 ml kg-1 min-1 volunteered toparticipate in this study. All participants were healthy andnon-smoking. In order to avoid fatigue-related effects onthe test outcomes, we allowed no strenuous physicalactivity for 48 h prior to the measurements. We informedthe participants about all procedures involved and about theassociated risks. Subsequently, participants completed aroutine health questionnaire and gave their writteninformed consent. The experimental protocol was approvedby the ethics committee of the ETH Zurich and was per-formed in accordance with the ethical standards laid downin the Declaration of Helsinki for human experimentation.Study design and experimental setupEach participant performed one GXT on a cycle ergometer(Ergoselect 200 K, Ergoline, Bitz, Germany) and one WT(Ergomedic 894E Peak Bike, Monark, Vansbro, Sweden).The two tests were separated by at least 48 h and wereperformed in a randomised order. Each participant per-formed the two tests at the same daytime. During GXT andWT, cardiac output and stroke volume were estimated byinert gas rebreathing (InnocorTM, Innovision, Odense,Denmark). In addition, heart rate was continuously recor-ded (S610i, Polar Electro, Kempele, Finland). Before thetests, we informed the participants about the upcomingprocedures and they practiced the rebreathing techniquewith ambient air (Fontana et al. 2009). No additionalfamiliarisation trials were performed prior to GXT and WT.Prior to the start of the GXT, participants rested for2 min on the cycle ergometer. Subsequently, they startedpedalling at 100 W using a self-selected pedalling rate[70–90 revolutions per minute (rpm)], which was heldconstant (±5 rpm) throughout the test. Power wasincreased by 30 W for every 2 min until participantsstopped cycling or were unable to maintain pedalling ratewithin the given limits for more than 5 s (mean GXTduration 12.4 ± 2.5 min). We previously used the sameincremental protocol to show that test–retest reliability ofcardiac output and stroke volume during a GXT is high(Fontana et al. 2009). Furthermore, we demonstrated that at46 and 103 s after a power stage transition (54–69, 69–77and 77–85% peak power) both cardiac output and strokevolume are similar (Fontana et al. 2010), indicating thatless than 46 s are needed to reach a steady state for cardiacoutput and stroke volume. For WT, participants startedunloaded pedalling as fast as possible. As soon as theyreached 130 rpm, the computer interfaced with the testbike automatically loaded the ergometer with 7.5% of theparticipant’s body weight (Burgomaster et al. 2005). Par-ticipants were verbally encouraged to continue to pedal asfast as possible.Estimation of cardiac outputThe rebreathing manoeuvres during GXT were performedin accordance with our previously published protocol(Fontana et al. 2009). We manually set the rebreathingparameters to 3 l rebreathing volume and 10% bolus vol-ume (volume of gas mixture, consisting of nitrous oxide,sulphur hexafluoride and oxygen). During the rebreathingmanoeuvres, participants continued to spontaneouslybreathe, as their breathing frequency was already highenough while cycling. Breathing frequency was monitoredonline by the examinator and participants were given ver-bal feedback to maintain a constant breathing frequency.All participants cycled until the software of the InnocorTMindicated the end of the rebreathing. For WT, the exactpoint in time (averaged over all participants) of the firstbreath, which we used for fitting the regression line156 Eur J Appl Physiol (2011) 111:155–158123(calculation of cardiac output, represented by complete gasmixing), was 27 ± 2 s (range 24–32 s) after the beginningof the sprint bout (after loading). Given that the rebreathinglasted *3 s, a WT lasted 27–35 s. Using the end tidalnitrous oxide concentrations of at least two breaths, cardiacoutput could be estimated in all study participants duringthe final phase of WT, as well as at peak GXT. Thecoefficient of variation (CV) over repeated preliminarymeasurements of cardiac output during the final phase of aWT for the investigator was 8%. This is in agreement withvalues obtained for a GXT (95% confidence interval:5.5–9%, Fontana et al. 2009).CalculationsGXTWe calculated stroke volume at peak exercise by dividingcardiac output by the heart rate measured during therebreathing (10 s average), corresponding to the highest10 s average throughout the GXT (i.e. peak heart rate).WTWT stroke volume during the WT was obtained by divid-ing cardiac output by heart rate. Here, we used a 5 insteadof a 10 s mean because of the shorter test duration. Thecorresponding heart rate measurement started as soon asthe valve to the rebreathing bag opened during cardiacoutput determination.Statistical analysisStatistical analyses were performed with SPSS software(version 16.0, SPSS, Chicago, IL, USA). Normality ofln-transformed data was ascertained by Q–Q plots. Forcomparisons of cardiac output, stroke volume and heartrate between GXT and the WT, we used Student’s pairedt test. Results are presented as mean ± standard deviation.Statistical significance was set at P \ 0.05.ResultsCardiac output at (or immediately before) the end of WTand GXT was similar (Table 1). Furthermore, strokevolume was higher (34 ± 31%), whereas heart rate(-22 ± 12%) was lower at the end of WT compared toGXT. Power (460 ± 54 vs. 286 ± 38 W; P \ 0.001) andpedalling rate (89 ± 9 vs. 77 ± 5 rpm; P = 0.002) duringWT rebreathings were significantly higher than duringGXT rebreathings.DiscussionIn the present study, we found that cardiac output is similarat the end of WT compared to the point in time of voli-tional exhaustion during GXT in healthy young men. Incontrary to cardiac output, stroke volume was significantlyhigher and heart rate was significantly lower for WT thanGXT. Our results contrast with the data of Sagiv et al.(2000), who found that both cardiac output and strokevolume were significantly higher for GXT than WT. Weascribe the divergent results to the unnatural (i.e. fixedupper body) WT condition used by Sagiv et al. (2000).Having shown that a single WT is capable of increasingcardiac output to maximal levels, we have provided novel,scientific insight into the mechanistic bases possiblyunderlying the increase in peak oxygen consumption whichis observed after 2–3 weeks of WT training programmes(Burgomaster et al. 2008; Hazell et al. 2010). In fact, ourresults suggest that the observed increase in peak oxygenconsumption after a WT training programme (Burgomasteret al. 2008; Hazell et al. 2010) might originate from anincrease in peak cardiac output.There are a few considerations pertinent to the estimationof cardiac output that are warranted. First, the absorption ofnitrous oxide by the blood, and hence the calculation ofpulmonary blood flow (equal to cardiac output when there isno pulmonary shunt flow), can be affected not only byventilation inhomogeneity but also by flow inhomogeneity.If breathing frequency during the rebreathing manoeuvres isnot constant, the slope of the regression line through end-tidal gas concentrations could yield a wrong estimate ofcardiac output. Only in 5 out of 30 rebreathing manoeuvresparticipants could not maintain a constant breathing fre-quency. For those rebreathings, we manually moved theregression line to 2–3 breaths with a stable pulmonary bloodflow to correctly estimate cardiac output.Second, pulmonary blood flow equals cardiac outputonly if there is no significant pulmonary shunt flow.Eldridge et al. (2004) showed that arterio-venous intra-pulmonary shunts develop at about 59% peak oxygenconsumption and persist at all subsequent power stages.Table 1 Cardiac output, stroke volume and heart rate in 15 younghealthy men at the end of a Wingate test (WT), as well as at the pointin time of volitional exhaustion during a graded cycling exercise test(GXT)Wingatetest (WT)Graded cyclingexercise test (GXT)PCardiac output (l min-1) 18.2 ± 3.3 17.9 ± 2.6 0.744Stroke volume (ml) 127 ± 37 94 ± 15 \0.001Heart rate (beats min-1) 149 ± 26 190 ± 12 \0.001Eur J Appl Physiol (2011) 111:155–158 157123Thus, in both exercise modalities, arterio-venous intrapul-monary shunts may have developed. Assuming for eachparticipant a blood haemoglobin concentration of15 g dl-1 and considering the respective arterial oxygensaturations (data not shown), we found that during a GXT,the estimated arterio-venous intrapulmonary shunt fractiontended to be higher (6.0 ± 2.7%) than during a WT(1.9 ± 2.7%). However, even when considering thesepossible differences in estimated arterio-venous intrapul-monary shunt flow, our findings presented in Table 1 donot significantly change.Finally, we want to address the issue that maximalstroke volume might have been underestimated during theGXT. It appears that during a GXT with constant powerincrements, stroke volume reaches maximal values alreadyat 64% peak power and remains at this level untilexhaustion (Calbet et al. 2007; Fontana et al. 2010). Incontrast, for GXT protocols with varying power incrementsit has been shown that stroke volume is maximal at 80%and subsequently decreases to reach a significantly lowervalue at exhaustion (Mortensen et al. 2005). Besides dif-ferences in exercise protocols, levels of exertion, exercisemode, sex, age and training status also might lead to dif-ferent responses in stroke volume. Given the fact that weused a GXT with constant power increments and that theparticipants’ sex, age as well as training status was similarin the study by Calbet et al. (2007), we believe that wereport (near-)maximal values for stroke volume in thepresent study.We conclude that a single, unrestricted WT produces ahaemodynamic response which is characterised by similarcardiac output, higher stroke volume and lower heart ratecompared to peak exercise during a GXT in young men.Conflict of interest None.ReferencesBurgomaster KA, Hughes SC, Heigenhauser GJ, Bradwell SN, GibalaMJ (2005) Six sessions of sprint interval training increasesmuscle oxidative potential and cycle endurance capacity inhumans. J Appl Physiol 98:1985–1990Burgomaster KA, Howarth KR, Phillips SM, Rakobowchuk M,Macdonald MJ, McGee SL, Gibala MJ (2008) Similar metabolicadaptations during exercise after low volume sprint interval andtraditional endurance training in humans. J Physiol (Lond)586:151–160Calbet JA, Gonza´lez-Alonso J, Helge JW, Sondergaard H, Munch-Andersen T, Boushel R, Saltin B (2007) Cardiac output and legand arm blood flow during incremental exercise to exhaustion onthe cycle ergometer. J Appl Physiol 103:969–978Daussin FN, Ponsot E, Dufour SP, Lonsdorfer-Wolf E, Doutreleau S,Geny B, Piquard F, Richard R (2007) Improvement of VO2max bycardiac output and oxygen extraction adaptation during inter-mittent versus continuous endurance training. Eur J Appl Physiol101:377–383Eldridge MW, Dempsey JA, Haverkamp HC, Lovering AT, Hokan-son JS (2004) Exercise-induced intrapulmonary arteriovenousshunting in healthy humans. J Appl Physiol 97:797–805Fick A (1870) U¨ber die Messung des Blutquantums in denHerzventrikeln. Sitzung Phys med Gesell Wu¨rzburg 14:16Fontana P, Boutellier U, Toigo M (2009) Reliability of measurementswith InnocorTMduring exercise. Int J Sports Med 30:747–753Fontana P, Boutellier U, Toigo M (2010) Non-invasive haemody-namic assessments using InnocorTMduring standard gradedexercise tests. Eur J Appl Physiol 108:573–580Hazell TJ, MacPherson REK, Gravelle BMR, Lemon PWR (2010) 10or 30-s sprint interval training bouts enhance both aerobic andanaerobic performance. Eur J Appl Physiol. doi:10.1007/s00421-010-1474-yHelgerud J, Høydal K, Wang E, Karlsen T, Berg P, Bjerkaas M,Simonsen T, Helgesen C, Hjorth N, Bach R, Hoff J (2007)Aerobic high-intensity intervals improve VO2max more thanmoderate training. Med Sci Sports Exerc 39:665–671Mortensen SP, Dawson EA, Yoshiga CC, Dalsgaard MK, DamsgaardR, Secher NH, Gonzalez-Alonso J (2005) Limitations tosystemic and locomotor limb muscle oxygen delivery anduptake during maximal exercise in humans. J Physiol (Lond)566:273–285Sagiv M, Ben-Sira D, Goldhammer E, Soudry M (2000) Leftventricular contractility and function at peak aerobic andanaerobic exercises. Med Sci Sports Exerc 32:1197–1201158 Eur J Appl Physiol (2011) 111:155–158123

Cardiac output but not stroke volume is similar in a Wingate and $$ \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} $$ test in young men

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Cardiac output but not stroke volume is similar in a Wingate and $\dot{V}{\text{O}}_{{ 2 {\text{peak}}}}$ test in young men

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Cardiac output but not stroke volume is similar in a Wingate and V˙O2peak \dot{V}{\text{O}}_{{ 2 {\text{peak}}}} V˙O2peak​ test in young men

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Cardiac output but not stroke volume is similar in a Wingate and $\dot{V}{\text{O}}_{{ 2 {\text{peak}}}}$ test in young men