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O2 during repeated bouts of heavy knee extension exercise in humans
1 Department of Exercise Science and Physiology, School of Health Sciences, Hiroshima Prefectural Women's University, Hiroshima 734–8558, Japan2 Laboratory of Health and Exercise Science, Hiroshima Institute of Technology, Hiroshima 731–5193, Japan3 Laboratory of Physical Activity and Health Evaluation, National Institute of Health and Nutrition, Tokyo 162–8636, Japan4 Laboratory for Applied Physiology, Kobe Design University, Kobe 651–2196, Japan5 Laboratory for Human Science and Biomedical Engineering, National Institute of Advanced Industrial Science and Technology, Tsukuba 305–8563, Japan.
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Abstract |
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O2 kinetics at the onset of subsequent heavy exercise. This might be due to improved muscle perfusion via acidosis-induced vasodilating effects. However, it is difficult to measure the blood flow (BF) to the working muscles (via the femoral artery) during cycling exercise. We therefore selected supine knee extension (KE) exercise as an alternative, and investigated whether the faster O2 kinetics in the 2nd bout was matched by proportionally faster BF kinetics to the exercising muscle. Nine healthy subjects (aged 21–44 years) volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate: 70–75% of peak power) separated by a 6-min baseline rest (EX1 to EX2). During the protocol, a pulsed Doppler ultrasound technique was utilized to continuously measure the BF in the right femoral artery. The protocol was repeated at least 6 times to characterize the precise kinetics. In agreement with previous studies using cycling exercise, the O2 kinetics in the 2nd bout were facilitated compared with that in the 1st bout [mean ±S.D. of the ‘effective’ time constant (
): EX1, 68.6 ± 15.9, versus EX2, 58.0 ± 14.4 s. Phase II-: EX1, 48.7 ± 9.0, versus EX2, 41.2 ± 13.3 s. Empirical index of the slow component (
O2(6–3)): EX1, 78 ± 44, versus EX2, 57 ± 36 ml min–1 (P < 0.05)]. However, no substantial difference was observed for the facilitation of the femoral artery BF response to the 1st and 2nd exercise bouts [i.e. the ‘effective’ of the femoral artery BF: EX1, 40.8 ± 16.9, versus EX2, 39.0 ± 17.1 s (P > 0.05)]. It was concluded that the faster pulmonary O2 kinetics during heavy KE exercise following prior heavy exercise was not associated with a similar modulation in the BF to the working muscles.
(Received 24 September 2003;
accepted after revision 23 January 2004; first published online 17 February 2004)
Corresponding author Y. Fukuba: Department of Exercise Science and Physiology, School of Health Sciences, Hiroshima Prefectural Women's University, 1-1-71, Ujina-higashi, Minami-ku, Hiroshima 734–8558, Japan. Email: fukuba{at}hirojo-u.ac.jp
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Introduction |
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O2) during ‘moderate’ intensity square-wave cycling exercise (i.e. work rates below the lactate threshold; LT) approaches its steady state with an exponential time course (phase II) after a short delay (phase I) and attains a steady state (phase III) within 2–3 min in normal healthy individuals (e.g. see Whipp & Ward, 1990 for a review). It has been suggested that the time constant () for phase II O2 during moderate exercise reflects that of muscle O2 consumption (mO2; Grassi et al. 1996). Since it is also closely related to the intramuscular [phosphocreatine] ([PCr]), ‘metabolic inertia’ is thought to be its primary determinant (Chance et al. 1986; Mahler, 1985; Meyer, 1988; Rossiter et al. 1999). During ‘heavy’ intensity exercise (i.e. supra-LT work rates), however, the O2 response is more complex. The response consists of two main components: a fundamental phase II component, still well described by a single-exponential, and a subsequent delayed phase yielding a slowly developing supplemental rise in O2 which has been termed the O2‘slow’ component (Poole et al. 1988; Whipp, 1994).
While the physiological determinant(s) of the O2 response during square-wave exercise in the supra-LT domain is (are) currently debated (e.g. Grassi, 2001; Hughson et al. 2001; Tschakovsky & Hughson, 1999), it has been suggested that O2 delivery may be of a greater importance in modulating the O2 kinetics during heavy intensity exercise than during moderate intensity exercise (Grassi et al. 2000; MacDonald et al. 1998; Whipp & Ward, 1990). Support for this notion is, in part, derived from the demonstration that the O2 response may be facilitated when heavy intensity exercise (usually cycling) is preceded by a ‘priming’ bout of identical intensity (Gerbino et al. 1996; MacDonald et al. 1997). For normal healthy subjects, such a modulation may only be brought about during exercise in the heavy intensity domain, and not in the moderate domain. It was proposed that this adjustment of the O2, seen on the transition to a 2nd exercise bout, may be due to improved muscle perfusion consequent to the vasodilatory effects of the residual lactic acidaemia still present at the onset of the 2nd bout (Gerbino et al. 1996).
Concurrent measurements of the muscle blood flow (BF) and the whole body O2 can provide strong support for the influence of the BF on the O2 slow component. This has only been performed using hand-grip exercise, although the constraints of the experimental protocol did not allow estimation of the kinetic parameters of the BF and O2 temporal responses (MacDonald et al. 2001). Furthermore, hand-grip exercise activates a relatively small muscle mass that may have a different circulatory/respiratory adaptation than systemic cycling exercise which engages a much larger muscle mass (e.g. Saltin, 1985; Shephard et al. 1988). This may limit the usefulness of the small muscle model for interpreting the O2 kinetics of large muscle groups. In fact, hand-grip exercise did not induce a distinct O2 slow component (MacDonald et al. 2001). Therefore, we selected, as an alternative, supine bilateral knee extension (KE) exercise and measured the temporal profiles of the pulmonary O2 and femoral artery BF during repeated bouts of heavy KE exercise. The use of KE provides a large exercising muscle mass that enables valid and reliable BF measurements with concurrent hip joint stabilization. We therefore hypothesized that the faster O2 kinetics in the 2nd bout would be matched by proportionally faster BF kinetics to the exercising muscle.
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Methods |
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Nine healthy subjects (5 women and 4 men; mean (S.D.) age, 29.1 (9.1) years; height, 165.8 (7.6) cm; weight, 58.9 (14.0) kg) volunteered to participate in this study. The subjects were aware of all the testing procedures and gave informed consent to participate as approved by the ethics committee of the local institution (in accordance with the Declaration of Helsinki).
Exercise Protocols
The knee extension (KE) exercise was conducted in a supine position with the hip extended to approximately 150° with a thigh supporter. To minimize the effects of body movement, each subject was strapped to the table with a belt placed across the iliac spines, allowing unimpeded BF through the femoral artery. The bilateral KE exercise involved lifting and lowering a weight at 1-s intervals (i.e. 60 cycles per min) for each leg in an alternating pattern. The weight was connected to the ankle by a wire and pulley mechanism. Timed audio signals provided the subjects with a constant exercise cadence. Soft rubber was used to cushion the heel during knee flexion to minimize eccentric muscle activation and ensure that concentric contractions dominated the muscle activation pattern. The range of motion during knee extension was regulated by a bar that the subjects' toes had to touch. The subjects were given continuous verbal feedback to ensure a consistent lifting length of the load for accurate and reproducible work rate calculations. The average lifting distance for this KE exercise protocol was 16.5 ± 1.5 cm.
First, the subjects performed a stepwise incremental KE exercise test (0.5 kg increase every 30 s from 0.5 kg) until exhaustion. This protocol resulted in a peak O2 of 1113 ± 407 ml min–1 and a peak work rate of 18.3 ± 3.3 W for each leg. The main experimental protocol consisted of two consecutive 6-min KE exercise bouts in the same position as the incremental bout separated by a 6-min baseline supine rest (EX1 to EX2). The work rate selected was approximately 70–75% of the peak power based on each subject's ability to sustain the 6-min duration double-bout of exercise and whether the O2 slow component could be discerned. To characterize the precise kinetics, numerous tests were required, and each subject repeated the protocol at least six occasions (i.e. 6–13 times) at the same time on different days and each test was separated by at least 2 days to avoid the training effect. Although there was concern regarding a possible training effect on the constancy of the O2 responses (due to the frequent repetitions), no systematic changes in the kinetic parameters (see below) of O2 were found in any of the subjects with increasing number of repetitions.
Measurements
Ventilatory and gas exchange responses were determined breath-by-breath using a computerized metabolic measuring system (RM-300, Minato Medical Co., Osaka, Japan). Prior to each exercise test, a hot-wire flow-sensor and gas analysers were calibrated by inputting a known volume of air (at several mean flow rates) and gas mixtures of known concentrations, respectively. The heart rate (HR) was monitored by a cardiotachogram (BP-306; Colin, Komaki, Japan). A second-by-second time course was calculated for each variable by interpolation and then stored on disks for further analysis.
The femoral artery BF was obtained using simultaneous pulsed and echo Doppler ultrasound to measure the mean blood velocity (MBV) and femoral artery diameter, from a site 
2–3 cm distal to the right inguinal ligament. The femoral artery blood velocity was obtained with the pulsed Doppler system (EUB-415; Hitachi Medico, Japan) by using a 3.5 MHz probe with an insonation angle of 55–60°. The use of this machine had at least two advantages. The first was that a real-time cross-sectional image (i.e. B mode echo) could be displayed every 4 s with the real-time Doppler spectral display and sound, and thus the angle of the pulse and the location of the targeted vessel could be continually visually confirmed. The second was a modification that allowed all Doppler spectral signals to the display to be simultaneously digitized and recorded every 10 ms. This allowed instantaneous mean BF to be accurately determined without any of the bias that can occur with the more common visually inspected hand-tracing technique. B mode echo images of the right femoral artery were obtained with the same probe. Longitudinal images of the arterial vessel were recorded on videotape and analysed to calculate the artery diameter with on-screen calipers. Vessel diameter was measured during the contraction/relaxation phases at rest and during exercise, that is, three times at rest, every 10 s during the first and second minutes of exercise, and then at 1-min intervals to the end of the exercise, similar to previously utilized methods (e.g. MacDonald et al. 1998; Rådegran, 1997). The mean BF was calculated on a second-by-second basis by multiplying the MBV by the calculated cross-sectional area of the artery. No systematic changes in the diameter were noticed during the protocol for any of the subjects. Validation of the simultaneous pulsed and echo Doppler ultrasound system with our automatic data-acquisition system for measuring the BF was performed by in vitro calibration. This was conducted by utilizing a blood-mimicking test fluid (Model 707, ATS Laboratories, Bridgeport, CT, USA). The system was calibrated 16 times by inputting a known volume (100 ml) of the test fluid via a syringe through Tygon plastic tubes (10 mm diameter) at various flow profiles (approximately 5–20 ml s–1). Comparison between the calculated flow volume (i.e. the total area under the mean velocity curve multiplied by the cross-sectional area of the tube) by the Doppler ultrasound system and the known volume (i.e. 100 ml), revealed a good agreement with no apparent bias and a mean error of ± 8%.
Estimation of O2, BF and HR responses
The temporal O2, BF and HR profiles at the onset of heavy KE exercise were quantified by a cluster of empirical and model-based indices during both 1st and 2nd 6-min square-wave bouts (i.e. EX1 and EX2). The baseline was an average of the first minute prior to the exercise onset. The temporal profiles were fitted to models based on the following equation:
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O2, BF, or HR at time t; BL is the baseline value at rest, and A, Td, and are the amplitude, time delay, and time constant parameters, respectively (subscripts p and s represent ‘primary’ and ‘slow’ component, respectively, see below). For the first model, the second exponential term of equation 1 was set to zero (i.e. mono-exponential model) and the entire response (i.e. 0 s to 360 s) was considered. This allowed conventional overall estimation of the mean response time [MRT = time constant () + time delay (Td)] for the O2, BF and HR (providing a broad description of these variable dynamics, using the MRT as a ‘parameter of convenience’).
Then, the mono-exponential model was also fitted to the data excluding phase I (i.e. 20 s to 360 s; Whipp et al. 1982), and the time constants of the O2 and the BF were established (the so-called ‘effective’; e.g. Gerbino et al. 1996). It has been shown that there is a bias in the O2 residuals resulting from a mono-exponential fitting during supra-LT leg cycling exercise due to the influence of the slow component (e.g. Barstow & Molé, 1991; Casaburi et al. 1989; Paterson & Whipp, 1991). Thus the same O2 and BF data (i.e. 20 s to 360 s) were also fitted with equation 1 where the second term was allowed to be freely variable, i.e. a double-exponential model incorporating two amplitudes (primary, Ap; and slow, As, components), two time constants (p and s), and two time delays (Tdp and Tds). Fitting was performed using a non-linear least-squares regression technique (Marquardt–Levenberg Algorithm in Sigma Plot 2000, Jandel Scientific, Chicago, IL, USA). The increment in the O2 between minutes 3 and 6 of the 6-min exercise bout (O2(6–3)) was also measured to estimate the magnitude of the O2 slow component empirically (and also BF(6–3) in the case of the BF).
Statistics
The values are expressed as means ±S.D. The F-test was used to decide whether double-exponential fitting led to a significant reduction in the residual summed squared error term for each response, compared with mono-exponential fitting (Motulsky & Ransnas, 1987). Since the estimated parameters and variables were found to be normally distributed, the differences between the variables and parameters (by bout) were examined by the Student's paired-comparison t test. The time–serial changes in the variables (every 20-s average) were tested with respect to the differences between EX1 and EX2 by repeated measures ANOVA with time. When a significant difference was detected, this was further examined by Tukey's post hoc test. All statistical analyses were performed with SPSS for Windows (SPSS Inc.) and Sigma Plot (2000) (Jandel Scientific). Statistical significance was accepted at P < 0.05.
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Results |
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O2 data much better than the mono-exponential model. However, for the BF data, the double-exponential model fitting did not significantly reduce the residuals compared to the mono-exponential model (see Figs 1 and 2). This indicated that the BF data did not exhibit a significant slow component (Fig. 2). Individually, this was true in 7 of 9 subjects in the first bout and 8 of 9 subjects in the second bout. We therefore omitted the results from double-exponential fitting of the BF with low confident estimates from Table 1.
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O2 and BF
Examples of the O2, HR and femoral artery BF responses of a representative subject during the repeated bouts of KE exercise are shown in Fig. 1. The 1st bout of heavy KE exercise had a distinguishable O2 slow component (as shown in the top panel of Figs 1 and 2). Figure 3 illustrates the superposition of the O2, CO2, HR and BF responses from the group mean (i.e. n= 9) for every 20 s of the transition to both the 1st and 2nd exercise bouts. The temporal profile of O2 after the onset of the 2nd bout of KE exercise was essentially higher than that in the 1st bout, while the baseline O2 was not different. In contrast, the CO2 data showed a slightly, but significantly, decreased development during the latter half of the 2nd bout of exercise. The HR was substantially elevated throughout 2nd bout, including the duration prior to the onset. The BF showed a very similar temporal response for the 1st and 2nd bouts on the transition to heavy KE exercise after the first 20 s. The empirical index of the O2 slow component, O2(6–3), in the 2nd bout (57 ± 36 ml min–1) was significantly diminished compared with that in the 1st bout (78 ± 44 ml min–1; Table 1). A similar index for BF, BF(6–3), did not show any statistical difference between the 1st and 2nd bouts and was not discernibly different from zero (EX1, 0.04 ± 0.10, versus EX2, 0.03 ± 0.09 l min–1; Table 1).
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O2 and BF kinetics
The overall O2 kinetics for the exercise evaluated by mono-exponential fitting was discernibly faster for the 2nd bout than for the 1st bout as evaluated by either the MRT (EX1, 72.1 ± 14.3, versus EX2, 60.6 ± 13.3 s) or effective (EX1, 68.6 ± 15.9, versus EX2, 58.0 ± 14.4 s; Table 1). The double-exponential fitting, partitioning the response into the primary and slow components of the O2 response, revealed that the facilitation of the primary O2 component was still manifest in the 2nd bout (p; EX1, 48.7 ± 9.0, versus EX2, 41.2 ± 13.3; Table 1), whereas the amplitude (Ap) did not show any difference.
In contrast to the case for the O2 kinetics, the BF kinetics did not show any significant difference between the 1st and 2nd bouts in either the MRT (EX1, 39.2 ± 16.1, versus EX2, 40.2 ± 15.7 s) or effective (EX1, 40.8 ± 16.9, versus EX2, 39.0 ± 17.1 s; Table 1). The baseline BF just prior to the 2nd bout was substantially higher than that in the 1st bout, and this resulted in a significant reduction in the amplitude (A) in the 2nd bout (Table 1). Since the BF responses in both the 1st and 2nd bouts were well described by the mono-exponential model fitting (see the example in Fig. 2), we did not include the estimated kinetic parameters from the inappropriate double-exponential fitting in the results (Table 1). These features were typical of both the individual and the group responses, as seen in Figs 1 to 3. The HR kinetics using the MRT showed no statistical difference between the 1st and 2nd bouts (EX1, 30.0 ± 18.9, versus EX2, 31.3 ± 19.2 s). The ‘effective’ between the O2 and the BF by mono-exponential fitting were significantly different. That is, the BF was essentially faster than the O2 in both the 1st and 2nd bouts (EX1: O2, 68.6 ± 15.9, versus BF, 40.8 ± 26.9. EX2: O2, 58.0 ± 14.4, versus BF, 39.0 ± 17.1 s; P < 0.05). If the comparison was limited to phase II (i.e. using p in the O2), a significant difference was recognized in the 1st bout (BF-effective : 40.8 ± 26.9, versusO2-p, 48.7 ± 9.0 s; P < 0.05), but not in the 2nd bout (BF-effective : 39.0 ± 17.1, versusO2-p, 41.2 ± 13.3 s).
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Discussion |
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O2 response to KE exercise was facilitated by a prior identical bout, while the BF to the exercising muscles (i.e. the BF in the femoral artery) was unchanged between the bouts. Similar to previous studies (e.g. Gerbino et al. 1996; MacDonald et al. 1997), repeated supra-LT square-wave exercise facilitated the O2 response, but in the present study, there was no comparable facilitation of the BF as evaluated by both kinetic and empirical parameters and time serial changes in the variables (Table 1; Figs 1 and 3). The BF has been suggested to be limiting in the 1st bout transition (e.g. MacDonald et al. 1997), and therefore during the 2nd bout of the repeated bout protocol, a facilitated BF to the exercising limb has been suggested to mediate the acceleration of the O2 response (e.g. Gerbino et al. 1996). Against this hypothesis, the time course of the BF was not demonstrably accelerated after the onset of the 2nd bout of exercise, despite the substantially faster primary component and the reduced slow component of the O2, as estimated by double-exponential fittings. Furthermore, whereas there was no distinguishable development of a BF slow component from the 3rd to the 6th minute of exercise in either the 1st or 2nd bouts, there was a marked O2 slow component during the 1st bout, which was significantly reduced during the 2nd bout (i.e. the relative ratio of the slow component to Ap; EX1, 15.6 ± 7.8, versus EX2, 11.7 ± 7.3%). These findings are, in general, inconsistent with the notion that circulatory dynamics appear to play a controlling role in the adjustment of the pulmonary O2 during high-intensity exercise with a large muscle mass.
The physiological mechanism(s) underlying the ‘facilitated’O2-kinetics during repeated bouts of identical heavy exercise may be linked to the aetiology of the complex O2 kinetics manifest in the supra-LT exercise domain, mainly reflected in the adaptation of the slow component (i.e. between the 1st and 2nd bouts). Similar to moderate intensity exercise, there have been two main lines of thought proposed to determine the O2 response at the onset of supra-LT exercise: (a) the rate of O2 transport to the exercising muscle (vascular limitation), or (b) the ability of the exercising muscle to utilize O2 (metabolic inertia) (Grassi, 2001; Hughson, 1990; Hughson et al. 2001; Mahler, 1985; Tschakovsky & Hughson, 1999; Whipp & Ward, 1990).
Originally, Gerbino et al. (1996) speculated that a circulatory limitation contributed to the slowed O2 kinetics during supra-LT work intensities after demonstrating an appreciably facilitated O2 response during the 2nd bout of exercise following a prior identical supra-LT ‘conditioning’ bout. This hypothesis of a circulatory limitation during heavy intensity exercise has since been supported by several studies. For example, MacDonald et al. (1997) showed that enhanced O2 delivery, by hyperoxic inspiration, accelerated the MRT of the O2 during heavy leg cycling exercise, although the of the primary component remained unaffected. In addition, when heavy KE exercise was performed in the supine position, compared to the upright position, these authors showed that a slowed femoral artery BF was associated with a slower O2 response (MacDonald et al. 1998). Similarly, Grassi et al. (2000) were able to elicit a faster adjustment of the mO2 in the canine gastrocnemius by artificially increasing the muscle BF during ‘peak’ stimulations, whereas a similar effect was not found during exercise that elicited 60–70% of the O2,max (Grassi et al. 1998). Furthermore, recent studies (MacDonald et al. 2001; Perrey et al. 2001; Van Beekvelt et al. 2001) using single or repeated bouts of hand-grip exercise (presumably in the heavy intensity domain), demonstrated that the mO2 and BF manifested similar response adaptations. In other words, improved O2 delivery was associated with a facilitation of the mO2 response on the transition to a 2nd bout of hand-grip exercise following an identical ‘conditioning’ bout, such that the forearm mO2 during the first minute of the 2nd bout of exercise was elevated compared to that in the 1st bout with a concomitant increase in the BF to the forearm (MacDonald et al. 2001). However, due to the constraints of the experimental mode, the authors could not estimate the kinetic parameters of these changes, and there was no substantial slow component of the O2 in this exercise model (see Figure 2 in MacDonald et al. 2001).
On the other hand, in humans, impositions to adjust the limb oxygen delivery prior to heavy-intensity exercise, such as lower body positive pressure (Williamson et al. 1996) or by a manoeuvre to induce a reactive hyperemia (Walsh et al. 2002), have similarly failed to alter kinetic parameters of the O2 during a single supra-LT cycling exercise bout. Furthermore, Fukuba et al. (2002) found that a comparable systemic residual lactic acidosis (generated by exercising a different muscle group, i.e. arm) had no effect on the subsequent O2 kinetics at the onset of heavy intensity leg cycling exercise, despite the potential beneficial effects of peripheral vasodilatation and an expected rightward shift of the oxygen dissociation curve. These studies are inconsistent with a substantial role for the central and/or peripheral BF in determining the O2 response at the onset of heavy exercise. The results in the present study are consistent with this interpretation.
It appears that the dynamics of the cardiac output or BF are consistently faster than the O2 at the onset of both moderate (De Cort et al. 1991; Grassi et al. 1996) and heavy intensity (MacDonald et al. 1998) exercise. In the present study, we also showed that the BF dynamics at the onset of either 1st or 2nd bout was faster than the O2 response estimated by mono-exponential fitting (‘effective’ and MRT in Table 1). Furthermore, Endo et al. (2003),, recently demonstrated that a circulatory attenuating manipulation by cold face stimulation (CFS) applied at the onset of a second bout of supra-LT cycling exercise had no effect on the O2 response at the onset of the second bout. This result did not support the hypothesis that the O2 response at the onset of the 2nd bout of exercise would be suppressed by centrally and/or peripherally attenuating O2 delivery by CFS manipulation. All these observations, including the results of the present study, support the metabolic inertial hypothesis for determining the characteristics of the O2 response at the initial onset of heavy intensity exercise, while Tordi et al. (2003) most recently demonstrated that, during exercise that elicited 97% of peak O2, a faster primary was manifest when cardiac output was increased by prior repeated-30 s-‘sprint’ cycling exercise.
Behnke et al. (2002) have shown that, in the rat intact-spinotrapezius muscle, a faster overall decrease in the microvascular PO2 in the 2nd bout of contraction was indicative of a relatively faster O2 than the BF response. In other words, there was faster O2 extraction in the 2nd bout of contraction. Thus, alterations in muscle metabolism facilitate the O2 in excess of the BF and can occur without elevation of the resting or contracting BF per se. Supporting this notion, BF/O2 in the primary phase of the 1st bout was approximately 5.5 [i.e. (2 x 1.38)/0.49 from the mean values in Table 1] which is very close to the ordinary value for the O2 and cardiac output in cycling exercise (e.g. Whipp et al. 1996), but was reduced in the 2nd bout to 3.7 [(2 x 0.93)/0.49] due to the elevated baseline BF just prior to the 2nd bout in the present study. This suggests an altered relationship between the O2 and the BF, i.e. an increased a-v O2 difference, which may be of great mechanistic importance. The elevated baseline BF may ‘prime’ the muscle with a higher microvascular PO2 and facilitate the kinetics in the absence of faster kinetics per se. Mizuno et al. (2003) recently demonstrated that there was relatively uniform distribution of the regional perfusion to metabolism ratio and O2 extraction in the quadriceps femoris muscle using a novel technique, positron emission tomography, when they were measured in the recovery from, not during, single leg exhaustive cycling exercise.
In contrast to most previous studies with a repeated bouts protocol using a cycle ergometer in which the facilitated O2 in the 2nd bout was mainly ascribed to the reduction in the slow component, the present study demonstrated a significant facilitation of the ‘primary’ component of the O2 (i.e. p) at the onset of the 2nd bout compared with the 1st bout. This is consistent with the results in a recent study by Rossiter et al. (2001) using rhythmic alternative-leg KE exercise and magnetic resonance spectroscopy. While we are currently unable to explain the different results derived from the cycling and KE exercises, the muscle mass utilized, exercise intensity, and exercise modality may all be contributory. In particular, the exercise modality, that is, the difference between the leg cycle ergometry versus the KE exercise used in the present study and Rossiter et al. (2001), may be important, since the primary kinetics of the O2 (e.g. p) was substantially slower in KE exercise [approximate mean values: 49 and 41 s in the 1st and 2nd bouts, respectively, in both the present study and Rossiter et al. (2001)] compared with those in the studies using conventional leg cycle ergometry [e.g. approximately 23 and 25 s in either the 1st or 2nd bout in Burnley et al. (2000) and Fukuba et al. (2002)]. In addition, a substantially different muscle usage pattern between heavy cycling and KE exercise (Richardson et al. 1998) or with a different domain of exercise intensity of cycling (Endo et al. 2003a) has been demonstrated by magnetic resonance imaging. Further studies are needed to resolve this issue.
The mechanism(s) underlying the facilitated O2 response (manifest as either a facilitation of the fundamental p, a reduction in the slow component, or both) at the onset of the 2nd bout of exercise during repeated exercise therefore remain(s) to be elucidated. Rossiter et al. (2001) suggested that the O2 slow component during the repeated bouts protocol in humans was related to an intramuscular event linked to [PCr] degradation, which was in accordance with the demonstration of Poole et al. (1991) that approximately 80–90% of the pulmonary O2 slow component could be accounted for by the associated increase in the leg O2. Consequently, the control of the O2 slow component is commonly ascribed to factors related to the exercising limb, rather than to the rest of the body. Therefore, we believe that the mechanisms proposed to explain the facilitated O2 in the 2nd bout are more likely to be ascribed to an intramuscular event, such as the pattern of motor unit recruitment and/or fatigue (Barstow et al. 1996; Rossiter et al. 2002), intracellular factors other than O2 availability (Hogan, 2001) which may arise from either activation of the pyruvate dehydrogenase complex (Howlett & Hogan, 2003; Rossiter et al. 2003; Timmons et al. 1998), and/or be related to the attenuation of the blood lactate increase (Fukuba et al. 2002; Gerbino et al. 1996), or altered phosphate-mediated feedback control (Rossiter et al. 2001).
In summary, this study demonstrated that, whereas the pulmonary O2 was accelerated substantially at the onset of square-wave heavy intensity KE exercise following an identical 1st bout of KE, the BF to the exercising muscles did not show a similar response. This is contrary to our original hypothesis and suggests that the marked adaptation of the O2 kinetics during the 2nd bout of heavy exercise is not associated with an O2-delivery related mechanism. Rather, these data implicate mechanisms that are more proximally related to the event(s) within the exercising muscles in mediating this phenomenon.
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