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1 Departments of Kinesiology and Anatomy and Physiology, Kansas State University, 66506-0302, Manhattan, KS, USA
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Abstract |
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to O2 uptake
ratio) after prior contractions that did not alter blood [lactate] have been considered to be a consequence of faster
kinetics. However, in humans, prior exercise below the lactate threshold does not affect the pulmonary
kinetics. To clarify this apparent discrepancy, we examined the effects of prior moderate exercise on the kinetics of muscle oxygenation (deoxyhaemoglobin, [HHb]
) and pulmonary
in humans. Eight subjects performed two bouts (6 min each) of moderate-intensity cycling separated by 6 min of baseline pedalling. Muscle (vastus lateralis) oxygenation was evaluated by near-infrared spectroscopy and
was measured breath-by-breath. The time constant (
) of the primary component of
was not significantly affected by prior exercise (21.5 ± 9.2 versus 25.6 ± 9.7 s; Bout 1 versus 2, P= 0.49). The time delay (TD) of [HHb] decreased (11.6 ± 2.6 versus 7.7 ± 1.5 s; Bout 1 versus 2, P < 0.05) and [HHb] increased (7.0 ± 3.5 versus 10.2 ± 4.6 s; Bout 1 versus 2, P < 0.05), while the mean response time (TD +) did not change (18.6 ± 2.7 versus 17.9 ± 3.9 s) after prior moderate exercise. Thus, prior moderate exercise resulted in shorter onset and slower rate of increase in [HHb] during subsequent exercise. These data suggest that prior exercise altered the dynamic interaction between
and
following the onset of exercise.
(Received 3 December 2004;
accepted after revision 26 January 2005; first published online 11 February 2005)
Corresponding author T. J. Barstow: Department of Kinesiology, 1A Natatorium, Kansas State University, Manhattan, KS, 66506-0302, USA. Email: tbarsto{at}ksu.edu
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Introduction |
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kinetics will become faster in the second exercise transition (Korzeniewski & Zoladz, 2004). However, in humans, a prior period of moderate exercise had no effects on the kinetics of the primary component of pulmonary oxygen uptake 
(Gerbino et al. 1996; Burnley et al. 2000), which has been predicted (Barstow et al. 1990) and shown (Grassi et al. 1996; Rossiter et al. 1999) to be a surrogate of 
kinetics, during subsequent moderate exercise. On the other hand, the time delay to the onset of fall in microvascular O2 pressure (PO2mv) decreased during electrical stimulations of rat spinotrapezius muscle performed 10 min after prior contractions that did not elicit an increase in blood lactate concentration (Behnke et al. 2002). As PO2mv is considered to be directly proportional to 
, the results of the PO2mv kinetics were interpreted to show that prior muscle contraction resulted in faster 
kinetics in the rat muscle (Behnke et al. 2002), which is in contrast with human studies but in agreement with theoretical predictions (Korzeniewski & Zoladz, 2004).
Simulated responses of 
and muscle blood flow 
to exercise suggest that muscle O2 extraction (Ca–vO2) (and PO2mv) are very sensitive to subtle changes in the dynamic balance between 
and 
(where 
; Ferreira et al. 2005). Therefore, divergences between interpretations based on 
in humans (Gerbino et al. 1996; Burnley et al. 2000) and PO2mv in rats (Behnke et al. 2002) might depend, in part, on the sensitivity of the technique used to assess the response. In humans, the time course of O2 extraction in the muscle microcirculation can be estimated non-invasively by the deoxyhaemoglobin concentration ([HHb]) signal from near-infrared spectroscopy (NIRS) (Grassi et al. 2003; DeLorey et al. 2004). Thus, the apparent controversy surrounding the interpretation of 
kinetics (Gerbino et al. 1996; Burnley et al. 2000) versusPO2mv kinetics (Behnke et al. 2002) can be addressed by investigating the effects of prior moderate exercise on the 
and [HHb] kinetics (roughly similar to PO2mv (t)) measured simultaneously in exercising humans.
Behnke et al. (2002) speculated that if 
kinetics were faster following prior contractions, the unchanged PO2mv profile (i.e. unaltered time constant) after the time delay would suggest that 
(O2 delivery) was accelerated in proportion with the speeding of 
. In contrast, in humans the kinetics of muscle blood flow during supine, heavy exercise were not altered after prior exercise performed above the lactate threshold (Fukuba et al. 2004). However, due to the highly oscillatory characteristic of blood flow in the femoral artery, the fast-, primary- and slow- phases of 
kinetics could not be discerned, making it difficult to ascertain any effects of prior exercise on specific components of the 
dynamics. Acute exercise enhances the vascular responsiveness to acetylcholine (an endothelium-dependent vasodilator) (Cheng et al. 1999; Jen et al. 2002) which appears to be related to the elevated blood flow during the exercise session (Jen et al. 2000). Therefore, it is possible that moderate exercise primes the vascular system leading to a faster 
response for subsequent exercise.
Thus, the purpose of the present study was to examine the effects of prior exercise below the LT on the dynamics of [HHb] (as a surrogate for O2 extraction (t)) in the human muscle microcirculation during subsequent exercise at the same intensity. Specifically, we tested the hypothesis that the overall kinetics of [HHb] would become faster (i.e. shorter time delay but invariant time constant) with prior moderate exercise, which as suggested by Behnke et al. (2002) could indicate accelerated muscle oxygen uptake and blood flow kinetics.
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Methods |
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The protocol included three visits to the laboratory. The first visit was used to determine the peak oxygen uptake 
, estimated LT and the work rate for the constant work-rate tests. All exercise tests were performed on an electronically braked cycle ergometer (Corival 400, Lode, the Netherlands). The incremental (ramp) exercise test was performed at 60 r.p.m. with work rate increments of 15–30 W min–1 (based on verbal assessment of fitness) until volitional exhaustion. 
was defined as the highest 
achieved during the test averaged over a 15-s interval. The LT was estimated from gas exchange measurements using the V-slope method, ventilatory equivalents and end-tidal gas tensions (Wasserman et al. 1973; Beaver et al. 1986). To study the effects of repeated bouts of moderate exercise, a work rate calculated to elicit 90% of the LT 
(90% LT) was determined. On each of the two subsequent visits, subjects performed two bouts at the predetermined work rate for 6 min, with 6 min of recovery pedalling at 20 W after each bout. The first bout was preceded by 4 min of baseline pedalling at 20 W. It has been shown that this protocol results in a similar blood lactate concentration before each exercise transition (Burnley et al. 2000).
Pulmonary gas exchange (
and 
), minute expired ventilation 
and heart rate (HR) were measured breath-by-breath (CardiO2, Medical Graphics Corporation, Saint Paul, MN, USA). Before each exercise test the volume signal was calibrated with a 3-l syringe, while the O2 and CO2 analysers were calibrated with gases of known concentration.
Muscle oxygenation was evaluated by a frequency-domain multidistance (FDMD) NIRS system (OxiplexTS, ISS, Champaign, IL, USA). The principles and algorithms utilized in the equipment were reviewed by Gratton et al. (1997). The NIRS probe consisted of eight light-emitting diodes operating at two wavelengths (four at each wavelength; 690 and 830 nm) and one detector fibre bundle, with source-detector separations of 2.0, 2.5, 3.0 and 3.5 cm. The modulation frequency of the light-source intensity was 110 MHz and the cross-correlation frequency for heterodyne detection was 5 kHz. The output frequency for data storage was selected as 31.25 Hz. The probe was positioned longitudinally on the vastus lateralis muscle 
15 cm above the patella, bonded to the skin with skin cement (Skin-Bond, Smith & Nephew, Largo, FL, USA) and secured with Velcro straps around the thigh. No movement of the probe was observed in any exercise test. The near-infrared spectrometer was calibrated on each test day following the manufacturer's recommendations.
The FDMD NIRS provides measurement of absolute concentration (in µM) of oxy- ([HbO2]), deoxyhaemoglobin ([HHb]) and reduced scattering coefficient (µ'S, cm–1). The [HHb] and [HbO2] reported here were calculated incorporating the dynamic measurement of µ'S made continuously throughout the exercise test. Total haemoglobin concentration ([THb]) was determined as the sum of [HHb] and [HbO2].
Data analysis
The stored pulmonary 
(
, breath-by-breath) and NIRS data (31.25 Hz) were converted to second-by-second values, and for each subject, the data were time-aligned to the start of exercise and averaged to generate a single data set for each bout (i.e. two transitions for Bouts 1 and 2). The [HHb] has been considered a proxy of O2 extraction (Grassi et al. 2003; DeLorey et al. 2004), as the [HHb] kinetics are similar to those of Ca–vO2 determined in exercising humans (Grassi et al. 1996) and dog gastrocnemius (Grassi et al. 2002). Therefore, as the NIRS signal originates from the microcirculation (Liu et al. 1995), [HHb] is considered to reflect the balance between 
and 
in the capillaries. The kinetics of [HHb] and 
were then determined by non-linear regression using a least-squares technique (Marquadt-Levenberg, SigmaPlot 2001, Jandel Scientific). The model used for fitting the responses consisted of a single-exponential with a time delay
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| (1) |
or [HHb], BSL is baseline, A is amplitude, TD is the time delay and p is the time constant of primary component. To determine the kinetics of the primary component of 
(approximating the muscle 
kinetics), the first 25 s of data were ignored in the curve-fitting routine (Gerbino et al. 1996). For [HHb], the data were fitted from 30 s of baseline pedalling to 90 s following the increase in work rate. The [HHb] kinetics are relatively fast (mean response time 17 s; Grassi et al. 2003); therefore, the [HHb] response is predicted to be almost complete within 90 s (i.e. 98% of the response achieved in less than 70 s). Further, minor slow changes in [HHb] from 90 to 360 s were often observed, which, if included in the monoexponential fitting, led to distortion of the initial TD and time constant of the early, primary response that we sought to accurately describe (e.g. Fig. 1).
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of the response (ANOVA repeated measures). Therefore, we ensemble-averaged the transitions to increase the confidence of parameter estimation in the non-linear regression analysis. Under these conditions, the confidence interval for the TD of [HHb] was on average equal to estimated TD ± 10% (range 5–20%, n= 9 subjects) and for [HHb] it was equal to estimated ± 20% (range 10–35%, n= 7 subjects). In two subjects the 95% confidence interval (CI) was estimated ± 70%; but exclusion of these subjects did not alter the primary results of our study. The relatively high 95% CI for [HHb] in some subjects suggests that an exponential model might not be the best description of [HHb] response. However, the exponential function would provide quantitative information on the time course of [HHb] response after the delay phase. A different description of [HHb] kinetics must await development of specific mathematical models. Statistical analysis
A Student's paired t test was used to compare means between the two exercise bouts for each variable or parameter of interest. Statistical significance was declared when P < 0.05. All tests were conducted using a commercial statistical software (NCSS 2000, NCSS Statistical Software, Kaysville, UT, USA). Values are reported as mean ±S.D., unless stated otherwise.
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Results |
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were 50.6 ± 4.6 ml kg–1 min–1 and the estimated LT occurred at 57.8 ± 7.6%
. The work rate for the constant work-rate tests was 122 ± 31 W, eliciting a 
equal to 88 ± 6.2% LT. There was a small, but significant (P < 0.05) increase in baseline THb from Bout 1 (78.7 ± 23.2 µM) to Bout 2 (81.8 ± 25.1 µM), while no changes were seen in baseline 
between the two exercise bouts (Table 1). Moreover, as previously observed (Gerbino et al. 1996; Burnley et al. 2000), the time constant of the primary component of 
kinetics was not significantly affected by prior moderate exercise (Table 1; Fig. 2).
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, Figs 3 and 4). The baseline [HHb] for Bout 2 was slightly, but significantly lower than for Bout 1, while the amplitude of response for [HHb] during Bout 2 was greater than during Bout 1. As a consequence, the ‘steady state’[HHb] (i.e. [HHb], BSL +A) was not significantly different between bouts (Table 1). The TD of [HHb] decreased significantly (34%) when comparing Bouts 1 and 2 (Fig. 3A). The of [HHb] became longer in the second bout (46%, Fig. 3B), while the mean response time (MRT, + TD) of [HHb] was not significantly different between bouts (Fig. 3C).
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Discussion |
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and 
following the onset of exercise.
Prior exercise and pulmonary 
kinetics
Substantial effects of prior exercise on the pulmonary 
characteristics are observed when heavy exercise is performed after a bout of high intensity exercise (above the LT) (Gerbino et al. 1996; Burnley et al. 2000; Rossiter et al. 2001; Scheuermann et al. 2001). In contrast, invariant kinetics of the primary component of pulmonary 
during subsequent moderate exercise (Gerbino et al. 1996; Burnley et al. 2000) have been considered evidence that prior exercise (moderate or heavy) does not alter the kinetics of muscle 
in the moderate domain. Our present results for the kinetics of the primary component of 
are in agreement with these previous studies. Pulmonary 
kinetics are a useful non-invasive means of assessing the time course of muscle 
response (Barstow et al. 1990; Grassi et al. 1996; Rossiter et al. 1999); however, the characteristic breath-by-breath noise of 
response could mask minor, but physiologically important, changes in muscle 
kinetics (Hughson et al. 2001).
Effects of prior exercise on the dynamics of PO2 and O2 extraction
In isolated single myocytes, prior stimulation shortened the time delay to the onset of decrease in intracellular PO2 in subsequent stimulations (Hogan, 2001), which was regarded as an indication of faster activation of oxidative phosphorylation in the consecutive period of muscle stimulation. It is important to note that in this elegant model, the absence of myoglobin and vascular supply, and use of high extracellular PO2 levels (Behnke et al. 2001) may limit its appropriateness for comparison with findings from human studies (Gerbino et al. 1996; Burnley et al. 2000).
In the rat spinotrapezius muscle (with preserved blood supply), Behnke et al. (2002) showed that the time delay of PO2mv decreased while the time constant was unchanged when muscle contractions were repeated after a 10-min recovery period. The alterations in PO2mv dynamics 
were then interpreted as a speeding of 
after prior contractions of moderate intensity (Behnke et al. 2002), which contradicted the interpretation based on pulmonary 
kinetics in humans. In the present study, we extended the findings of Behnke et al. (2002) to human muscle by showing that a bout of moderate exercise resulted in an earlier onset of increase in [HHb] (34% shorter time delay), and a prolonged time constant of [HHb] (46% longer ), where [HHb] is assumed to be an index of muscle capillary O2 extraction. Similar results were observed by DeLorey et al. (2004) when moderate exercise was performed after heavy exercise, although the changes in [HHb] did not reach significance. In contrast, Wilkerson et al. (2004) reported a slower [HHb] but no change in the TD of [HHb] during perimaximal-intensity exercise repeated after prior multiple sprint exercise. The cause of the inconsistency among studies regarding the effects of prior exercise on [HHb] kinetics is unclear. However, differences in duration of the prior exercise bout, recovery period between subsequent transitions, and/or intensity of the subsequent exercise might be possible explanations.
Interpretation of changes in [HHb] kinetics
Although in the present study the overall kinetics of [HHb] represented by the MRT were not modified by prior exercise, this does not directly indicate a lack of effect of prior exercise on 
and 
dynamics. Inasmuch as similar overall kinetics may be achieved by different interactions between the monoexponential 
and biphasic 
responses (e.g. Fig. 5), the individual parameters (TD and ) need to be considered to interpret the effects of prior exercise on the estimated time course of O2 extraction.
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kinetics after prior moderate exercise, as implied by analysis of pulmonary 
; and (2) faster 
kinetics in the second transition of moderate exercise, as suggested by Behnke et al. (2002) and Korzeniewski & Zoladz (2004). Based on these two possibilities we simulated responses using data from the present study to clarify the dynamic balance between 
and 
that would predict the observed [HHb] kinetics (Fig. 5).
The simulations predicted that if 
kinetics remained unchanged, the shorter TD of [HHb] would be the consequence of a smaller increase in 
during the initial phase (first 15–25 s), while the longer [HHb] would result from a shorter duration of the initial fast phase of 
response, such that the increase in 
during Phase 2 would emerge earlier in the transition after prior moderate exercise. In contrast, if 
kinetics were faster in the second exercise bout, the shorter TD of [HHb] could be explained by accelerated O2 uptake and unchanged kinetics of the initial 
response (Phase 1); in this case, the longer [HHb] would reflect a shorter duration of Phase 1 of 
and a faster increase in 
during Phase 2 (Fig. 5). Thus, the [HHb] profile would be explained by faster overall kinetics of 
accompanying the speeding of 
kinetics.
Effects of prior exercise on the dynamics of muscle blood flow
Skeletal muscle capillary hypaeremia following the onset of exercise consists of two phases (Kindig et al. 2002). The cause of the initial (fast) phase (15–25 s) of 
remains controversial, with a muscle-pump effect and rapid vasodilatation considered important determinants of Phase 1 of 
(Tschakovsky & Sheriff, 2004). A possible mechanism underlying the shorter TD of [HHb] would be a smaller increase in 
during the initial fast phase of the response (Fig. 5C). A residual hypaeremia after prior exercise could blunt the early 
response; however, data from previous studies indicate that blood flow would have recovered to its baseline pre-exercise value 6 min after a bout of moderate exercise (Van Beekvelt et al. 2001). The observations here of small, but significant differences in baseline [HHb] (1.3%) and total haemoglobin concentration (4%) preceding each transition suggest some residual hypaeremia. However, the unchanged TD of [HHb] after prior multiple sprint exercise, where the NIRS signal indicated existence of substantial hypaeremia, suggests that this mechanism is less likely to explain our results (Wilkerson et al. 2004).
The two scenarios considered above to explain the [HHb] kinetics after prior exercise suggested that the second phase of 
kinetics began (or emerged) earlier after prior moderate exercise. In addition, simulating faster 
kinetics required a concomitant speeding of 
kinetics in order to appropriately reproduce the [HHb] response, as suggested by Behnke et al. (2002) from the PO2mv profile. The 
response after 15–25 s probably involves interaction of neurohumoral, metabolic and endothelial factors (Shoemaker & Hughson, 1999; Clifford & Hellsten, 2004). Exercise-induced release of nitric oxide blunted pharmacologically induced sympathetic vasoconstriction 6 min after exercise (Patil et al. 1993). Moreover, acute exercise increased the vascular sensitivity to acetylcholine (Cheng et al. 1999; Jen et al. 2002) and these effects appear to be caused in part by the elevated blood flow during the exercise period (Jen et al. 2000). However, these observations were made after exercise of high-intensity (Patil et al. 1993; Cheng et al. 1999; Jen et al. 2002) and long duration (Patil et al. 1993). It remains to be demonstrated whether moderate-intensity exercise of short duration has similar effects on the human muscle vascular system. Obviously, faster kinetics of muscle capillary blood flow after prior moderate exercise needs to be confirmed experimentally, and elucidation of mechanisms underlying this response must await further investigation. Nevertheless, our data and those of Behnke et al. (2002) suggest that prior moderate exercise modifies the dynamics of O2 exchange in the microcirculation, possibly by inducing faster 
, with concomitantly faster 
, kinetics.
Altogether, the simulations shown in Fig. 5 predicted a tight coupling between the dynamics of 
and 
. This has been shown in other studies of transitions from unloaded baseline exercise (Grassi et al. 1996; Koga et al. 2005; Ferreira et al. 2005). This temporal association does not support or refute either the O2 delivery (Hughson et al. 2001) or ‘metabolic inertia’ hypothesis (Grassi, 2001) as the factor limiting 
kinetics following the onset of exercise (for discussion see Ferreira et al. 2005). During moderate exercise muscle 
kinetics were not limited by O2 delivery (MacDonald et al. 1997; Grassi et al. 1998a,b). Thus, the similar overall kinetics of 
and 
appears to be determined by mechanisms that are not simply characterized as the rate of increase in O2 uptake being limited by the dynamics of O2 supply.
Faster 
kinetics induced by prior exercise
Several pieces of evidence indicate that during moderate exercise 
kinetics are not limited by O2 delivery (MacDonald et al. 1997; Grassi et al. 1998a,b), implying that there is a metabolic inertia determining the rate of increase in 
. If the 
kinetics were faster in the second exercise bout, it would suggest a priming of the intramuscular metabolic rate-limiting step(s). The putative faster 
kinetics were not apparent in the primary component of the 
response (average of two transitions), hence, this possible speeding of 
kinetics is probably small, if present. However, it should not be considered irrelevant, as it would be sufficient to change significantly the dynamics of estimated O2 extraction. Prior exercise could augment the provision of acetyl groups to the tricarboxylic acid (TCA) cycle by activating the pyruvate dehydrogenase complex (PDC) (Campbell-O'Sullivan et al. 2002). However, the PDC does not appear to be the primary site of metabolic inertia regarding muscle and pulmonary 
kinetics (Grassi et al. 2002; Rossiter et al. 2003; Koppo et al. 2004) or PCr kinetics (Rossiter et al. 2003).
A recent computer model of oxidative phosphorylation, in which skeletal muscle PCr was defined as an important determinant of 
kinetics, predicts that 5–6 min after a bout of moderate exercise muscle PCr would remain reduced from pre-exercise levels, and that 
kinetics would be faster in a subsequent exercise bout (Korzeniewski & Zoladz, 2004). Although this model contains limitations (e.g. no inclusion of glycolysis), interventions that decrease muscle creatine content (Meyer, 1989) or inhibit PCr breakdown (Gustafson & Van Beek, 2002; Kindig et al. 2005) result in a speeding of 
or PCr kinetics, consistent with model predictions. It is difficult to determine whether a residual decrease in muscle PCr would contribute to the possible acceleration of the adjustment of 
after prior moderate exercise. In some studies using different exercise modes from the present one, muscle PCr content appeared to be reduced to a small extent, 5–6 min after low to moderate exercise (Laurent et al. 1992; Yoshida & Watari, 1993; McCreary et al. 1996). In contrast, other studies have shown that muscle PCr had achieved pre-exercise levels within 6 min of recovery from moderate exercise (Rossiter et al. 2002), but in this study, several consecutive transitions were ensemble averaged. Muscle PCr was restored to resting values 5–10 min after heavy-intensity exercise (Sahlin et al. 1979, 1997), where greater PCr breakdown is observed compared to moderate exercise (e.g. Rossiter et al. 2002). Therefore, it is presently unclear whether changes in the baseline muscle PCr stores are involved in the hypothetical speeding of 
kinetics; however, the possibility of faster muscle 
kinetics following prior moderate exercise deserves to be further investigated.
Methodological considerations
In this study we assumed that the time course of [HHb] was directly proportional to that of Ca–vO2. These assumptions and their limitations were discussed in detail in previous studies (Grassi et al. 2003; Ferreira et al. 2005). Briefly, the kinetics of [HHb] (Grassi et al. 2003; present study) are similar to those of Ca–vO2 in the isolated dog muscle in situ (Grassi et al. 2002), and to direct measurements of leg Ca–vO2 when the mean transit time of blood from capillaries to femoral vein is considered (Grassi et al. 1996). To date, there is only indirect evidence to support this assumption and direct confirmation in humans is difficult because, in theory, it requires isolation of venous outflow from the exercising muscle.
To determine the kinetics of [HHb], we used 90 s of data for non-linear regression analysis. In subjects for whom [HHb] had not achieved a steady state, but was undergoing minor changes (as in Fig. 1), the [HHb] would have been different if we had analysed the total exercise duration (360 s) using a monoexponential model. However, we believe our approach was justified because we were interested in reliably determining the time delay and time constant for the initial portion of the [HHb] response (as shown in Fig. 1).
Finally, we used two transitions ensemble-averaged to reduce breath-to-breath noise of pulmonary 
responses, as in the study of Burnley et al. (2000). The remaining equivalent of breath-to-breath noise might still limit the possibility of detecting minor effects of prior exercise on 
kinetics. However, the primary focus of our study was the time course of [HHb] and for such, the average of two transitions appeared sufficient.
Conclusion
In summary, we have demonstrated that prior moderate exercise affects the temporal characteristic of [HHb] response (and presumably O2 extraction) by decreasing the time to onset of increase in [HHb] and prolonging the time constant such that the overall kinetics (mean response time) remained unchanged. This [HHb] response could either be a consequence of lower amplitude and shorter duration of Phase 1 of 
, or could reflect the speeding of both 
and 
overall kinetics during the subsequent exercise transition. If 
kinetics were indeed faster in the second transition, the effects were probably small, so as to be undetected in the primary component of 
kinetics of one (Gerbino et al. 1996) or two transitions ensemble-averaged (Burnley et al. 2000; present study). Nevertheless, our results, in agreement with a previous animal study (Behnke et al. 2002), indicate that the effects of prior activity on the metabolic and vascular responses of contracting skeletal muscle are not confined to transitions performed in the heavy exercise-intensity domain.
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and [HHb] responses to repeated exercise bouts
kinetics before and after prior moderate exercise 
kinetics of a representative subject before (Bout 1; •) and after prior moderate exercise (Bout 2; 
). Note that in this example, where two transitions were averaged, small changes in the kinetics of muscle 
might be masked by the breath-by-breath noise of pulmonary 
(
kinetics (from 20–25 s to end exercise) were similar, as reported previously (
kinetics estimated from time constant (
kinetics without prior moderate exercise (Bout 1, 
response estimated from 
and [HHb] (
. The estimated blood flow response was biphasic, with an initial fast phase lasting 15–25 s (Phase 1) followed by a slower increase in 
to the steady state (Phase 2) (
kinetics; and (2) faster muscle 
kinetics after prior moderate exercise. A–C, simulation of similar muscle 
kinetics before and after prior moderate exercise (A, superimposed responses). For this situation, the shorter time delay of [HHb] is the consequence of a smaller increase of 
during Phase 1, while the slower time constant of [HHb] appears to be determined primarily by the earlier onset (or emergence) of Phase 2 of 
(C,
kinetics after prior moderate exercise (D, 
during Phase 2 (F, 
(mean response time, MRT) were tightly coupled to the dynamics of muscle 
(as 
). Thus, the speeding of muscle 
in D would have to be accompanied by an obligatorily faster 
response after prior exercise. See text for further details.