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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/ locate / resphys io l
nfluence of duty cycle on the power-duration relationship:bservations and potential mechanisms
.M. Broxtermana,b,∗, C.J. Adea,b, S.L. Wilcoxa, S.J. Schlupa, J.C. Craiga, T.J. Barstowa
Department of Kinesiology, Kansas State University, Manhattan, KS, USADepartment of Anatomy and Physiology, Kansas State University, Manhattan, KS, USA
r t i c l e i n f o
rticle history:ccepted 28 November 2013
eywords:ritical power
a b s t r a c t
The highest sustainable rate of aerobic metabolism [critical power (CP)] and the finite amount of workthat 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 exhaustionto determine CP and W’ for 50% and 20% duty cycles, while brachial artery blood flow (QBA) and
xercise toleranceuscle blood flowuscle contraction
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 significantlydifferent (50% duty cycle: 452 ± 141 J vs. 20% duty cycle: 432 ± 130 J; p > 0.05). At the same power out-put, QBA and deoxy-[Hb + Mb] achieved higher end-exercise values for the 20% duty cycle (9.87 ± 1.73ml·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).
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These findings indicate th. Introduction
The notion of an increase in exercise duration with progres-ively decreasing power outputs dates back at least to the earlywentieth century (Hill, 1925, 1927) and potentially as early as theourth century (Whipp et al., 1996; Whipp et al., 1998). This robustower-duration relationship is now commonly characterized using
hyperbolic mathematical model to obtain the asymptote (criti-al power, CP) and the curvature constant (W’) (Hill, 1993; Jonest al., 2010; Whipp et al., 1982). CP demarcates the boundaryetween the heavy- and severe-exercise intensity domains, as it ishe highest intensity in which a physiological steady-state can bechieved (i.e., for oxygen uptake (VO2 ) (Poole et al., 1988); bloodow (Copp et al., 2010); intramuscular concentrations of phos-hocreatine [PCr], inorganic phosphate [Pi], and hydrogen ion [H+]Jones et al., 2008)). W’ represents a finite work capacity that cane performed above CP and has traditionally been associated with
anaerobic’ metabolism (Coats et al., 2003; Ferguson et al., 2007;ukuba et al., 2003; Miura et al., 1999; Miura et al., 2000; Monodnd Scherrer, 1965). This interpretation is supported by [Pi], [H+],nd [PCr] consistently achieving ‘critical levels’ upon exhaustionChidnok et al., 2013; Jones et al., 2008; Poole et al., 1988; Vanhatalo
t al., 2010). Alternatively, W’ may be determined by the magni-ude of the severe-domain (i.e., the range between CP and VO2 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).
569-9048/$ – see front matter © 2013 Elsevier B.V. All rights reserved.ttp://dx.doi.org/10.1016/j.resp.2013.11.010
ood flow influences CP, but not W’.© 2013 Elsevier B.V. All rights reserved.
associated with the VO2 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’ 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 flow) 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 influence on blood flow as a
siology & Neurobiology 192 (2014) 102– 111 103
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Figure 1. Displacement profiles for the 50% and 20% duty cycles. Schematic rep-resentation of the specific contraction components for each duty cycle (Panel A). The50% duty cycle consisted of a 0.6 s concentric contraction period, a 0.3 s isometrictransition period, a 0.6 s eccentric contraction period, and a 1.5 s relaxation period.The 20% duty cycle consisted of a 0.6 s concentric contraction period and a 2.4 s
R.M. Broxterman et al. / Respiratory Phy
esult of blood vessel compression, increased impedance to bloodow, and possible occlusion of blood flow (Hoelting et al., 2001;utjemeier et al., 2005; Robergs et al., 1997; Sadamoto et al., 1983).he muscle contraction-relaxation cycle yields rhythmic alter-tions in intramuscular pressure, and therefore blood flow, withhe majority of blood flow occurring during the relaxation periodhen intramuscular pressure is low (Barcroft and Dornhorst, 1949;
olkow et al., 1970; Robergs et al., 1997; Walloe and Wesche, 1988).obergs et al. (1997) suggesting that the relaxation period bloodow may be important in determining the attainment of a steady-tate metabolic rate. The muscle contraction duty cycle (time underension/total contraction time) directly impacts blood flow, suchhat with high duty cycles (longer time under tension relativeo total contraction time) blood flow to the active skeletal mus-le becomes limited (Bellemare et al., 1983; Buchler et al., 1985),hile blood flow is not compromised at low duty cycles (shorter
ime under tension relative to total contraction time) even withncreased contraction frequencies (Ferreira et al., 2006; Osada andadegran, 2002; Sjogaard et al., 2002). Collectively, these resultsemonstrate that the muscle contraction duty cycle directly influ-nces blood flow to the active skeletal muscle.
To the best of our knowledge there are no reports till datehat have examined the influence of alterations in blood flow dueo the muscle contraction-relaxation cycle on the parameters ofhe power-duration relationship. Therefore, the aim of the currenttudy was to manipulate blood flow using muscle contraction dutyycles in order to assess the dependence of CP and W’ on bloodow. We hypothesized that: 1) CP would be higher for the 20% dutyycle than the 50% duty cycle, while W’ would remain unchanged,urther, when the same power output was repeated at both dutyycles, 2) blood flow would be higher for the 20% duty cycle thanhe 50% duty cycle, but, 3) deoxy-[Hb + Mb] and EMG (electromyo-raphy) measurements would achieve similar end-exercise valuesor both duty cycles.
. Methods
.1. Subjects
Eight healthy men (age: 24.8 ± 2.5 years, height: 173.7 ± 4.6 cm;eight: 77.1 ± 14.6 kg) volunteered to participate in this study.
ubjects reported to the Human Exercise Physiology Laboratoryith at least 24 h between testing sessions and having abstained
rom vigorous activity within that 24 h period. All experimentalrocedures in the present study were approved by the Institutionaleview Board of Kansas State University and conformed to the stan-ards set forth by the Declaration of Helsinki. Prior to testing, eachubject was informed of the overall protocol along with the poten-ial risks involved. Each subject then provided written informedonsent and completed a health history evaluation.
.2. Experimental Protocol
All testing was performed on a custom-built handgrip ergome-er. The handrail of the ergometer was attached to a pneumaticylinder by means of a cable-pulley system and provided a fixedinear displacement of 4 cm. Resistance was set by pressurizinghe pneumatic cylinder and work was accomplished by compress-ng the air within the cylinder when the handrail was moved.ower output was calculated as P = Rdf · k−1, where P is powern Watts (W), R is resistance in kg, d is displacement in meters, f
s contraction frequency, and k is the constant 6.12 for the con-ersion of kg·m·min−1 to W. When seated at the ergometer theubject grasped the handrail so that the forearms were at approxi-ately heart level and the elbows were slightly bent. A contractionrelaxation period. A displacement profile for a representative subject throughout acontraction cycle for each duty cycle is shown in Panel B.
frequency of 20 contractions·min−1 was utilized for both dutycycles so that each total contraction cycle duration was main-tained at 3.0 s. Thus any set resistance would produce the samepower output for both duty cycles. The 50% duty cycle consistedof a 1.5 s contraction period (in which the handrail was raisedwith concentric muscle contraction and lowered with eccentricmuscle contraction) followed by a 1.5 s relaxation period. The20% duty cycle consisted of a 0.6 s contraction period (in whichthe handrail was raised with concentric muscle contraction andthen immediately released) followed by a 2.4 s relaxation period(Figure 1). Both duty cycles had the same duration of concen-tric contraction and total contraction cycle, while the 20% dutycycle had no eccentric contraction period and therefore a longerduration of time without muscle tension. The eccentric contrac-tion period duration was altered specifically to minimize anymetabolic differences between duty cycles, while emphasizingblood flow differences (see Discussion). Audio recordings set withthe specific timing for each duty cycle were used along with feed-back provided by an investigator monitoring the tests to ensure
correct timing. Subjects completed three familiarization trialsper duty cycle prior to data collection to aid in correct, consis-tent production of the contraction-relaxation timing. All testing
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04 R.M. Broxterman et al. / Respiratory Phy
essions were continued until exhaustion, determined as the inabil-ty to complete three consecutive contraction cycles.
A peak incremental test for each duty cycle was completed in randomized order during the initial two testing sessions. Theseests were initiated at 1.0 W and the power output was increased by.5 W·min−1 until exhaustion. The peak power (Ppeak) was recordeds the highest power output for which at least 30 s of the stageas completed. The Ppeak was utilized to determine the power
utputs for the subsequent constant-power testing sessions thatould elicit exhaustion between 2–15 min. Subjects completed ainimum of three randomly ordered constant-power tests per duty
ycle in which the time-to-exhaustion (Tlim) was recorded. After thenitial three constant-power tests, the data were fit with the two-arameter hyperbolic model and the goodness-of-fit was analyzed.
f the goodness-of-fit data did not meet the a priori criteria (see Datanalysis) a fourth testing session was conducted in an attempt to
ower the parameter standard error values. A power output thatlicited exhaustion between 2–5 min for the 50% duty cycle wasepeated for the 20% duty cycle, such that any differences in thehysiological responses between duty cycles could be examinedithout the confounding influence of different power outputs (i.e.,etabolic rates).
.3. Measurements
.3.1. Doppler ultrasoundThe raw blood velocity profiles were measured using Doppler
ltrasound (Vivid 3, GE Medical Systems, Milwaukee, WI, USA)perating in pulse wave mode at a Doppler frequency of 4.0 MHzith a phased linear array transducer probe operating at an imag-
ng frequency of 6.7 MHz, and were stored for post-hoc analysis. Forll testing sessions the Doppler gate was set to the full width of therachial artery to ensure complete isonation and all Doppler veloc-
ty measurements were corrected for the angle of isonation, whichas adjusted to be less than 60 degrees. Measurements were made
–5 cm above the antecubital fossa to avoid the bifurcation of therachial artery. A bifurcation was not seen in the two-dimensional
mage, suggesting that all Doppler measurements were made ateast 1 cm from the bifurcation, as previously utilized in our labo-atory (Ade et al., 2012). Brachial artery diameters were measuredn the transverse axis using two-dimensional sonography.
.4. Near-infrared spectroscopy
The oxygenation characteristics of the flexor digitorum superfi-ialis were determined using a frequency-domain multi-distanceIRS (Near-infrared spectroscopy) system (Oxiplex TS, ISS, Cham-aign, IL, USA). The principles and algorithms of the NIRSechnology were reviewed by Gratton et al. (1997) and have pre-iously been described by Ferreira et al. (2006). Briefly, this deviceonsists of eight light-emitting diodes (LED) operating at wave-engths of 690 and 830 nm (four LEDs per wavelength) with oneetector fiber bundle and LED-detector separation distances of.0, 2.5, 3.0, and 3.5 cm. The NIRS data were collected at 50 Hznd stored for post-hoc analysis. After locating the flexor digitorumuperficialis of the right arm using EMG and palpation, the NIRSrobe was secured longitudinally along the belly of the muscle.he position of the probe was then marked with indelible ink foreproducible placement throughout the study. The NIRS probe was
alibrated prior to each test according to the manufacturer’s rec-mmendations using a calibration block with known absorptionnd scattering coefficients. Calibration was confirmed on a separatelock with different absorption and scattering coefficients.& Neurobiology 192 (2014) 102– 111
2.5. Electromyography
Surface electromyography (EMG) measurements were obtainedfrom the flexor digitorum superficialis in the left forearm. The singledifferential EMG electrode (Trigno EMG, Delsys Inc., Boston, MA,USA) consists of four silver contact bars (5 × 1 mm) arranged in a2 × 2 orientation. The electrode was positioned over the belly of themuscle, as determined by palpation and strong electrical activitywhen the fingers were flexed, but not with ulnar or radial devia-tion. This site was then marked with indelible ink for reproducibleplacement of the electrode throughout the study. The EMG datawere sampled at 1000 Hz and stored for post-hoc analysis.
2.6. Data Analysis
2.6.1. Determination of the power-duration relationshipThe parameters of the power-duration relationship (CP and
W’) were determined with the two-parameter hyperbolic modelt = W’/(P–CP), where t is time in s, W’ is the finite work capacityin Joules (J), P is power in W, and CP is critical power in W. Thedata from the initial three constant-power tests were fit with thehyperbolic model and the goodness-of-fit was assessed. A fourthconstant-power test was conducted if the parameter standard error(SE) was greater than 10% of the parameter value for either CP or W’.When applied to whole-body exercise (i.e., cycling) this ‘acceptable’margin of error allows for the anaerobic work capacity to be accu-rately estimated by W’ (Hill, 1993). There has been no establishedmargin of error for small muscle mass exercise (i.e., handgrip) andtherefore we chose to use the 10% cut-off.
2.7. Doppler Ultrasound
Mean blood velocity (Vmean; cm·s−1) was defined as the time-averaged mean velocity over each 3 s contraction cycle. Brachialartery blood flow (QBA) was calculated using the product of Vmean
and vessel cross-sectional area (CSA). Brachial artery diameterswere measured every minute throughout each test and were usedto calculate vessel CSA in cm2 (CSA = �r2). The QBA data were ana-lyzed using one contraction cycle (i.e., 3 s) at the time points of 0,46.5, and 91.5 s, while three consecutive contraction cycles (i.e., 9s) were utilized at the end of each subsequent minute, at the equiv-alent time within the 20% duty cycle to the time of end-exercise forthe 50% duty cycle (matched-time), and at end-exercise. QBA datawere also measured 9 s postexercise using a 3 s average.
2.8. NIRS
The NIRS data were processed using 3 s averages throughouteach testing session. During the first minute of exercise and at91.5 s the NIRS data were analyzed for each contraction cycle,while 3 consecutive contraction cycles were used for each sub-sequent minute, at 50% matched-time, and at end-exercise. At 9s postexercise the NIRS data were analyzed using a 3 s average.The deoxy-[hemoglobin + myoglobin] (deoxy-[Hb + Mb]) is rela-tively insensitive to changes in blood-volume (De Blasi et al.,1993; Ferrari et al., 1997; Grassi et al., 2003) and has been usedto reliably estimate the fractional oxygen extraction (De Blasiet al., 1994; DeLorey et al., 2003; Ferrari et al., 1997; Ferreiraet al., 2006; Grassi et al., 2003). The device used in the presentstudy provides absolute concentrations (�M) for deoxy-[Hb + Mb]and oxygenated-[hemoglobin + myoglobin] (oxy-[Hb + Mb]), which
may be combined to provide total-[hemoglobin + myoglobin](total-[Hb + Mb]). The dynamic reduced scattering coefficientswere measured throughout the tests and were incorporated in allof the NIRS data calculations.
siology & Neurobiology 192 (2014) 102– 111 105
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Figure 2. A representative subject’s power-duration relationship for the twoduty cycles. Two-parameter hyperbolic fits to the 50% duty cycle (solid line) andthe 20% duty cycle (dashed line) data are shown. The asymptote of each modelrepresents critical power (CP) and the curvature constant represents W’.
Figure 3. Brachial artery blood flow responses for the two duty cycles at thesame absolute power output. Mean and standard error exercise brachial artery
R.M. Broxterman et al. / Respiratory Phy
.9. EMG
The raw EMG data were processed with a band-pass filter30–300 Hz) and each electrical burst corresponding to a muscleontraction was detected using a custom-designed computer pro-ram. The EMG signal amplitude characteristics were analyzed viantegrated EMG (iEMG), a measure of motor unit recruitment and
otorneuron firing rate, which typically increases as the muscleatigues (Enoka and Stuart, 1992; Fulco et al., 1996). The EMGignal frequency characteristics were analyzed via mean power fre-uency (MPF), a measure of the muscle action potential conductionelocity, which typically shifts to lower frequencies as the muscleatigues (Hagg, 1992). During the first minute of exercise and at1.5 s the EMG data were analyzed for each contraction cycle, afterhich the end of each subsequent minute, 50% matched-time, and
nd-exercise were analyzed using three consecutive contractionycles.
.10. Estimation of oxygen consumption
To investigate the relationship between O2 delivery and O2xtraction across duty cycles we used the model put forth by Wag-er and colleagues (Roca et al., 1992; Wagner, 1996, 2011), which
ntegrates perfusive O2 delivery (Fick Principle, VO2 max = Q (arterial-enous O2 content difference), where Q is blood flow) and diffusive2 capacity (Fick’s Law of Diffusion, VO2 = DO2 (PcapO2 − PmitO2),here DO2 is the oxygen diffusing capacity of the muscle, PcapO2
s the partial pressure of oxygen within the microcirculation, andmitO2 is the partial pressure of oxygen within the mitochon-ria). The intersection of these two relationships yields the VO2peakor those conditions. The mechanisms for the discrepancy in CPetween duty cycles in the current study can be further exploredsing this model under a few assumptions. The assumptions wereeld constant between duty cycles to reduce systematic error, sohat any differences in the model would be attributable to dif-erences in the deoxy-[Hb + Mb] and QBA values. It was assumedhat the deoxy-[Hb + Mb] signal reflects only deoxy-[Hb] [n.b., were aware that the signal contains deoxy-[Mb] as well (Davis andarstow, 2013)] and that the entire signal arises solely from theuscle (i.e., not from any intervening adipose or skin tissue). With
hese assumptions the deoxy-[Hb] may be converted into an esti-ated VO2 . The deoxy-[Hb] values are in units of �mole heme/l
issue, where the tissue is assumed to be muscle. These deoxy-[Hb]nits can be converted into �mole heme/� blood using the conver-ion 1.36% capillary blood volume/muscle volume (derived from00 cap/mm2, 28.3 �m2 CSA, and a coefficient of 1.2 correcting forortuosity and branching of the capillaries (Richardson et al., 1993)).hese units can then be converted into mole O2/� blood assuming
mole O2/mole heme and further to � O2/� blood using the conver-ion 22.4 � O2/mole O2. VO2 values in � O2/min may then be obtainedy multiplying this value by the measured QBA values. The QBA andeoxy-[Hb + Mb] responses for each duty cycle (Figures 3 and 4)ere fit with exponential models which were then integrated torovide the VO2 response throughout each duty cycle.
.11. Statistical analysis
Ppeak, CP, and W’ were compared across duty cycles using paired-tests. Main effects for QBA, deoxy-[Hb + Mb], total-[Hb + Mb], VO2 ,EMG, and MPF were tested using two-way ANOVA with repeated
easures (duty cycle × time) for the same power output constant-
ower tests for each duty cycle. When a significant main effect wasetected, a Tukey’s post-hoc analysis was conducted. Differencesere considered statistically significant when p < 0.05 and all datare presented as mean ± SD unless otherwise noted.
blood flow (QBA) data (Panel A), and end-exercise and 9 s postexercise (Panel B) forthe 50% and 20% duty cycles. † significantly different from the 50% duty cycle end-exercise, p < 0.001. ‡ significantly different from the 50% end-exercise time, p < 0.001.* significantly different from 20% duty cycle at 91.5 s, p < 0.001.
106 R.M. Broxterman et al. / Respiratory Physiology
Figure 4. Deoxygenated-[hemoglobin + myoglobin] response for the two dutycycles at the same power output. Mean and standard error deoxygenated-[hemoglobin + myoglobin] (deoxy-[Hb + Mb]) data (Panel A), and end-exercise and9fe
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The deoxy-[Hb + Mb] increased to a significantly higher value at
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s postexercise (Panel B) for the 50% and 20% duty cycles. † significantly differentrom 50% end-exercise, p < 0.05. ‡ significantly different from the 50% duty cyclend-exercise time, p < 0.001.
. Results
.1. Power-duration relationship
As determined from the a priori goodness-of-fit criteria,he power-duration relationships were determined using four
onstant-power tests in all of the subjects for the 50% duty cyclend in four of the subjects for the 20% duty cycle. The resultingE values as a percent of the parameter value were 4.6 ± 6.1% forable 1rachial artery diameter and blood velocity data.
50% duty cycle
Diameter (cm) Vmean(cm·s−1)
Baseline 0.45 ± 0.04 11.4 ± 4.56
46.5 s 0.46 ± 0.04 35.6 ± 10.6b2
91.5 s 0.46 ± 0.03 41.6 ± 9.62b2
Matched-time — —
End-exercise 0.48 ± 0.03b1,c1 43.0 ± 6.88b2
mean, mean blood velocity; Matched-time, equivalent time-point within the 20% duty cya significantly different from 50% duty cycle.b significantly different from baseline within duty cycle.c significantly different from 46.5 s within duty cycle.d significantly different from 91.5 s within duty cycle.
evel of significance: 1p < 0.05 and 2p < 0.001.
& Neurobiology 192 (2014) 102– 111
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-ficient of determination values for the 50% and 20% duty cycleswere 0.98 ± 0.02 and 0.98 ± 0.02, respectively. CP was significantlylower 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 and 20% duty cycle: 432 ± 130 J; coeffi-cient of variation = 13.9%) (Figure 2). There was a significant 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 significantly 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 repeatedfor both duty cycles was 6.2 ± 0.8 W, which equated to a sig-nificantly higher relative power output for the 50% duty cycle(109 ± 8.4% Ppeak) than the 20% duty cycle (93.7 ± 7.5% Ppeak;p < 0.001). This power output was also significantly higher as a per-centage of CP for the 50% duty cycle (165 ± 37.3%) than the 20%duty cycle (125 ± 14.4%; p = 0.003). The Tlim for the 50% duty cycle(201 ± 52.1 s) was significantly shorter than the 20% duty cycle(501 ± 314 s; p = 0.017).
3.3. QBA
The brachial artery diameter and Vmean data are presentedin Table 1. QBA increased significantly between 91.5 s and end-exercise for the 20% duty cycle, while QBA did not increase forthe 50% duty cycle, such that at matched-time (50% duty cycle:7.37 ± 1.76 ml·s−1; 20% duty cycle: 9.26 ± 1.99 ml·s−1; p = 0.001)and end-exercise (50% duty cycle: 7.37 ± 1.76 ml·s−1; 20% dutycycle: 9.87 ± 1.73 ml·s−1; p < 0.001) the 50% duty cycle QBA wassignificantly lower than the 20% duty cycle (Figure 3A). At 9 s pos-texercise, QBA was not significantly different from end-exercisewithin the 20% duty cycle, but had significantly increased aboveend-exercise within the 50% duty cycle (p = 0.008), such that QBAwas no longer significantly different between duty cycles (20%duty cycle: 11.3 ± 2.8 ml·s−1; 50% duty cycle: 10.6 ± 3.4 ml·s−1)(Figure 3B).
3.4. NIRS
end-exercise for the 20% duty cycle (51.7 ± 4.7 �M) than the 50%duty cycle (44.3 ± 2.4 �M; p = 0.03) (Figure 4A). At 9 s postexer-cise there was no significant difference (albeit marginally) between
20% duty cycle
Diameter (cm) Vmean(cm·s−1)
0.46 ± 0.03 12.1 ± 6.850.46 ± 0.03 36.6 ± 6.56b2
0.47 ± 0.03 41.3 ± 7.62b2
0.48 ± 0.03 50.1 ± 11.7a1,b2,c2,d1
0.51 ± 0.04a2,b2,c2,d2 49.1 ± 8.18a1,b2,c2,d1
cle test to that of end-exercise for the 50% duty cycle.
R.M. Broxterman et al. / Respiratory Physiology & Neurobiology 192 (2014) 102– 111 107
Figure 5. Mean electromyography response for the two duty cycles at the samepower output. Group mean and standard error for integrated electromyography(iEMG) (Panel A) and mean power frequency (MPF) (Panel B). † significantly differentfrom the 50% duty cycle end-exercise, p < 0.01. ‡ significantly different from 50%esp
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Figure 6. Estimated oxygen uptake response of the two duty cycles at thesame power output. Mean and standard error exercise estimated oxygenuptake (VO2 ; determined from brachial artery blood flow and deoxygenated-[hemoglobin + myoglobin]; see Methods for assumptions) (Panel A), and end-exercise and 9 s postexercise (Panel B) for the 50% and 20% duty cycles. Theintegrated VO2 response was determined from the integration of exponential modelfits to the brachial artery blood flow and deoxygenated-[hemoglobin/myoglobin]
nd-exercise time, p < 0.001. * significantly different from the 50% duty cycle at theame time points, p < 0.05. # significantly different from the 50% duty cycle at 60 s, < 0.05.+ significantly different from the 50% duty cycle at 90 s and 120 s, p < 0.05.
uty cycles for the deoxy-[Hb + Mb] (20% duty cycle: 52.3 ± 16.7M; 50% duty cycle: 45.8 ± 9.19 �M; p = 0.054) (Figure 4B).hroughout exercise the total-[Hb + Mb] increased within eachuty cycle and no significant difference was detected between dutyycles.
.5. EMG
Within the 20% duty cycle, iEMG did not change significantlyhroughout the test (Figure 5A). During the 50% duty cycle, the iEMGrogressively increased until end-exercise, resulting in significantifferences between duty cycles at 120 s (p = 0.017), matched-timep < 0.001), and end-exercise (p = 0.002). The MPF did not changeignificantly during the 20% duty cycle test, while it continuallyecreased throughout the 50% duty cycle test (Figure 5B). Thisesulted in a significantly higher MPF for the 20% duty cycle atatched-time (p = 0.005) and end-exercise (p = 0.008).
.6. VO2
The integration of the QBA and deoxy-[Hb + Mb] values esti-ated VO2 data that qualitatively increased with similar time
data. † significantly different from the 50% duty cycle end-exercise, p < 0.001. ‡ sig-nificantly different from the 50% end-exercise time, p < 0.001. * significantly differentfrom 20% duty cycle at 91.5 s, p < 0.001.
courses and amplitudes for both duty cycles until approximately90 s (as seen for QBA, Figure 3 and deoxy-[Hb + Mb], Figure 4), afterwhich the 20% duty cycle VO2 increased beyond that of the 50% dutycycle (Figure 6). VO2 significantly increased between 91.5 s and end-exercise for the 20% duty cycle, while VO2 did not increase for the50% duty cycle, such that at matched-time (50% duty cycle: 32 ± 9ml O2·min−1; 20% duty cycle: 43 ± 11 ml O2·min−1; p = 0.003) andend-exercise (50% duty cycle: 32 ± 9 ml O2·min−1; 20% duty cycle:50 ± 1 ml O2·min−1; p = 0.001) the 50% duty cycle VO2 was lowerthan the 20% duty cycle (Figure 7). The model analysis resultedin DO2 values of 1.02 ml−1·min−1·mmHg−1 for the 50% duty cycleand 1.72 ml−1·min−1·mmHg−1 for the 20% duty cycle. At 9 s pos-texercise the VO2 values were not significantly different betweenduty cycles (50% duty cycle 50 ± 13 ml O2·min−1 and 20% duty cycle53 ± 17 ml O2·min−1; p = 0.612).
4. Discussion
Consistent with our first hypothesis, CP was higher for the 20%duty cycle than the 50% duty cycle, while W’ was not differentbetween duty cycles. When the same power output was completed
108 R.M. Broxterman et al. / Respiratory Physiology
Figure 7. Diagram of estimated oxygen uptake as a function of microvascularPO2 for each duty cycle. The model integrates perfusive oxygen delivery (Fick Prin-ciple, curved lines) and diffusive oxygen delivery (Fick’s Law, straight lines fromorigin) to yield VO2 peak
values for the specific conditions of each duty cycle. Exercisewas carried out to the limit of tolerance (Tlim) at the same absolute power out-put (6.5 ± 0.9 W) for each duty cycle. VO2 was estimated using brachial artery bloodflow (QBA) and the deoxygenated-[hemoglobin + myoglobin] (deoxy-[Hb + Mb]) (SeeDiscussion for details). The percent change in QBA and the diffusive oxygen capac-ity (DO2 ) from the 50% duty cycle to the 20% duty cycle was estimated to be 69%and 34%, respectively, which together predicted a 56% higher VO2 peak
for the 20%
duty cycle. The 20% duty cycle allowed for a higher QBA (possibly due to the longerrr
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33% of systemic values at rest and increases to systemic values at
elaxation time) and a higher DO2 (possibly due to increased longitudinal capillaryecruitment) than the 50% duty cycle.
or both duty cycles, QBA was higher for the 20% duty cycle than the0% duty cycle, consistent with our second hypothesis. In contrasto our third hypothesis, however, deoxy-[Hb + Mb] achieved higheralues for the 20% duty cycle, while the iEMG was lower and thePF higher for the 20% duty cycle than the 50% duty cycle.In characterizing the power-duration relationship, Monod and
cherrer (1965) considered CP to be dependent upon muscle bloodow (i.e., O2 delivery). Since this seminal publication, CP has beenemonstrated to be dependent upon O2 delivery (blood flow ×rterial O2 content) by manipulating inspired O2 concentrationso reveal that CP is lowered with hypoxia (Dekerle et al., 2012;
oritani et al., 1981) and elevated with hyperoxia (Vanhatalo et al.,010). The current study has extended these findings by manipulat-
ng O2 delivery via altered blood flow with the use of two differentuty cycles for muscle contraction, demonstrating that CP is loweror the 50% duty cycle than the 20% duty cycle as a result of reducedlood flow. In addition, O2 extraction was altered with duty cycles the 50% duty cycle deoxy-[Hb + Mb] was lower than the 20%uty cycle. These differences in blood flow and deoxy-[Hb + Mb]easured between the duty cycles performed at the same power
utput, would be anticipated for the other exercise tests as well.onsistent with this, CP was lower for the 50% duty cycle than the0% duty cycle. These findings support that CP reflects the high-st rate of O2 utilization which is matched by O2 delivery, that theuscle contraction duty cycle directly influences CP.The deterministic mechanisms of W’ have traditionally been
ssociated with intramuscular ‘anaerobic’ energy productiondepletion of the intramuscular energy stores (Jones et al., 2008;
iura et al., 1999; Miura et al., 2000; Monod and Scherrer, 1965)nd/or metabolite accumulation (Coats et al., 2003; Ferguson et al.,007; Fukuba et al., 2003; Jones et al., 2008)). In the current study,uscle contraction duty cycle-induced alterations in O2 delivery
QBA) and O2 extraction (deoxy-[Hb + Mb]) did not alter W’. Thendings of the current study are consistent with those whereypoxia led to a decrease in CP, while not altering W’ (Dekerle
& Neurobiology 192 (2014) 102– 111
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 definition of W’ as a work capacity that isdetermined by the magnitude of the severe-intensity domain hasemerged in the literature (Burnley and Jones, 2007; Vanhatalo et al.,2010). This definition postulates that the parameters determiningthe severe-intensity domain (VO2 max and CP) dictate W’.
It is worth noting that this definition implies VO2 max is involvedin determining W’, despite the power-duration relationship beingdetermined by (and assumed to hold true for) work rates in theextreme-intensity domain where exhaustion ensues (and theoret-ically W’ is completely utilized) prior to the attainment of VO2 max .The magnitude of the severe-intensity domain was not determinedin the current study, as the VO2 at CP was not measured. However,implications may be drawn from examining the power outputsassociated with the boundaries of the severe-intensity domain.Ppeak and CP were both approximately 1.0 W lower for the 50% dutycycle than the 20% duty cycle, which implies that the magnitude ofthe severe domain, and therefore W’, was unaltered. This is consis-tent with hypoxia resulting in a concomitant 29 W reduction in thepower output at VO2 peak
,with a 30 W reduction in CP and no changein W’ (Dekerle et al., 2012). An unaltered magnitude of W’ witha lower CP would necessitate a faster rate of W’ utilization at thesame power output and a decrease in time-to-exhaustion (as seenin the present study), as ‘critical levels’ (Poole et al., 1988; Joneset al., 2008; Vanhatalo et al., 2010) of the ‘anaerobic’ substancesassociated with fatigue would be achieved earlier in the exercisebout. Collectively, these findings support that the magnitude of W’is not dependent on O2 delivery or O2 extraction per se, rather thesedetermine the rate at which W’ is utilized, via alterations in VO2 maxand CP.
The VO2 peakvalues from the current study are similar to previ-
ously reported directly measured values for handgrip exercise of∼30–50 ml O2·min−1 (Richards et al., 2012; Van Beekvelt et al.,2001). From the model analysis, it was found that the changein DO2 (69%) was double the change in QBA (34%) between dutycycles. The DO2 /Q ratio is indicative of O2 extraction (Poole et al.,2011; Roca et al., 1992), and therefore the increased DO2 /Q ratiofor the 20% duty cycle in the current study would explain theincreased deoxy-[Hb + Mb] compared to the 50% duty cycle. A possi-ble mechanism for the increased diffusive O2 capacity (DO2 = A/T x(solubility/
√molecular weight), where A is the surface area for
diffusion and T is the thickness of the membrane across whichdiffusion occurs) for the 20% duty cycle may be due to enhancedlongitudinal recruitment of capillary surface area (Poole et al.,2011). Increased red blood cell velocity and fractional O2 extractionincrease the length of a capillary involved in O2 exchange (‘longitu-dinal recruitment’) (Poole et al., 2011), which may be a mechanismfor increasing capillary surface area, and thus DO2, during exercise.In the current study, brachial artery blood velocity was signifi-cantly faster and brachial artery diameter was significantly largerfor the 20% duty cycle than the 50% duty cycle (Table 1). Assum-ing that duty cycle did not alter the microvascular volume, theincreased brachial artery blood flow (Vmean × CSA) for the 20% dutycycle evinces an increased red blood cell velocity in the capillar-ies, leading to increased longitudinal recruitment. The increased O2extraction despite the increased blood flow for the 20% duty cyclesuggests that red blood cell transit time was not limiting (consis-tent with Richardson et al. (1993b)), but rather served to augmentO2 extraction. The surface area for gas exchange in the capillary isalso determined by capillary hematocrit, which is approximately
maximal exercise (Kindig et al., 2002). However, total-[Hb + Mb]was not significantly different between duty cycles, suggesting thatmicrovascular hematocrit was similar between conditions. Thus,
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R.M. Broxterman et al. / Respiratory Phy
oth the increased O2 delivery and O2 extraction for the 20% dutyycle likely contributed to the higher CP and estimated VO2 peak
thanhe 50% duty cycle.
The underlying end-exercise metabolic state of the muscle wasxamined by analyzing the data immediately upon recovery toemove the influence of the muscle contraction. The increase in˙ BA with no physiological change in deoxy-[Hb + Mb] (despite slighttatistical differences) during recovery for the 50% duty cycle abovehe end-exercise value suggests that QBA was limited during exer-ise (possibly due to the decreased relaxation time), while the lackf increase during recovery for the 20% duty cycle suggests that thisontraction style was not limiting. Importantly, both duty cyclesere performed at the same power output and therefore, simi-
ar metabolic rates would be expected. However, the VO2 modelemonstrates that this was not the case, as the estimated VO2 peak
as low for the 50% duty cycle. The fact that the 50% duty cycle˙ O2 increased (as a result of the increase in QBA) in recovery to aalue not different from the 20% duty cycle suggests that the sameetabolic rate may have been ‘wanted’ by the muscles for both
uty cycles, but the limitations imposed on O2 delivery (QBA) and O2xtraction (deoxy-[Hb + Mb]) for the 50% duty cycle prevented thisetabolic rate from being achieved. As a result, the aerobic energy
ontribution would be diminished for the 50% duty cycle (reflecting decreased CP) while requiring a greater anaerobic energy con-ribution for any power output above CP. This would result in theaster utilization of W’ and earlier occurrence of exhaustion, as seenn the present study.
Despite being performed at the same power output, the iEMGnd MPF profiles differed between the 20% and 50% duty cycles. Inontrast to the current study, Burnley et al. (2012) reported thatsometric knee-extension exercise at various intensities above CPielded similar end-exercise EMG values. However, these findingsay not directly relate to the current study due to differences in
he mode of exercise (knee-extension vs. handgrip), contractiontyle (isometric vs. dynamic), and duty cycle (constant duty cycle vs.ltered duty cycle). The EMG profiles in the current study may haveiffered between duty cycles as a result of differences in the relative
ntensity and the duration of the tests, as these have been demon-trated to affect the EMG response (Camic et al., 2010; Perry et al.,001; Petrofsky, 1979). Amann (2011) suggested that the accumu-
ation of metabolites within the muscle may lead to increased firingates of the group III/IV afferents, resulting in the inability to volun-arily produce the required force despite the muscle being capablef generating it. In addition, exhaustion for supra-CP power outputsas been linked to the attainment of critical levels for intramus-ular energy stores and metabolites ([PCr], [H+], and [Pi]) (Poolet al., 1988; Vanhatalo et al., 2010), which may directly impair forceroduction (Fitts, 2008). Therefore, EMG differences between dutyycles in the current study may be a consequence of increased fir-ng rates of the group III/IV afferents and/or the attainment of aritical level of intramuscular [PCr], [H+], and [Pi] at different levelsf muscle activation. During handgrip exercise the flexor digitorumuperficialis and flexor digitorum profundus are the primary mus-les activated and used throughout the exercise test (Mizuno et al.,994), and the fiber type composition of these muscles are ∼50%ype I (Hwang et al., 2013; Johnson et al., 1973). The EMG data fromhe current study suggest that the 50% duty cycle led to a greaterecruitment of Type II fibers and/or induced more fatigue of thesebers than the 20% duty cycle. The limitation of O2 delivery and2 extraction in the 50% duty cycle may have led to greater muscleber fatigue, thus requiring the recruitment of more muscle fiberso maintain the requisite power output. The current study demon-
trated that at exhaustion the muscles were in different states ofotor unit recruitment and action potential conduction velocities,etween the two duty cycles.
& Neurobiology 192 (2014) 102– 111 109
The findings 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 thatcomparisons among different protocols need to be made withregard to the specific contraction protocol so as to prevent misinter-pretation. In application, altering the biomechanics of locomotionto provide a shorter duty cycle may lead to higher levels of sus-tainable performance. In running, decreasing the ground-contacttime (i.e., duty cycle) may permit higher blood flow and O2 extrac-tion values, leading to improved performance. In a clinical setting,a shorter duty cycle in ambulation may allow higher intensitiesof ‘exercise’ to be maintained, such that activities of daily liv-ing become less fatiguing, increasing the patient’s quality of life.For cycling, the power output (but not the metabolic rate (Barkeret al., 2006)) associated with CP has consistently been demon-strated to be lower with high pedal cadences (≥ 100 rpm) thanlow pedal cadences (≤ 60 rpm), while W’ has not been affectedwhen fitting the data with the hyperbolic model used in the cur-rent study (Barker et al., 2006; Carnevale and Gaesser, 1991; Hillet al., 1995; McNaughton and Thomas, 1996). The pedal frequen-cies used in these studies would vary the time under tension forthe muscle, as the force generation by the muscle decreases withincreasing pedal cadences (McCartney et al., 1983; Sargeant et al.,1981), and therefore would alter O2 delivery by producing lessblood flow impedance (Hagberg et al., 1981). The finding thatW’ was not altered by duty cycle in the current study is in linewith the pedal cadence manipulation studies and cumulativelythe data support that W’ is independent of O2 delivery. Impor-tantly, the subjects of the studies examining the effect of pedalcadence on the power-duration relationship were noncyclists. Astrained cyclists tend to select higher pedal cadences ((Hagberget al., 1981; Pugh, 1974; Sargeant, 1994 see Table 1) than non-cyclists (Hagberg et al., 1981), it is not known if experiencedcyclists would demonstrate similar decreases in CP with high pedalcadences.
Several experimental limitations are pertinent when interpre-ting the findings from the current study. In order to vary theduty cycle while maintaining the 3 s contraction cycle duration,the eccentric contraction component was omitted for the 20%duty cycle. The additional eccentric contraction of the 50% dutycycle may have contributed to metabolic differences betweenduty cycles. However, this does not seem likely as the estimatedVO2 peak
(along with peak QBA and deoxy-[Hb + Mb]) was higherfor the 20% duty cycle. In addition, eccentric contraction O2 con-sumption is approximately 20% that of concentric contraction(Abbott et al., 1952), and concentric contraction efficiency (mea-sured as ATP/contraction) is ∼15%, while eccentric efficiency is∼35% (Ryschon et al., 1997). Furthermore, the maintenance of ten-sion by the muscle requires less energy than the development oftension (Hamann et al., 2005; Russ et al., 2002). Therefore, themajor energy requiring component (concentric contraction) wasthe same between duty cycles, while the less energy demandingcomponent (eccentric contraction) differed. Another limitation ofthe current study was that VO2 was not directly measured. Rather itwas estimated using the deoxy-[Hb + Mb] and QBA values. We rec-ognize that the assumptions may have limited the accuracy of theabsolute values. Nevertheless, any contribution of these assump-tions to the detected differences was minimized by holding theassumptions constant between duty cycles. The integration of thedeoxy-[Hb + Mb] and QBA responses allowed for the estimation oftime course changes in VO for both duty cycles. However, due to
2the limited number of deoxy-[Hb + Mb] and QBA data points for theexponential fits, no statistical kinetic analyses were conducted toprevent over interpretation of the data.
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10 R.M. Broxterman et al. / Respiratory Phy
In conclusion, the current study reveals that a relatively longuscle contraction duty cycle imposes limitations on blood flow
nd O2 extraction that ultimately leads to a decrease in exerciseolerance. CP was lower for the 50% duty cycle than the 20% dutyycle, while W’ was not different. The 20% duty cycle resulted in ele-ated QBA and deoxy-[Hb + Mb] than the 50% duty cycle and uponemoval of the contraction impedance, QBA and deoxy-[Hb + Mb]ncreased for the 50% duty cycle to values not different from thosef the 20% duty cycle. These findings suggest that O2 delivery and2 extraction were limited for the 50% duty cycle, possibly due to aecreased relaxation time and less longitudinal recruitment of theapillary surface area, respectively. The EMG values also differedetween duty cycles, such that at exhaustion, the muscles were inifferent states of motor unit recruitment and action potential con-uction velocities. The 50% duty cycle appears to have limited thehysiological determinants of CP, resulting in a greater utilizationf W’ per contraction and less W’ restoration between contractionst the same power output. This resulted in a decreased exerciseolerance compared to the 20% duty cycle. The findings of the cur-ent study support the notion that CP is determined by the highestustainable rate of aerobic ATP production, which in turn is influ-nced by O2 delivery and O2 extraction. In contrast, the magnitudef W’ appears to be determined (at least in part) by mechanismshat are independent of O2 delivery and O2 extraction, while theate of W’ utilization is affected by O2 delivery and O2 extractionia alterations in CP.
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