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1 Department of Kinesiology, Kansas State University, Manhattan, KS 66506-0302, USA
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Abstract |
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to those of femoral artery blood flow 
and estimated muscle oxygen uptake 
. Nine healthy subjects performed a series of transitions from rest to moderate (below estimated lactate threshold, 6 min bouts) knee extension exercise. Pulmonary oxygen uptake 
was measured breath by breath, 
was measured continuously using Doppler ultrasound, and deoxyhaemoglobin ([HHb]) was estimated by near-infrared spectroscopy over the rectus femoris throughout the tests. The time course of 
was estimated by rearranging the Fick equation (i.e. 
), (arterio – venous O2 difference) using the primary component of 
to represent 
and [HHb] as a surrogate for (a
–
v)O2. The overall kinetics of 
(mean response time, MRT, 13.7 ± 7.0 s), 
(
, 27.8 ± 9.0 s) and 
(MRT, 41.4 ± 19.0 s) were significantly (P < 0.05) different from each other. We conclude that for moderate intensity knee extension exercise, conduit artery blood flow 
kinetics may not be a reasonable approximation of blood flow kinetics in the microcirculation 
, the site of gas exchange. This temporal dissociation suggests that blood flow may be controlled differently at the conduit artery level than in the microcirculation.
(Received 29 November 2005;
accepted after revision 16 March 2006; first published online 23 March 2006)
Corresponding author T. J. Barstow: 1A Natatorium, Kansas State University, Manhattan, KS 66506-0302, USA. Email: tbarsto{at}ksu.edu
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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. However, there is controversy regarding whether the kinetics of 
are limited by oxygen delivery or by some other intrinsic (intramuscular) mechanism (Grassi, 2001; Hughson et al. 2001). Adequacy of oxygen delivery has previously been assessed by a comparison of the temporal profiles of limb or muscle blood flow 
and 
(Shoemaker et al. 1994; Grassi, 2000). Previous research has shown the kinetics of 
to be either faster than (Macdonald et al. 1997; Grassi et al. 1998; Behnke et al. 2002a) or similar to 
(Grassi et al. 1996; Koga et al. 2005). Owing to technical limitations, however, this conclusion has been based on measurement of blood flow either through conduit arteries (Hughson et al. 1996; Bangsbo et al. 2000) or through the capillary bed of isolated muscles (Behnke et al. 2002a). It is presently unknown whether the characteristics of limb (conduit artery) blood flow following exercise onset are representative of blood flow in the microcirculation where gas exchange actually occurs. Therefore, clarifying the relationship between 
and capillary blood flow 
is critical to furthering our understanding of the mechanisms that govern the balance between O2 delivery and 
in health and disease.
Estimates of the kinetics of 
can be made by rearranging the Fick equation to solve for blood flow 
(arterio – venous O2 difference) and using the primary component of pulmonary oxygen uptake 
during phase 2 and [HHb] derived from near-infrared spectroscopy (NIRS) to represent 
and (a
–
v)O2, respectively (Ferreira et al. 2005a,d). These estimates have yielded a temporal response of 
that is similar to that of 
following the onset of cycling exercise (Ferreira et al. 2005d).
Estimates of 
have not been compared with limb blood flow measurements collected simultaneously. Thus, it is presently unknown whether conduit artery blood flow can be used to estimate 
and, by inference, the kinetics of capillary oxygen delivery. Any discrepancy that may exist between the kinetic responses of blood flow in the limb and in the microcirculation could have serious implications for the use of limb blood flow kinetics to evaluate the adequacy of oxygen delivery at the site of gas exchange during transitional phases of exercise in health and disease. Therefore, the purpose of this study was to describe the relationship between the temporal profiles of leg blood flow 
, estimated 
and estimated 
in healthy human subjects following the onset of moderate intensity knee extension exercise, and to determine whether 
kinetics are a reasonable representation of 
kinetics. We hypothesized that the kinetics of (1) 
and (2) 
would be faster than those of 
, and that (3) the kinetics of 
would be similar to those of 
.
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Methods |
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Nine subjects (6 male, 3 female), age 31.3 ± 12.3 years (mean ± S.D.), height 1.72 ± 0.01 m, and weight 67.4 ± 7.5 kg, participated in this study. The subjects' adipose tissue thickness over the rectus femoris was 0.78 ± 0.22 cm, and mean femoral artery diameter was 1.01 ± 0.19 cm. Experimental procedures and all benefits and risks were explained to each subject, and written informed consent was obtained before any testing began. All procedures were approved by the Institutional Review Board for Research Involving Human Subjects at Kansas State University and followed the principles outlined in the Declaration of Helsinki.
Protocol
Each subject completed a minimum of five visits to the laboratory, with at least 1 day of rest between each visit. All visits consisted of two-leg dynamic knee extension exercise at a rate of approximately 40 contractions per minute (c.p.m.), with legs extended simultaneously for each kick (i.e. as a ‘dolphin kick’). On the first visit, an incremental test to volitional fatigue was completed on the knee extension ergometer to estimate lactate threshold and peak pulmonary oxygen consumption 
for this mode of exercise. On each subsequent visit the subjects completed three 6 min constant work rate exercise bouts at a moderate work rate selected to elicit a metabolic rate of approximately 80% lactate threshold, each separated by 6 min rest. This protocol was performed four to six times by each subject.
Measurements
During each test, pulmonary oxygen consumption and other ventilatory and gas exchange variables were measured using an open-circuit breath-by-breath system (CardiO2, Medical Graphics, St Paul, MN, USA). The volume signal was calibrated before each test using a 3 l syringe, and the O2 and CO2 analysers were calibrated using two gases of known composition.
Blood velocity through the right femoral artery 
was measured continuously using Doppler ultrasound (Model 500-V, Multigon Industries, Mt. Vernon, NY, USA) with the transducer operating at a frequency of 4 MHz and the isonation angle fixed at 45 deg. The probe was positioned flat against the skin above and parallel to the common femoral artery, proximal (
2 cm) to the bifurcation, as confirmed using a 2-D ultrasound imaging system (Vivid 3-Pro, GE, Rochester, MN, USA). Femoral artery diameter (DFA) at this position was measured at rest in each subject, also using 2-D ultrasound imaging. Femoral artery blood flow 
was calculated as follows:
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| (1) |
Muscle capillary O2 extraction (as deoxyhaemoglobin concentration, [HHb]) was determined using a frequency-domain multidistance NIRS system (OxiplexTS, ISS, Champaign, IL, USA) during the incremental exercise tests and each subject's first two constant work rate test sessions. This device operated at two wavelengths (690 and 830 nm) with light source–detector separation distances of 2.0, 2.5, 3.0 and 3.5 cm for each wavelength. Data were stored at 31.25 Hz. The probe was placed longitudinally along the belly of the right rectus femoris, which has been shown to produce electromyogram activity similar to that of the vastus medialis and vastus lateralis during concentric knee extension exercise (Pincivero et al. 2006). It was then bound to the skin, which had previously been shaved and dried, with skin cement (Skin-Bond, Smith & Nephew, Largo, FL, USA), and secured using a Velcro elastic strap around the thigh. Probe position was marked to ensure accurate repositioning on each test day. The NIRS probe was calibrated each day according to the manufacturer's recommendations.
Data analysis
The breath-by-breath 
data were first converted to second-by-second values; then the 
and 
(at 200 Hz) were each time aligned to the onset of exercise for each exercise bout and ensemble averaged across bouts for each subject to generate a single data set for each variable. These averaged responses were then filtered using a low-pass filter with cut-off frequencies of 0.075 Hz for 
and 0.2 Hz for 
(SigmaPlot 2001, Jandel Scientific; Ferreira et al. 2006). Kinetic analysis was conducted using non-linear regression with a least squares technique (Marquardt–Levenberg and SigmaPlot 2001). Pulmonary oxygen uptake responses were fitted as follows:
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| (2) |
the time constant of each exponential response. The initial component of 
was described up to TDP, where the amplitude of the response (AI') was calculated as 
. The overall amplitude of the response was calculated as AP'
=
AI'
+
AP. Femoral artery blood flow data were also fitted in this manner, while [HHb] was described as a monoexponential response up to its peak value, in a manner similar to the initial component of 
in eqn (2).
In three subjects, the phase 1 response of 
was such a high percentage of the total increase (mean = 63%) that accurate determination of the phase 2 time constant was precluded. Previous studies using a cycle ergometer have shown that the phase 2 time constant is similar for transitions from a baseline of rest or very light exercise (Whipp et al. 1982). Based on this, these three subjects subsequently performed four to five bouts of exercise with a baseline of unloaded knee extension (estimated to be approximately 7 W) followed by an immediate transition to the preset resistance on the knee extension ergometer. In each case, this reduced the relative amplitude of the phase 1 response of 
and increased the relative amplitude for phase 2. Subsequent curve fitting produced more physiologically realistic time constants.
The estimated 
response following the onset of exercise was calculated from the kinetics of 
and the [HHb] data as described in detail previously (Ferreira et al. 2005a,d). The kinetics of the primary component of 
have been predicted (Barstow et al. 1990) and shown (Grassi et al. 1996; Rossiter et al. 1999) to closely approximate those of muscle 
. The [HHb] response determined by NIRS has been used to estimate the dynamic response of muscle capillary oxygen extraction (i.e. 
; DeLorey et al. 2003; Grassi et al. 2003). By rearranging the Fick equation, the temporal characteristics of 
were estimated using the ratio of 
to [HHb] as shown below (Ferreira et al. 2005d):
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| (3) |
The temporal characteristics of this 
response were described using a three component exponential equation:
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| (4) |
and 
was determined as:
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| (5) |
Statistical analysis
Significant differences between means were determined using repeated measures analysis of variance, followed when appropriate with the Tukey–Kramer post hoc test for pairwise comparisons. Relationships between two variables were analysed using the Pearson product–moment correlation. Statistical tests were performed using NCSS 2000 software (NCSS Statistical Software, Kaysville, UT, USA). For all comparisons, significance was declared when P < 0.05.
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Results |
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of 1460 ± 390 ml min–1 (21.6 ± 5.1 ml kg–1 min–1) and a peak heart rate of 166 ± 21 beats min–1 during the incremental knee extension exercise test, at a peak work rate of 53.7 ± 9.4 W. Their estimated lactate threshold occurred at a 
of 1040 ± 260 ml min–1, or 71.5 ± 7.8% of 
. Work rates for the constant work rate tests averaged 23.8 ± 5.7 W, or approximately 83.2 ± 13.6% lactate threshold heart rate 98.0 ± 13.3%, and contraction frequency 39.2 ± 0.7%.
Average pulmonary 
, 
, [HHb], tissue oxygenation ([HbO2]) and total haemoglobin for the three exercise transitions performed during each constant work rate test by a representative subject are shown in Fig. 1. Estimated 
, [HHb] and the resultant estimated 
for a representative subject are shown in Fig. 2, while the comparison between 
and 
for the same subject is shown in Fig. 3. Noticeable overshoots were seen in four (of 9) subjects for phase 2 of 
and in six subjects for [HHb] (see Fig. 2).
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, 
, 
and [HHb] are presented in Table 1. The MRT of 
was significantly faster than 
and 
kinetics, while the kinetics of 
were also significantly faster than the MRT of 
(Fig. 4). The relationships between kinetic parameters [MRT of 
versus
of 
; MRT of 
versus
of 
(Fig. 5) and MRT of 
versus MRT of 
(Fig. 6)] were not significant (P > 0.05).
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Discussion |
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, estimated 
and estimated 
in healthy human subjects following the onset of upright knee extension exercise, and to determine whether 
kinetics are a reasonable representation of 
kinetics. The major findings are as follows. Consistent with our first hypothesis, the kinetics (as MRT) of 
for moderate exercise were significantly faster than those of 
( for 
). In contrast to our second and third hypotheses, however, the kinetics of 
were significantly slower than those of 
and 
.
While measurements of capillary blood flow have been made in isolated animal muscle preparations (Kindig et al. 1999, 2002), direct measurement in humans has been problematic. Recently, Ferreira and coworkers (Ferreira et al. 2005a,b,c,d) have proposed a non-invasive method to estimate 
kinetics in exercising humans using [HHb] derived from NIRS. During cycling exercise, the MRT of 
was found to be similar to of 
for both moderate and heavy exercise (Ferreira et al. 2005d). Similar results were generally observed in the present study for subjects whose of 
values were relatively fast (Fig. 5A). However, unlike the results for cycling (Ferreira et al. 2005d), subjects with slower 
kinetics displayed disproportionally longer MRT of 
. The reason(s) for this discrepancy are unclear at present. Ferreira and coworkers examined oxygenation of the vastus lateralis during cycling, which may have different patterns of motor unit recruitment, fibre type distribution, blood flow and/or oxygen extraction than that of the rectus femoris during knee extension exercise as studied here. In addition, the cycle exercise protocol used by Ferreira and coworkers (Ferreira et al. 2005b,d) used an unloaded-to-loaded exercise transition, while in the present study rest-to-exercise transitions were performed, with the exception of three subjects who also performed unloaded-to-loaded exercise solely for determination of 
kinetics. The underlying mechanisms for the observed discrepancies must await further investigation.
The relationship between the kinetics of 
and 
seen in the present study is similar to previous results in which conduit artery blood flow has been shown to increase more rapidly than 
(Hughson et al. 1996; MacDonald et al. 1998). These observations, as well as results indicating a similar temporal profile of 
and 
(Hughson et al. 1996; Koga et al. 2005), have been interpreted as evidence that bulk O2 delivery 
does not limit 
kinetics following the onset of exercise. However, the temporal discrepancy between 
and 
shown here, and predicted by DeLorey et al. (2003), suggests it may not be appropriate to use 
to represent the kinetics of oxygen delivery to the microcirculation in assessing the dynamic adequacy of 
to 
matching. As the kinetics of 
approach or become slower relative to those of 
, it is possible that there is a smaller reserve of capillary O2 available to the muscle, so that at some point O2 delivery would transiently limit (slow) the increase in 
following the onset of exercise. At present it is not possible to determine from the time course of 
alone whether its slower rate of adjustment in some subjects may limit the increase in 
following the onset of exercise, since the amplitudes of both responses are also critical to this assessment, and the units of 
are arbitrary (see assumptions below).
In the present study, overshoots were seen in several subjects for [HHb] and 
. An overshoot in the [HHb] response was seen in six subjects. This overshoot has been shown previously, and may be eliminated either by prior exercise or by application of a topical vasodilating ointment (Maehara et al. 1997). An overshoot in [HHb] is equivalent to an undershoot in microvascular partial pressure of O2, which has been seen in rat models of both heart failure and diabetes (Behnke et al. 2002b; Diederich et al. 2002). Since subjects for the present study were generally healthy, this overshoot may have been caused by regional differences in [HHb] or the mode of exercise employed here. Overshoots in 
have been reported following, but not prior to, a short-term training programme (Shoemaker et al. 1994). The underlying cause of the 
overshoots seen in four subjects in the present study is unclear, but the response was consistent between transitions.
Assumptions
The assumptions associated with estimation of 
have been summarized previously (Ferreira et al. 2005a,b,c,d). Pertinent to the present study, the relative contributions to [HHb] from the arterioles, capillaries and venules are not clear, nor is it clear whether this weighted distribution remains constant throughout the transition from rest to exercise (McCully & Hamaoka, 2000; Ferreira et al. 2005d). However, it has been estimated that in the rat diaphragm capillaries comprise 84% of the vascular space (Poole et al. 1995), indicating that the majority of the NIRS signal is likely to reflect capillary oxygen extraction. Evidence also shows that, in the brain, the fractional contribution of arterial and venous blood values to tissue saturation remains relatively constant throughout the physiological range of O2 saturation values for the tissues (Chance et al. 2003).
Another consideration is the relative contribution of [HHb] from cutaneous and subcutaneous adipose tissue microvasculature, and whether this contribution is constant (Maehara et al. 1997). However, the vascular volume of these tissues is substantially less than that of skeletal muscle, so the relative contribution is likely to be small, although contribution by these tissues to the overshoot cannot be ruled out (Maehara et al. 1997). The small sampling volume of the NIRS probe determines the oxygenation state of only a small (relatively superficial) portion of the working muscle. Owing to potential regional differences in fibre type distribution, motor unit recruitment and muscle blood flow, it is unclear whether the area sampled is representative of the entire muscle (Boushel et al. 2001). However, concentric knee extension exercise has been shown to elicit similar recruitment patterns for the rectus femoris, vastus medialis and vastus lateralis (Pincivero et al. 2006), suggesting that the rectus femoris is representative of the muscle group involved in the exercise task. Furthermore, phosphocreatine kinetics of the knee extensor group as a whole reflect those of pulmonary 
during knee extension exercise (Rossiter et al. 1999). Thus, examination of microvascular oxygen exchange and calculation of 
in the rectus femoris is likely to be kinetically representative of the other heads of the vastus during knee extension exercise. It is also unclear whether the onset of movement accompanying rest-to-exercise transitions introduces error into the NIRS signal following the onset of exercise.
As illustrated in Fig. 1, the baseline of [HHb] is slightly elevated during subsequent bouts of exercise, but the kinetic response following the onset of exercise appears similar in all three bouts. Since 
is indistinguishable among the three bouts, the individual estimates of 
would be very similar. Note, in contrast, that [HbO2] appears to be quite sensitive to warm-up exercise, possibly owing, in part, to changes in skin blood flow, which make it less informative in assessing the relationship between 
and 
(Maehara et al. 1997; DeLorey et al. 2003; Grassi et al. 2003).
Discrepancy between 
and 
Assuming the discrepancy between conduit artery 
and microcirculation 
kinetics to be real (but see discussion of assumptions above), the fundamental question emerges, ‘Where is the blood flow seen in the femoral artery going, if not through the capillaries of the contracting muscle?’ Since the circulation below the knee was not occluded in the present study, 
is a measurement of blood flow to the entire leg, including active muscle and inactive tissues in both the upper and lower leg.
During phase 1, the increase in blood flow is thought to be mediated through a combination of the muscle pump, which probably results from pressure changes within the intramuscular vasculature with each contraction cycle, and rapid vasodilatation. Evidence of vasodilatation has been seen within the first 5 s of exercise (Wunsch et al. 2000; Saunders & Tschakovsky, 2004; Tschakovsky & Sheriff, 2004; Tschakovsky et al. 2004), but the mechanism(s) for this has not been determined (Shoemaker et al. 1997; Brock et al. 1998; Radegran & Saltin, 1999; Hamann et al. 2004). The muscle pump would, and rapid vasodilatation might, cause an indiscriminate increase in blood flow to all parts of the contracting muscle. Phase 2 of the blood flow increase is tightly coupled to metabolic activity, and may be controlled in part by H+, adenosine, ATP, nitric oxide, potassium, prostaglandins and/or a number of other metabolites (Delp & Laughlin, 1998). It appears that, like phase 1, vasodilatation during phase 2 is controlled by multiple mechanisms in combination (Clifford & Hellsten, 2004).
Blood flow to the contracting muscles (and more specifically the contracting motor units) is also achieved by a functional sympatholysis, which directs the increasing blood flow to the sites of active metabolism (Buckwalter & Clifford, 2001; Tschakovsky & Hughson, 2003; Wray et al. 2004). The time course for the increase in 
-adrenergic vasoconstriction of the vasculature of inactive tissue could potentially cause a delay before redistribution of flow towards contracting muscle and motor units was fully achieved. The decrease in renal blood flow following the onset of mild exercise seen in conscious baboons, which may reflect the time course of sympathetic vasoconstrictor outflow, can take up to 1.5 min (Hohimer & Smith, 1979). Given the systemic nature of sympathetic vasoconstrictor outflow (Wray et al. 2004), a similar time course is possible in the inactive tissue of the legs. Consistent with this, direct measurement of muscle sympathetic nerve activity (MSNA) showed a lag of at least 1 min before it increased following exercise onset in both exercising and non-exercising muscles (Hansen et al. 1994). However, muscle sympathetic nerve activity, as evidenced by plasma noradrenaline levels, does not increase until 50%
(for review see Laughlin et al. 1996). Therefore, it is at present unclear whether muscle sympathetic nerve activity (i.e. -adrenergic vasoconstriction) is activated during moderate intensity exercise such as that performed in the present study, and, if it is, whether its temporal profile could contribute to the difference seen here between 
and 
.
Conclusions
We have shown that for moderate intensity exercise: (1) the kinetics of 
are significantly faster than those of 
; (2) the kinetics of 
are slower than those of 
; and (3) the kinetics of 
are slower than those of 
. Our finding regarding the difference in 
and 
kinetics for this mode of exercise, as predicted by DeLorey et al. (2003), indicates that the time course of adjustment of limb blood flow may not be a reasonable representation of blood flow in the microcirculation for conditions such as those used here.
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(in l min–1) after filtering in the frequency domain. B, limb blood flow (
, in ml min–1) after filtering in the frequency domain. C, deoxyhaemoglobin concentration ([HHb], µM). D, oxyhaemoglobin concentration ([HbO2], µM). E, total haemoglobin (Hb, µM).
(in l min–1) estimated from kinetic parameters of pulmonary 
. B, deoxyhaemoglobin concentration ([HHb], µM). C, estimated 
profile obtained from 
divided by [HHb]. The amplitude of 
is displayed in arbitrary units (a.u.; 
and 
responses for the subject shown in 
compared to 
.
, 
, 
and [HHb] for moderate exercise
, 
and 
, there is no time delay, so 
(P < 0.05). BSignificantly different from MRT of 
(P < 0.05).
(A) and 
(B) with 
for moderate exercise 
and 
for moderate exercise