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

  • View

  • Download

Embed Size (px)

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

  • 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: (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


    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


    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 (elect