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J Appl Physiol 105: 538-546, 2008. First published May 29, 2008; doi:10.1152/japplphysiol.90357.2008
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Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise from an elevated baseline

Fred J. DiMenna,1 Daryl P. Wilkerson,1 Mark Burnley,2 and Andrew M. Jones1

1School of Sport and Health Sciences, University of Exeter, Exeter, Devon; and 2Department of Sport and Exercise Science, Aberystwyth University, Ceredigion, United Kingdom

Submitted 4 March 2008 ; accepted in final form 23 May 2008


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
It has been suggested that the slower O2 uptake (VO2) kinetics observed when exercise is initiated from an elevated baseline metabolic rate are linked to an impairment of muscle O2 delivery. We hypothesized that "priming" exercise would significantly reduce the phase II time constant ({tau}) during subsequent severe-intensity cycle exercise initiated from an elevated baseline metabolic rate. Seven healthy men completed exercise transitions to 70% of the difference between gas exchange threshold (GET) and peak VO2 from a moderate-intensity baseline (90% GET) on three occasions in each of the "unprimed" and "primed" conditions. Pulmonary gas exchange, heart rate, and the electromyogram of m. vastus lateralis were measured during all tests. The phase II VO2 kinetics were slower when severe exercise was initiated from a baseline of moderate exercise compared with unloaded pedaling (mean ± SD {tau}, 42 ± 15 vs. 33 ± 8 s; P < 0.05), but were not accelerated by priming exercise (42 ± 17 s; P > 0.05). The amplitude of the VO2 slow component and the change in electromyogram from minutes 2 to 6 were both significantly reduced following priming exercise (VO2 slow component: from 0.47 ± 0.09 to 0.27 ± 0.13 l/min; change in integrated electromyogram between 2 and 6 min: from 51 ± 35 to 26±43% of baseline; P < 0.05 for both comparisons). These results indicate that the slower phase II VO2 kinetics observed during transitions to severe exercise from an elevated baseline are not altered by priming exercise, but that the reduced VO2 slow component may be linked to changes in muscle fiber activation.

oxygen uptake kinetics; phase II time constant; oxygen uptake slow component; work-to-work transition

AFTER A SHORT DELAY, PULMONARY oxygen uptake (VO2) rises exponentially when external work rate is increased during cycle ergometer exercise (58, 60). The time constant ({tau}) describing this "fundamental" (phase II) response has been shown to closely reflect the kinetics of O2 consumption in the contracting muscles (1, 22). With appropriate caveats, the study of pulmonary VO2 kinetics can, therefore, provide useful insight into the factors that regulate and/or limit muscle oxidative metabolism in the transition from one work rate to another (59). This information is important because slow VO2 kinetics (as is observed in older age, deconditioning, and a variety of disease states) obligate a greater rate of substrate-level phosphorylation, resulting in a greater perturbation to muscle homeostasis and a reduction in exercise tolerance (29).

The phase II {tau} has been reported to be greater (i.e., the VO2 kinetics are slower) when a step transition to a higher work rate is initiated from a metabolic rate that exceeds that recorded during "unloaded" pedaling (5, 15, 25, 26, 40, 61, 62). For example, the phase II {tau} has been reported to be ~60% longer when severe-intensity exercise commences from a moderate-intensity work rate rather than from unloaded pedaling (61). The cause of the slower VO2 kinetics during such "work-to-work" transitions is unclear. However, it has been suggested that the altered balance between parasympathetic and sympathetic control of heart rate (HR) (and thus cardiac output) might reduce muscle O2 delivery and restrict the VO2 kinetics during work-to-work transitions (25, 26). Another possible explanation for the slower VO2 kinetics during work-to-work transitions is that they reflect the metabolic properties of the muscle fiber pool contributing to force production (5, 31, 61, 62). This will be dictated by Henneman's "size principle" (24), which posits that fibers are recruited in an orderly fashion, with smaller, more oxidative fibers recruited first. There is evidence that fibers that are higher in the recruitment hierarchy, which would be isolated in a work-to-work transition, have slower VO2 kinetics as well as a greater O2 cost of contraction relative to lower order fibers (12, 50, 64).

"Priming" exercise has been used extensively as an intervention to test the hypothesis that VO2 kinetics are rate limited by O2 availability (29), with it having been demonstrated that prior high-intensity exercise increases muscle blood flow and indexes of muscle oxygenation before and during subsequent exercise (6, 13, 14, 19, 31, 35). Priming exercise typically results in an "overall" speeding of VO2 kinetics during subsequent high-intensity exercise [as assessed with the mean response time (MRT); Refs. 9, 21, 39]. This speeding is generally attributable to a reduction in the amplitude of the so-called "VO2 slow component" and is often associated with an increased amplitude of the VO2 fundamental component (3, 6–8, 17, 32, 55, 63). However, a reduction in the phase II {tau} has also been reported in some cases (13, 23, 27).

It has been proposed that the VO2 slow component is related to an alteration in fiber recruitment (possibly the progressive activation of less efficient high-order fibers) as heavy/severe exercise proceeds (2, 16, 36, 37, 46, 52, 56). However, the emergence of the VO2 slow component at ~120 s of high-intensity exercise might also reflect the existence of much slower VO2 kinetics in high-order fibers that are recruited at, or close to, the onset of exercise (44, 61). Priming exercise might augment fiber recruitment during the initial stages of subsequent exercise, thereby attenuating the need for further fiber recruitment (6, 10) and/or speed the kinetics in the initially recruited fibers by alleviating any local blood flow to metabolic rate heterogeneity (21). In either case, an increased VO2 fundamental component amplitude and a reduced VO2 slow component would be anticipated, with the latter being associated with a reduction in neuromuscular activity [as reflected in the integrated electromyogram (iEMG)]. However, a reduction in the phase II {tau} would only be expected if an O2 delivery limitation, extant in the control condition, were resolved by the priming intervention.

From the above, it is clear that using priming exercise in conjunction with the work-to-work model is potentially useful for exploring the mechanistic bases to both the slower phase II VO2 kinetics that are apparent during work-to-work exercise transitions and the VO2 slow-component phenomenon that is present during heavy/severe exercise. The results of such a study potentially have implications for understanding, and resolving, the slow VO2 kinetics that are evident in a number of patient populations and that have been suggested to be related, at least in part, to inadequate muscle O2 delivery (46). The purpose of the present investigation was, therefore, to determine the influence of priming exercise on VO2 kinetics and neuromuscular activation during moderate-to-severe-intensity exercise transitions. We hypothesized that the phase II {tau} would be longer when severe exercise was initiated from a baseline of moderate exercise compared with a baseline of unloaded pedaling. We further hypothesized that prior severe-intensity priming exercise would 1) significantly reduce the phase II {tau}; and 2) significantly reduce both the amplitude of the VO2 slow component and the change in iEMG between 2 and 6 min ({Delta}iEMG6-2) during a subsequent moderate-to-severe exercise transition.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects.   Seven male subjects (mean ± SD age 31 ± 8 yr, stature 1.80 ± 0.06 m, mass 83.2 ± 4.9 kg) volunteered and gave written, informed consent to participate in this study, which had been approved by the local Research Ethics Committee. The subjects were all recreationally active and were familiar with the exercise mode and experimental procedures used in the present study. On test days, subjects were instructed to report to the laboratory in a rested state, having completed no strenuous exercise within the previous 24 h, and having abstained from food, alcohol, and caffeine for the preceding 3 h.

Experimental procedures.   All testing was completed in an air-conditioned laboratory at a temperature of 21 ± 2°C. The subjects visited the laboratory on seven occasions over a 4-wk period to perform exercise tests on an electronically braked cycle ergometer (Lode Excalibur Sport, Groningen, the Netherlands). Testing was conducted at the same time of day (±2 h) for each subject. On the first visit, the subjects completed a ramp incremental exercise test for determination of peak VO2 (VO2peak) and gas exchange threshold (GET). On each of six subsequent visits, subjects completed bouts of severe-intensity exercise (at a work rate calculated to require 70% of the difference between the GET and VO2peak, i.e., 70% "{Delta}"), initiated from a baseline of moderate-intensity exercise (90% GET). The protocol is illustrated in Fig. 1. In M->S Unprimed (M, moderate intensity; S, severe intensity), the work-to-work transition was completed in the absence of any prior exercise; in M->S Primed, the work-to-work transition was preceded by a bout of severe-intensity exercise (70% {Delta}) (U->S, where U is unloaded) and a rest period of 5 min. Each of the two conditions was presented to subjects three times in random order, and each laboratory visit was separated by at least 48 h.


Figure 1
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  		Fig. 1. Schematic illustration of the experimental protocol. U->S involved 3 min of unloaded cycling followed by an abrupt transition to a severe-intensity work rate. M->S Unprimed and M->S Primed each involved 3 min of unloaded cycling, followed by 4 min of moderate-intensity exercise, and then 6 min of severe-intensity exercise. M->S Primed was performed after U->S and 5 min of rest.

 
The ramp incremental exercise test consisted of 3 min of pedaling at 0 W, followed by a continuous ramped increase in work rate of 30 W/min until the subject was unable to continue. The subjects cycled at 80 rpm, and saddle and handlebar heights were recorded. The same pedal rate and settings were reproduced on subsequent tests. The VO2peak was defined as the highest 30-s mean value recorded before the subject's volitional termination of the test; "secondary criteria" were not used to verify that a "true" maximum had been obtained (47). The GET was determined from a cluster of measures, including 1) the first disproportionate increase in carbon dioxide output (VCO2) from visual inspection of individual plots of VCO2 vs. VO2; 2) an increase in expiratory ventilation (VE)/VO2 with no increase in VE/VCO2; 3) an increase in end-tidal O2 tension with no fall in end-tidal CO2 tension. The work rates that would require 90% of the GET (moderate exercise, M) and 70% of the difference ({Delta}) between the GET and VO2peak (severe exercise, S) were estimated, with account taken of the MRT of the VO2 response to ramp exercise (assumed to approximate two-thirds of the ramp rate, i.e., 20 W) (57). These work rates were subsequently applied during the work-to-work transitions completed in both the unprimed and primed state.

The subjects returned to the laboratory on six occasions to perform one of the following protocols: 1) 3 min of "unloaded" cycling at 20 W, 4 min of moderate-intensity cycling, and 6 min of severe-intensity cycling; and 2) 3 min of "unloaded" cycling at 20 W, 6 min of severe-intensity cycling, 5 min of passive rest, 3 min of "unloaded" cycling at 20 W, 4 min of moderate-intensity cycling, and 6 min of severe-intensity cycling (Fig. 1). The first protocol provided data for transitions to severe-intensity exercise from a moderate-intensity baseline without priming (M->S Unprimed). The second protocol provided data for transitions to severe-intensity exercise from an unloaded baseline (U->S), and from a moderate-intensity baseline after priming (M->S Primed). The VO2 responses from like transitions were averaged before any analysis being performed to enhance the signal-to-noise ratio and improve confidence in the parameters derived from the model fits (38, 59).

During all tests, pulmonary gas exchange and ventilation were measured continuously using a portable gas analysis system (MetaMax 3B, Cortex Biophysik, Leipzig, Germany). A DVT turbine digital transducer measured inspired and expired airflow, while an electrochemical cell O2 analyzer and ND infrared CO2 analyzer simultaneously measured expired gases. Subjects wore a nose clip and breathed through a low-dead space, low-resistance mouthpiece that was securely attached to the volume transducer. The inspired and expired gas volume and gas concentration signals were continuously sampled via a capillary line connected to the mouthpiece. The gas analyzers were calibrated before each test with gases of known concentration, and the turbine volume transducer was calibrated using a 3-liter syringe (Hans Rudolph, Kansas City, MO). Pulmonary gas exchange and ventilation were calculated and displayed breath by breath. HR was measured every breath during all tests using short-range radiotelemetry (Polar S610, Polar Electro Oy, Kempele, Finland). During one of the three trials under each condition, a blood sample from a fingertip was collected into a capillary tube over the 20 s preceding any step transition in work rate and within the last 20 s of exercise and subsequently analyzed to determine blood [lactate] (where brackets denote concentration) (YSI 1500, Yellow Springs Instruments, Yellow Springs, OH). Blood lactate accumulation ({Delta}blood [lactate]) was calculated as the difference between blood [lactate] at end exercise and blood [lactate] at baseline.

Neuromuscular activity of the m. vastus lateralis of the left leg was measured using bipolar surface EMG. The leg was initially shaved and cleaned with alcohol around the belly of the muscle, and graphite snap electrodes (Unilect 40713, Unomedical, Stonehouse, UK) were adhered to the prepared area in a bipolar arrangement (interelectrode distance: 40 mm). A ground electrode was positioned on the rectus femoris equidistant from the active electrodes. The sites of electrode placement (20 cm superior to the lateral tibial head) were chosen according to the recommendations provided in the EMG software (Mega Electronics). To secure electrodes and wires in place and to minimize movement during cycling, an elastic bandage was wrapped around the subject's leg. Pen marks were made around the electrodes to enable reproduction of the placement in subsequent tests. The EMG signal was recorded using a ME3000PB Muscle Tester (Mega Electronics).

EMG measurements at a sampling frequency of 1,000 Hz were recorded throughout all exercise tests. The bipolar signal was amplified (amplifier input impedance > 1 M{Omega}), and data were collected online in raw form and stored on a personal computer using MegaWin software (Mega Electronics). The raw EMG data were subsequently exported as an ASCII file and digitally filtered using Labview 8.2 (National Instruments, Newbury, UK). Initially, the signals were filtered with a 20-Hz high-pass, second-order Butterworth filter to remove contamination from movement artifacts. The signal was then rectified and low-pass filtered at a frequency of 50 Hz to produce a linear envelope. The average iEMG was calculated for 15-s intervals throughout exercise, with these values normalized to the average measured during 15–180 s of unloaded cycling before the initial transition. Therefore, all iEMG data are presented as a percentage of the initial unloaded cycling phase. Data from repeat trials were averaged, and {Delta}iEMG6–2 was defined as the difference between the average iEMG over the last 15 s of exercise and the average from 105–120 s.

Data analysis procedures.   The breath-by-breath VO2 data from each test were initially examined to exclude errant breaths caused by coughing, swallowing, sighing, etc., and those values lying more than 4 SDs from the local mean (defined using a five-breath rolling average) were removed. The breath-by-breath data were subsequently linearly interpolated to provide second-by-second values, and, for each individual, identical repetitions from the three conditions were time aligned to the start of exercise and ensemble averaged. The first 20 s of data after the onset of exercise (i.e., the phase I response) were deleted (59, 60), and a nonlinear least squares algorithm was used to fit the data, as described in the following biexponential equation:

Formula
where VO2(t) is the absolute VO2 at a given time t; VO2baseline is the mean VO2 in the baseline period; Ap, TDp, and {tau}p are the amplitude, time delay, and time constant, respectively, describing the phase II increase in VO2 above baseline; and As, TDs, and {tau}s are the amplitude of, time delay before the onset of, and time constant describing the development of the VO2 slow component, respectively. An iterative process was used to minimize the sum of the squared errors between the fitted function and the observed values. VO2baseline was defined as the mean VO2 measured over the final 90 s of exercise preceding the step transition to severe exercise. The end-exercise VO2 was defined as the mean VO2 measured over the final 30 s of severe exercise. The absolute Ap was defined as the sum of VO2baseline and Ap. Because the asymptotic value (As) of the exponential term describing the VO2 slow component may represent a higher value than is actually reached at the end of the exercise, the actual amplitude of the VO2 slow component at the end of exercise was defined as As. The amplitude of the slow component was also described relative to the entire VO2 response.

To provide information on the "overall" VO2 kinetics, with no distinction made for the various phases of the response, we also fitted a single-exponential curve without time delay to the data from the onset to the end of exercise. The MRT so derived was used to calculate the O2 deficit (O2D) using the equation:

Formula
In addition, for all three conditions, the functional "gain" of the phase II VO2 response was computed by dividing the asymptotic Ap response by the {Delta}work rate. The functional gain of the entire response was calculated in a similar manner.

We also modeled the HR response to exercise in each of the three conditions. For this analysis, breath-by-breath data were linearly interpolated to provide second-by-second values, and, for each individual, identical repetitions from the three conditions were time aligned to the start of exercise and ensemble averaged. A nonlinear least squares monoexponential model without time delay was used to fit the data, with the fitting window commencing at t = 0 and constrained at the time delay before the onset of the VO2 slow component (see above). The phase II HR {tau} so derived provides information on the overall response dynamics in the absence of any HR "slow component".

Statistics.   The parameters derived from the modeling of the VO2 and HR data and the EMG data were analyzed using one-way repeated-measures analysis of variance with Fisher's least significant difference tests, as appropriate, to identify the location of statistically significant differences between the three conditions. Paired t-tests were used to compare kinetics parameters between VO2 and HR within conditions. Paired t-tests were also used to compare the average iEMG at 120 s with the average at end exercise within conditions. Pearson product-moment correlation coefficients were used to assess the relationships between changes in the parameters of the VO2 kinetics, HR kinetics, and iEMG response. Significance was accepted at P < 0.05. Results are reported as means ± SD.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
The subjects' VO2peak was 45 ± 5 ml·kg–1·min–1, with the GET occurring at 20 ± 4 ml·kg–1·min–1 (46 ± 6% VO2peak). The peak work rate attained in the incremental test was 359 ± 42 W, and the work rate at the GET was 102 ± 26 W. The work rates calculated for moderate and severe exercise were 92 ± 23 and 266 ± 38 W, respectively.

Blood [lactate] and HR.   The baseline blood [lactate] was significantly greater for M->S Primed compared with the other two conditions (U->S, 0.6 ± 0.2; M->S Unprimed, 1.2 ± 0.2; M->S Primed, 3.5 ± 1.7 mM; P < 0.05). There was no significant difference in {Delta}blood [lactate] between the three conditions (U->S, 5.1 ± 1.5; M->S Unprimed, 5.1 ± 1.1; M->S Primed, 3.6 ± 1.6 mM), although it tended to be lower in M->S Primed compared with the other two conditions (P = 0.08). The baseline HR was significantly different between the three conditions (79 ± 6, 98 ± 10, and 116 ± 10 beats/min for U->S, M->S Unprimed, and M->S Primed, respectively; Table 1), and these differences persisted during exercise (Fig. 2). The pertinent parameters of the HR kinetics in each of the three conditions are reported in Table 1, and the group mean HR response at 30-s intervals is illustrated in Fig. 2. The HR phase II {tau} was similar between the three conditions (U->S, 37 ± 14 s; M->S Unprimed, 36 ± 17 s; M->S Primed, 42 ± 12 s; Table 1).


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  		Table 1. Heart rate kinetics during U->S, M->S Unprimed, and M->S Primed

 

Figure 2
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  		Fig. 2. Heart rate response at 30-s intervals during baseline cycling and severe exercise. {circ}, U->S condition; {blacksquare}, M->S Unprimed condition; {triangleup}, M->S Primed condition. Values are means ± SE. *Significant difference between all three conditions (P < 0.05); #significant difference between M->S Primed and the other two conditions (P < 0.05).

 
VO2 kinetics.   The parameters of the VO2 response in each of the three conditions are reported in Table 2 and are illustrated for a representative subject in Fig. 3. As per the experimental design, the baseline VO2 was significantly higher for the M->S transitions compared with the U->S transition; however, the baseline VO2 was also significantly higher for the M->S Primed compared with the M->S Unprimed condition. The phase II {tau} was significantly longer for the M->S transitions compared with the U->S transition (P < 0.05), but there was no significant difference between the M->S Unprimed and M->S Primed conditions (U->S, 33 ± 8 s; M->S Unprimed, 42 ± 15 s; M->S Primed, 42 ± 17 s; Table 2). The change (slowing) of the VO2 phase II {tau} between U->S and M->S Unprimed was not significantly correlated with the change in HR kinetics (r = 0.38). The Ap was significantly lower for both M->S transitions compared with the U->S transition. However, phase II gain was significantly greater for M->S Primed compared with U->S.


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  		Table 2. VO2 kinetics during U->S, M->S Unprimed, and M->S Primed

 

Figure 3
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  		Fig. 3. Pulmonary O2 uptake (VO2) response following the onset of severe exercise in a representative subject. {blacksquare}, U->S condition; {circ}, M->S Unprimed condition; bullet, M->S Primed condition. Vertical dotted line represents the abrupt transition to the higher work rate. Note that the phase II VO2 kinetics are markedly slower when the transition is initiated from a higher baseline metabolic rate without priming. After priming, there is no change in the phase II time constant, but the overall VO2 response is faster due to an elevation in phase II absolute amplitude and a reduction in the amplitude of the VO2 slow component. See text for further details.

 
The VO2 slow component was greatest for U->S, least for M->S Primed, and intermediate for M->S Unprimed, with all conditions significantly different from one another (U->S, 0.62 ± 0.20 l/min; M->S Unprimed, 0.47 ± 0.09 l/min; M->S Primed, 0.27 ± 0.13 l/min; Table 2). The MRT was significantly longer in M->S Unprimed compared with U->S, but there was no difference between M->S Primed and U->S. The end-exercise VO2 was not significantly different between conditions. The end-exercise gain was significantly greater in M->S Unprimed compared with U->S, but was significantly reduced by priming exercise, such that there was no difference between M->S Primed and U->S (Fig. 4). When expressed in absolute terms, there was no significant difference in O2 deficit between U->S and M->S Unprimed, but the O2 deficit in M->S Primed was significantly lower than in the two other conditions. However, relative to the increase in work rate, O2 deficit was significantly greater for M->S Unprimed compared with U->S and M->S Primed.


Figure 4
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  		Fig. 4. Group mean VO2 response following the onset of severe exercise, where VO2 is expressed per unit change in work rate (i.e., gain). The solid line represents the U->S condition; the short-dashed line represents the M->S Unprimed condition; and the long-dashed line represents the M->S Primed condition. Note that the elevation in end-exercise gain that is present when severe-intensity exercise is initiated from a moderate-intensity baseline is reduced after priming.

 
iEMG.   For U->S and M->S Unprimed, the mean iEMG at the end of exercise was significantly greater than the value measured at 120 s of exercise. However, for M->S Primed, there was no significant difference in the mean iEMG at the end of exercise compared with that at 120 s of exercise. The {Delta}iEMG6-2 during severe exercise was significantly lower in M->S Primed compared with the other two conditions (54 ± 43, 51 ± 35, and 26±43% increase relative to the baseline value for U->S, M->S Unprimed, and M->S Primed, respectively). The group mean iEMG response at minutes 2 and 6 and the group mean {Delta}iEMG6–2 for the three conditions are illustrated in Fig. 5.


Figure 5
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  		Fig. 5. Group mean integrated electromyogram (iEMG) response during severe exercise. Top: percentage of baseline iEMG measured at minute 2 (open bars) and minute 6 (solid bars) for each of the three conditions. *Significant difference between minute 2 and minute 6 within condition (P < 0.05). Bottom: change in iEMG ({Delta}iEMG) between 2 and 6 min for each of the three conditions. #Significant difference between M->S Primed and the other two conditions (P < 0.05). Error bars were excluded for clarity.

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The principal original findings of this investigation were that the performance of severe-intensity priming exercise 1) did not alter the phase II {tau}, but 2) did significantly reduce both the amplitude of the VO2 slow component and the {Delta}iEMG6-2, during severe-intensity exercise initiated from a moderate-intensity baseline. These results indicate that the slower phase II VO2 kinetics observed during moderate-to-severe exercise transitions are not related to a muscle O2 delivery limitation. The results also suggest that the reduced VO2 slow component observed following priming exercise is linked to altered motor unit recruitment patterns.

Consistent with our first hypothesis, the phase II VO2 kinetics were slower when severe-intensity cycle exercise was initiated from a baseline of moderate-intensity cycling compared with a baseline of unloaded cycling: the phase II {tau} was ~27% longer during M->S Unprimed compared with U->S. Similar results have been reported previously. For example, Wilkerson and Jones (62) reported that initiating heavy-intensity cycling from a moderate-exercise baseline lengthened the phase II {tau} from 27 to 48 s. In an earlier study, investigating severe-intensity cycling (requiring ~100% VO2peak), Wilkerson and Jones (61) reported that the phase II {tau} became progressively longer when the transition was initiated from a baseline of light, moderate, or heavy exercise. Slower phase II VO2 kinetics have also been reported during exercise transitions within the upper compared with the lower region of the moderate-intensity domain (5, 40) and when moderate exercise commences from very light exercise compared with rest (25, 26). Moreover, markedly slower intramuscular [phosphocreatine] kinetics have been reported when high-intensity, knee-extension exercise transitions were initiated from a moderate-intensity exercise baseline compared with rest (31). Since the muscle [phosphocreatine] kinetics and pulmonary VO2 kinetics demonstrate similar temporal characteristics (52), these latter data indicate that the mechanism responsible for the slower phase II VO2 kinetics in work-to-work transitions reside within the contracting muscles.

It has been suggested that slower phase II VO2 kinetics during work-to-work transitions reflect a shift in the balance from rapid parasympathetic withdrawal to slower sympathetic activation of HR and cardiac output (25, 26). It was argued that slower cardiac output kinetics could limit O2 delivery to contracting muscles, thereby restricting the rate at which VO2 rises to meet the increase in metabolic demand (25, 26). MacPhee et al. (40) provided support for this suggestion by showing that slower phase II VO2 kinetics were associated with slower leg blood flow kinetics when moderate-intensity, knee-extension exercise was initiated from an elevated baseline metabolic rate. However, the leg blood flow kinetics in that study (mean {tau} of 39 s) were still appreciably faster than the phase II VO2 kinetics (mean {tau} of 52 s), which would not be expected if bulk O2 delivery kinetics were limiting muscle VO2. It should be noted, however, that conduit artery blood flow kinetics might not accurately reflect blood flow kinetics in the muscle microvasculature (18). An alternative proposition is that the slower phase II VO2 kinetics during work-to-work exercise reflect the fact that such transitions functionally isolate the oxidative metabolic properties of the population of muscle fibers recruited to meet the increased energetic demand (5, 31, 61, 62).

In the present study, we used priming exercise to investigate the O2 dependency of the strikingly slower VO2 kinetics observed during work-to-work transitions. Priming exercise (particularly when of high-intensity and resulting in a metabolic acidosis) would be predicted to result in muscle vasodilatation and a right shift of the oxyhemoglobin dissociation curve and thus to increase both convective and diffusive components of muscle O2 delivery (21). Indeed, priming exercise has been shown to increase cardiac output, muscle blood flow, and muscle oxygenation before and during subsequent exercise (6, 14, 19, 31, 35, 63). That similar effects are likely to have occurred in the present study is evidenced by the significantly higher HR recorded both at baseline and throughout exercise, and the significantly elevated baseline blood [lactate] in the M->S Primed compared with the M->S Unprimed condition.

Despite the likelihood that muscle O2 availability was enhanced, however, and in contrast to our hypothesis, the phase II {tau} was not altered by priming exercise (M->S Unprimed, 42 ± 15 s; M->S Primed, 42 ± 17 s). We, therefore, conclude that the slower VO2 kinetics observed when high-intensity exercise is initiated from an elevated baseline metabolic rate are not mechanistically linked to a muscle O2 delivery insufficiency. The lack of an effect of priming exercise on the phase II {tau} during the moderate-to-severe exercise transition reported herein is consistent with the majority of previous studies that have focused on the effect of priming exercise on VO2 kinetics during transitions from unloaded pedaling to heavy- or severe-intensity upright cycle exercise in healthy young subjects (e.g., Refs. 6–9, 17, 19, 27, 32, 34, 43, 53, 55, 63). However, when muscle O2 delivery is compromised in the control condition and relatively slow phase II VO2 kinetics are present, such as during heavy cycle exercise in the supine position (27), and during heavy arm crank exercise performed above the level of the heart (33), priming exercise has been shown to reduce the phase II {tau}. That this effect did not occur in the present study, therefore, indicates that the slow phase II VO2 kinetics observed in the M->S Unprimed condition were not related to an O2 delivery limitation.

MacPhee et al. (40) reported slower HR kinetics when a transition to moderate-intensity knee extension exercise was initiated from an elevated baseline. In contrast, we observed no lengthening of the HR {tau} for M->S Unprimed compared with U->S, despite a significant elevation of baseline HR (Fig. 2). Wilkerson and Jones (61) also reported an invariant HR {tau} for transitions to severe-intensity cycle exercise from light, moderate, and heavy baselines. The explanation for the different findings is unclear, but is probably related to differences in both the exercise modality and particularly the range of exercise intensities investigated (transitions to severe-intensity exercise would be predominantly sympathetically driven, regardless of baseline metabolic rate). It is of interest, however, that the slower phase II VO2 kinetics observed for M->S Unprimed compared with U->S in the present study occurred in the absence of an associated slowing of HR kinetics.

Our data are consistent with the suggestion that slower VO2 kinetics during work-to-work transitions are related to factors within the contracting muscle, such as the metabolic properties of the population of muscle fibers recruited across the transient (31). According to Henneman's size principle (24), only a fraction of the population of motor units typically required for a given work rate will be recruited when the transition is made from an elevated baseline metabolic rate, and that fraction will reside at the higher end of the recruitment hierarchy. These higher order fibers will typically possess a lower oxidative capacity, a reduced microvascular pressure head for O2, slower VO2 kinetics, higher total creatine content, a greater propensity for "anerobic" metabolism, a reduced efficiency, and greater fatiguability, compared with fibers positioned lower in the recruitment hierarchy (4, 12, 50, 64). Interestingly, in addition to the slower VO2 kinetics, the end-exercise gain (which reflects muscle efficiency) and the O2 deficit incurred relative to the change in work rate (which provides an indication of the relative contribution of O2-independent metabolism to energy transfer) were both significantly greater for M->S Unprimed than for U->S. These results are similar to previous reports (5, 40, 61, 62) and are also suggestive of an amplified expression of the response characteristics of higher order muscle fibers during work-to-work transitions.

The MRT was significantly greater in M->S Unprimed compared with U->S, but priming reduced the MRT such that there was no significant difference between M->S Primed and U->S. This occurred primarily as a consequence of a reduction in the amplitude of the VO2 slow component (consistent with our hypothesis), although the absolute amplitude of the fundamental component of the VO2 response was also increased by priming. A reduction in the amplitude of the VO2 slow component is a consistent finding in studies that have investigated the influence of priming exercise on VO2 kinetics during subsequent high-intensity exercise (3, 6–9, 17, 19, 21, 27, 32, 34, 39, 51, 55, 63). Precisely why this occurs is unclear, but potential mechanisms include an increased homogeneity of local muscle perfusion relative to metabolic rate, improved muscle carbon substrate availability, and alterations in motor unit recruitment profiles: mechanisms that might not be mutually exclusive (29).

In the present study, the reduction in the VO2 slow component coincided with a significant reduction in {Delta}iEMG6-2, suggesting that the smaller slow component might have been mechanistically linked to reduced neuromuscular activity. Indeed, during both the U->S and the M->S Unprimed conditions, the iEMG increased significantly between 2 and 6 min of exercise, whereas, in the M->S Primed condition, iEMG did not change significantly over this same time frame. Our results suggesting an association between neuromuscular activation and the VO2 slow component are consistent with some previous studies (6, 41, 42), but not others (11, 20, 55). Given the variability associated with measurement of iEMG, it is perhaps unsurprising that inconsistent results have been reported. Even in our study, the reduction in the amplitude of the VO2 slow component with priming was not significantly correlated with the {Delta}iEMG6-2 (r = 0.28). However, other evidence indicates that the VO2 slow component is linked to increased motor unit recruitment. For example, the transverse relaxation time of muscle protons from magnetic resonance images (T2, believed to represent muscle fiber recruitment) increases in a number of thigh muscles during high-intensity exercise and appears to be temporally associated with the VO2 slow component (16, 54). Moreover, Krustrup et al. (37) reported that both type I and type II fibers were recruited from close to the onset of severe-intensity exercise and that the development of the VO2 slow component was associated with the continued recruitment of both fiber types.

While it appears reasonable to assume that the VO2 slow component is associated in some way with the recruitment of higher order (perhaps type II) fibers with poor efficiency (2, 6, 16, 36, 37, 44, 48, 49, 52, 53), it is presently unclear whether the association derives from a progressive recruitment of higher-order fibers as exercise proceeds, from the slow kinetics and/or the effects of fatigue on these fibers if they are recruited near the onset of exercise, or through a combination of these processes (44, 61). The reduction in the VO2 slow component following priming exercise in the present study might, therefore, have occurred through a number of potential mechanisms. One possibility is that priming exercise resulted in the activation of more motor units at subsequent exercise onset, thereby decreasing the need to recruit additional motor units (and the O2 cost associated with that activation) as exercise proceeded (6, 37). However, unlike in the study of Burnley et al. (6), the iEMG at 2 min of exercise was not significantly increased by priming exercise in the present study (Fig. 5). Another possibility is that greater and/or more homogenous muscle O2 delivery reduced the rate of fatigue development and thus the extent of additional motor unit recruitment required to maintain force production, again with a consequent reduction in the O2 cost of exercise (44). Finally, if the VO2 slow component reflects, at least in part, the slower VO2 kinetics of high-order fibers recruited at exercise onset (61), then priming exercise might have speeded VO2 kinetics in these fibers such that they reached their individual "steady-state" values more rapidly. However, if this latter effect did occur, then it was insufficient to impact measurably on the phase II {tau}.

In conclusion, the most important finding in this investigation was that significantly slower phase II VO2 kinetics observed when severe-intensity exercise was initiated from an elevated baseline metabolic rate were not altered when the transient was preceded by a bout of high-intensity priming exercise. However, the amplitude of the VO2 slow component and the {Delta}iEMG6-2 of exercise were significantly reduced following priming exercise. These results suggest that the slower phase II VO2 kinetics evident during moderate-to-severe exercise transitions are not related to an O2 delivery limitation across the transient, but are rather linked to intramuscular factors, such as the metabolic properties of the population of muscle fibers recruited.


   FOOTNOTES
 

Address for reprint requests and other correspondence: A. M. Jones, School of Sport and Health Sciences, St. Luke's Campus, Univ. of Exeter, Heavitree Rd., Exeter, Devon EX1 2LU, United Kingdom (e-mail: a.m.jones{at}exeter.ac.uk)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
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