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School of Sport and Health Sciences, University of Exeter, St. Luke's Campus, Exeter, United Kingdom
Submitted 13 April 2006 ; accepted in final form 9 July 2006
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONREFERENCES |
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O2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean ± SD age 24 ± 7 yr; body mass 75.0 ± 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant (
) of the O2 response in phase 2 (bout 1: 29 ± 10 vs. bout 2: 28 ± 4 s; P = 0.91) but reduced the amplitude of the O2 slow component (bout 1: 0.45 ± 0.16 vs. bout 2: 0.22 ± 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 (bout 1: 38 ± 18 vs. bout 2: 24 ± 9 s; P = 0.03) but did not alter the amplitude of the O2 slow component (bout 1: 0.40 ± 0.29 vs. bout 2: 0.41 ± 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 O2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.
O2 dynamics; O2 slow component; phase 2 time constant; prior exercise; O2 delivery limitation; muscle energetics
O2) increases with finite kinetics, such that a steady state is reached after 2–3 min for work rates that do not engender a significant lactic acidosis [that is, below the lactate threshold (LT)], or considerably later (or not at all) for work rates above the LT (4, 43, 59, 63). The limitation to the O2 kinetics could occur at any point in the O2 transport pathway: from convective O2 transport to muscle (comprising arterial oxygenation, hemoglobin concentration, cardiac output, and muscle blood flow and its distribution), through diffusive O2 conductance (related to muscle capillarity and the O2 gradient from capillary to mitochondria), to the rate of O2 consumption in the myocytes (influenced by mitochondrial density, oxidative enzyme activity, muscle fiber type, and substrate supply). The control and limitations to O2 kinetics are likely to be influenced by a variety of factors, including the type of subject studied (including their age and fitness) and the type of exercise performed (including its intensity, body position, and muscle mass recruited) (32, 57).
A number of experimental interventions have been employed in an effort to determine the principal limiting factor(s) to O2 kinetics in humans (32), among them being the utilization of "priming" exercise (10, 16, 21, 34, 36, 41, 45, 51, 52, 54). Early studies demonstrated that the O2 response to exercise differed markedly depending on the extent of any prior activity (see Ref. 11 for review). In an influential study, Gerbino et al. (21) systematically examined the influence of initial bouts of either moderate (<LT) or heavy (>LT) upright cycle exercise on the O2 response to subsequent bouts of either moderate or heavy exercise. These authors reported that prior exercise of either intensity had no effect on O2 kinetics during moderate exercise, that prior moderate exercise had no effect on O2 kinetics during heavy exercise, but that prior heavy exercise resulted in significantly faster "overall" O2 kinetics during heavy exercise. Gerbino et al. postulated that the effects they observed might be attributed to an enhanced muscle O2 availability consequent to a greater muscle vasodilatation and rightward shift of the oxyhemoglobin (HbO2) dissociation curve resulting from the residual acidemia and elevated muscle temperature. Subsequent studies using the same exercise model (i.e., upright cycle ergometer exercise) demonstrated that the overall "speeding" of the O2 response during heavy exercise reported by Gerbino et al. was not related to any alteration in the phase 2 time constant () but, rather, was caused by a reduction in the amplitude of the O2 slow component (often with an increased O2 amplitude in the fundamental phase of the response) (5, 8–10, 16, 34, 36, 45, 52, 54). Because the amplitudes of both the fundamental and slow components of the O2 response to heavy exercise appear to be associated with muscle fiber-type recruitment profiles (3, 38, 47, 48), these studies suggested that the performance of prior heavy exercise might have altered local (i.e., muscle metabolic) factors in such a way as to modify muscle fiber recruitment during subsequent heavy exercise (8, 11).
Evidence from most prior exercise studies, as well as other sources, therefore implies that muscle O2 supply does not normally limit O2 kinetics during heavy-intensity upright cycle exercise, at least in young, healthy subjects with relatively high aerobic fitness (32). In contrast, there is evidence that muscle O2 delivery can limit O2 kinetics in other exercise modes or in other populations (15, 23, 26, 32, 46, 53). For example, reductions in muscle perfusion pressure during cycle exercise in the supine position (30, 42) and during arm exercise where the arms are positioned at or above the level of the heart (29, 35) are associated with slower phase 2 O2 kinetics relative to the respective control conditions. In these situations, enhancing muscle O2 delivery can result in a speeding of the phase 2 O2 kinetics (26, 27, 35, 40, 46).
Whether the performance of prior heavy exercise does result in an increased muscle blood flow and/or faster muscle blood flow kinetics during subsequent exercise is somewhat controversial (2, 8, 16, 19, 20, 37, 44, 56). The deoxyhemoglobin (HHb) concentration ([HHb]) signal derived from near-infrared spectroscopy (NIRS) reflects the balance between O2 delivery and O2 utilization in the field of interrogation and has been used to noninvasively estimate O2 extraction in the skeletal muscle microcirculation and to provide an indication of the adequacy (or otherwise) of muscle O2 supply (15, 18, 22, 62). If the performance of prior heavy exercise improves muscle O2 availability, one would expect NIRS evidence of an increased total Hb in the field of interrogation [i.e., the sum of the oxygenated Hb and myoglobin (Mb) and the deoxygenated Hb and Mb, suggestive of hyperemia]. An enhanced muscle O2 supply might also result in slower [HHb] kinetics, although this effect might be difficult or impossible to discern if priming exercise also enhances muscle O2 extraction.
The available evidence (reviewed above) therefore suggests that the extent to which the performance of prior heavy exercise might impact on the phase 2 O2 kinetics depends, at least in part, on body position and its attendant effects on muscle perfusion pressure (35, 46, 51). The purpose of the present study was to test this possibility by comparing the influence of prior heavy cycle exercise on O2 kinetics during subsequent heavy cycle exercise performed in both the upright and supine positions. We used NIRS to noninvasively estimate changes in muscle O2 delivery and utilization brought about by the performance of prior exercise in both body positions. Our specific hypotheses were that 1) prior heavy exercise would result in hyperemia (as estimated by NIRS) and therefore greater muscle O2 availability in both body positions; 2) the of the phase 2 O2 kinetics would be greater during supine than upright heavy cycle exercise in the initial "control" exercise bout; 3) the phase 2 would be significantly reduced by prior heavy exercise in the supine, but not the upright, position; and 4) the amplitude of the O2 slow component would be reduced in both body positions.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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Procedures.
All testing was completed in a well-ventilated laboratory at a temperature of 20–22°C. The subjects attended the laboratory on six occasions over a 3-wk period to perform exercise tests on an electronically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands). The first two visits were used to establish maximal O2 (O2 max) and to estimate the gas-exchange threshold (GET) during cycle exercise performed in both the upright and supine positions. On each of the four subsequent visits, subjects completed two bouts of heavy exercise (at a work rate calculated to require 50% of the difference between the GET and O2 max established during upright exercise; i.e., 50% "
") separated by 10 min of recovery. On two occasions, this protocol was completed in the upright position, and on two other occasions it was completed in the supine position. To create the latter condition, the ergometer was tipped backward by 90° and fixed against a wall. Subjects lay supine on a secure mat inside a custom-built restraint that enabled them to produce force on the pedals without sliding backward during the exercise tests. Fixed handgrips were available, and the feet were strapped to the pedals in both conditions. In this way, the cycling position was similar in the upright and supine conditions, with the exception that the legs were positioned just above the level of the heart in the supine position. The conditions were presented to the subjects in random order, and each laboratory visit was separated by 1–4 days.
During the first visit to the laboratory, after measurement of height and body mass, subjects performed a "ramp" incremental exercise test (in either the upright or supine position) to determine O2 max and GET. The ramp tests consisted of 3 min of pedaling at 0 W, followed by a continuous ramped increase in work rate of 30 W/min until the limit of tolerance. The pedal rate selected by each of the subjects in the first ramp test (typically 80–85 rev/min) was employed during all subsequent tests. All gas-exchange and ventilatory variables were averaged and displayed every 10 s. The O2 max was determined as the highest O2 measured over 30 s, and the GET was estimated by the V-slope method (6). During upright exercise, the work rate corresponding to 50% was calculated using linear regression of O2 vs. work rate with account taken of the lag in O2 relative to work rate that exists during ramp incremental exercise (58). This work rate was subsequently applied during the constant-work-rate protocols completed in both the upright and supine positions.
The constant-work-rate protocols began with 3 min of pedaling at 0 W, after which the 50% work rate was abruptly applied and subjects continued exercising for a further 6 min. After 7 min of passive rest, the subjects completed an identical exercise bout, again comprising 3 min of pedaling at 0 W and 6 min of heavy exercise at 50% . This "double-step" test was completed four times in total: twice in the upright position and twice in the supine position. This enabled us to average the O2 responses from the tests performed in the same body position and thus enhance the signal-to-noise ratio and improve confidence in the parameters derived from the model fits (39).
During all tests, pulmonary gas exchange and ventilation were measured breath by breath with subjects wearing a nose clip and breathing through a low-dead-space, low-resistance mouthpiece and impeller turbine assembly (Jaeger Triple V). The inspired and expired gas volume and gas concentration signals were continuously sampled at 100 Hz, the latter using paramagnetic (O2) and infrared (CO2) analyzers (Jaeger Oxycon Pro, Hoechberg, Germany) via a capillary line connected to the mouthpiece. The gas analyzers were calibrated before each test with gases of known concentration and the turbine volume transducer was calibrated by using a 3-liter syringe (Hans Rudolph, Kansas City, MO). The volume and concentration signals were time aligned by accounting for the delay in the capillary gas transit and the analyzer rise time relative to the volume signal. Pulmonary gas exchange and ventilation were calculated and displayed breath by breath. Heart rate (HR) was measured every 5 s in all tests using short-range radiotelemetry (Polar S610, Polar Electro Oy, Kempele, Finland). During the double-step tests, blood was collected from a fingertip into glass capillary tubes immediately before and immediately after the two 6-min periods of heavy exercise for subsequent determination of whole blood lactate concentration ([lactate]; YSI 1500, Yellow Springs Instruments, Yellow Springs, OH). Blood lactate accumulation was calculated as the difference between the blood [lactate] measured at 6 min of exercise and the blood [lactate] measured at baseline.
During one of the test days in each condition, the oxygenation status of the right vastus lateralis muscle was monitored by use of a commercially available NIRS system (model Heo-200, OMRON, Tokyo, Japan). In our hands, this device provides highly reproducible [HHb] responses when the same subject performs like transitions on different days (coefficient of variation for of the [HHb] response of 
4–7%; D. P. Wilkerson and A. M. Jones, unpublished observations). The system consisted of a probe attached to a data logger that received NIRS signals at 2 Hz. The probe consisted of two light-emitting diodes and two photodetectors, which detected photons at wavelengths of 840 nm (HbO2) and 760 nm (HHb). With this device, the optodes are separated by 3 cm and the penetration depth is at least 1.5 cm (manufacturer's instructions). After shaving and cleaning of the lower one-third of the vastus lateralis muscle, the probe was secured to the skin at 10–12 cm above the knee joint with a Velcro strap and adhesive tape. Pen marks were made above and below the Velcro strap and around the probe to check for any movement of the device during exercise and to enable reproduction of the probe position in subsequent tests. The probe gain was set with the subject at rest in a seated position, and NIRS data were collected continuously during both bouts of exercise. The data were subsequently downloaded onto a personal computer, and the resulting text files were stored on disk for later analysis. The NIRS data represented a relative gain based on the optical density measured in the first datum collected and could not, therefore, be used to estimate absolute tissue O2 saturation. We summed the HbO2 and HHb signals to provide an estimate of total Hb (and, therefore, blood volume) in the field of interrogation. We also modeled the [HHb] data to provide information on the balance between muscle O2 supply and utilization (see Modeling of O2 and HHb data). It should be noted here that the NIRS signals might also partly reflect oxygenated and deoxygenated Mb as well as Hb (see Ref. 18 for discussion).
Modeling of O2 and HHb data.
The breath-by-breath data from the step exercise tests were used to estimate the O2 kinetics. The data were first manually filtered to remove outlying breaths, defined as breaths deviating by more than three standard deviations from the preceding five breaths. The data were subsequently interpolated to provide second-by-second values and, for each individual, the two data sets from each of the upright and supine cycling conditions were time aligned and averaged.
The first 20 s of data after the onset of exercise (i.e., the phase 1 response) were deleted and a nonlinear least squares algorithm was used to fit the data, as described in the following biexponential equation:
 | (1) |
O2 (t) represents the absolute O2 at a given time t; O2baseline represents the mean O2 in the baseline period; Ap, TDp, and p represent the amplitude, time delay, and time constant, respectively, describing the fundamental or primary increase in O2 above baseline; and As, TDs, and s represent the amplitude, time delay, and time constant describing the development of the O2 slow component, respectively. An iterative process was used to minimize the sum of the squared errors between the fitted function and the observed values. Because the asymptotic value (As) of the exponential term describing the O2 slow component may represent a higher value than is actually reached at the end of the exercise, the actual amplitude of the O2 slow component at the end of exercise was used and defined as As'. The magnitude of the O2 slow component was also quantified by calculating the difference between O2 at 2 min and 6 min of exercise.
To provide further information on the effect of the prior exercise on muscle oxygenation, we also modeled the [HHb] responses to exercise. We chose to model [HHb] because this variable is relatively insensitive to alterations in blood volume (see Ref. 18 for review). A biexponential model with delay similar to that described in Eq. 1 above was used, with the exception that the fitting window commenced at the onset of exercise (i.e., at time 0). The TD and of the [HHb] response over the "fundamental" phase of the response were summed to provide an indication of the overall response dynamics in the absence of any "slow component" (MRTf). Furthermore, the [HHb] dynamics for the entire response were modeled with a monoexponential function commencing at the onset of exercise and with the time delay term set to zero (MRTt).
Statistics.
Paired t-tests were used to compare the physiological responses to ramp exercise in the upright and supine positions. A 2 (bout 1 vs. bout 2) x 2 (upright vs. supine) repeated-measures ANOVA was used to evaluate the O2, blood lactate, and HR data in the double-step tests. Significant differences were further analyzed by post hoc Bonferroni-adjusted paired t-tests. Pearson's product moment correlation coefficient was used to explore the relationship between the differences in phase 2 in the upright and supine positions and the effects of prior exercise. Significance was accepted at P < 0.05. Data are presented as means ± SD.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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O2 max and the peak work rate were significantly lower during supine compared with upright cycling, but the GET was not different during exercise in the two body positions. The absolute work rate calculated to require 50% during upright exercise (212 ± 17 W) required 72% during supine exercise.
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blood [lactate] values were not significantly different between upright and supine exercise for either the first or the second exercise bouts. However, the baseline blood [lactate] was significantly greater, and the blood [lactate] was significantly smaller, for the second compared with the first exercise bout, in both the upright and supine positions. Similarly, the baseline, end-exercise, and HR values were not significantly different between upright and supine exercise for either the first or the second exercise bouts. However, the baseline and end-exercise HR values were higher in the second compared with the first exercise bout for both upright and supine exercise. The HR was significantly smaller in the second exercise bout compared with the first exercise bout during upright cycling but there was no significant difference during supine cycling (Table 2).
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of the [HHb] signal was significantly different when the first (control) exercise bout in the upright position was compared with the first exercise bout in the supine position. However, the MRTf (i.e., TD + over the fundamental phase) tended to be faster during supine compared with upright exercise (upright: 20 ± 3 vs. supine: 17 ± 3 s; P = 0.07). Furthermore, the total change in [HHb] appeared to be appreciably greater over the fundamental phase of the response during supine exercise (Fig. 1). One striking difference between the two body positions in the respective control conditions was in the incidence and relative magnitude of a [HHb] slow component. A [HHb] slow component was evident in all of the eight subjects and represented 20 ± 12% of the total response during upright exercise but was only observed in five of the subjects and represented just 8 ± 7% of the total response during supine exercise. Therefore, the overall [HHb] kinetics tended to be slower during upright compared with supine exercise (MRTt; upright: 42 ± 21 vs. supine: 24 ± 12 s; P = 0.07; see Fig. 1), suggesting that muscle O2 supply might have been compromised in the supine position (see DISCUSSION).
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of the [HHb] kinetics in either the upright or the supine position (Table 3). The 95% confidence intervals (CIs) for the estimation of the fundamental were 3 ± 1 and 3 ± 0 s for the first and second bout, respectively, of both upright and supine exercise. Prior exercise also had no significant effect on the [HHb] slow component during upright exercise. However, during supine exercise, the [HHb] slow component that was observed in five of the subjects in the first exercise bout was eliminated in the second exercise bout (Fig. 1). The MRTt was not significantly altered by prior exercise either in the upright or the supine position (Table 3).
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O2 kinetics during the first and second bouts of upright exercise are shown in Table 4, whereas the O2 response of a representative subject during upright exercise is shown in Fig. 3 and the group mean O2 response is shown in Fig. 4. During upright cycling, prior exercise resulted in a significantly elevated baseline O2, and a significant reduction in the amplitude of the O2 slow component (bout 1: 0.45 ± 0.16 vs. bout 2: 0.22 ± 0.14 l/min; P = 0.006). The increase in O2 between 2 min and 6 min of exercise was also significantly reduced in the second bout compared with the first (Table 4). However, the phase 2 was not significantly affected by prior exercise (bout 1: 29 ± 10 vs. bout 2: 28 ± 4 s; P = 0.91). The 95% CIs for the estimation of the phase 2 were 4 ± 2 and 3 ± 1 for bouts 1 and 2, respectively. In three subjects, the phase 2 was shorter in bout 2, and in the other five subjects the phase 2 was longer in bout 2. The amplitude of the fundamental phase of the O2 response tended to be greater after prior exercise (bout 1: 1.78 ± 0.18 vs. bout 2: 1.84 ± 0.16 l/min; P = 0.09), and this difference was significant when expressed in absolute terms (i.e., as baseline O2 + fundamental component amplitude; bout 1: 2.49 ± 0.25 vs. bout 2: 2.66 ± 0.20 l/min; P = 0.003). The end-exercise O2 was not significantly different between the first and second exercise bouts (Table 4).
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O2 kinetics during the first and second bouts of supine exercise are shown in Table 4, whereas the O2 response of a representative subject during supine exercise is shown in Fig. 3 and the group mean O2 response is shown in Fig. 4. The influence of prior exercise on O2 kinetics during supine cycling differed from that observed during upright cycling. During supine cycling, prior exercise also resulted in a significant elevation of baseline O2 (Table 4). However, unlike upright exercise, prior exercise resulted in a significant 37% reduction in the phase 2 during supine cycling (bout 1: 38 ± 18 vs. bout 2: 24 ± 9 s; P = 0.03). The 95% CIs for the estimation of the phase 2 were 2 ± 1 and 3 ± 2 for bouts 1 and 2, respectively. In seven subjects, the phase 2 was shorter in bout 2, and in the other subject, it was identical in bouts 1 and 2. Prior exercise had no significant effect on the amplitude of the O2 response in the fundamental phase (bout 1: 1.65 ± 0.30 vs. bout 2: 1.59 ± 0.19 l/min; P = 0.43), or in the slow component phase (bout 1: 0.40 ± 0.29 vs. bout 2: 0.41 ± 0.20 l/min; P = 0.86). Interestingly, however, prior exercise resulted in a significantly earlier "appearance" of the O2 slow component during supine exercise (bout 1: 127 ± 58 vs. bout 2: 88 ± 46 s; P = 0.03) so that the difference in O2 between 2 min and 6 min of exercise was less in the second exercise bout (bout 1: 0.43 ± 0.20 vs. bout 2: 0.32 ± 0.11 l/min; P = 0.03). Again, the end-exercise O2 was not significantly different between the first and second exercise bouts (Table 4).
There were no statistically significant differences in O2 kinetics between upright and supine exercise when the responses to the first exercise bout were compared, although the phase 2 tended to be greater during supine exercise (upright: 29 ± 10 vs. supine: 38 ± 18 s; P = 0.15). When the second exercise bouts performed in the upright and supine positions were compared, the amplitude of the fundamental O2 response was greater (upright: 1.84 ± 0.16 vs. supine: 1.59 ± 0.19 l/min; P = 0.02) and the amplitude of the O2 slow component was lower (upright: 0.22 ± 0.14 vs. supine: 0.41 ± 0.20 l/min; P = 0.02) in the upright position, but there were no other significant differences. The extent of the reduction of the phase 2 after prior exercise in the supine position was correlated with the difference in the phase 2 between upright and supine exercise in the first exercise bout (r = 0.87; P = 0.005); that is, subjects who had appreciably slower phase 2 O2 kinetics during supine compared with upright exercise in the "control" condition evidenced a greater speeding of the phase 2 O2 kinetics after prior exercise in the supine position.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONREFERENCES |
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O2 response to subsequent heavy exercise but that the effects evoked varied according to whether the exercise was performed in the upright or the supine position. Specifically, in the upright position, prior heavy exercise had no effect on the phase 2 but led to a substantial (50%) reduction in the amplitude of the O2 slow component during subsequent heavy exercise. In contrast, in the supine position, prior heavy exercise caused a significant reduction in the phase 2 but had no effect on the amplitude of the O2 slow component during subsequent heavy exercise. NIRS data indicated that the blood volume in the field of interrogation was increased following the performance of prior heavy exercise (i.e., that there was a relative hyperemia), but the effects on the [HHb] kinetics were again somewhat different depending on the body position adopted. The results were consistent with our hypothesis that prior heavy exercise would result in a speeding of the phase 2 O2 kinetics during supine exercise, in which muscle perfusion pressure is likely reduced and muscle O2 availability might be compromised (26, 30, 42), but not during upright exercise. However, the results were not consistent with our hypothesis that prior heavy exercise would reduce the amplitude of the O2 slow component in both body positions.
Comparison of upright and supine exercise.
During ramp incremental exercise, the O2 max and peak work rate attained were lower by 13 and 15%, respectively, during supine compared with upright cycling. These results agree very well with previous reports (1, 30, 33). However, in these previous studies it was also reported that the GET was significantly reduced during supine exercise, whereas there was no significant difference in our study. A reduction in O2 max during ramp incremental exercise in the supine position is consistent with the existence of reduced muscle perfusion pressure in this mode of exercise (55).
There were no significant differences in O2 kinetics between upright and supine exercise when the first (control) bout in each series was compared (see Table 4). The phase 2 was 31% longer during supine compared with upright exercise, but interindividual variability in response precluded the attainment of statistical significance. Koga et al. (33) also did not report a significant difference in the phase 2 during heavy cycle exercise performed in the upright and supine positions. However, these authors reported that the amplitude of the fundamental O2 response was smaller and the amplitude of the O2 slow component response was greater in supine exercise, such that the "mean response time" was significantly greater during supine compared with upright exercise. This is consistent with the general finding that O2 kinetics is slower during supine than during upright exercise (14, 26, 30, 42). These findings have generally been attributed to a reduction in the pressure head for muscle O2 delivery during supine exercise in which the "gravitational assist" to muscle blood flow is absent. The tendency for faster overall [HHb] kinetics and the greater absolute change in [HHb] during supine compared with upright exercise observed in the present study (Fig. 1) is consistent with this notion.
Influence of prior exercise on muscle oxygenation. In the present study, we hypothesized that the metabolic acidosis caused by a prior bout of heavy exercise would enhance muscle O2 availability in a subsequent exercise bout by enabling a greater vasodilatation and thence muscle blood flow, and also through a Bohr shift of the HbO2 dissociation curve (21). Consistent with this, blood [lactate] and HR were both significantly elevated in the baseline period preceding the second exercise bout in both body positions. Alterations in the NIRS-derived total Hb signal (which provides an index of the blood volume in the area of interrogation) also suggests that muscle O2 supply was enhanced in the second exercise bout (Fig. 2). This interpretation would be consistent with several other studies that have either directly (2, 37) or indirectly (8, 15, 19, 23, 28, 56) assessed muscle blood flow and O2 supply during various forms of exercise. Despite the indirect evidence of enhanced muscle oxygenation following priming exercise in the present study, the [HHb] kinetics was essentially unchanged. Because [HHb] kinetics reflect a dynamic balance between the local rate of O2 delivery and utilization (15), these data might be interpreted to indicate that the potentially greater blood volume and/or flow matched, or was matched by, greater muscle O2 utilization following the performance of prior exercise (i.e., that the intrinsic muscle oxidative "metabolic inertia" was reduced).
An interesting feature of the NIRS data was the greater initial (and total) change in [HHb], and the lower incidence and smaller magnitude of a [HHb] slow component, during supine compared with upright exercise (Fig. 1). With the assumption that the [HHb] signal reliably reflects muscle O2 extraction (18, 22), these results suggest that muscle O2 extraction was greater throughout exercise in the supine position. In situations in which muscle O2 extraction is initially high (and perhaps near maximal), an increased muscle O2 availability (such as that evoked by the performance of prior heavy exercise) might be expected to speed the O2 response to exercise, as was indeed observed in the present study. The [HHb] data indicate that, during supine cycling, the O2 slow component is associated with a relatively greater increase in muscle blood flow and a relatively smaller increase in muscle O2 extraction, relative to upright cycling. It should be noted, however, that interpretation is complicated by the fact that the relative intensity of exercise was higher during supine exercise (see below), and it is therefore unclear to what extent these observations are a function of the exercise modality per se.
Influence of prior exercise on O2 kinetics during upright cycling.
During upright heavy cycle exercise, the performance of prior heavy exercise had no significant effect on the phase 2 but resulted in a significant reduction in the O2 slow component amplitude and a significant increase in the absolute amplitude of the fundamental phase of the response. These results are entirely consistent with a large number of previous studies (e.g., 5, 8–10, 16, 34, 36, 45, 52, 54). The lack of an effect of prior heavy exercise on the phase 2 during subsequent heavy exercise in the upright position has been interpreted to indicate that muscle O2 availability is not limiting the O2 kinetics in these circumstances. The reduced O2 slow component (which is often associated with an elevated amplitude in the fundamental phase of the response) following heavy exercise, however, might itself be linked to an enhancement of muscle O2 availability. Indeed, several studies have suggested that the amplitudes of the fundamental and/or slow components might be related to differences in muscle O2 delivery (convective and/or diffusive), or the homogeneity of its distribution (21, 24, 33, 41, 60). However, Endo et al. (17) have recently reported that the facilitated O2 kinetics (mainly ascribed to a reduced O2 slow component amplitude) in the second of two bouts of heavy cycle exercise was not attenuated when the central circulation was slowed using facial cooling, suggesting that the effects of prior exercise on the O2 slow component might be ascribed more to changes in peripheral (metabolic) factors than to altered muscle O2 supply (see also Refs. 7, 25).
Campbell-O'Sullivan et al. (12) reported that the performance of prior exercise reduced muscle phosphocreatine depletion and lactate accumulation during subsequent exercise and suggested that the lag in oxidative ATP production was linked to a limitation in the delivery or availability of acetyl groups to the mitochondria. However, Sahlin et al. (52) observed no change in the phase 2 during the second of two bouts of heavy exercise despite there being a sixfold higher acetylcarnitine concentration before the second bout. Although the pharmacological activation of the pyruvate dehydrogenase complex with dichloroacetate has the potential to delay or reduce the O2 slow component during heavy exercise in humans (31, 50), it neither reduces the phase 2 nor increases the amplitude of the fundamental component of O2 (i.e., the characteristics of the prior exercise effect). Alterations in substrate delivery or availability are therefore an unlikely explanation for the physiological effects of prior exercise. An alternative explanation is that fatigue in some muscle fibers as a result of the performance of prior heavy exercise might alter muscle fiber recruitment patterns in such a way as to impact on the O2 kinetics during subsequent exercise. It has been reported that muscle fiber-type distribution and fiber recruitment profiles are related to O2 kinetics (3, 38, 47, 48). Burnley et al. (8) demonstrated that the increased amplitude of the O2 fundamental component and the reduced amplitude of the O2 slow component in the second of two bouts of heavy upright cycle exercise was associated with an increased integrated electromyogram (iEMG) in the first 2 min of exercise and a reduced rate of increase in iEMG over the remainder of the exercise period; however, significant changes in iEMG have not been found in other studies (54, 56).
Influence of prior exercise on O2 kinetics during supine cycling.
Consistent with our hypothesis, in the supine position, the performance of prior heavy exercise resulted in a significant reduction in the phase 2 . We interpret these results to indicate that O2 kinetics across the exercise transient were partially constrained by muscle O2 availability in the first exercise bout and that this limitation was negated by the performance of prior heavy exercise. This argument is supported by evidence that the speeding of the phase 2 O2 kinetics after prior exercise in the supine position was significantly correlated with the extent to which the phase 2 O2 kinetics were slower during supine compared with upright exercise in the first (control) exercise bout.
Our results are consistent with a number of earlier studies that reported that enhancing muscle O2 supply can speed O2 kinetics in situations in which O2 kinetics might be O2 supply limited in the control condition (15, 23, 26, 27, 35, 40, 46, 51, 53). Hughson et al. (26) showed that the application of lower body negative pressure during supine exercise, which restored the arterial-to-venous perfusion pressure gradient, enabled a speeding of O2 kinetics to values that were not different from those measured during upright exercise. Furthermore, Perrey et al. (46) reported that an increase in forearm blood flow brought about by a combination of leg occlusion and calf exercise resulted in a more rapid increase in O2 during dynamic handgrip exercise when the subjects lay supine with the arm extended at heart level. Also, several studies have reported that prior heavy exercise resulted in faster phase 2 O2 kinetics during subsequent heavy exercise performed in the prone (51) or supine (16, 20) positions, in which the hydrostatic gradient to blood flow will be absent in the control condition. Interestingly, however, in the studies of Fukuba et al. (20) and Endo et al. (16), the faster O2 kinetics was not accompanied by faster muscle blood flow kinetics. Richardson et al. (49) have reported that, for plantar flexion exercise performed in the prone position, some regions of the contracting muscle can be relatively underperfused or overperfused relative to the local metabolic rate. Therefore, one explanation for our results is that prior heavy exercise resulted in a more appropriate distribution of blood flow within the working muscles during subsequent heavy exercise in the supine position. This would be consistent with the results of MacDonald et al. (42), who reported that although the slower O2 kinetics measured during supine compared with upright cycle exercise was accompanied by relatively slower muscle blood flow kinetics (estimated by Doppler ultrasound techniques), the muscle blood flow kinetics were still faster than O2 kinetics in both body positions. These data suggest that blood flow distribution in the exercising muscles, rather than bulk muscle O2 delivery per se, might have been limiting in the supine position (42).
If, however, the faster phase 2 O2 kinetics after prior heavy exercise in the supine position can be partially attributed to a better matching of perfusion to local metabolic rate, it is unclear why the amplitude of the O2 slow component was not significantly altered by prior exercise. In this latter regard, our results contrast with those of Rossiter et al. (51), who reported that the slow components in both muscle phosphocreatine concentration (assessed via magnetic resonance spectroscopy) and pulmonary O2 were reduced after prior heavy exercise during leg extension exercise performed in the prone position. Our results are, however, in accord with those of Koppo and Bouckaert (35). These authors reported that prior heavy exercise reduced the O2 slow component (but did not change the phase 2 ) when arm crank exercise was performed below the level of the heart but did not alter the O2 slow component (but led to a reduced phase 2 ) when the exercise was performed above heart level. If, as discussed earlier, the altered O2 slow component response following priming exercise reflects different muscle fiber recruitment profiles during upright cycle exercise (8, 11), then it is difficult to explain why an equivalent effect was not observed during supine cycle exercise (presuming that prior heavy exercise has similar effects on muscle fatigue and fiber recruitment profiles irrespective of body position). However, although we made every effort to equate the mechanics of upright and supine cycling in the present study, the possibility that the exercise modes invoke somewhat different fiber (and, indeed, muscle) recruitment profiles cannot be dismissed.
One notable difference between the conditions in the present study was the relative intensity of exercise. Subjects exercised at the same absolute work rate in both body positions: this was equivalent to 50% during upright exercise (75% of mode-specific O2 max after the fundamental phase rising to 88% of mode-specific O2 max at the end of exercise) and 72% during supine exercise (85% of mode-specific O2 max after the fundamental phase rising to 100% of mode-specific O2 max at the end of exercise). It is feasible that this difference in relative exercise intensity might have differentially affected muscle fiber recruitment profiles in both the first and second bouts of exercise. The higher relative exercise intensity in the supine position might be expected to result in greater muscle fatigue in the first bout of exercise with, consequently, a greater requirement for the recruitment of higher order (perhaps type IIx) fibers during subsequent exercise to maintain power output. In this scenario, the "positive" effects of prior heavy exercise such as improved muscle perfusion might be offset by the greater residual fatigue, obligating a greater or earlier recruitment of lower efficiency fibers after the onset of subsequent exercise. Support for this suggestion comes from the study of Tordi et al. (56), who reported that "fatiguing" prior exercise reduced the time delay preceding the "emergence" of the O2 slow component (from 121 to 96 s) but did not reduce its amplitude during subsequent upright cycle exercise requiring >85% O2 max. Although interindividual variability precluded the attainment of statistical significance, iEMG appeared to be substantially greater during constant-work-rate exercise following the performance of multiple-sprint exercise, at least in the vastus lateralis and vastus medialis (see Fig. 3 in ref. 56). This is the only study, to date, that has reported that prior high-intensity exercise can speed the phase 2 O2 kinetics during heavy cycle exercise in the upright position. It is possible, therefore, that the similarity of our results to those of Tordi et al. (56) for supine, although not upright, cycle exercise (i.e., reduced phase 2 , shorter TDs, and unchanged O2 slow component amplitude) is related to the high relative exercise intensity studied (i.e., >85% O2 max).
The results of the present study appear to provide evidence in favor of an O2 delivery limitation during supine exercise that is negated by the physiological effects of prior heavy exercise, which include a relative hyperemia and a right-shifted HbO2 dissociation curve. However, it should also be considered that prior exercise might influence muscle metabolic processes during subsequent exercise (irrespective of body position) by altering, for example, the activity of rate-limiting oxidative enzymes or one or more of the putative regulators of mitochondrial respiration such as the concentration of ADP or creatine, the phosphorylation potential, or Ca2+ concentration (see Ref. 11 for review). Indeed, in animal models, both Hogan (25) and Behnke et al. (7) reported that prior contractile activity resulted in faster activation of muscle oxidative metabolism that was not related to changes in muscle O2 availability. Why this same effect has been so rarely reported in humans, at least for upright cycle exercise, is unclear. One possibility is that a priming of oxidative metabolism in previously active fibers is offset by slower kinetics in higher order fibers that are recruited to maintain power output during subsequent exercise (61), with the net effect being no change in the phase 2 .
In conclusion, the effects of priming exercise on O2 kinetics during heavy cycle exercise differed according to whether the exercise was performed in the upright or the supine position. In the upright position, prior heavy exercise did not alter the phase 2 but resulted in a significant reduction in the amplitude of the O2 slow component, consistent with previous studies (5, 8–10, 16, 34, 36, 45, 52, 54). In the supine position, prior heavy exercise resulted in a significant reduction in the phase 2 (to a value that was not different from that measured during upright exercise) but did not alter the amplitude of the O2 slow component. We interpret these data to indicate that the fundamental component O2 kinetics are not O2 delivery limited during upright cycle exercise in healthy young subjects but, rather, are principally regulated by intracellular factors. In contrast, a lower muscle perfusion pressure in the supine position results in the "superimposition" of an O2 availability limitation that can be negated by the enhanced muscle vasodilatation and right-shifted HbO2 dissociation curve that attends the performance of prior heavy exercise. We speculate that the reduction in the amplitude of the O2 slow component after prior heavy exercise during upright but not supine cycling was related, at least in part, to differences in the relative intensity of exercise between the two body positions.
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O2 and heart rate kinetics in cycling: transitions from an elevated baseline. J Appl Physiol 90: 2081–2087, 2001.O2 kinetics during heavy exercise are related to changes in muscle activity. J Appl Physiol 93: 167–174, 2002.O2 kinetics. In: Oxygen Uptake Kinetics in Sport, Exercise and Medicine, edited by Jones AM and Poole DC. London and New York: Routledge, 2005, p. 230–260.O2 and femoral artery blood flow and their relationship during repeated bouts of heavy exercise. Eur J Appl Physiol 95: 418–430, 2005.[CrossRef][ISI][Medline]O2 kinetics at the onset of high-intensity exercise. J Appl Physiol 95: 1623–1631, 2003.O2 kinetics in heavy exercise is not altered by prior exercise with a different muscle group. J Appl Physiol 92: 2467–2474, 2002.O2 during repeated bouts of heavy knee extension exercise in humans. Exp Physiol 89: 243–253, 2004.
) and second bout (
) of heavy cycle exercise performed in the upright (top) and supine (bottom) positions in a representative subject. Vertical line represents the transition from "unloaded" to "loaded" cycling. AU, arbitrary units. Brackets denote concentration. Note the faster overall [HHb] kinetics in the first exercise bout in the supine compared with the upright position. The [HHb] "slow component" was significantly attenuated by the performance of prior exercise in the supine position.
