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Respiratory Physiology & Neurobiology 192 (2014) 102–111 Contents lists available at ScienceDirect Respiratory Physiology & Neurobiology j our na l ho me pa g e: www.elsevier.com/locate/resphysiol Influence of duty cycle on the power-duration relationship: Observations and potential mechanisms R.M. Broxterman a,b,, C.J. Ade a,b , S.L. Wilcox a , S.J. Schlup a , J.C. Craig a , T.J. Barstow a a Department of Kinesiology, Kansas State University, Manhattan, KS, USA b Department of Anatomy and Physiology, Kansas State University, Manhattan, KS, USA a r t i c l e i n f o Article history: Accepted 28 November 2013 Keywords: Critical power exercise tolerance muscle blood flow muscle contraction a b s t r a c t The highest sustainable rate of aerobic metabolism [critical power (CP)] and the finite amount of work that can be performed above CP (W’ [curvature constant]) were determined under two muscle con- traction duty cycles. Eight men completed at least three constant-power handgrip tests to exhaustion to determine CP and W’ for 50% and 20% duty cycles, while brachial artery blood flow ( ˙ Q BA ) and deoxygenated-[hemoglobin + myoglobin] (deoxy-[Hb + Mb]) were measured. CP was lower for the 50% duty cycle (3.9 ± 0.9 W) than the 20% duty cycle (5.1 ± 0.8 W; p < 0.001), while W’ was not significantly different (50% duty cycle: 452 ± 141 J vs. 20% duty cycle: 432 ± 130 J; p > 0.05). At the same power out- put, ˙ Q BA and deoxy-[Hb + Mb] achieved higher end-exercise values for the 20% duty cycle (9.87 ± 1.73 ml·s 1 ; 51.7 ± 4.7 M) than the 50% duty cycle (7.37 ± 1.76 ml·s 1 , p < 0.001; 44.3 ± 2.4 M, p < 0.03). These findings indicate that blood flow influences CP, but not W’. © 2013 Elsevier B.V. All rights reserved. 1. Introduction The notion of an increase in exercise duration with progres- sively decreasing power outputs dates back at least to the early twentieth century (Hill, 1925, 1927) and potentially as early as the fourth century (Whipp et al., 1996; Whipp et al., 1998). This robust power-duration relationship is now commonly characterized using a hyperbolic mathematical model to obtain the asymptote (criti- cal power, CP) and the curvature constant (W’) (Hill, 1993; Jones et al., 2010; Whipp et al., 1982). CP demarcates the boundary between the heavy- and severe-exercise intensity domains, as it is the highest intensity in which a physiological steady-state can be achieved (i.e., for oxygen uptake ( ˙ V O 2 ) (Poole et al., 1988); blood flow (Copp et al., 2010); intramuscular concentrations of phos- phocreatine [PCr], inorganic phosphate [Pi], and hydrogen ion [H + ] (Jones et al., 2008)). W’ represents a finite work capacity that can be performed above CP and has traditionally been associated with ‘anaerobic’ metabolism (Coats et al., 2003; Ferguson et al., 2007; Fukuba et al., 2003; Miura et al., 1999; Miura et al., 2000; Monod and Scherrer, 1965). This interpretation is supported by [Pi], [H + ], and [PCr] consistently achieving ‘critical levels’ upon exhaustion (Chidnok et al., 2013; Jones et al., 2008; Poole et al., 1988; Vanhatalo et al., 2010). Alternatively, W’ may be determined by the magni- tude of the severe-domain (i.e., the range between CP and ˙ V O 2 max ) (Burnley and Jones, 2007; Vanhatalo et al., 2010) and has been Corresponding author. Tel.: +785 532 5114; fax: +785 532 6486. E-mail address: [email protected] (R.M. Broxterman). associated with the ˙ V O 2 slow component (Ferguson et al., 2007; Jones et al., 2003; Murgatroyd et al., 2011; Vanhatalo et al., 2011). This interpretation is supported by several studies that demon- strated a decrease in W’ with interventions that increased CP (Jenkins and Quigley, 1992; Vanhatalo et al., 2008; Vanhatalo et al., 2010). It has been speculated that these decreases in W’ were a result of the interventions increasing CP disproportionately to ˙ V O 2 max and therefore decreasing the magnitude of the severe- domain (Burnley and Jones, 2007; Vanhatalo et al., 2010). Although the mechanism(s) determining W’ are not fully understood, it is clear that exercise tolerance for any activity performed at an inten- sity above CP is limited by the magnitude of W’ with exhaustion ensuing upon complete utilization of W’ if the power output is not reduced to an intensity equal to or below CP. Monod and Scherrer (1965), in originally characterizing the power-duration relationship, suggested that CP is dependent upon the circulatory conditions in the muscle, while W’ is determined by intramuscular ‘anaerobic’ (with the exception of O 2 stores) mecha- nisms. Subsequent experiments have revealed that CP is dependent upon the rate of aerobic ATP production (i.e., O 2 delivery and O 2 uti- lization) (Dekerle et al., 2012; Hill, 1993; Jones et al., 2010; Moritani et al., 1981; Vanhatalo et al., 2010), while W’ (at least in part) is dependent upon ‘anaerobic’ ATP production (Heubert et al., 2005; Jenkins and Quigley, 1993; Miura et al., 1999; Miura et al., 2000; Smith et al., 1998). Thus, any intervention altering O 2 delivery (i.e., reduced blood flow) to the active skeletal muscle would be expected to alter CP, with presumably no (or little) affect on W’. The increased intramuscular pressure accompanying muscle contraction can exhibit a profound influence on blood flow as a 1569-9048/$ see front matter © 2013 Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/j.resp.2013.11.010

Influence of duty cycle on the power-duration relationship: Observations and potential mechanisms

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  • Respiratory Physiology & Neurobiology 192 (2014) 102 111

    Contents lists available at ScienceDirect

    Respiratory Physiology & Neurobiology

    j our na l ho me pa g e: www.elsev ier .com/

    Inuen reObserv

    R.M. Bro J.C. a Department ob Department o

    a r t i c l

    Article history:Accepted 28 N

    Keywords:Critical powerexercise toleramuscle blood muscle contra

    ic me [curletedd 20bin] (

    duty vs. 2ed hi

    dutyw in

    1. Introdu

    The notion of an increase in exercise duration with progres-sively decreasing power outputs dates back at least to the earlytwentieth century (Hill, 1925, 1927) and potentially as early as thefourth centpower-duraa hyperbolical power, et al., 2010between ththe highestachieved (iow (Coppphocreatine(Jones et albe performanaerobic Fukuba et aand Scherreand [PCr] c(Chidnok etet al., 2010tude of the (Burnley an

    CorresponE-mail add

    ted 2Jones et al., 2003; Murgatroyd et al., 2011; Vanhatalo et al., 2011).This interpretation is supported by several studies that demon-strated a decrease in W with interventions that increased CP(Jenkins and Quigley, 1992; Vanhatalo et al., 2008; Vanhatalo et al.,

    1569-9048/$ http://dx.doi.oury (Whipp et al., 1996; Whipp et al., 1998). This robusttion relationship is now commonly characterized usingc mathematical model to obtain the asymptote (criti-CP) and the curvature constant (W) (Hill, 1993; Jones; Whipp et al., 1982). CP demarcates the boundarye heavy- and severe-exercise intensity domains, as it is

    intensity in which a physiological steady-state can be.e., for oxygen uptake (VO2) (Poole et al., 1988); blood

    et al., 2010); intramuscular concentrations of phos- [PCr], inorganic phosphate [Pi], and hydrogen ion [H+]., 2008)). W represents a nite work capacity that caned above CP and has traditionally been associated withmetabolism (Coats et al., 2003; Ferguson et al., 2007;l., 2003; Miura et al., 1999; Miura et al., 2000; Monodr, 1965). This interpretation is supported by [Pi], [H+],onsistently achieving critical levels upon exhaustion

    al., 2013; Jones et al., 2008; Poole et al., 1988; Vanhatalo). Alternatively, W may be determined by the magni-severe-domain (i.e., the range between CP and VO2 max )d Jones, 2007; Vanhatalo et al., 2010) and has been

    ding author. Tel.: +785 532 5114; fax: +785 532 6486.ress: [email protected] (R.M. Broxterman).

    2010). It has been speculated that these decreases in W werea result of the interventions increasing CP disproportionately toVO2 max and therefore decreasing the magnitude of the severe-domain (Burnley and Jones, 2007; Vanhatalo et al., 2010). Althoughthe mechanism(s) determining W are not fully understood, it isclear that exercise tolerance for any activity performed at an inten-sity above CP is limited by the magnitude of W with exhaustionensuing upon complete utilization of W if the power output is notreduced to an intensity equal to or below CP.

    Monod and Scherrer (1965), in originally characterizing thepower-duration relationship, suggested that CP is dependent uponthe circulatory conditions in the muscle, while W is determined byintramuscular anaerobic (with the exception of O2 stores) mecha-nisms. Subsequent experiments have revealed that CP is dependentupon the rate of aerobic ATP production (i.e., O2 delivery and O2 uti-lization) (Dekerle et al., 2012; Hill, 1993; Jones et al., 2010; Moritaniet al., 1981; Vanhatalo et al., 2010), while W (at least in part) isdependent upon anaerobic ATP production (Heubert et al., 2005;Jenkins and Quigley, 1993; Miura et al., 1999; Miura et al., 2000;Smith et al., 1998). Thus, any intervention altering O2 delivery(i.e., reduced blood ow) to the active skeletal muscle would beexpected to alter CP, with presumably no (or little) affect on W.

    The increased intramuscular pressure accompanying musclecontraction can exhibit a profound inuence on blood ow as a

    see front matter 2013 Elsevier B.V. All rights reserved.rg/10.1016/j.resp.2013.11.010ce of duty cycle on the power-durationations and potential mechanisms

    xtermana,b,, C.J. Adea,b, S.L. Wilcoxa, S.J. Schlupa, f Kinesiology, Kansas State University, Manhattan, KS, USAf Anatomy and Physiology, Kansas State University, Manhattan, KS, USA

    e i n f o

    ovember 2013

    nceowction

    a b s t r a c t

    The highest sustainable rate of aerobthat can be performed above CP (Wtraction duty cycles. Eight men compto determine CP and W for 50% andeoxygenated-[hemoglobin + myogloduty cycle (3.9 0.9 W) than the 20%different (50% duty cycle: 452 141 Jput, QBA and deoxy-[Hb + Mb] achievmls1; 51.7 4.7 M) than the 50%These ndings indicate that blood o

    ction associalocate / resphys io l

    lationship:

    Craiga, T.J. Barstowa

    tabolism [critical power (CP)] and the nite amount of workvature constant]) were determined under two muscle con-

    at least three constant-power handgrip tests to exhaustion% duty cycles, while brachial artery blood ow (QBA) anddeoxy-[Hb + Mb]) were measured. CP was lower for the 50%

    cycle (5.1 0.8 W; p < 0.001), while W was not signicantly0% duty cycle: 432 130 J; p > 0.05). At the same power out-gher end-exercise values for the 20% duty cycle (9.87 1.73

    cycle (7.37 1.76 mls1, p < 0.001; 44.3 2.4 M, p < 0.03).uences CP, but not W.

    2013 Elsevier B.V. All rights reserved.

    with the VO slow component (Ferguson et al., 2007;

  • R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111 103

    result of blood vessel compression, increased impedance to bloodow, and possible occlusion of blood ow (Hoelting et al., 2001;Lutjemeier et al., 2005; Robergs et al., 1997; Sadamoto et al., 1983).The muscle contraction-relaxation cycle yields rhythmic alter-ations in inthe majoritwhen intramFolkow et aRobergs et ow may bstate metabtension/totathat with hto total concle becomewhile bloodtime underincreased cRadegran, 2demonstratences blood

    To the bthat have eto the musthe power-study was tcycles in orow. We hycycle than tfurther, whcycles, 2) bthe 50% dutgraphy) mefor both du

    2. Method

    2.1. Subject

    Eight heweight: 77Subjects rewith at leasfrom vigoroproceduresReview Boadards set fosubject wastial risks inconsent and

    2.2. Experim

    All testinter. The hacylinder bylinear displthe pneumaing the airPower outpin Watts (Wis contractiversion of ksubject grasmately hear

    . Displacement proles for the 50% and 20% duty cycles. Schematic rep-ion of the specic contraction components for each duty cycle (Panel A). They cycle consisted of a 0.6 s concentric contraction period, a 0.3 s isometricn period, a 0.6 s eccentric contraction period, and a 1.5 s relaxation period.

    duty cycle consisted of a 0.6 s concentric contraction period and a 2.4 sn period. A displacement prole for a representative subject throughout aion cycle for each duty cycle is shown in Panel B.

    ncy of 20 contractionsmin1 was utilized for both dutyso that each total contraction cycle duration was main-

    at 3.0 s. Thus any set resistance would produce the same output for both duty cycles. The 50% duty cycle consisted5 s contraction period (in which the handrail was raisedoncentric muscle contraction and lowered with eccentric

    contraction) followed by a 1.5 s relaxation period. Thety cycle consisted of a 0.6 s contraction period (in whichndrail was raised with concentric muscle contraction andmediately released) followed by a 2.4 s relaxation period

    1). Both duty cycles had the same duration of concen-ntraction and total contraction cycle, while the 20% dutyad no eccentric contraction period and therefore a longern of time without muscle tension. The eccentric contrac-eriod duration was altered specically to minimize anyolic differences between duty cycles, while emphasizingow differences (see Discussion). Audio recordings set withcic timing for each duty cycle were used along with feed-rovided by an investigator monitoring the tests to ensuret timing. Subjects completed three familiarization trialsty cycle prior to data collection to aid in correct, consis-roduction of the contraction-relaxation timing. All testingtramuscular pressure, and therefore blood ow, withy of blood ow occurring during the relaxation perioduscular pressure is low (Barcroft and Dornhorst, 1949;

    l., 1970; Robergs et al., 1997; Walloe and Wesche, 1988).al. (1997) suggesting that the relaxation period bloode important in determining the attainment of a steady-olic rate. The muscle contraction duty cycle (time underl contraction time) directly impacts blood ow, suchigh duty cycles (longer time under tension relativetraction time) blood ow to the active skeletal mus-s limited (Bellemare et al., 1983; Buchler et al., 1985),

    ow is not compromised at low duty cycles (shorter tension relative to total contraction time) even withontraction frequencies (Ferreira et al., 2006; Osada and002; Sjogaard et al., 2002). Collectively, these resultse that the muscle contraction duty cycle directly inu-

    ow to the active skeletal muscle.est of our knowledge there are no reports till datexamined the inuence of alterations in blood ow duecle contraction-relaxation cycle on the parameters ofduration relationship. Therefore, the aim of the currento manipulate blood ow using muscle contraction dutyder to assess the dependence of CP and W on bloodpothesized that: 1) CP would be higher for the 20% dutyhe 50% duty cycle, while W would remain unchanged,en the same power output was repeated at both dutylood ow would be higher for the 20% duty cycle thany cycle, but, 3) deoxy-[Hb + Mb] and EMG (electromyo-asurements would achieve similar end-exercise valuesty cycles.

    s

    s

    althy men (age: 24.8 2.5 years, height: 173.7 4.6 cm;.1 14.6 kg) volunteered to participate in this study.ported to the Human Exercise Physiology Laboratoryt 24 h between testing sessions and having abstainedus activity within that 24 h period. All experimental

    in the present study were approved by the Institutionalrd of Kansas State University and conformed to the stan-rth by the Declaration of Helsinki. Prior to testing, each

    informed of the overall protocol along with the poten-volved. Each subject then provided written informed

    completed a health history evaluation.

    ental Protocol

    g was performed on a custom-built handgrip ergome-ndrail of the ergometer was attached to a pneumatic

    means of a cable-pulley system and provided a xedacement of 4 cm. Resistance was set by pressurizingtic cylinder and work was accomplished by compress-

    within the cylinder when the handrail was moved.ut was calculated as P = Rdf k1, where P is power), R is resistance in kg, d is displacement in meters, f

    on frequency, and k is the constant 6.12 for the con-gmmin1 to W. When seated at the ergometer theped the handrail so that the forearms were at approxi-t level and the elbows were slightly bent. A contraction

    Figure 1resentat50% duttransitioThe 20%relaxatiocontract

    frequecycles tainedpowerof a 1.with cmuscle20% duthe hathen im(Figuretric cocycle hduratiotion pmetabblood the speback pcorrecper dutent p

  • 104 R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111

    sessions were continued until exhaustion, determined as the inabil-ity to complete three consecutive contraction cycles.

    A peak incremental test for each duty cycle was completed ina randomized order during the initial two testing sessions. Thesetests were i0.5 Wminas the highwas comploutputs forwould eliciminimum ocycle in whiinitial threeparameter hIf the goodnAnalysis) a lower the pelicited exhrepeated fophysiologicwithout themetabolic r

    2.3. Measur

    2.3.1. DoppThe raw

    ultrasound operating inwith a phasing frequenall testing sbrachial artity measurewas adjuste25 cm abobrachial artimage, suggleast 1 cm fratory (Adein the trans

    2.4. Near-in

    The oxycialis were NIRS (Near-paign, IL, technologyviously beeconsists of lengths of 6detector b2.0, 2.5, 3.0and stored supercialisprobe was The positioreproduciblcalibrated pommendatiand scatteriblock with

    2.5. Electromyography

    Surface electromyography (EMG) measurements were obtainedfrom the exor digitorum supercialis in the left forearm. The single

    ntialonsisrient, as the his sient amp

    ata A

    Deter parere dPCPes (Jom tolic nt-poas greappli

    of eestim

    of ere w

    opple

    an bled mbloossel easu

    ulatesingnd 9

    utilime w% dulso m

    IRS

    NIRestin

    the 3 cot mixercoxy-insenFerraably 19942006roviygene c[Hb +eas

    NIRSnitiated at 1.0 W and the power output was increased by1 until exhaustion. The peak power (Ppeak) was recordedest power output for which at least 30 s of the stageeted. The Ppeak was utilized to determine the power

    the subsequent constant-power testing sessions thatt exhaustion between 215 min. Subjects completed af three randomly ordered constant-power tests per dutych the time-to-exhaustion (Tlim) was recorded. After the

    constant-power tests, the data were t with the two-yperbolic model and the goodness-of-t was analyzed.ess-of-t data did not meet the a priori criteria (see Datafourth testing session was conducted in an attempt toarameter standard error values. A power output thataustion between 25 min for the 50% duty cycle wasr the 20% duty cycle, such that any differences in theal responses between duty cycles could be examined

    confounding inuence of different power outputs (i.e.,ates).

    ements

    ler ultrasound blood velocity proles were measured using Doppler(Vivid 3, GE Medical Systems, Milwaukee, WI, USA)

    pulse wave mode at a Doppler frequency of 4.0 MHzed linear array transducer probe operating at an imag-cy of 6.7 MHz, and were stored for post-hoc analysis. Foressions the Doppler gate was set to the full width of theery to ensure complete isonation and all Doppler veloc-ments were corrected for the angle of isonation, whichd to be less than 60 degrees. Measurements were madeve the antecubital fossa to avoid the bifurcation of theery. A bifurcation was not seen in the two-dimensionalesting that all Doppler measurements were made atrom the bifurcation, as previously utilized in our labo-

    et al., 2012). Brachial artery diameters were measuredverse axis using two-dimensional sonography.

    frared spectroscopy

    genation characteristics of the exor digitorum super-determined using a frequency-domain multi-distanceinfrared spectroscopy) system (Oxiplex TS, ISS, Cham-USA). The principles and algorithms of the NIRS

    were reviewed by Gratton et al. (1997) and have pre-n described by Ferreira et al. (2006). Briey, this deviceeight light-emitting diodes (LED) operating at wave-90 and 830 nm (four LEDs per wavelength) with oneer bundle and LED-detector separation distances of, and 3.5 cm. The NIRS data were collected at 50 Hzfor post-hoc analysis. After locating the exor digitorum

    of the right arm using EMG and palpation, the NIRSsecured longitudinally along the belly of the muscle.n of the probe was then marked with indelible ink fore placement throughout the study. The NIRS probe wasrior to each test according to the manufacturers rec-ons using a calibration block with known absorptionng coefcients. Calibration was conrmed on a separatedifferent absorption and scattering coefcients.

    differeUSA) c2 2 omusclewhen tion. Tplacemwere s

    2.6. D

    2.6.1. The

    W) wt = W/(in Jouldata frhyperbconsta(SE) wWhen marginrately margintherefo

    2.7. D

    Meaveragartery and vewere mto calclyzed u46.5, as) werealent tthe 50were a

    2.8. N

    Theeach t91.5 swhile sequens posteThe detively 1993; to reliet al., et al., study pand oxmay b(total-were mof the EMG electrode (Trigno EMG, Delsys Inc., Boston, MA,ts of four silver contact bars (5 1 mm) arranged in aation. The electrode was positioned over the belly of thedetermined by palpation and strong electrical activityngers were exed, but not with ulnar or radial devia-te was then marked with indelible ink for reproducibleof the electrode throughout the study. The EMG dataled at 1000 Hz and stored for post-hoc analysis.

    nalysis

    mination of the power-duration relationshipameters of the power-duration relationship (CP andetermined with the two-parameter hyperbolic model), where t is time in s, W is the nite work capacity), P is power in W, and CP is critical power in W. Thehe initial three constant-power tests were t with themodel and the goodness-of-t was assessed. A fourthwer test was conducted if the parameter standard errorater than 10% of the parameter value for either CP or W.ed to whole-body exercise (i.e., cycling) this acceptablerror allows for the anaerobic work capacity to be accu-ated by W (Hill, 1993). There has been no establishedrror for small muscle mass exercise (i.e., handgrip) ande chose to use the 10% cut-off.

    r Ultrasound

    ood velocity (Vmean; cms1) was dened as the time-ean velocity over each 3 s contraction cycle. Brachiald ow (QBA) was calculated using the product of Vmeancross-sectional area (CSA). Brachial artery diametersred every minute throughout each test and were used

    vessel CSA in cm2 (CSA = r2). The QBA data were ana- one contraction cycle (i.e., 3 s) at the time points of 0,1.5 s, while three consecutive contraction cycles (i.e., 9ized at the end of each subsequent minute, at the equiv-ithin the 20% duty cycle to the time of end-exercise for

    ty cycle (matched-time), and at end-exercise. QBA dataeasured 9 s postexercise using a 3 s average.

    S data were processed using 3 s averages throughoutg session. During the rst minute of exercise and atNIRS data were analyzed for each contraction cycle,nsecutive contraction cycles were used for each sub-nute, at 50% matched-time, and at end-exercise. At 9ise the NIRS data were analyzed using a 3 s average.[hemoglobin + myoglobin] (deoxy-[Hb + Mb]) is rela-sitive to changes in blood-volume (De Blasi et al.,ri et al., 1997; Grassi et al., 2003) and has been usedestimate the fractional oxygen extraction (De Blasi; DeLorey et al., 2003; Ferrari et al., 1997; Ferreira; Grassi et al., 2003). The device used in the presentdes absolute concentrations (M) for deoxy-[Hb + Mb]ated-[hemoglobin + myoglobin] (oxy-[Hb + Mb]), whichombined to provide total-[hemoglobin + myoglobin]

    Mb]). The dynamic reduced scattering coefcientsured throughout the tests and were incorporated in all

    data calculations.

  • R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111 105

    2.9. EMG

    The raw EMG data were processed with a band-pass lter(30300 Hz) and each electrical burst corresponding to a musclecontractiongram. The Eintegrated Emotorneurofatigues (Ensignal freququency (MPvelocity, whfatigues (H91.5 s the Ewhich the eend-exerciscycles.

    2.10. Estim

    To invesextraction aner and colintegrates pvenous O2 cO2 capacitywhere DO2is the partiaPmitO2 is thdria). The infor those cbetween duusing this mheld constathat any diferences inthat the deoare aware tBarstow, 20muscle (i.e.these assummated VO2 .tissue, wheunits can besion 1.36% 400 cap/mmtortuosity aThese units1 mole O2/msion 22.4 Oby multiplydeoxy-[Hb +were t wiprovide the

    2.11. Statis

    Ppeak, CPt-tests. MaiiEMG, and Mmeasures (dpower testsdetected, awere considare present

    . A representative subjects power-duration relationship for the twoles. Two-parameter hyperbolic ts to the 50% duty cycle (solid line) and

    duty cycle (dashed line) data are shown. The asymptote of each modelts critical power (CP) and the curvature constant represents W.

    . Brachial artery blood ow responses for the two duty cycles at thesolute power output. Mean and standard error exercise brachial arteryw (QBA) data (Panel A), and end-exercise and 9 s postexercise (Panel B) forand 20% duty cycles. signicantly different from the 50% duty cycle end-, p < 0.001. signicantly different from the 50% end-exercise time, p < 0.001.antly different from 20% duty cycle at 91.5 s, p < 0.001. was detected using a custom-designed computer pro-MG signal amplitude characteristics were analyzed viaMG (iEMG), a measure of motor unit recruitment andn ring rate, which typically increases as the muscleoka and Stuart, 1992; Fulco et al., 1996). The EMGency characteristics were analyzed via mean power fre-F), a measure of the muscle action potential conductionich typically shifts to lower frequencies as the muscle

    agg, 1992). During the rst minute of exercise and atMG data were analyzed for each contraction cycle, afternd of each subsequent minute, 50% matched-time, ande were analyzed using three consecutive contraction

    ation of oxygen consumption

    tigate the relationship between O2 delivery and O2cross duty cycles we used the model put forth by Wag-leagues (Roca et al., 1992; Wagner, 1996, 2011), whicherfusive O2 delivery (Fick Principle, VO2 max = Q (arterial-ontent difference), where Q is blood ow) and diffusive

    (Ficks Law of Diffusion, VO2 = DO2(PcapO2 PmitO2),is the oxygen diffusing capacity of the muscle, PcapO2l pressure of oxygen within the microcirculation, ande partial pressure of oxygen within the mitochon-tersection of these two relationships yields the VO2peakonditions. The mechanisms for the discrepancy in CPty cycles in the current study can be further exploredodel under a few assumptions. The assumptions werent between duty cycles to reduce systematic error, sofferences in the model would be attributable to dif-

    the deoxy-[Hb + Mb] and QBA values. It was assumedxy-[Hb + Mb] signal reects only deoxy-[Hb] [n.b., wehat the signal contains deoxy-[Mb] as well (Davis and13)] and that the entire signal arises solely from the, not from any intervening adipose or skin tissue). Withptions the deoxy-[Hb] may be converted into an esti-

    The deoxy-[Hb] values are in units of mole heme/lre the tissue is assumed to be muscle. These deoxy-[Hb]

    converted into mole heme/ blood using the conver-capillary blood volume/muscle volume (derived from2, 28.3 m2 CSA, and a coefcient of 1.2 correcting for

    nd branching of the capillaries (Richardson et al., 1993)). can then be converted into mole O2/ blood assumingole heme and further to O2/ blood using the conver-2/mole O2. VO2 values in O2/min may then be obtaineding this value by the measured QBA values. The QBA and

    Mb] responses for each duty cycle (Figures 3 and 4)th exponential models which were then integrated toVO2 response throughout each duty cycle.

    tical analysis

    , and W were compared across duty cycles using pairedn effects for QBA, deoxy-[Hb + Mb], total-[Hb + Mb], VO2 ,PF were tested using two-way ANOVA with repeateduty cycle time) for the same power output constant-

    for each duty cycle. When a signicant main effect was Tukeys post-hoc analysis was conducted. Differencesered statistically signicant when p < 0.05 and all dataed as mean SD unless otherwise noted.

    Figure 2duty cycthe 20%represen

    Figure 3same abblood othe 50% exercise* signic

  • 106 R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111

    Figure 4. Deocycles at the[hemoglobin +9 s postexercifrom 50% endend-exercise t

    3. Results

    3.1. Power-

    As detethe power-constant-poand in fourSE values a

    CP and 12.7 8.7% for W with the 50% duty cycle and 1.6 1.4%for CP and 10.8 11.7% for W% with the 20% duty cycle. The coef-cient of determination values for the 50% and 20% duty cycleswere 0.98 0.02 and 0.98 0.02, respectively. CP was signicantlylower for the 50% duty cycle (3.9 0.9 W) than the 20% duty cycle(5.1 0.8 W; p < 0.001), while W was not signicantly different(50% duty cycle: 452 141 J and 20% duty cycle: 432 130 J; coef-cient of variation = 13.9%) (Figure 2). There was a signicant inversecorrelation between the percent change in CP versus the percentchange in W between the 50% and 20% duty cycles (r = 0 83,p = 0.01), but not for the absolute changes in CP versus W (r = 0.61,p = 0.11).

    3.2. Equivalent power output tests

    The Ppeak from the incremental test was signicantly lowerfor the 50% duty cycle (5.7 0.7 W) than the 20% duty cycle(6.7 0.8 W; p < 0.001). The mean power output that was repeated

    th duty cycles was 6.2 0.8 W, which equated to a sig-tly h

    8.4%01). Te of ycle (

    52.1 314

    Table 1Brachial artery

    Baseline 46.5 s91.5 s Matched-timEnd-exercise

    Vmean, mean ba signicantb signicantc signicantd signicant

    Level of signifor bonican(109 p < 0.0centagduty c(201 (501 xygenated-[hemoglobin + myoglobin] response for the two duty same power output. Mean and standard error deoxygenated-

    myoglobin] (deoxy-[Hb + Mb]) data (Panel A), and end-exercise andse (Panel B) for the 50% and 20% duty cycles. signicantly different-exercise, p < 0.05. signicantly different from the 50% duty cycleime, p < 0.001.

    duration relationship

    rmined from the a priori goodness-of-t criteria,duration relationships were determined using fourwer tests in all of the subjects for the 50% duty cycle

    of the subjects for the 20% duty cycle. The resultings a percent of the parameter value were 4.6 6.1% for

    3.3. QBA

    The brain Table 1.exercise fothe 50% du7.37 1.76 and end-excycle: 9.87signicantltexercise, Qwithin the end-exerciswas no londuty cycle:(Figure 3B)

    3.4. NIRS

    The deoend-exercisduty cycle cise there w

    diameter and blood velocity data.

    50% duty cycle

    Diameter (cm) Vmean(cms1) 0.45 0.04 11.4 4.56 0.46 0.04 35.6 10.6b20.46 0.03 41.6 9.62b2

    e 0.48 0.03b1,c1 43.0 6.88b2

    lood velocity; Matched-time, equivalent time-point within the 20% duty cycle test to thaly different from 50% duty cycle.ly different from baseline within duty cycle.ly different from 46.5 s within duty cycle.ly different from 91.5 s within duty cycle.cance: 1p < 0.05 and 2p < 0.001.igher relative power output for the 50% duty cycle Ppeak) than the 20% duty cycle (93.7 7.5% Ppeak;his power output was also signicantly higher as a per-CP for the 50% duty cycle (165 37.3%) than the 20%125 14.4%; p = 0.003). The Tlim for the 50% duty cycle

    s) was signicantly shorter than the 20% duty cycles; p = 0.017).

    chial artery diameter and Vmean data are presentedQBA increased signicantly between 91.5 s and end-r the 20% duty cycle, while QBA did not increase forty cycle, such that at matched-time (50% duty cycle:mls1; 20% duty cycle: 9.26 1.99 mls1; p = 0.001)ercise (50% duty cycle: 7.37 1.76 mls1; 20% duty

    1.73 mls1; p < 0.001) the 50% duty cycle QBA wasy lower than the 20% duty cycle (Figure 3A). At 9 s pos- BA was not signicantly different from end-exercise20% duty cycle, but had signicantly increased abovee within the 50% duty cycle (p = 0.008), such that QBAger signicantly different between duty cycles (20%

    11.3 2.8 mls1; 50% duty cycle: 10.6 3.4 mls1).

    xy-[Hb + Mb] increased to a signicantly higher value ate for the 20% duty cycle (51.7 4.7 M) than the 50%(44.3 2.4 M; p = 0.03) (Figure 4A). At 9 s postexer-as no signicant difference (albeit marginally) between

    20% duty cycle

    Diameter (cm) Vmean(cms1)0.46 0.03 12.1 6.850.46 0.03 36.6 6.56b20.47 0.03 41.3 7.62b20.48 0.03 50.1 11.7a1,b2,c2,d10.51 0.04a2,b2,c2,d2 49.1 8.18a1,b2,c2,d1

    t of end-exercise for the 50% duty cycle.

  • R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111 107

    Figure 5. Meapower output(iEMG) (Panel from the 50% end-exercise tsame time poip < 0.05.+ signi

    duty cyclesM; 50% Throughoutduty cycle acycles.

    3.5. EMG

    Within tthroughoutprogressivedifferences (p < 0.001), signicantlydecreased tresulted in matched-ti

    3.6. VO2

    The intemated VO2n electromyography response for the two duty cycles at the same. Group mean and standard error for integrated electromyographyA) and mean power frequency (MPF) (Panel B). signicantly differentduty cycle end-exercise, p < 0.01. signicantly different from 50%ime, p < 0.001. * signicantly different from the 50% duty cycle at thents, p < 0.05. # signicantly different from the 50% duty cycle at 60 s,cantly different from the 50% duty cycle at 90 s and 120 s, p < 0.05.

    for the deoxy-[Hb + Mb] (20% duty cycle: 52.3 16.7duty cycle: 45.8 9.19 M; p = 0.054) (Figure 4B).

    exercise the total-[Hb + Mb] increased within eachnd no signicant difference was detected between duty

    he 20% duty cycle, iEMG did not change signicantly the test (Figure 5A). During the 50% duty cycle, the iEMGly increased until end-exercise, resulting in signicantbetween duty cycles at 120 s (p = 0.017), matched-timeand end-exercise (p = 0.002). The MPF did not change

    during the 20% duty cycle test, while it continuallyhroughout the 50% duty cycle test (Figure 5B). Thisa signicantly higher MPF for the 20% duty cycle atme (p = 0.005) and end-exercise (p = 0.008).

    gration of the QBA and deoxy-[Hb + Mb] values esti-data that qualitatively increased with similar time

    Figure 6. Estsame power uptake (VO2 ; [hemoglobin +exercise and integrated VO2ts to the bradata. signicnicantly diffefrom 20% duty

    courses and90 s (as seewhich the 2cycle (Figurexercise for50% duty cyml O2minend-exercis50 1 ml Othan the 20in DO2 valuand 1.72 mtexercise thduty cycles53 17 ml

    4. Discussi

    Consisteduty cycle between duimated oxygen uptake response of the two duty cycles at theoutput. Mean and standard error exercise estimated oxygendetermined from brachial artery blood ow and deoxygenated-

    myoglobin]; see Methods for assumptions) (Panel A), and end-9 s postexercise (Panel B) for the 50% and 20% duty cycles. Theresponse was determined from the integration of exponential modelchial artery blood ow and deoxygenated-[hemoglobin/myoglobin]antly different from the 50% duty cycle end-exercise, p < 0.001. sig-rent from the 50% end-exercise time, p < 0.001. * signicantly different

    cycle at 91.5 s, p < 0.001.

    amplitudes for both duty cycles until approximatelyn for QBA, Figure 3 and deoxy-[Hb + Mb], Figure 4), after0% duty cycle VO2 increased beyond that of the 50% dutye 6). VO2 signicantly increased between 91.5 s and end-

    the 20% duty cycle, while VO2 did not increase for thecle, such that at matched-time (50% duty cycle: 32 91; 20% duty cycle: 43 11 ml O2min1; p = 0.003) ande (50% duty cycle: 32 9 ml O2min1; 20% duty cycle:2min1; p = 0.001) the 50% duty cycle VO2 was lower% duty cycle (Figure 7). The model analysis resultedes of 1.02 ml1min1mmHg1 for the 50% duty cyclel1min1mmHg1 for the 20% duty cycle. At 9 s pos-e VO2 values were not signicantly different between

    (50% duty cycle 50 13 ml O2min1 and 20% duty cycleO2min1; p = 0.612).

    on

    nt with our rst hypothesis, CP was higher for the 20%than the 50% duty cycle, while W was not differentty cycles. When the same power output was completed

  • 108 R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111

    Figure 7. DiagPO2 for each dciple, curved lorigin) to yieldwas carried oput (6.5 0.9 Wow (QBA) andDiscussion for ity (DO2 ) fromand 34%, resp

    duty cycle. Threlaxation timrecruitment) t

    for both dut50% duty cyto our thirdvalues for tMPF higher

    In charaScherrer (19ow (i.e., Odemonstratarterial O2to reveal thMoritani et2010). The cing O2 delivduty cyclesfor the 50% blood ow.as the 50%duty cycle. measured boutput, woConsistent 20% duty cest rate of Omuscle con

    The deteassociated (depletion Miura et aland/or met2007; Fukumuscle con(QBA) and Ondings ofhypoxia led

    et al., 2012; Moritani et al., 1981). In contrast, hyperoxia led to anincrease in CP and, interestingly, a decrease in W (Vanhatalo et al.,2010). A more recent denition of W as a work capacity that is

    ined by the magnitude of the severe-intensity domain hased in

    Thisere-

    worrmininede-in isgnitcurreationted nd CPhan tere dith h

    outp(Dekr CP owepres2008ted ollecepenine .VO2 epor0 ml

    From(69%

    TheRocaram of estimated oxygen uptake as a function of microvascularuty cycle. The model integrates perfusive oxygen delivery (Fick Prin-ines) and diffusive oxygen delivery (Ficks Law, straight lines fromVO2 peak values for the specic conditions of each duty cycle. Exercise

    ut to the limit of tolerance (Tlim) at the same absolute power out-) for each duty cycle. VO2 was estimated using brachial artery blood

    the deoxygenated-[hemoglobin + myoglobin] (deoxy-[Hb + Mb]) (Seedetails). The percent change in QBA and the diffusive oxygen capac-

    the 50% duty cycle to the 20% duty cycle was estimated to be 69%ectively, which together predicted a 56% higher VO2 peak for the 20%

    e 20% duty cycle allowed for a higher QBA (possibly due to the longere) and a higher DO2 (possibly due to increased longitudinal capillaryhan the 50% duty cycle.

    y cycles, QBA was higher for the 20% duty cycle than thecle, consistent with our second hypothesis. In contrast

    hypothesis, however, deoxy-[Hb + Mb] achieved higherhe 20% duty cycle, while the iEMG was lower and the

    for the 20% duty cycle than the 50% duty cycle.cterizing the power-duration relationship, Monod and65) considered CP to be dependent upon muscle blooddelivery). Since this seminal publication, CP has been

    determemerg2010).the sev

    It isin detedetermextremically WThe main the implicassociaPpeak acycle tthe sevtent wpowerin W a lowesame pin the et al., associabout. Cis not ddetermand CP

    Theously r3052001).in DO2cycles.2011; 2ed to be dependent upon O2 delivery (blood ow content) by manipulating inspired O2 concentrationsat CP is lowered with hypoxia (Dekerle et al., 2012;

    al., 1981) and elevated with hyperoxia (Vanhatalo et al.,urrent study has extended these ndings by manipulat-ery via altered blood ow with the use of two different

    for muscle contraction, demonstrating that CP is lowerduty cycle than the 20% duty cycle as a result of reduced

    In addition, O2 extraction was altered with duty cycle duty cycle deoxy-[Hb + Mb] was lower than the 20%These differences in blood ow and deoxy-[Hb + Mb]etween the duty cycles performed at the same poweruld be anticipated for the other exercise tests as well.with this, CP was lower for the 50% duty cycle than theycle. These ndings support that CP reects the high-2 utilization which is matched by O2 delivery, that thetraction duty cycle directly inuences CP.rministic mechanisms of W have traditionally beenwith intramuscular anaerobic energy productionof the intramuscular energy stores (Jones et al., 2008;., 1999; Miura et al., 2000; Monod and Scherrer, 1965)abolite accumulation (Coats et al., 2003; Ferguson et al.,ba et al., 2003; Jones et al., 2008)). In the current study,traction duty cycle-induced alterations in O2 delivery2 extraction (deoxy-[Hb + Mb]) did not alter W. The

    the current study are consistent with those where to a decrease in CP, while not altering W (Dekerle

    for the 20%increased dble mechan(solubility/diffusion adiffusion oclongitudina2011). Increincrease thedinal recruifor increasiIn the currcantly fastefor the 20%ing that duincreased bcycle evincies, leadingextraction dsuggests thtent with RO2 extractioalso determ33% of systmaximal exwas not signmicrovascu the literature (Burnley and Jones, 2007; Vanhatalo et al., denition postulates that the parameters determiningintensity domain (VO2 max and CP) dictate W.th noting that this denition implies VO2 max is involveding W, despite the power-duration relationship being

    by (and assumed to hold true for) work rates in thetensity domain where exhaustion ensues (and theoret-

    completely utilized) prior to the attainment of VO2 max .ude of the severe-intensity domain was not determinednt study, as the VO2 at CP was not measured. However,s may be drawn from examining the power outputswith the boundaries of the severe-intensity domain.

    were both approximately 1.0 W lower for the 50% dutyhe 20% duty cycle, which implies that the magnitude ofomain, and therefore W, was unaltered. This is consis-

    ypoxia resulting in a concomitant 29 W reduction in theut at VO2 peak ,with a 30 W reduction in CP and no changeerle et al., 2012). An unaltered magnitude of W withwould necessitate a faster rate of W utilization at ther output and a decrease in time-to-exhaustion (as seenent study), as critical levels (Poole et al., 1988; Jones; Vanhatalo et al., 2010) of the anaerobic substanceswith fatigue would be achieved earlier in the exercisetively, these ndings support that the magnitude of Wdent on O2 delivery or O2 extraction per se, rather thesethe rate at which W is utilized, via alterations in VO2 max

    peakvalues from the current study are similar to previ-

    ted directly measured values for handgrip exercise of O2min1 (Richards et al., 2012; Van Beekvelt et al.,

    the model analysis, it was found that the change) was double the change in QBA (34%) between dutyDO2/Q ratio is indicative of O2 extraction (Poole et al.,

    et al., 1992), and therefore the increased DO2/Q ratio duty cycle in the current study would explain theeoxy-[Hb + Mb] compared to the 50% duty cycle. A possi-ism for the increased diffusive O2 capacity (DO2 = A/T xmolecular weight), where A is the surface area for

    nd T is the thickness of the membrane across whichcurs) for the 20% duty cycle may be due to enhancedl recruitment of capillary surface area (Poole et al.,ased red blood cell velocity and fractional O2 extraction

    length of a capillary involved in O2 exchange (longitu-tment) (Poole et al., 2011), which may be a mechanismng capillary surface area, and thus DO2, during exercise.ent study, brachial artery blood velocity was signi-r and brachial artery diameter was signicantly larger

    duty cycle than the 50% duty cycle (Table 1). Assum-ty cycle did not alter the microvascular volume, therachial artery blood ow (Vmean CSA) for the 20% dutyes an increased red blood cell velocity in the capillar-

    to increased longitudinal recruitment. The increased O2espite the increased blood ow for the 20% duty cycleat red blood cell transit time was not limiting (consis-ichardson et al. (1993b)), but rather served to augmentn. The surface area for gas exchange in the capillary isined by capillary hematocrit, which is approximatelyemic values at rest and increases to systemic values atercise (Kindig et al., 2002). However, total-[Hb + Mb]icantly different between duty cycles, suggesting thatlar hematocrit was similar between conditions. Thus,

  • R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111 109

    both the increased O2 delivery and O2 extraction for the 20% dutycycle likely contributed to the higher CP and estimated VO2 peak thanthe 50% duty cycle.

    The underlying end-exercise metabolic state of the muscle wasexamined bremove theQBA with nostatistical dthe end-execise (possibof increase dcontractionwere perfolar metaboldemonstratwas low foVO2 increasvalue not dmetabolic rduty cycles,extraction (metabolic rcontributioa decreasedtribution fofaster utilizin the prese

    Despite and MPF prcontrast to isometric kyielded simmay not dirthe mode ostyle (isomealtered dutydiffered betintensity anstrated to a2001; Petrolation of merates of the tarily produof generatinhas been licular energet al., 1988;production cycles in thing rates ofcritical leveof muscle asupercialiscles activate1994), and Type I (Hwathe currentrecruitmenbers than O2 extractiober fatigueto maintainstrated thatmotor unit between th

    The ndings of the present study have direct implicationsfor past and future studies, as well as direct application foractivities performed above CP. The different values for CP, QBA,deoxy-[Hb + Mb], and EMG between duty cycles emphasize that

    rison to thon. Ivide le pe.e., dlues,ter drcisecomeling2006

    to bdal ttinudy 995ed inscleing p

    andows nohe pta su

    the e on

    cyc1981s (Has woues.eral e nycle centrycle.may ycles(alo

    20%ion it et as ARysc

    the (Haenere b

    nentrenttima

    thatte vao theption[Hb ourseitedntiat ovey analyzing the data immediately upon recovery to inuence of the muscle contraction. The increase in

    physiological change in deoxy-[Hb + Mb] (despite slightifferences) during recovery for the 50% duty cycle abovercise value suggests that QBA was limited during exer-ly due to the decreased relaxation time), while the lackuring recovery for the 20% duty cycle suggests that this

    style was not limiting. Importantly, both duty cyclesrmed at the same power output and therefore, simi-ic rates would be expected. However, the VO2 modeles that this was not the case, as the estimated VO2 peakr the 50% duty cycle. The fact that the 50% duty cycleed (as a result of the increase in QBA) in recovery to aifferent from the 20% duty cycle suggests that the sameate may have been wanted by the muscles for both

    but the limitations imposed on O2 delivery (QBA) and O2deoxy-[Hb + Mb]) for the 50% duty cycle prevented thisate from being achieved. As a result, the aerobic energyn would be diminished for the 50% duty cycle (reecting

    CP) while requiring a greater anaerobic energy con-r any power output above CP. This would result in theation of W and earlier occurrence of exhaustion, as seennt study.being performed at the same power output, the iEMGoles differed between the 20% and 50% duty cycles. Inthe current study, Burnley et al. (2012) reported thatnee-extension exercise at various intensities above CPilar end-exercise EMG values. However, these ndingsectly relate to the current study due to differences inf exercise (knee-extension vs. handgrip), contractiontric vs. dynamic), and duty cycle (constant duty cycle vs.

    cycle). The EMG proles in the current study may haveween duty cycles as a result of differences in the relatived the duration of the tests, as these have been demon-ffect the EMG response (Camic et al., 2010; Perry et al.,fsky, 1979). Amann (2011) suggested that the accumu-tabolites within the muscle may lead to increased ringgroup III/IV afferents, resulting in the inability to volun-ce the required force despite the muscle being capableg it. In addition, exhaustion for supra-CP power outputsnked to the attainment of critical levels for intramus-y stores and metabolites ([PCr], [H+], and [Pi]) (Poole

    Vanhatalo et al., 2010), which may directly impair force(Fitts, 2008). Therefore, EMG differences between dutye current study may be a consequence of increased r-

    the group III/IV afferents and/or the attainment of al of intramuscular [PCr], [H+], and [Pi] at different levelsctivation. During handgrip exercise the exor digitorum

    and exor digitorum profundus are the primary mus-d and used throughout the exercise test (Mizuno et al.,the ber type composition of these muscles are 50%ng et al., 2013; Johnson et al., 1973). The EMG data from

    study suggest that the 50% duty cycle led to a greatert of Type II bers and/or induced more fatigue of thesethe 20% duty cycle. The limitation of O2 delivery andn in the 50% duty cycle may have led to greater muscle, thus requiring the recruitment of more muscle bers

    the requisite power output. The current study demon- at exhaustion the muscles were in different states ofrecruitment and action potential conduction velocities,e two duty cycles.

    comparegardpretatito protainabtime (ition vaa shorof exeing beFor cycet al., stratedlow pewhen rent stet al., 1cies usthe muincreas1981),blood W wawith tthe datantly,cadenctrainedet al., cyclistcyclistcadenc

    Sevting thduty cthe ecduty ccycle duty cVO2 peakfor thesumpt(Abbotsured 35% (sion bytensionmajor the samcompothe curwas esognizeabsolutions tassumdeoxy-time cthe limexponeprevens among different protocols need to be made withe specic contraction protocol so as to prevent misinter-n application, altering the biomechanics of locomotiona shorter duty cycle may lead to higher levels of sus-rformance. In running, decreasing the ground-contactuty cycle) may permit higher blood ow and O2 extrac-

    leading to improved performance. In a clinical setting,uty cycle in ambulation may allow higher intensities to be maintained, such that activities of daily liv-

    less fatiguing, increasing the patients quality of life., the power output (but not the metabolic rate (Barker)) associated with CP has consistently been demon-e lower with high pedal cadences ( 100 rpm) than

    cadences ( 60 rpm), while W has not been affectedg the data with the hyperbolic model used in the cur-(Barker et al., 2006; Carnevale and Gaesser, 1991; Hill; McNaughton and Thomas, 1996). The pedal frequen-

    these studies would vary the time under tension for, as the force generation by the muscle decreases withedal cadences (McCartney et al., 1983; Sargeant et al.,

    therefore would alter O2 delivery by producing less impedance (Hagberg et al., 1981). The nding thatt altered by duty cycle in the current study is in lineedal cadence manipulation studies and cumulativelypport that W is independent of O2 delivery. Impor-subjects of the studies examining the effect of pedal

    the power-duration relationship were noncyclists. Aslists tend to select higher pedal cadences ((Hagberg; Pugh, 1974; Sargeant, 1994 see Table 1) than non-gberg et al., 1981), it is not known if experiencedld demonstrate similar decreases in CP with high pedal

    experimental limitations are pertinent when interpre-dings from the current study. In order to vary thewhile maintaining the 3 s contraction cycle duration,ic contraction component was omitted for the 20%

    The additional eccentric contraction of the 50% dutyhave contributed to metabolic differences between. However, this does not seem likely as the estimatedng with peak QBA and deoxy-[Hb + Mb]) was higher

    duty cycle. In addition, eccentric contraction O2 con-s approximately 20% that of concentric contractional., 1952), and concentric contraction efciency (mea-TP/contraction) is 15%, while eccentric efciency ishon et al., 1997). Furthermore, the maintenance of ten-

    muscle requires less energy than the development ofmann et al., 2005; Russ et al., 2002). Therefore, thegy requiring component (concentric contraction) wasetween duty cycles, while the less energy demanding

    (eccentric contraction) differed. Another limitation of study was that VO2 was not directly measured. Rather itted using the deoxy-[Hb + Mb] and QBA values. We rec-

    the assumptions may have limited the accuracy of thelues. Nevertheless, any contribution of these assump-

    detected differences was minimized by holding thes constant between duty cycles. The integration of the+ Mb] and QBA responses allowed for the estimation of

    changes in VO2 for both duty cycles. However, due to number of deoxy-[Hb + Mb] and QBA data points for thel ts, no statistical kinetic analyses were conducted tor interpretation of the data.

  • 110 R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102 111

    In conclusion, the current study reveals that a relatively longmuscle contraction duty cycle imposes limitations on blood owand O2 extraction that ultimately leads to a decrease in exercisetolerance. CP was lower for the 50% duty cycle than the 20% dutycycle, whilevated QBA aremoval of increased foof the 20% dO2 extractiodecreased rcapillary subetween dudifferent staduction velphysiologicof W per coat the sametolerance corent study ssustainableenced by O2of W appeathat are indrate of W uvia alteratio

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    Influence of duty cycle on the power-duration relationship: Observations and potential mechanisms1 Introduction2 Methods2.1 Subjects2.2 Experimental Protocol2.3 Measurements2.3.1 Doppler ultrasound

    2.4 Near-infrared spectroscopy2.5 Electromyography2.6 Data Analysis2.6.1 Determination of the power-duration relationship

    2.7 Doppler Ultrasound2.8 NIRS2.9 EMG2.10 Estimation of oxygen consumption2.11 Statistical analysis

    3 Results3.1 Power-duration relationship3.2 Equivalent power output tests3.3 QBA3.4 NIRS3.5 EMG3.6 VO2

    4 DiscussionReferences