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J Appl Physiol 103: 771-778, 2007. First published May 10, 2007; doi:10.1152/japplphysiol.01061.2006
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Prior exercise speeds pulmonary O2 uptake kinetics by increases in both local muscle O2 availability and O2 utilization

Darren S. DeLorey,1,2 John M. Kowalchuk,1,2,3 Aaron P. Heenan,1,2 Gregory R. duManoir,1,2 and Donald H. Paterson1,2

1Canadian Centre for Activity and Aging, 2School of Kinesiology; and 3Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada

Submitted 21 September 2006 ; accepted in final form 4 May 2007


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 NOTE ADDED IN PROOF
 GRANTS
 REFERENCES
 
The effect of prior exercise on pulmonary O2 uptake (VO2p), leg blood flow (LBF), and muscle deoxygenation at the onset of heavy-intensity alternate-leg knee-extension (KE) exercise was examined. Seven subjects [27 (5) yr; mean (SD)] performed step transitions (n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity ({Delta}50%, 8 min; HVY 2) KE exercise. VO2p was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O2Hb)-, deoxy (HHb)-, and total (Hbtot) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 VO2p, LBF, and HHb data were fit with a monoexponential model. The time delay (TD) from exercise onset to an increase in HHb was also determined and an HHb effective time constant (HHb – MRT = TD + {tau}) was calculated. Prior heavy-intensity exercise resulted in a speeding (P < 0.05) of phase 2 VO2p kinetics [HVY 1: 42 s (6); HVY 2: 37 s (8)], with no change in the phase 2 amplitude [HVY 1: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the VO2p slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O2Hb and Hbtot were elevated throughout the on-transient following prior heavy-intensity exercise. The {tau}LBF [HVY 1: 39 s (7); HVY 2: 47 s (21); P = 0.48] and HHb-MRT [HVY 1: 23 s (4); HVY 2: 21 s (7); P = 0.63] were unaffected by prior exercise. However, the increase in HHb [HVY 1: 21 µM (10); HVY 2: 25 µM (10); P < 0.001] and the HHb-to-VO2p ratio [(HHb/VO2p) HVY 1: 14 µM·l–1·min–1 (6); HVY 2: 17 µM·l–1·min–1 (5); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 {tau}VO2p was the result of both elevated local O2 availability and greater O2 extraction evidenced by the greater HHb amplitude and HHb/VO2p ratio following prior heavy-intensity exercise.

near-infrared spectroscopy; muscle O2 utilization; muscle blood flow; VO2 kinetics; slow component

IN 1996, Gerbino et al. (20) demonstrated that completion of a bout of heavy-intensity exercise (above the estimated lactate threshold) resulted in an acceleration of pulmonary O2 uptake (VO2p) kinetics during a subsequent heavy-intensity exercise bout. Gerbino et al. (20) argued that the faster VO2p kinetics were the result of an improvement in muscle O2 delivery consequent to the vasodilatory effects of a metabolic acidosis from the previous exercise bout; however, an improvement in muscle O2 delivery was not established experimentally. Since this initial investigation, several studies (19, 24, 27, 28, 30, 35) confirmed that a bout of prior heavy-intensity warm-up exercise can speed VO2p kinetics at the onset of a subsequent heavy-intensity exercise bout, whereas others have shown no effect of prior heavy exercise on VO2p kinetics, or an increase in the amplitude of the phase 2 response with no change in the rate of VO2p adaptation (5–8, 36, 37).

In an attempt to elucidate the role of O2 delivery in the control of VO2p kinetics, a number of investigations (14, 19, 24, 28, 30) compared the adaptation of limb blood flow to that of either limb or pulmonary VO2 after a prior bout of heavy-intensity exercise. MacDonald et al. (28) and Hughson et al. (24) reported a speeding of VO2p kinetics following prior heavy-intensity exercise that was associated with an elevation of limb blood flow prior to the onset of and throughout the subsequent exercise transition. In contrast, others (14, 19), including our laboratory (30), reported a speeding of phase 2 VO2p kinetics without an increased limb blood flow. While baseline blood flow was elevated prior to the exercise transition, the time constant, or amplitude of the blood flow response during the exercise transient were such that bulk limb blood flow/O2 delivery was not different following a prior bout of heavy-intensity exercise. The contrasting findings of these studies do not allow a consensus to be reached regarding the role of muscle O2 delivery in the control of VO2p (and muscle O2 consumption) kinetics and warrant further investigation in this area.

A limitation of previous studies is the inability to investigate the effect of prior exercise on the adaptation of muscle O2 delivery at the site of O2 exchange within the microvasculature of the active muscle of the dynamically exercising human. The technique of near-infrared spectroscopy (NIRS) provides noninvasive and continuous monitoring of relative concentration changes in deoxy (HHb)-, oxy (O2Hb)-, and total (Hbtot) hemoglobin/myoglobin in the microvasculature (small arterioles, capillaries, and venules) (4) of the muscle. The NIRS-derived HHb signal reflects the balance between O2 delivery and O2 utilization in the region of NIRS interrogation and provides information on the time course of local muscle O2 utilization when combined with the measurement of VO2p kinetics (13). Moreover, conduit artery leg blood flow/O2 delivery kinetics and NIRS-derived O2Hb and Hbtot data provide important information on the effect of priming exercise on bulk O2 delivery to the exercising limb and the distribution of blood flow and local matching of O2 delivery to O2 utilization within the active muscle.

Additionally, exercise in the heavy-intensity domain is characterized by a progressive increase in VO2p throughout the "steady state" of the exercise bout, which has been termed the VO2p slow component. The mechanism(s) responsible for the slow component have not been identified. However, several studies (5–8, 36) have demonstrated that a bout of priming exercise reduces the amplitude of the VO2p slow component during subsequent exercise. Whether changes in local muscle O2 delivery and O2 utilization accompany the reduced VO2p slow component following priming exercise has not been investigated. The simultaneous measurement of VO2p, leg blood flow (LBF), and local muscle oxygenation during the repeated bouts of heavy-intensity exercise may help to identify the factor(s) responsible for the control of the VO2p slow component.

Therefore, the purpose of the present study was to investigate the effect of prior heavy-intensity exercise on the adaptation of VO2p, leg blood flow, and muscle deoxygenation at the onset of a subsequent heavy-intensity exercise bout in young adults. A secondary purpose of the present study was to investigate the effect of prior heavy-intensity exercise on the VO2p slow component as well as LBF and local muscle O2 delivery to O2 utilization matching during the slow component. We hypothesized that 1) prior heavy-intensity exercise would speed VO2p kinetics during subsequent heavy-intensity exercise and that the speeding would be associated with an enhancement of local muscle O2 availability; 2) prior exercise would decrease the amplitude of the VO2p slow component with a greater local muscle O2 delivery for a given O2 utilization reflected in a reduced muscle deoxygenation during the VO2p slow component.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 NOTE ADDED IN PROOF
 GRANTS
 REFERENCES
 
Subjects.   Seven healthy, physically active young men (age: 26 ± 5 yr) volunteered and gave written informed consent to participate in the study. All procedures were approved by the University Ethics Committee for Research on Human Subjects.

Protocol.   Subjects reported to the laboratory on four separate occasions. All testing was performed on a custom-built, double-leg, knee-extension (KE) ergometer as described previously (3, 29). Subjects performed an incremental work rate test to volitional fatigue for the determination of peak power output, estimated lactate threshold ({theta}L), and peak O2 uptake (VO2peak). Testing began at an initial work rate of 18 W and was incremented by 6 W every 2 min until the subjects were unable to continue or were unable to maintain contraction frequency at 30/min. Estimated lactate threshold ({theta}L) was determined by visual inspection and defined as the VO2 at which VCO2 began to increase out of proportion in relation to VO2, with a systematic rise in VE/VO2p and PETO2 while VE/VCO2 and PETCO2 were stable. Following the incremental exercise test, subjects returned to the laboratory on three separate occasions to perform heavy-intensity exercise transients at a work rate chosen to elicit a VO2p corresponding to {theta}L plus 50% of the difference between {theta}L and VO2peak ({Delta}50). Each transient was 8 min in duration and was preceded by 2 min of rest, 4 min of passive exercise, and followed by 8 min of passive exercise recovery. All exercise was performed at a cadence of 30 contractions per minute (cpm) for each leg in an alternating pattern. To facilitate passive exercise, each of the subjects' legs were secured to the lever arms of the KE ergometer. Passive exercise was used to minimize mechanical inertia during the transition from passive exercise and to control for the potential effects of the muscle pump on muscle blood flow and VO2p.

Measurements.   Gas exchange measurements were similar to those described previously (1). Briefly, inspired and expired flow rates were measured using a low dead space (90 ml) bidirectional turbine (Alpha Technologies VMM 110), which was calibrated prior to each test using a syringe of known volume (3.01 liters). Expired gases were sampled continuously at the mouth and analyzed for concentrations of O2, CO2, and N2 by mass spectrometry (Innovision, Amis 2000) after calibration with precision-analyzed gas mixtures. Changes in gas concentration were aligned with gas volumes by measuring the time delay for a square-wave bolus of gas passing the turbine to the resulting changes in fractional gas concentrations as measured by the mass spectrometer. Data collected every 20 ms were transferred to a computer, which aligned concentrations with volume data to build a profile of each breath. Breath-by-breath alveolar gas exchange was calculated using algorithms of Beaver et al. (2). Heart rate (HR) was monitored continuously by electrocardiogram and arterial saturation was monitored by pulse oximetry (Nonin).

Femoral artery mean blood velocity (MBV) was measured from the right leg using pulsed-Doppler ultrasonography (GE/VingMed, System 5). Data were acquired continuously with a 4- to 5-MHz probe with a 45° angle of insonation placed on the skin surface 2–3 cm distal to the inguinal ligament. The ultrasound gate was maintained at full width to ensure complete insonation of the entire vessel cross-section with constant intensity (21). Beat-by-beat MBV was calculated by integrating the total area under the MBV profile. MBV data were recorded at 100 Hz and stored on a computer for subsequent analysis. Femoral artery diameter was measured continuously by echo-Doppler ultrasound (7.5-MHz probe) in triplicate at rest. Previous reports from our laboratory (11, 29) and others (32) have demonstrated that femoral artery diameter does not change from the resting value at any time point of an exercise transient, therefore the three measures of vessel diameter (during diastole) at rest were averaged to obtain a femoral artery diameter for each subject. LBF was calculated as LBF (ml/min) = MBV (cm/s)·{Pi}r2·60, where r is the radius of the femoral artery. Leg O2 delivery was calculated as the product of LBF and CaO2. CaO2 was estimated as the product of SaO2 from pulse oximetry and the O2 content of Hb, assuming an arterial [Hb] of 15.0 g/100 ml and an O2 carrying capacity of 1.34 ml/g Hb. Since the interpretation of O2 delivery relative to O2 utilization was with regard to the rate and amplitude of the response, rather than an absolute value for O2 delivery, between subject differences in this estimate would not affect the results.

Local muscle oxygenation profiles of the quadriceps vastus lateralis muscle group were made with NIRS (Hamamatsu NIRO 300, Hamamatsu Photonics KK) as described previously (13). Briefly, optodes were placed on the belly of the muscle midway between the lateral epicondyle and greater trochanter of the femur. The optodes were housed in an optically dense plastic holder, thus ensuring that the position of the optodes, relative to each other, was fixed and invariant. The optode assembly was secured on the skin surface with tape and then covered with an optically dense, black vinyl sheet, thus minimizing the intrusion of extraneous light and loss of NIR transmitted light from the field of interrogation. The thigh, with attached optodes and covering, was wrapped with an elastic bandage, to minimize movement of the optodes while still permitting freedom of movement. This preparation essentially prevented any optode movement relative to the skin surface.

The intensity of incident and transmitted light was recorded continuously and, along with the relevant specific extinction coefficients and estimated optical pathlength, used for online estimation and display of the changes from the resting baseline of O2Hb, HHb, and Hbtot hemoglobin. The raw attenuation signal (in OD units) was transferred to computer and stored for further analysis. Values for O2Hb, HHb, and Hbtot are reported as a delta ({Delta}) from baseline in micromolar units assuming a differential pathlength (DPF) factor of 3.83 (25). Small (5–7%) wavelength (690 and 830 nm)-dependent changes in DPF have been reported during incremental exercise (15). Whether the DPF changes during constant load exercise transitions, or during repeated bouts of heavy-intensity exercise and at the wavelengths utilized in the present study (775, 810, 850, and 910 nm), has not been established.

Analysis.   Breath-by-breath gas exchange data were interpolated to 1-s intervals, filtered for aberrant data points, and then ensemble averaged in 5-s time bins to yield a single response for each subject. Phase 2 VO2p kinetics were determined from the phase 1-phase 2 interface, to the time point where the model fit departed from monoexponentiality and the sum of least-squares residuals increased (defined as the phase 2-phase 3 interface) by the use of a monoexponential model of the form:

Formula 1(1)
where Y represents Formula 1O2p at any time (t); b is the baseline value of Y at the point in time from which the data were fitted; A is the amplitude of the increase in Y above the baseline value; {tau} is the time constant defined as the duration of time through which Y increases to a value equivalent to 63% of A, and TD is the time delay. The phase 1–2 and phase 2–3 interfaces were determined according to the method of Rossiter et al. (34). The amplitude of the slow component of Formula 1O2p (phase 3) was calculated as the difference between end-exercise Formula 1O2p and the phase 2 Formula 1O2p amplitude.

Beat-by-beat HR data were filtered for aberrant beats, time aligned, and averaged to 5-s time bins. HR data were then fit with a monoexponential model of the form in Eq. 1 from exercise onset to the time point representing the phase 2-phase 3 interface for Formula 1O2p to determine the rate of adaptation of HR during the primary adaptive phase of Formula 1O2p. The amplitude of the increase in HR from the end of model fitting to end exercise was also calculated.

MBV data were filtered, time aligned, and interpolated to 2-s intervals (corresponding to one contraction cycle). LBF was calculated for each contraction cycle, then averaged into 5-s time bins. Subsequently, LBF data were fit with a monoexponential model of the form in Eq. 1 from exercise onset to the time point representing the phase 2-phase 3 interface for Formula 1O2p to determine the rate of adaptation of LBF during the primary adaptive phase of Formula 1O2p.

The NIRS-derived O2Hb, HHb, and Hbtot data were time aligned and ensemble averaged to 5-s time bins to yield a single response for each subject. The time to the onset of an increase in HHb was determined as the first point greater than one standard deviation above the mean of the baseline. This analysis was performed on each individual trial prior to averaging and the TD for all three trials were averaged. Subsequently, HHb data were fit with a monoexponential model of the form in Eq. 1 from the time of initial increase in HHb to the time point representing the phase 2-phase 3 interface for Formula 1O2p to determine the rate of adaptation of muscle deoxygenation during the primary adaptive phase of Formula 1O2p. While we are not certain that the underlying processes determining muscle deoxygenation are exponential in nature, visual inspection of the NIRS-derived HHb signal and analysis of least-squares residuals, suggested that fitting with a monoexponential model would yield a reasonable estimate of the time course of muscle deoxygenation (i.e., an effective {tau}). The amplitude of the increase in HHb from the end of model fitting to end exercise was also calculated. The O2Hb and Hbtot signals did not approximate an exponential response, thus these data were not modeled; however, the response of these signals was qualitatively compared with the HHb data at corresponding time intervals. The Hbtot and O2Hb signals represent the time course and magnitude of change in Hbtot and O2Hb concentration relative to a baseline value in the local area of muscle interrogated by NIRS. The Hbtot signal reflects the balance between local muscle blood flow, the effect of muscular contraction on vascular Hb volume, vasodilation, hemoconcentration, and capillary recruitment. Factors such as hemoconcentration, capillary recruitment, local vasodilation, and/or an increase in local muscle blood flow may contribute to an increase in Hbtot during exercise, whereas increased muscle pressure and vascular compression associated with muscular contraction may decrease Hbtot in the local area of muscle interrogated by NIRS. In addition to the above factors, O2Hb will be influenced by the local metabolic rate. During repeated constant-load exercise that is associated with a marked local vasodilation, change in Hbtot and O2Hb most likely reflect changes in local muscle blood flow.

Statistics.   The effect of prior exercise on Formula 1O2p, LBF, and HHb kinetics was determined by paired t-test. Comparison of Formula 1O2p, LBF, and HHb kinetics within a condition was by one-way repeated-measures ANOVA. Relationships among key variables were determined by Pearson product correlation. All data are presented as means and SD. A P value <0.05 was considered statistically significant.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 NOTE ADDED IN PROOF
 GRANTS
 REFERENCES
 
Subjects were 1.84 m (0.06) tall and had a body mass of 80 kg (9). During incremental alternate-leg KE exercise to volitional exhaustion, subjects achieved a peak work rate (WR) of 132 W (19) and an absolute and relative Formula 1O2peak of 2.76 l/min (0.35) and 35 ml·kg–1·min–1 (5), respectively. The mean WR for heavy-intensity exercise was 100 W (18) and this elicited an end exercise Formula 1O2p (HVY 1) of 2.1 l/min (0.3), which was 76% (10) of Formula 1O2peak and a Formula 1O2p of {Delta}46% (17).

O2 uptake kinetics.   The adaptation of Formula 1O2p at the onset of heavy-intensity exercise following no warm-up (HVY 1) and a heavy-intensity warm-up (HVY 2) for a representative subject is illustrated in Fig. 1. A Formula 1O2p slow component characteristic of heavy-intensity exercise performed above {theta}L was present in all subjects during both HVY 1 and HVY 2.


Figure 1
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  		Fig. 1. Adaptation of pulmonary O2 uptake (Formula 1O2p) during the on-transient of heavy-intensity exercise following no prior exercise ({circ}) and following a bout of prior heavy-intensity exercise ({blacktriangleup}) for a representative subject. Solid vertical line represents exercise onset.

 
Phase 2 Formula 1O2p kinetics increased at a faster rate (P = 0.014) during HVY 2 [{tau}Formula 1O2p: 37 s (8)] compared with HVY 1 [{tau}Formula 1O2p: 42 s (6); Table 1]. The pretransition baseline Formula 1O2p during passive knee-extension was greater (P = 0.002) in HVY 2 [0.49 (0.05)] compared with HVY 1 [0.43 (0.05)]. The amplitude of phase 2 Formula 1O2p was not different (P = 0.11) between HVY 1 [1.43 l/min (0.21)] and HVY 2 [1.48 l/min (0.21)]. Additionally, the gain ({Delta}Formula 1O2p/{Delta}WR) of the phase 2 Formula 1O2 response was not different (P = 0.10) between HVY 1 [14.3 ml·min–1/W (0.8)] and HVY 2 [14.7 ml·min–1/W (0.7)]. A Formula 1O2p slow component was present in all subjects during HVY 1 and HVY 2 and the time of onset [HVY 1: 226 s (25); HVY 2: 223 s (34)] and amplitude [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)] of the slow component were not different between conditions. The resulting end exercise Formula 1O2p was lower (P < 0.05) in HVY 1 [2.04 l/min (0.35)] compared with HVY 2 [2.15 l/min (0.40)].


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  		Table 1. Kinetic parameters for VO2p, leg blood flow and muscle deoxygenation

 
Heart rate.   The rate of adaptation of HR ({tau}HR) was not different (P = 0.18) between HVY 1 [37 s (16)] and HVY 2 [52 s (17)]. Baseline HR was elevated (P < 0.01) prior to HVY 2 [82 beats/min (10)] compared with HVY 1 [71 beats/min (7)]. The amplitude of the increase in HR during the period corresponding to the phase 2 Formula 1O2p response was similar (P = 0.53) during HVY 1 [49 beats/min (12)] and HVY 2 [51 beats/min (11)]. During the time period associated with the Formula 1O2p slow component, HR increased in all subjects during both conditions; however, there was a tendency for the increase in HR (P = 0.06) to be larger in HVY 1 [14 beats/min (7)] compared with HVY 2 [11 beats/min (5)]. End exercise HR was greater (P < 0.01) during HVY 2 [143 beats/min (14)] compared with HVY 1 [134 beats/min (14)].

LBF.   The mean femoral artery diameter was 10.0 mm (0.7) at rest. The adaptation of LBF and calculated leg O2 delivery during HVY 1 and HVY 2 for a representative subject is illustrated in Fig. 2. The rate of adaptation of LBF ({tau}LBF) was not different between HVY 1 (39 ± 7 s) and HVY 2 (47 ± 21 s; Table 1). Baseline LBF (LBF·2) was elevated (P < 0.01) prior to HVY 2 [1.70 l/min (0.42)] compared with HVY 1 [0.92 l/min (0.31)]. The amplitude of the increase in LBF (LBF·2) was similar (P = 0.21) during HVY 1 [7.16 l/min (1.83)] and HVY 2 [6.75 l/min (0.89)]. There was a tendency for the increase in LBF per increase in Formula 1O2p (LBF·2/Formula 1O2p) to be lower during HVY 2 [4.8 (1.2)] compared with HVY 1 [5.3 (1.2)]; however, this difference did not reach statistical significance (P = 0.07). During the time period associated with the Formula 1O2p slow component, LBF increased in all subjects during both conditions; however, the increase in LBF was larger (P = 0.026) in HVY 1 [0.58 l/min (0.34)] compared with HVY 2 [0.14 l/min (0.27)]. The end exercise LBF was similar between HVY 1 [8.66 l/min (1.90)] and HVY 2 [8.58 l/min (1.60)].


Figure 2
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  		Fig. 2. Adaptation of leg blood flow (top) and leg O2 delivery (bottom) during the on-transient of heavy-intensity exercise following no prior exercise ({circ}) and following a bout of prior heavy-intensity exercise ({blacktriangleup}) for a representative subject. Solid vertical line represents exercise onset.

 
NIRS.   The adaptation of {Delta}HHb, {Delta}O2Hb, and {Delta}Hbtot during HVY 1 and HVY 2 for a representative subject is illustrated in Fig. 3. The pretransition baseline [HHb] was not different between HVY 1 [–8 µM (2)] and HVY 2 [–8 µM (2)]. The time delay prior to an increase in {Delta}HHb was shorter (P < 0.01) at the onset of HVY 2 [7 s (1)] compared with HVY 1 [11 s (2)]. Following the time delay, {Delta}HHb increased with an effective {tau}HHb [HVY 1: 11 s (4); HVY 2: 16 s (6); P = 0.10] and MRT-HHb [HVY 1: 23 s (4); HVY 2: 22 s (7); P = 0.63)] both being similar between HVY 1 and HVY 2. The amplitude of increase in {Delta}HHb during the period corresponding to the phase 2 Formula 1O2p response was greater (P < 0.01) in HVY 2 [25 µM (10)] compared with HVY 1 [21 µM (10); Table 1]. Additionally, the increase in {Delta}HHb for a given increase in Formula 1O2p ({Delta}Formula 1O2p) was also larger (P = 0.004) during HVY 2 [17 µM·l–1·min–1 (5)] compared with HVY 1 [14 µM·l–1·min–1 (6); Fig. 4]. During the time period associated with the Formula 1O2p slow component, HHb increased in all subjects during both conditions; however, the increase in {Delta}HHb was larger (P < 0.05) during HVY 1 [7 µM (2)] compared with HVY 2 [4 µM (2)].


Figure 3
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  		Fig. 3. Adaptation of deoxy (HHb; top)-, oxy (O2Hb; middle )-, and total hemoglobin/myoglobin (Total Hb; bottom) during the on-transient of heavy-intensity exercise following no prior exercise ({circ}) and following a bout of prior heavy-intensity exercise ({blacktriangleup}) for a representative subject. Solid vertical line represents exercise onset.

 

Figure 4
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  		Fig. 4. Increase in muscle deoxygenation (HHb) per increase in phase 2 (Formula 1O2p) during heavy-intensity exercise following no prior exercise (HVY 1) and following a bout of prior heavy-intensity exercise (HVY 2). *P < 0.01; values are mean (SD).

 
Baseline O2Hb and Hbtot were elevated prior to the onset of HVY 2 compared with HVY 1 [{Delta}O2Hb: HVY2 – HVY1 = 11 µM increase (3); P < 0.01; {Delta}Hbtot: HVY2 – HVY1 = 10 µM increase (4); P < 0.01; Fig. 5]. O2Hb and Hbtot remained elevated throughout the exercise transient and at end exercise, O2Hb and Hbtot were 3 µM (1) and 4 µM (2) greater during HVY 2 compared with HVY 1, respectively.


Figure 5
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  		Fig. 5. Increase in baseline oxygenated (O2Hb) and total (Hbtot) hemoglobin/myoglobin (HVY 2 pretransition baseline minus HVY 1 pretransition baseline) following a bout of prior heavy-intensity exercise. *P < 0.01; values are mean (SD).

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
NOTE ADDED IN PROOF
 GRANTS
 REFERENCES
 
The purpose of the present study was to examine the effect of prior heavy-intensity exercise on the adaptation of Formula 1O2p, LBF/O2 delivery, and muscle deoxygenation during the on-transient of a subsequent heavy-intensity exercise bout in young adults. The main findings of this study were the following: 1) phase 2 Formula 1O2p kinetics were faster (by ~10%) following prior heavy-intensity exercise; 2) conduit artery LBF and leg O2 delivery were elevated prior to the onset of subsequent exercise; however, throughout the exercise transient LBF and leg O2 delivery were not different between the two exercise bouts throughout the exercise transient, whereas local muscle O2 availability (i.e., Hbtot and O2Hb) was increased prior to and throughout the subsequent exercise transient; 3) a larger increase in local muscle deoxygenation (~20% but with no change in kinetics) was observed during the time period corresponding to phase 2 of the Formula 1O2p response of subsequent heavy-intensity exercise, suggesting an increase in local muscle O2 extraction; and thus, collectively, these findings suggest that the speeding of phase 2 Formula 1O2p kinetics was due to an improvement in both local muscle O2 availability (indicated by a higher Hbtot and O2Hb) and O2 utilization (greater HHb); and 4) following prior exercise, the time of onset and amplitude of the Formula 1O2p slow component were not altered; however, the slow component increase in HHb was significantly smaller during HVY 2 compared with HVY 1 consistent with a greater local O2 delivery relative to O2 utilization, indicative of changes in the regional distribution of muscle blood flow since the bulk LBF/Formula 1O2p ratio was lower during HVY 2 (0.80) compared with HVY 1 (3.15).

The speeding of Formula 1O2p kinetics without a coincident increase in on-transient leg blood flow/O2 delivery following prior heavy-intensity in the present study is consistent with recent findings from our laboratory. During single-leg knee-extension exercise, Paterson et al. (30) reported a speeding of Formula 1O2p kinetics without faster leg O2 delivery kinetics following prior heavy-intensity exercise. Fukuba et al. (19) also reported that prior heavy-intensity knee-extension exercise speeds Formula 1O2p kinetics without a concomitant speeding or increase in leg blood flow throughout the subsequent exercise bout. In contrast, Hughson et al. (24) reported a speeding of Formula 1O2p kinetics that was associated with an increase in LBF during the exercise transient of repeated bouts of heavy-intensity knee extension/flexion exercise. Additionally, MacDonald et al. (28), utilizing a wrist flexion exercise model, also reported faster Formula 1O2 kinetics that were accompanied by faster limb blood flow kinetics following heavy-intensity warm-up exercise.

The reason for the disparate findings regarding bulk limb blood flow in the above studies is not clear; however, a potential explanation is that prior exercise improved muscle O2 delivery in all of the above studies either through an increase in bulk O2 delivery to the limb or through an improvement in the matching of local O2 delivery and O2 utilization within the muscle microvasculature that was undetectable by measurement of limb blood flow at the conduit artery.

In the present study, LBF and leg O2 delivery were elevated prior to the onset of HVY 2 (Fig. 2). However, throughout the exercise transient, LBF and leg O2 delivery were not different between the two heavy-intensity exercise bouts, suggesting that an improvement in bulk (conduit artery) blood flow/O2 delivery was not responsible for the faster Formula 1O2 kinetics. Despite the similar bulk leg blood flow, local [O2Hb] and [Hbtot] were elevated prior to and throughout HVY 2 compared with HVY 1, indicating increased local O2 availability and suggesting that the distribution of blood flow to active muscle was improved following prior exercise. We previously reported (9, 10, 13) a very rapid time course of muscle deoxygenation in the exercise transient, suggesting a slow adjustment of local muscle flow to the sites of local muscle O2 utilization. Subsequently, Ferreira et al. (17) using the time course of Formula 1O2p and HHb to estimate capillary blood flow kinetics noted a close relationship between {tau}Formula 1O2p and the mean response time of estimated capillary blood flow kinetics. Faster Formula 1O2p kinetics following a bout of heavy-intensity exercise being due to improved distribution of local blood flow and matching to O2 utilization is consistent with these earlier studies, indicating that microcirculatory blood flow may increase at a slower rate than local muscle O2 consumption. Therefore, a mismatch between O2 delivery and O2 utilization within an active muscle at the onset of exercise appears highly likely and a bout of prior exercise may serve to improve the matching of O2 delivery to metabolically active muscle fibers. Microvascular units are not well spatially matched to motor units, such that a single motor unit may be supplied by several different microvascular units, and muscle fibers within a motor unit may receive their vascular supply from more than one microvascular unit (39). Thus flow must increase to relatively large regions of muscle to perfuse the capillaries associated with each muscle fiber of a motor unit (18). Additionally, the precise delivery of O2 to active muscle fibers may be influenced by capillary recruitment (23), ascending vasodilation (38), sympatholysis (12), and venular-arteriolar feedback (22) that are, or may be, time-dependent processes. The present data indicate a more efficient regional distribution of LBF to metabolically active muscle fibers following the prior warm-up exercise.

Studies that previously reported a speeding of Formula 1O2p kinetics without an improvement in limb blood flow following priming exercise argued that the faster Formula 1O2p kinetics may be due to the alleviation of a diffusion limitation and/or changes in enzyme activation or substrate provision (14, 19, 30). In the present study, the kinetics of HHb were not different between HVY 1 and HVY 2; however, a larger increase (i.e., amplitude) in local muscle HHb was observed during phase 2 of the Formula 1O2p response during HVY 2 compared with HVY 1 suggestive of an increase in local O2 utilization (extraction) following prior heavy-intensity exercise. A metabolic acidosis accompanies exercise in the heavy-intensity domain, resulting in a rightward shift of the oxyhemoglobin dissociation curve enabling a greater off-loading of O2 from Hb at a given PO2 and may account for the greater muscle deoxygenation (HHb) during HVY 2. In this regard, Ferreira et al. (16) utilized computer simulations to investigate the relationship between muscle O2 uptake, blood flow (Q), and venous O2 content (CvO2) dynamics. In their analysis of exercise transients characterized by monoexponential blood flow dynamics (as in the present study where the exercise transient was initiated from a baseline of passive exercise), a number of CvO2 profiles can exist at a given Q/Formula 1O2.

Formula 1O2p slow component.   An additional goal of the present study was to determine if the Formula 1O2p slow component and bulk leg blood flow and the matching of local muscle O2 delivery and O2 utilization were altered during the Formula 1O2p slow component by prior heavy-intensity exercise. A Formula 1O2p slow component was evident in all subjects during both HVY 1 and HVY 2 and the time of onset and amplitude of the Formula 1O2p slow component was not affected by prior exercise. The slow component also represented a similar percentage of the total Formula 1O2p response in both HVY 1 and HVY 2. Our laboratory also previously reported no effect of prior heavy-intensity exercise on the Formula 1O2p slow component during single-leg knee-extension exercise (30). In contrast, others reported a decreased amplitude or elimination of the Formula 1O2p slow component following prior exercise (5–8, 36). The exercising muscle may account for as much as ~90% of the Formula 1O2p slow component (31, 33), and recent studies have argued that the progressive recruitment of less efficient type II muscle fibers may be responsible for the increased O2 consumption during the Formula 1O2p slow component (26, 34).

In the present study, LBF during the time period associated with the Formula 1O2p slow component increased 580 ml/min (single LBF·2) during HVY 1 and the increase was reduced to 140 ml/min (single LBF·2) during HVY 2. As a result, the Q/Formula 1O2p ratio during the Formula 1O2p slow component decreased from 3.15 during HVY 1 to 0.80 during HVY 2. Paterson et al. (30) also reported a smaller increase in leg blood flow and a lower Q/Formula 1O2p ratio during the Formula 1O2p slow component following prior heavy-intensity exercise. The accumulated evidence from Paterson et al. (30) and the present study suggest that prior heavy-intensity exercise may improve the matching of muscle O2 delivery to muscle O2 utilization during the slow component of subsequent heavy-intensity exercise or that a rightward shift of the oxyhemoglobin dissociation curve may facilitate the off loading of O2 from Hb, thereby reducing the need to increase O2 delivery.

Within a region of the vastus lateralis muscle an increase in HHb was also observed during the time period corresponding to the Formula 1O2p slow component in both HVY 1 and HVY 2 in the present study. The increase in HHb suggests that the local balance between muscle O2 delivery and utilization was altered during the slow component and suggests an increase in local O2 extraction during the slow component. However, the increase in HHb was smaller (P < 0.05) during HVY 2 (3.6 µM) compared with HVY 1 (6.5 µM), which suggests an improved matching of muscle O2 delivery to O2 utilization within the exercising muscle and is consistent with the LBF data. Collectively, these results suggest that muscle O2 consumption, muscle blood flow, and muscle deoxygenation all increase throughout the Formula 1O2p slow component and that prior exercise resulted in an improved matching of local O2 delivery to O2 utilization during the Formula 1O2p slow component. Moreover, the present data measured with noninvasive techniques at the level of the muscle microcirculation, indicating that both increased O2 delivery and O2 extraction contribute to the increase in Formula 1O2p during the slow component are consistent with the findings of Poole et al. (31) utilizing thermodilution measures of leg blood flow and blood sampled across the exercising limb during cycling exercise.

In conclusion, the results of the present investigation suggest that the speeding of heavy-intensity Formula 1O2p kinetics following prior warm-up exercise was the result of both elevated local O2 availability and greater O2 extraction. Importantly, the elevated local O2 availability was accomplished in the absence of an increase in bulk O2 delivery to the limb, suggesting that the increase in local O2 availability was achieved through an improved matching of O2 delivery to metabolically active muscle fibers following prior heavy-intensity exercise. A Formula 1O2 slow component was evident in all subjects and was accompanied by evidence of increases in limb O2 delivery, local O2 availability, and O2 extraction during HVY 1 and HVY 2. The amplitude and time of onset of the Formula 1O2p slow component was not different between exercise bouts; however, the matching of local O2 delivery to O2 utilization appeared to be improved during the slow component of subsequent heavy-intensity exercise.


   NOTE ADDED IN PROOF
TOP
 ABSTRACT
 METHODS
 RESULTS
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GRANTS
 REFERENCES
 
The authors of this article point out that certain data in this article were also published in the now retracted article "Dynamics of pulmonary O2 uptake, leg blood flow and muscle deoxygenation during heavy-intensity exercise in young adults" in the journal Experimental Physiology. Specifically, data related to the first heavy-intensity exercise transition were used in this paper as the "baseline control" to which the responses during the subsequent heavy-intensity exercise bout were compared; these data were also used for the purpose of examining the relationships of Formula 1O2, leg blood flow, and muscle deoxygenation during the (first) transition to heavy exercise in these subjects. The APS ethical policy states, "The journals of the APS accept only papers that are original work, no part of which has been submitted for publication elsewhere except as brief abstracts. When submitting a paper, the corresponding author should include copies of related manuscripts submitted or in press elsewhere." The authors did not alert the Editors of the Journal of Applied Physiology or Experimental Physiology to the existence of the other paper so that they would be aware of the duplicated data, and for this we apologize.


   GRANTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 NOTE ADDED IN PROOF
 GRANTS
REFERENCES
 
This study was supported by Natural Science and Engineering Research Council of Canada (NSERC) grants. Additional support was provided by a University of Western Ontario Academic Development Fund Grant and infrastructure support of the Canadian Foundation for Innovation and Ontario Innovation Trust. D. S. DeLorey was supported by Doctoral research scholarships from NSERC and the Canadian Institutes of Health Research.


   FOOTNOTES
 

Address for reprint requests and other correspondence: D. H. Paterson, Canadian Centre for Activity and Aging, School of Kinesiology, The Univ. of Western Ontario, London, Ontario, Canada N6A 3K7 (e-mail: dpaterso{at}uwo.ca)

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.


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