The effects of short recovery duration on VO 2 and ... - Springer Link

Eur J Appl Physiol (2012) 112:1907–1915 DOI 10.1007/s00421-011-2152-4

ORIGINAL ARTICLE

The effects of short recovery duration on VO2 and muscle deoxygenation during intermittent exercise Glen R. Belfry • Donald H. Paterson Juan M. Murias • Scott G. Thomas

•

Received: 29 April 2011 / Accepted: 25 August 2011 / Published online: 17 September 2011 Ó Springer-Verlag 2011

Abstract This study compared the oxygen uptake (VO2) and muscle deoxygenation (DHHb) of two intermittent protocols to responses during continuous constant load cycle exercise in males (24 year ± 2, n = 7). Subjects performed three protocols: (1) 10 s work/5 s active recovery (R), R at 20 W (INT1): (2) 10 s work/5 s R, R at moderate intensity (INT2); and (3) continuous exercise (CONT), all for 10 min, on separate days. The work rate of CONT and the 10 s work of INT1 and INT2 were set within the heavy intensity domain. VO2 and DHHb data were filtered and averaged to 5 s bins. Average VO2 (80–420 s) was highest during CONT (3.77 L/min), lower in INT2 (3.04 L/min), and lowest during INT1 (2.81 L/min), all (p \ 0.05). Average DHHb (80–420 s) was higher during CONT (p \ 0.05) than both INT exercise protocols (CONT; 25.7 ± 0.9 a.u. INT1; 16.4 ± 0.8 a.u., and INT2; 15.8 ± 0.8 a.u.). The repeated changes in metabolic rate elicited oscillations in DHHb in both intermittent protocols, whereas oscillations in VO2 were only observed during INT1. The greater DHHb during CONT suggests a reduction in oxygen delivery compared to oxygen consumption relative to INT. The higher VO2 for INT 2 versus INT 1 and similar DHHb during INT suggests an increase in oxygen delivery during INT 2. Thus the different demands of

Communicated by David C. Poole. G. R. Belfry (&) D. H. Paterson J. M. Murias Faculty of Health Sciences, School of Kinesiology, University of Western Ontario, Thames Hall, London, ON N6A 3K7, Canada e-mail: [email protected] S. G. Thomas Graduate Department of Exercise Sciences, University of Toronto, Toronto, ON, Canada

INT1, INT2, and CONT protocols elicited differing physiological responses to a similar heavy intensity power output. These intermittent exercise models seem to elicit an elevated O2 delivery condition compared to CONT. Keywords DHHb/VO2 O2 delivery to O2 utilization Heavy intensity work Muscle pump

Introduction Numerous sports demand short duration work periods interspersed with short duration recovery periods. Observations based on time motion analysis of track pursuit cycling (Schumacher and Mueller 2002), rugby (Gabbett 2005), middle distance running (Billat et al. 2009) and ballet (Twitchett et al. 2009) have documented rapid variations in power output (PO) and VO2 in competition. During laboratory conditions, step changes in PO result in exponential increases (on-kinetics) and decreases (offkinetics) in muscle VO2. Intermittent exercise including repeated short work and shorter recovery periods is, in essence, a series of brief ‘‘square wave’’ exercise bouts. This model of exercise requires rapid adjustments in oxygen delivery and utilization. Determinants of on–off VO2 and deoxyhaemoglobin (DHHb) kinetics in response to long duration square wave constant load exercise at various intensities have been examined (Barstow et al. 1996; DeLorey et al. 2004; Grassi et al. 1998b; Murias et al. 2010b; Paterson and Whipp 1991; Rossiter et al. 2002). The investigation of oxygen uptake and delivery responses to rapidly fluctuating intermittent exercise has received little attention (Christensen and Saltin 1960). Furthermore, the influence of the recovery period on these characteristics on the work period has been ignored. In this study we

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examine the effect of intensity of brief (5 s) recovery period activity on these variables. Light-intensity continuous exercise increases muscle blood flow due to, among other factors, muscle pump action (Barcroft and Dornhorst 1949; Folkow and Waaler 1970; Lutjemeier et al. 2005). Furthermore, it has been suggested that as the exercise intensity continues to increase, a threshold is reached where impedance to blood flow occurs due to the continued increase in pressure generated from contraction. It would seem that the inclusion of light-intensity short recovery periods during high-intensity continuous exercise may reduce contractile pressures that impair blood flow and thus facilitate O2 delivery and distribution during both the recovery period and the subsequent work period (Lutjemeier et al. 2005; Sadamoto et al. 1983). Moreover, increasing the work intensity of these recovery periods may facilitate a further enhancement of local blood flow due to increased action of the muscle pump during the higher intensity recovery and subsequent work period. Although technical limitations make the measurement of rapid changes in blood flow within the muscle challenging in humans, recent studies have shown that an estimation of changes in muscle O2 delivery can be obtained using near-infrared spectroscopy (NIRS) derived deoxyhaemoglobin concentration (DHHb) data in combination with measures of VO2 (DiMenna et al. 2010; Harper et al. 2008; Murias et al. 2010a; Murias et al. 2010b). Using this methodology, temporal adjustments in muscle O2 delivery during periods of work and recovery can be derived and insights can be gained into the mechanisms controlling the adjustments in muscle O2 utilization during intermittent exercise. Thus, the goal of this study was to compare the responses and mechanisms explaining the adjustments of VO2 between a continuous constant load exercise (CONT) and intermittent exercise including light-intensity recovery periods (INT 1) and moderate-intensity recovery periods (INT 2), with matched intensities of work periods between the two INT and the CONT protocols. It was hypothesized that: (1) the inclusion of the recovery periods during INT exercise will elicit a reduced DHHb/VO2 versus CONT reflecting an improved balance of O2 delivery to utilization; (2) the light-intensity recovery exercise during INT 1 will elicit a higher DHHb/VO2 versus the moderate recovery exercise of INT 2 reflecting enhanced blood flow distribution relative to oxygen demand during the INT 2 recovery and work periods; and (3) an increased contribution of oxidative phosphorylation to the energy demands during the work periods will be observed with moderateintensity recovery (INT 2) compared to light-intensity recovery (INT 1).

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Eur J Appl Physiol (2012) 112:1907–1915

Methods Subjects Seven adult males, 24 ± 4 years of age, volunteered and gave written consent to participate in the study (see Table 1) which was approved by The University Review Board for Research Involving Human Subjects. All subjects were healthy and physically active (1–3 times per week of moderate-intensity activities). Testing protocol Subjects were asked to refrain from ingesting caffeine in the 3 h prior to their testing sessions. The subjects performed a series of cycle ergometer tests (Lode Corival 400; Lode B.V., Groningen, Holland) on four separate days. Testing Day 1: One incremental ramp test to fatigue, 25 W/min was performed. This test was used to determine VO2max and the gas-exchange threshold (VET). VET was defined as the VO2 at which CO2 production (VCO2) began to increase out of proportion in relation to VO2 with a systematic rise in minute ventilation-to-VO2 ratio and endtidal PO2 whereas minute ventilation-to-VCO2 ratio and end-tidal PCO2 were stable. Data for this analysis began after accounting for the delay between VO2 and work rate (the cardiodynamic phase) during the incremental ramp test to fatigue. The tests were randomized on the following days of testing. Testing Day 2: Subjects performed a 3 min 20 W cycling warm-up followed immediately by 40 cycles (10 min) of the 10 s high-intensity: 5 s light-intensity recovery at 20 W (INT 1) protocol. This was followed immediately by a 10 min warm-down period at 50 W. Testing Day 3: A minimum of 48 h after Testing Day 2 the subjects returned to the laboratory and performed a 3 min 20 W warm-up followed immediately by 40 cycles (10 min) of 10 s heavy intensity: 5 s moderate-intensity (INT 2) protocol. This was followed immediately by a 10 min warm-down period at 50 W. The work rate during the 10 s heavy work period for both INT 1 and INT 2 was set at VET plus 50% of the difference between the VO2 at the VET and VO2max (D50%) of each subject. The work rate during the 5 s recovery of INT 2 was set at 50% of the difference between the subject’s 20 W cycling VO2 and gas-exchange threshold VO2 (D50% VET). Testing Day 4: Subjects returned to the laboratory a minimum of 48 h after Testing Day 3 and performed a 3 min 20 W warm-up followed immediately by a continuous constant load exercise at an identical power output to the 10 s work period of their INT protocols. Subjects were asked to maintain this power output until volitional fatigue or were stopped at 10 min. This was followed immediately by a 10 min warm-down period at 50 W.


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Table 1 Subject characteristics and exercise performances Age (years)

Height (cm)

Mass (kg)

VO2max (L min-1)

Peak PO (W)

VET (L min-1)

PO at VET (W)

27

188

92

4.40

395

2.90

230

27

183

88

4.67

413

3.66

295

24

179

80

3.52

327

2.07

158

24

185

94

3.50

310

2.47

210

23

183

80

3.32

358

2.24

168

23

175

71

4.02

335

2.37

163

21

172

69

2.68

249

1.73

120

Avg

24

181

82

3.73

341

2.49

192

SD

2

6

10

0.68

55

0.63

58

VO2max maximal oxygen uptake, PO power output, Peak PO power output at VO2max, VET ventilatory threshold, PO at VET power output at ventilatory threshold

Measurements Inspired and expired gases were measured breath-by-breath using a mass spectrometer and volume turbine, while simultaneous measures of deoxygenated haemoglobin (DHHb) were collected using NIRS throughout each test. Gas-exchange measurements have been previously described in detail (Babcock et al. 1994). Briefly, inspired and expired flow rates were measured with a low deadspace (90 mL) bidirectional turbine (Alpha Technologies VMM 110), and inspired and expired gases were sampled continuously at the mouth and analysed for concentrations of O2, CO2, and N2 by mass spectrometry (Perkin Elmer 1100). Changes in gas concentration were aligned with gas volumes by measuring the time delay for a square-wave bolus of gas passing the turbine to the resulting changes in fractional gas concentrations. Data collected every 20 ms were transferred to a computer, which aligned concentrations with volume data to build a profile of each breath. Breath-by-breath alveolar gas exchange was calculated using algorithms of Beaver et al. (1981). Heart rate (HR) was continuously monitored by electrocardiogram. NIRS measurements have been described in detail previously (DeLorey et al. 2003). Briefly, local muscle oxygenation profiles of the quadriceps vastuslateralis muscle were made with NIRS (Hamamatsu NIRO 300, Hamamatsu Photonics). Optodes were placed on the belly of the muscle midway between the lateral epicondyle and greater trochanter of the femur. The interoptode spacing was 5 cm. The optodes were housed in an optically dense plastic holder, thus ensuring that the position of the optodes, relative to each other, was fixed and invariant. The optode assembly was secured on the skin surface with tape and then covered with an optically dense, black vinyl sheet, thus minimizing the intrusion of extraneous light and loss of NIR-transmitted light from the field of interrogation. The thigh, with attached optodes and covering, was wrapped with an elastic bandage

to minimize movement of the optodes while still permitting freedom of movement for cycling. This preparation essentially prevented any optode movement relative to the skin surface. The intensity of incident and transmitted light was recorded continuously at 2 Hz and, along with the relevant specific extinction coefficients and optical path length, used for online estimation and display of the concentration changes from the zero-set during the resting baseline, deoxygenated (DHHb) haemoglobin. The raw attenuation signals (in optical density units) were transferred to a computer and stored for further analysis. Analysis The VO2 and NIRS profiles of the different exercise protocols were analysed from the onset to the end of exercise. Breath-by-breath gas-exchange data were filtered for aberrant data points (lying 4 SD beyond the local mean), interpolated to 1 s intervals, and then averaged into 5 s time bins to yield a single response for each subject. The arrival of the initial deoxygenated blood contributing to the measure of VO2 was detected by a combination of the first drop in PETO2 and RER. The previous VO2 data (i.e., the Phase 1 or cardiodynamic phase) were deleted. This time point, end of Phase 1, was utilized to time align the DHHb signal with the VO2 for purposes of observing the subsequent changes in the DHHb with the change in muscle VO2. The NIRS-derived DHHb data were averaged to 5 s time bins to yield a single response for each subject. Given the uncertainty of the optical pathlength in the vastuslateralis at rest and during exercise, NIRS data are presented as delta (D) arbitrary units (a.u.). NIRS-derived signal was zero set before the onset of exercise while subjects were quietly seated on the cycle ergometer. The three data points (5, 10, 15 s) of each 15 s cycle of INT exercise from 80–420 s were overlaid to observe the changes in VO2 and DHHb with the changes in work rate

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Statistical analysis Analysis of the results between each exercise condition (CONT, INT 1, INT2) on changes in VO2, and DHHb were calculated by two-way repeated-measures (RM) ANOVA. Significant differences were further tested by Student– Holman–Sidak, or Tukey post hoc analysis. Data are reported as mean ± SD unless otherwise presented. Statistical significance was declared when p \ 0.05.

Results Summary of the anthropometric characteristics and performance variables assessed during ramp incremental testing are presented in Table 1. The mean power outputs of the three exercise conditions were different (p \ 0.05) (CONT, 270 ± 43 W; INT 1, 185 ± 28 W (270 W with recovery 20 W); and INT 2, 209 ± 30 W (270 W with recovery 92 ± 5 W). The heart rates after 4 min of exercise were different (p \ 0.05) in all three exercise protocols (CONT, 162 ± 4 bpm; INT 1, 132 ± 3 bpm, and INT 2, 142 ± 3 bpm). The VO2 response for each of the exercise protocols are shown in Fig 1. The mean VO2 for the time period 80–420 s of the three exercise conditions was used to describe the ‘‘steady state’’ response after the initial onset of exercise. Average VO2 differed among all three exercise conditions [CONT 3.77 ± 0.61 L min-1, INT 1 2.81 ± 0.36 L min-1, and

123

4.5 4.0 3.5

VO2 (L/min)

during each 15 s cycle. It was assumed that the lowest mean 5 s VO2 within each 15 s cycle within each subject was a consequence of the lowest power output of each of the INT protocols and the two subsequent mean 5 s VO2 data were considered to be linked to the following two data points of the 10 s work period. The three mean VO2 data points of all the subjects, within each 15 s cycle of each of the intermittent exercise groups were then compared. The oxidative/substrate phosphorylation contribution to the 10 s INT was determined by the following method. Initially the expected O2 cost per Watt (W) for the supra threshold work rate during CONT was determined by the VO2 observed at the end of Phase 2 of the oxygen uptake kinetics profile. The VO2 after this point begins to increase, independent of a change in power output, as a function of the VO2 slow component (Paterson and Whipp 1991) and as such was deemed inappropriate for this analysis. This VO2 was used as the predicted VO2 of the 10 s work period of INT exercise. The difference between the highest actual 5 s average VO2 within the 15 s cycles of INT 1 and 2 exercises and the predicted VO2 was utilized to quantify the O2 deficit or the substrate phosphorylation contribution during the work periods.


3.0 2.5 2.0 1.5 1.0 0.5 0.0 0

30 60 90 120 150 180 210 240 270 300 330 360 390 420

time (s)

Fig. 1 VO2 during INT 1 (10 s work: 5 s recovery (20 W) cycling) (open circle), INT 2 (10 s work: 5 s recovery moderate cycling) (grey filled circle), and CONT (filled circle) (The overall VO2 between 80 s and 420 s was lower in INT 1 than INT 2 and both INT protocols were different than CONT; p \ 0.05)

INT 2 3.04 ± 0.49 L min-1 (p \ 0.05)]. Consecutive 15 s work and recovery cycles were overlaid between 80–420 s following exercise onset to give a mean VO2 response for each 5 s of the work (i.e., 0–5 s and 6–10 s) and recovery periods (i.e., 11–15 s) of both INT 1 and INT 2. VO2 was larger during both work periods compared to the recovery periods for INT 1 (p \ 0.05) (Fig. 2a). No differences in the VO2 response were observed between work and recovery during INT 2 (p [ 0.05) (Fig. 2b). The DHHb response for the CONT exercise condition differed from both INT protocols (p \ 0.05) from 80 s to 420 (CONT; 25.7 ± 0.9 a.u., INT 1; 16.4 ± 0.8 a.u., and INT 2; 15.8 ± 0.8 a.u.) (Fig. 3). The average DHHb over each 5 s of the 15 s work: recovery cycles were overlaid and analysed from 80 to 420 s. During INT 1 and INT 2, DHHb was the lowest during the 5 s of recovery and then was increased at 0–5 s and 5–10 s of work (p \ 0.05) (Fig. 4a, b). The ratio of the DHHb per unit VO2 (i.e., muscle deoxygenation level for a given VO2 also exhibited differences (p \ 0.05) amongst all conditions between 80 and 420 s (CONT 6.9 ± 0.18; INT 1, 5.6, ± 0.23; and INT 2, 4.9 ± 0.28) (Fig. 5). The calculated aerobic contribution at 10 s of the work period of INT 2 (88% ± 7.7) was greater than INT 1 (83% ± 7.6) (p \ 0.05).

Discussion The present study examined the effects of two different recovery periods on the oxygen consumption and muscle deoxygenation responses to heavy exercise. The major findings were: (1) a decreased DHHb and DHHb/VO2 during the work periods of INT 1 and INT 2 versus the

Fig. 2 Average oscillations in VO2 (±SE) INT 1 (a) and INT 2 (b) at 0–5 s work, 6–10 s work and recovery. Different from recovery (asterik) (p \ 0.05) from 80–420 s

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VO2 L/min

a

3.25

3.00

*

*

2.75

0-5 s work

6-10 s work

30 25 20

ΔHHb (a.u.)

3.25

3.00

2.75

2.50

2.50

15 10 5 0 -5 0

b

VO2 L/min


30 60 90 120 150 180 210 240 270 300 330 360 390 420

time (s)

Fig. 3 DHHb during INT 1 (10 s work: 5 s recovery) (open circle), INT 2 (10 s work: 5 s recovery 89 W moderate cycling) (grey filled circle), and CONT (filled circle). Differences between CONT and both INT conditions between 80 and 420 s (p \ 0.05)

CONT suggesting an improved, recovery-dependent matching of O2 delivery to O2 utilization during the work periods of intermittent versus continuous exercise, and (2) recovery at a moderate intensity (INT 2) elicits a higher VO2 for a similar DHHb compared to low-intensity recovery (INT 1) suggesting an intensity-dependent enhancement of the ratio of O2 delivery to oxygen utilization during both the work and recovery periods.

recovery

0-5 s work

6-10 s work recovery

20 mmHg versus 120 mmHg) that have been observed during passive knee-extension exercise (Ra˚degran and Saltin 1998). Similar findings (Walløe and Wesche 1988) have suggested that during a recovery duration comparable to that of INT exercise, elevated blood velocity is maintained until the next contraction. It is possible that this increased blood velocity and flow within the microvasculature would create a greater pressure head against the subsequent increase in intramuscular contraction pressures during the work period. This would result in greater muscle perfusion during INT compared to CONT. This facilitation for improved O2 delivery would explain the reduced DHHb/VO2 of INT versus CONT exercise observed in this research. This differs from earlier work in continuous versus intermittent exercise by Esse´n et al. (1977). They observed smaller femoral arterial-venous O2 differences and greater limb blood flow, during continuous versus intermittent exercise (15 s work: 15 s recovery). The discrepancies between the studies may be associated with the longer durations of the work and recovery periods of Essen’s intermittent exercise protocol which could elicit a greater fall in blood flow and lower O2 delivery. Taken together, our data suggest that this INT exercise elicits a recovery-dependent effect that improves microvascular blood flow distribution and/or O2 delivery during the work and recovery periods versus continuous exercise.

Decreased DHHb during the work of INT versus CONT

Improved blood flow distribution during INT 2 versus INT 1

In the present study, the higher DHHb/VO2 during CONT (Fig. 5) suggests a poorer matching of O2 delivery to O2 utilization relative to that achieved during the 10 s work periods of intermittent exercise. It has been shown previously that blood velocity increases (likely reflecting increases in blood flow) during the relaxation phase versus the contraction phase (2.54 m/s versus 0.57 m/s) of rhythmic exercise. Others (Ra˚degran and Saltin 1998) suggest that blood flow would be greater during the rest versus the work period during intermittent exercise. This increase in blood flow during INT may also be facilitated by the lower intramuscular pressures (i.e.,

In the present study, DHHb/VO2 was reduced during INT 2 (moderate-intensity recovery) compared to INT 1(lightintensity recovery), suggesting an improved blood flow distribution during INT 2. Differentially, Lutjemeier et al. (2005), observed increasing blood flow during light intensities which they attributed to muscle pump action. At moderate intensities this action disappeared. They utilized a variety of constant load knee-extension exercises with similar contraction frequencies (knee extension 40 kicks per min) as the current cycling protocol (80 rpm) (Lutjemeier et al. 2005; Sadamoto et al. 1983). Others (Walløe and Wesche 1988) have observed a similar muscle pump

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Fig. 4 Average oscillations in DHHb (±SE) INT 1 (a) and INT 2 (b) at 0–5 s work, 6–10 s work and recovery different from recovery (asterik) (p \ 0.05) from 80–420 s

a

b

17.5

17.0

ΔHHb (a.u.)

ΔHHb (a.u.)

17.0 16.5 16.0 15.5

Δ HHb/VO2

0-5 s work 6-10 s work recovery 8 7 6 5 4 3 2 1 0 -1 -2 -3 -4 60

120

180

240

300

360

420

Time (s)

Fig. 5 DHHb/VO2 during INT 1 (10 s work: 5 s recovery) (open circle), INT 2 (10 s work: 5 s recovery moderate cycling (89 W) (grey filled circle), and CONT (filled circle). All conditions were different from each other between 80 and 420 s (p \ 0.05)

enhancement of blood flow during knee-extension ramp exercise. The decreased blood flow during the light recovery in INT 1 may be a function of the reduced contractile pressures during cycling versus knee-extension exercise that would occur at light versus moderate-intensity exercise (Saltin 1985; Walløe and Wesche 1988). This may enhance the muscle pump effect during cycling exercise at moderate intensities as the contractile pressures are working against a reduced blood pressure. Subsequently an enhanced muscle pump effect may occur during INT 2 compared to INT 1. The Lutjemeier results are not necessarily directly transferable to cycling exercise because of the different exercise modality, although the attempt was made to account for the differences in work intensity to elicit similar muscle contractile pressures. Nevertheless, it is important to note that our data support the notion that both INT exercise protocols display similar increased O2 delivery conditions as has been observed within the light-intensity knee-extension exercise domain (Lutjemeier et al. 2005). Moreover, Ferreira et al. (2005a) showed that the drop in muscle capillary blood flow is larger upon the immediate cessation of moderate-intensity compared to light-intensity cycling and suggested that the removal of the muscle pump was responsible for this decline. In light of this, the inclusion of the moderate work rate during the recovery of INT 2

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16.0 15.5

14.5

14.5

0

16.5

15.0

15.0

-60

17.5

0-5 s work 6-10 s work

recovery

may increase the muscle pump effect and account for the decrease in DHHb/VO2 during INT2 compared to INT1. It is also known that increases in muscle blood flow occur through vasodilation independent of the muscle pump action (Andersen and Saltin 1985; Duling and Klitzman 1980; Harper et al. 2008; Laughlin and Korzick 2001). There is some controversy as to the time course of vasodilation to exercise [4 s (Bearden 2007; Gorczynski et al. 1978) to [20 s (Gorczynski et al. 1978)]. Changes may follow a two phase pattern with a rapid initial response (\5 s) and a delayed second phase ([20 s) (Rogers et al. 2006). Single contractions that increase arteriolar diameter by 5 s (Mihok and Murrant 2004; Van Teeffelen and Segal 2006) and increase red blood cell velocity in \5 s in mammals (Kindig et al. 2002) have been observed. The capacity of the microvasculature to quickly and sequentially adjust to changes in muscle contraction intensity has also been demonstrated in humans (Rogers et al. 2006). The symmetry of the blood flow response to increases and decreases of forearm exercise intensity were particularly notable. Rogers et al. (2006) suggested that these adjustments cannot be made during very fast variations in exercise intensity. It would seem plausible that the INT protocol utilized in the present study may elicit repeated changes in vasodilation and constriction with the fluctuations in work intensity with a net improvement in blood flow, but this has yet to be verified. The present data suggest that the greater muscle pump effect and/or the effects of higher power output during the recovery period increases vasodilation during the recovery periods of INT 2, which enhances O2 delivery during the subsequent 10 s work periods compared to INT 1. The higher metabolic stress of CONT was associated with a larger DHHb/VO2. This suggests a higher reliance on O2 extraction and compromised O2 delivery. The increased production of metabolites and production of vasodilators such as nitric oxide (Matsumoto et al. 1994) are expected to elicit greater vasodilation as intensity increases (Sarelius and Pohl 2010; Stowe et al. 1975). However, the relative reduction in blood flow distribution during CONT may result from muscle contraction-related impedance to flow. The different exercise protocols of the


current study elicited differing heart rate responses which could affect changes in perfusion pressure and subsequent microvascular blood flow in the working muscle. It would seem that the possible impedance to blood flow during CONT exercise has offset the effects of increased vasodilation or increased perfusion pressure (Walker et al. 2007). Greater aerobic contribution during the heavy intensity work period of INT 2 versus INT 1 despite higher power output The physiological response to recovery over short durations (5 s) encompasses several mechanisms. (1) An elevated VO2 for rephosphorylation of ADP to ATP and Cr to PCr, as well as the work for ventilatory buffering of CO2 via the carbonic anhydrase reaction (Jones 2008; Jones and Heigenhauser 1996) and the replenishment of muscle O2 stores (Christensen and Saltin 1960). Conversely the contribution from substrate level phosphorylation is required during the supra lactate threshold work periods of these INT protocols (Whipp and Wasserman 1972). The heavy intensity work rate of both INT protocols utilizes less oxidative contribution than that of the similar work rate during CONT exercise. Moreover, it would seem that the higher power output required during recovery (INT 2) and presumably less ATP available for recovery compared to INT 1 would demand a greater substrate level phosphorylation contribution to the subsequent work period (Peronnet and Thibault 1989). On the contrary, the calculated oxidative phosphorylation contribution (see ‘‘Methods’’) at 10 s of the work period of INT 2 (88% ± 7.7) was greater than INT 1 (83% ± 7.6) (p \ 0.05). Our data suggest that the increase in power output of the recovery period of INT 2 is accompanied by greater oxidative phosphorylation contribution during the 10 s work period to meet the energy demands. The elevated VO2 during INT2 may be associated with the speeding of VO2 kinetics over the recovery work transition compared to INT 1, as a function of the improved blood flow distribution at the onset of the work period that has been observed elsewhere (DiMenna et al. 2010; Ferreira et al. 2005a, 2005b, 2006, 2005c, 2005d; Harper et al. 2006; Hughson et al. 1996). In particular, Grassi et al. (2000) observed an *25% speeding in VO2 kinetics at the onset of a highintensity exercise in a model in which blood flow was elevated before the onset of exercise to meet the O2 requirements expected during an abrupt transition to highintensity exercise. It has been suggested that improved perfusion of Type 2 muscle fibres elicited the speeding in VO2 kinetics and that the oxidative ATP resynthesis within these Type 2 fibres may be particularly enhanced via changes in O2 delivery (Barstow et al. 1996; Krustrup et al. 2004). Based on previously reported observations, there

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could be similar fibre type composition between the gastrocnemius muscle group in the animal model used by Grassi et al. and the vastus muscle group in the subjects in the current study (Gollnick et al. 1972; Maxwell et al. 1977). The high relative power output (83% VO2peak) employed in the current study would require substantial recruitment of low oxidative, Type 2 fibres. DiMenna et al. (2010) also suggests that the enhanced blood flow during supine versus upright exercise, similar to the INT exercise in the present study, over comparable work–work transitions during upright exercise, speeds O2 kinetics. The improved blood flow distribution observed (increased DHHb/VO2) of INT 2 versus INT 1 may speed O2 kinetics. These speeded VO2 kinetics could be a factor in reducing the amplitude of the fluctuations in VO2 over the INT 2 work recovery transitions. Although we speculate that speeding of VO2 kinetics as a consequence of improved blood flow in Type 2 muscle fibres could be responsible for the responses observed in the present study, it has to be acknowledged that a number of studies suggest that VO2 on-kinetics are not necessarily improved by enhanced blood flow at the onset of the highintensity exercise (Delp 1999; Grassi et al. 1998a, b; Poole et al. 2008). Within the constraints of our data either scenario is possible. It is possible to utilize measures of DHHb as a proxy to reflect changes in PO2 (Behnke et al. 2001). Changes in PO2 has been observed to be the stimulus for changes in muscle VO2 (Barstow et al. 1994; Whipp and Wasserman 1972) at the onset of electrically stimulated muscle contractions (Behnke et al. 2001). Under rest-exercise transitions Behnke et al. (2001) observed a delayed (19 s) decrease in PO2 which they attributed to the delay in O2 delivery. A reduced time delay in the drop in muscle PO2 at the onset of exercise under intermittent exercise conditions similar to the present study (Behnke et al. 2002; Delp and Duan 1996). This was ascribed to an inherent speeding of oxidative phosphorylation. Over the light or moderate recovery: heavy intensity work transitions in the present study a delay in the DHHb (PO2) response was not observed. It is suggested that this immediate change in DHHb and presumably PO2 and VO2 reflects a virtually immediate rise in VO2 at the onset of the heavy intensity work periods of INT 2 indicative of a negligible (1–2 s) time delay of the on response of the oxidative machinery. The greater increases in DHHb/VO2 during the work periods of INT 1, versus INT 2 suggest a differing response to DHHb relative to QO2. The complex interactions of the differing exercise protocols on fibre type recruitment, fast acting and/or slower acting vasodilation, and VO2 kinetics makes it difficult to make strong suggestions on the proportionality of these different mechanisms to the DHHb/ VO2 response.

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We conclude that recurring short recovery periods of INT exercise results in an improved matching of O2 delivery to O2 utilization (improved muscle perfusion) during the subsequent work periods compared to continuous exercise performed at the same work rate. It was also shown that when a moderate exercise intensity, versus a light-intensity work rate, was utilized during the recovery period of this INT, an intensity-dependent improvement in O2 delivery to O2 utilization was observed during the work periods. Acknowledgments The authors would like to thank Brad Hansen for his technical expertise. Funding received from NSERC. Conflict of interest

The authors have no conflict of interest.

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