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1Applied Physiology Laboratory, Kobe Design University, Kobe, Japan; 3University of Leeds, Leeds, United Kingdom; 4Kobe University, Kobe, Japan; 5Hamamatsu Photonics K. K., Hamakita, Japan; and 2Department of Kinesiology, Anatomy, and Physiology, Kansas State University, Manhattan, Kansas
Submitted 12 June 2007 ; accepted in final form 19 September 2007
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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O2) kinetics, we adapted multi-optical fibers near-infrared spectroscopy (NIRS) to characterize the spatial distribution of muscle deoxygenation kinetics at exercise onset. Seven subjects performed cycle exercise transitions from unloaded to moderate [<gas exchange threshold (GET)] and heavy (>GET) work rates and the relative changes in deoxy(Hb + Mb), at 10 sites in the quadriceps, were sampled by NIRS. At exercise onset, the time delays in muscle deoxy(Hb + Mb) were spatially inhomogeneous [intersite coefficient of variation (CV), 3
56% for <GET, 221% for >GET]. The primary component kinetics (time constant) of muscle deoxy(Hb + Mb) reflecting increased O2 extraction were also spatially inhomogeneous (intersite CV, 648% for <GET, 747% for >GET) and faster (P < 0.05) than those of phase 2 pO2. However, the degree of dynamic intersite heterogeneity in muscle deoxygenation did not correlate significantly with phase 2 pO2 kinetics. In conclusion, the dynamics of quadriceps microvascular oxygenation demonstrates substantial spatial heterogeneity that must arise from disparities in the relative kinetics of O2 and O2 delivery increase across the regions sampled. near-infrared spectroscopy; oxygen uptake kinetics; muscle oxygen delivery; muscle oxygen utilization
O2, the product of arterial O2 content and blood flow) and O2 utilization (O2), i.e., O2/O2 ratio (or O2/O2, as deoxygenation). As such, the profile of muscle oxygenation, for example, following the onset of exercise can provide information regarding the adequacy of the vascular response and also the O2 pressures essential for driving blood-muscle O2 flux. Near-infrared spectroscopy (NIRS) has become an established technique for measurement of muscle oxygenation in health (9, 12, 14, 20, 21, 22, 25, 33), and it is plausible that it may yield mechanistic insights into muscle dysfunction and exercise intolerance in chronic diseases, for example, heart failure (5), peripheral vascular disease (34), and diabetes (37).
Typically, NIRS measurements have been made from a single site on the muscle of interest and interpretation of the NIRS response must therefore embrace the presumption that the muscle region sampled is representative of the active muscle mass as a whole. However, given that there is substantial heterogeneity in muscle blood flow (26, 27, 30, 36, 42, 44), motor unit recruitment (17), and fiber type distribution itself within and across muscles, it would be remarkable if a unitary O2/O2 relationship existed such that muscle deoxygenation state was uniform across the entire mass of the quadriceps during cycling exercise. Phosphorescence-quenching measurements of microvascular O2 pressures (PmvO2) indicate that, following the onset of contractions, slow- and fast-twitch muscle fibers have very different O2/O2 relationships (4, 35, 43). Specifically, PmvO2 falls faster and to a lower level in the microvasculature of fast-twitch fibers, raising the possibility that in fast-twitch muscle, or muscle regions in which these fibers predominate, muscle O2 flux may potentially constrain O2 kinetics at exercise onset. Thus, in human muscles, where there may be regional distribution of specific fiber types, it is conceivable that the predominance of fast-twitch fibers, when recruited, may, through their high O2/O2 ratios, have PmvO2s that are so low that blood-myocyte O2 flux is suboptimal and both muscle and pulmonary O2 kinetics are slowed.
From the above, it is likely that considerable heterogeneity of muscle oxygenation exists across the quadriceps muscle particularly in transient states where metabolic rate is changing rapidly. The previously used single-site NIRS is unable to resolve the extent, if any, of such heterogeneity, thereby limiting the inferences that can be drawn from human muscle oxygenation studies and also the diagnostic value of this technique in disease. To address these concerns, we developed a multioptical fiber NIRS method to establish the temporal profile of muscle oxygenation simultaneously at 10 different sites within the quadriceps. We tested the hypothesis that, at the onset of moderate or heavy cycling exercise, the dynamic profile of muscle deoxygenation would evidence significant heterogeneity across multiple measurement sites. If such heterogeneity is indeed present, it will present a novel opportunity to address whether O2 delivery may be limiting the speed of the O2 kinetics. Specifically, in the presence of spatially heterogeneous muscle deoxygenation kinetics, we tested the secondary hypothesis that greater intersite heterogeneity in the dynamics of deoxygenated (Hb + Mb) would be associated with a systematic slowing of the muscle O2 profile (phase 2 O2).
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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Seven healthy subjects (4 men, 3 women) (age 24.3 ± 3.3 yr; height 164 ± 12 cm; weight 54.8 ± 12.1 kg) participated in this study. After explanation of all procedures and possible risks and benefits of participation, each subject signed an informed consent form. The study was approved by the Human Subjects Committee of Kobe Design University.
Protocol
On each data-collection day, subjects reported to the laboratory at least 2 h after their last meal. They were asked to avoid caffeine and alcohol ingestion and strenuous exercise for 24 h before the test. The temperature and relative humidity of the laboratory were maintained at 22–24 °C and 50–65%, respectively. On the first visit, seat height and handlebar position on the cycle ergometer were recorded, and these were reproduced on subsequent tests.
Incremental Exercise Tests
The first visit was used to familiarize the subjects with testing procedures and to determine the peak O2, gas exchange threshold (GET), and work rates for the constant work rate tests. All exercise tests were performed on an electronically braked cycle. The incremental ramp exercise protocols, preceded by 4-min unloaded exercise on cycle ergometer, were performed in an upright position to estimate each individual's GET and peak O2. The work rate protocols for the ramp exercise tests were 25–30 W/min, and pedal frequency was held constant at 50 rpm. The O2 at the GET was estimated as the break point in the plot of CO2 output (CO2) against O2 (V-slope method).
Constant Work Rate Exercise Tests
Square-wave exercise transition tests were conducted on separate days. Each constant work rate exercise test was performed for 6 min. The moderate work rate corresponded to a O2 of 80% of the GET. The heavy exercise work rates were estimated to require a O2 equal to 40% of the difference (
) between the subject's GET and peak O2, i.e., a value of (GET + 0.40), based on the initial O2/work rate observed during the ramp exercise. The exercise was preceded by 4 min of unloaded exercise at a pedal frequency of 50 rpm. To minimize random noise and enhance the underlying response patterns for the moderate work rate tests, subjects performed a total of four to six exercise transitions. The number of repetitions was determined so as to produce an acceptable estimated confidence interval for the primary time constant of pulmonary O2, based on the ratio of the standard deviation (SD) of breath-by-breath fluctuation to the amplitude of the O2 response. Each subject was given at least 15 min of rest before starting the next exercise transition. For the heavy work rate tests, subjects normally performed two to four exercise transitions. Only one heavy exercise transition was performed on any single day.
Measurements
Pulmonary O2.
Subjects breathed through a low-resistance hot-wire flowmeter for measurement of inspiratory and expiratory flows (Minato-Medical AE-300S). The flowmeter was calibrated repeatedly by inputting known volumes of room air at various mean flows and flow profiles. Expired oxygen and carbon dioxide concentrations were determined by gas analysis (Minato-Medical AE-300S) from a sample drawn continuously from the mouthpiece. Precision-analyzed gas mixtures were used for calibration. Gas volume and concentration signals were time aligned by accounting for the delay in the sampling tube and the analyzer rise time relative to the volume signal. Alveolar gas exchange variables were calculated breath by breath (2). Heart rate (HR) was monitored continuously via a three-lead electrocardiogram.
Muscle deoxygenation.
Local muscle deoxygenation [deoxy(Hb + Mb)] profiles of the vastus lateralis and rectus femoris muscles were measured with multioptical fibers continuous wave near-infrared spectroscopy (CW-NIRS) [NIRO-200 with multifibers adaptor (MFA), Hamamatsu Photonics K. K.]. The optodes were housed in a plastic holder, thus ensuring that the position of the optodes, relative to each other, was fixed and invariant (Fig. 1). The most distal optode [channel 1 (CH1)] was placed on the lower third of the vastus lateralis muscle (10–12 cm above the knee joint) of the dominant limb, parallel to the major axis of the thigh. This location was chosen for a single-site NIRS measurement conducted by the previous studies (14, 15, 20, 25, 50). The optodes of CH2, CH6, and CH7 were placed on the rectus femoris, and the other optodes were placed on the vastus lateralis muscle. The interoptode spacing between emitter and receiver (e.g., E1-CH1 in Fig. 1) was 3 cm, and the surface area covered by the 10 probes was 6-cm width x 12-cm length. The depth of measured area was reported approximately half of the distance between the emitter and the receiver, 1.5 cm (7). The skin under the probes was previously carefully shaved. Pen marks were made over the skin to indicate the margins of the plastic holder to check for any downward sliding of the probe during cycling and for accurate probe repositioning. No sliding was observed in any subject at the end of each protocol. The optode assembly was secured on the skin surface with rubber holder and tape and then covered with a black cloth, thus minimizing the intrusion of stray 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 for cycling.
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) in concentration from baseline. The deoxy(Hb + Mb) signal can be regarded as being essentially blood-volume-insensitive during exercise (11, 12, 14, 25, 33). Thus the deoxy(Hb + Mb) signal obtained by NIRS has been used as an index of local O2 extraction reflecting the O2/O2 ratio principally in the capillaries (9, 11, 13, 14, 20, 22, 25, 33). The time course of deoxy(Hb + Mb) following the onset of exercise resembles qualitatively and quantitatively the arteriovenous O2 content difference observed in separate investigations (18, 20).
We have been able to demonstrate that this device provides highly reproducible deoxy(Hb + Mb) responses when the same subject performs like-transitions on different days. The coefficient of variation for the primary mean response time of the deoxy(Hb + Mb) was 3–7% (S. Koga, unpublished observations).
The fat thickness under each optode site was measured by B-mode ultrasound Doppler method (model Logiq 400; GE-Yokogawa Medical Systems) in the present study. The fat thickness on average for the 10 sites was 5.6 ± 1.3 mm.
Data Analysis
Individual responses of pulmonary O2 and deoxy(Hb + Mb) during the baseline-to-exercise transitions were time-interpolated to 1-s intervals and averaged across each transition for each subject and exercise condition. The response curve of pulmonary O2 was fit by a three-term exponential function that included amplitudes, time constants, and time delays, using nonlinear least-squares regression techniques (6, 14, 28). The computation of best-fit parameters was chosen by the program (Kaleida Graph) so as to minimize the sum of the squared differences between the fitted function and the observed response (9, 14, 16, 18, 25, 28, 29, 45). The first exponential term started with the onset of exercise, and the second and third terms began after independent time delays
 | (1) |
O2 (b) is the unloaded exercise baseline value; Ai, Ap, and As are the asymptotic amplitudes for the exponential terms; 
i, p, and s are the time constants; and TDp and TDs are the time delays.
The phase 1 O2 at the start of phase 2 (i.e., at TDp) was assigned the value for that time (Ai'):
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O2 response during moderate-intensity exercise reached a new steady state within 3 min after the onset of exercise in normal subjects, the slow exponential term invariably dropped out during the iterative-fitting procedure. The increment in O2 between the 2nd and 6th min relative to the overall increase at end exercise was calculated as an index of the slow component (SC).
The time-averaged NIRS signals were normalized such that the unloaded exercise baseline value was adjusted to zero, and thus the NIRS data are presented as a relative change from the baseline- to the end-exercise values. The time course of the initial and primary components of the deoxy(Hb + Mb) was evaluated by a two-component exponential curve-fitting procedure. The first exponential term started with the onset of exercise, and the second term began after an independent time delay.
 | (2) |
60 s during moderate exercise (9, 14, 20, 22) and 95% level of the primary component in 60 s (i.e., 10-s time delay plus 4 time constants) during heavy exercise (10, 14, 20, 25, 33). Visual inspection of the deoxy(Hb + Mb) signal and analysis of least-squares residuals suggested that fitting with a two-exponential model would provide a reasonable estimate of the initial and primary time course of muscle deoxygenation. We compared the TDp values in the present study with those of a single-exponential model (14, 20, 25, 33) and DeLorey et al. (9, 10; the TDp from the time of exercise onset to the first point greater than 1 SD above the mean of the baseline). At some sites there were no significant differences in the TDp for the three methods, while at others sites our method produced slightly shorter TDp (1–2 s). The TD and of the deoxy(Hb + Mb) response over the "primary" phase of the response were summed (MRTp) to provide an indication of the overall response dynamics in the absence of any "slow component" (25). Statistics
Data are presented as means ± SD. Intersite coefficient of variation [CV (%); 100·SD/mean of the 10 sites values] for each subject was calculated to show spatial heterogeneity of the TDp, p, and MRTp. To determine significant differences between two means, a two-tailed Student's paired t-test was performed. A repeated-measures ANOVA was performed to compare more than two means. When a significant difference was detected, this was further examined by Tukey's post hoc test. The relationship between two variables was analyzed by least-squares correlation. Significance was accepted when P < 0.05.
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RESULTS |
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The kinetic profiles of muscle deoxygenation for the 10 sites during 6-min moderate- and heavy-intensity exercise are shown in Table 1 (means ± SD of the 7 subjects, i.e, intersubject variability). Figure 2 shows the relative increases in muscle deoxygenation [deoxy(Hb + Mb)] and pulmonary O2 responses for the transition from unloaded to heavy exercise in two representative subjects. For some subjects, the muscle deoxygenation kinetics of the most distal site (S1), i.e., location used routinely in previous studies for single-site NIRS measurement (14, 20, 25, 50), differed substantially from some sites. The group mean (n = 7) time delays (TDp) were 9–10 s for <GET and 7 s for >GET among the sites. TDp of some sites (sites S4–S5, S6, S8–S9) were slightly but significantly shorter for above- compared with below-GET. However, the other sites showed no difference of TDp between the work rates.
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O2 occurred at a faster rate than that of O2 (see site S7 in Fig. 3 for most extreme example), while other sites evidenced a constant deoxy(Hb + Mb), implying that O2 and O2 increased in concert (e.g., site S3 in Fig. 3) following the onset of exercise. The TDps for each subject were spatially inhomogeneous (Table 2; intersite CV, 3–56% for <GET, 2–21% for >GET).
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After the initial TDp, averaging the 10 site values of [deoxy(Hb + Mb)], the primary component of the muscle deoxygenation kinetics (p, 911 s for <GET, 78 s for >GET, Table 1) and the mean response time (MRTp = TDp + p) were faster than those of phase 2 O2 kinetics (time constant of phase 2 O2, 28.0 ± 7.2 s for below GET and 28.8 ± 10.9 s for above GET, Fig. 2 and Table 3). When data for each single subject were examined individually, the primary component of [deoxy(Hb + Mb)] was not spatially homogeneous (Fig. 2). We quantified the degree of the spatial heterogeneity as the intersite CV of the p among the 10 sites (Table 2). The heterogeneity varied among the subjects (intersite CV, 6–48% for <GET, 7–47% for >GET). There was no significant difference of the intersite heterogeneity of p for above compared with below GET.
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O2/O2), the intersite CV of the MRTp was not associated with variations in the time constant of the muscle O2 (phase 2 O2) at the onset of moderate (r = 0.29) or heavy (r = 0.49) cycling exercise (both P > 0.05; Fig. 4). Further, the phase 2 O2 was not related to the primary MRT of deoxy(Hb + Mb) per se at the onset of moderate (r = 0.16) or heavy (r = 0.20) exercise (both P > 0.05).
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p, or MRTp for either moderate or heavy exercise. Further, for the comparison of the vastus lateralis vs. rectus femoris muscles, there were no significant differences of the TDp, p, or MRTp for moderate and heavy exercise. However, when data for each single subject were examined individually, the kinetic profiles of muscle deoxygenation were clearly not spatially homogeneous (Table 2). |
DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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O2 occurred at a faster rate than that of O2 as evidenced by a substantial transient decrease in deoxy(Hb + Mb) while others displayed profiles of oxygenation consistent with a more equal increase of O2 and O2 following the onset of exercise. The primary component kinetics of muscle deoxy(Hb + Mb) reflecting increased O2 extraction were spatially inhomogeneous and faster than those of pulmonary phase 2 O2 kinetics. However, the degree of dynamic heterogeneity in muscle deoxygenation (O2/O2) was not associated with any systematic variation of the pulmonary phase 2 O2 profile (close analog of muscle O2, Refs. 18, 28, 45) at the onset of moderate or heavy cycling exercise. Initial Component
During the initial component (typically 7–10 s following the onset of exercise), some sites showed a decrease (undershoot) in the [deoxy(Hb + Mb)] from the baseline, and the others remained constant before the subsequent exponential increase. These results suggest that in a single subject there is both microvascular O2/O2 matching (e.g., site S3 in Fig. 3) and mismatching (e.g., site S7 in Fig. 3; i.e., an excess of O2 in relation to the metabolic requirement) in some regions of the muscles such that kinetic profiles of the sites are not homogeneous. It is pertinent that NIRS technology cannot determine to what extent the differences in the deoxy(Hb + Mb) profile among sites reflects the behavior of O2 versus O2. However, our data do indicate that, in the first 7–10 s of exercise, the rate of increase in blood flow () was either similar to, or faster than, that of O2. Mechanistically, the unchanged or increased muscle oxygenation (the present study, 9, 10, 14, 18, 20, 25, 33) and PmvO2 (3) across the early phase of the transition suggests adequacy of O2 availability during this period, thereby, by default, providing support for an intracellular locus of control for O2 kinetics following exercise onset (1, 6, 16, 20, 28, 45, 49).
During the latter part of the primary phase, O2 delivery limitation may occur, and this would lead to distortion of exponentiality that may not be distinguished from breath-by-breath measurements (24; see discussion of the primary component). TDp of some sites was slightly but significantly shorter for above GET compared with below GET. These results are consistent with the findings by Ferreira et al. (14) and Grassi et al. (20). However, the other sites showed no difference of TDp between the work rates. The shorter period of TDp suggests a closer matching of O2 and O2 or relatively less abundant O2 during transitions to intense exercise. According to previous observations by Grassi et al. (19) in the isolated in situ muscle preparation, as well as by Scheuermann and Barstow (46) and Hughson et al. (23) in exercising humans, O2 availability could help control (together with intracellular enzymatic regulation) O2 kinetics during transitions to high-intensity exercise. There was no significant difference of the intersite heterogeneity of TDp for above GET compared with below GET.
Primary Component
After the initial TDp, the primary component of the muscle deoxygenation kinetics was faster than those of phase 2 O2 kinetics (Fig. 2 and Tables 1–3). These results are consistent with NIRS measurements made at a single site within the muscle of interest (9, 14, 20, 25). The primary component of [deoxy(Hb + Mb)] is not spatially homogeneous, and the degree of heterogeneity varied substantially among the subjects. Interestingly, there was no significant difference of the intersite heterogeneity of p for above GET compared with below GET.
It is possible that the adjustment of in the microcirculation of active skeletal muscles may differ from that measured in larger conduit arteries (22, 31). However, it remains unclear exactly how the microvascular is distributed following the onset of exercise. Since the muscle pump likely increases (phase 1; Ref. 47) within a muscle without regard for the metabolic requirements of the individual fibers or motor units, a microvascular mismatching of O2 with respect to O2 is likely to occur in some intramuscular regions, i.e., hyperperfusion in areas of the muscle that are inactive. As exercise continues, negative-feedback control of local vascular responses progresses towards a matching of O2/O2 (e.g., 8, 32).
Because inadequate O2 may slow muscle and pulmonary O2 kinetics (10, 21, 24, 32, 40, 48), we tested the secondary hypothesis that those subjects evidencing the greatest intersite heterogeneity in deoxygenated (Hb + Mb) (i.e., increased likelihood of some regions with inadequate O2 and higher O2/O2 ratio) at exercise onset would evince the slowest pulmonary kinetics. If the intra- and intermuscular heterogeneity of the dynamics of muscle oxygenation contributes to slow the kinetics of phase 2 O2 (i.e., O2 delivery limitation to O2 kinetics), these variables should have been directly and positively related. However, they were not (Fig. 4). Thus the heterogeneity of microvascular O2 delivery (in relation to O2 uptake) might not lead to O2 delivery limitation of the whole limb O2 kinetics during moderate and heavy exercise [see Hughson et al. (24)]. Further, in the present study, the phase 2 O2 was not related to the primary MRT of deoxy(Hb + Mb) per se. This result is consistent with the finding from NIRS measurements made at a single site within the muscle of interest (9, 20).
However, caution is required to interpret this finding. 1) The 10-channel NIRS allows investigation on a limited area of the superficial muscle (the surface area: 6-cm width x 12-cm length; and the depth: 1.5 cm). Thus it may be difficult to find the precise relation for the overall kinetics of the quadriceps muscle O2 and the metabolic and microvascular heterogeneities associated with skeletal muscle fiber type and fiber-type recruitment. While this concern remains to be further investigated, we believe that our present technique provides useful information regarding the heterogeneity of the dynamic profiles of muscle microvascular oxygenation. 2) In addition, since there is substantial heterogeneity in muscle blood flow, motor unit, and fiber type distribution itself within and across muscles, it is logical that heterogeneity of muscle oxygenation exists across the quadriceps muscle in transient states where metabolic rate is changing rapidly. At present, it cannot be ascertained how microvascular O2 delivery and metabolic regulation interact to determine the regional muscle O2 kinetics (3, 35). 3) Even if a whole mapping of the spatial and temporal distribution became available, the individual kinetic profiles would blend to produce a single kinetic response of the whole limb muscle O2 that would smooth and ultimately mask the local site profiles (49). For example, the average of two fiber compartment time constants, 20 s and 40 s , would be 30 s . The average of 25 s and 35 s also would be the same, 30 s. Thus the heterogeneity per se may not be necessarily related to kinetics of the whole limb muscle O2. 4) In addition, it is possible that intersubject variations in both heterogeneity and O2 kinetics were not large enough to establish a correlation between these variables. Thus the present data did not support the hypothesis, but at the same time rejecting the hypothesis may reflect a type II error. 5) Further, we do not know to what extent the absolute amplitudes of deoxy(Hb + Mb) of the different regions influence the temporal profile of the mean muscle PO2 and O2 (amplitude-weighting on the time constant distribution). To this point, site differences in thickness of the overlying adipose tissue may affect the absolute amplitudes of the NIRS signals independently of O2/O2 heterogeneities. Therefore, the definitive impact of different profiles of oxygenation on the whole limb and individual muscle O2 kinetics must await development of more powerful and comprehensive technologies.
Regarding the comparison of the distal vs. proximal site (i.e., S1 vs. S10 and average of S1–S3 vs. S8–S10), there were no significant differences of the TDp, p, and MRTp for moderate and heavy exercise. Mizuno et al. (36) found that blood flow, oxygen uptake, and oxygen extraction within the quadriceps femoris muscle were heterogeneous both at rest and during recovery from exhaustive exercise and that there is a systematic proximal-to-distal difference in these variables. Although the perfusion pressure and the muscle blood flow in the distal sites was expected to be lower than the proximal sites (27, 36), the limited area of the NIRS measurement in the present study did not show associated regional differences in the deoxy(Hb + Mb) kinetics. Further, for the comparison of the vastus lateralis vs. rectus femoris muscles, there were no significant differences of the TDp, p, and MRTp for moderate and heavy exercise.
Methodological Considerations
Reproducibility of the muscle oxygenation heterogeneity. The present study revealed the presence of heterogeneity with respect to the dynamics of muscle oxygenation within the quadriceps muscles of healthy subjects following the onset of exercise. Determination of whether such heterogeneity is altered by disease, training, or experimental perturbations depends on the reliability and reproducibility of the NIRS technique. Such considerations as the precise placement of the optodes, the area of the interrogation, and the day-to-day physiological variation are important. We used B-mode Doppler ultrasound echo images to ensure that the optodes were placed exactly on the desired locations of the vastus lateralis and rectus femoris muscles for each individual subject and that they were located in the same position on different days. In the present study, the multifiber CW-NIRS system provided highly reproducible deoxy(Hb + Mb) responses when the same subject performed like-transitions on different days: coefficient of variation for the primary mean response time of the deoxy(Hb + Mb) was 3–7% (S. Koga, unpublished observations).
The issue of contributions of muscles not sampled by the optodes, especially at higher work rates [i.e., influencing O2 but not the sampled deoxy(Hb + Mb)] is a further concern. For example, muscle deoxygenation in the deeper area of the muscles, where the slow-twitch muscle fibers might be more predominant, was not measurable.
Effect of optical path lengths on the relative kinetic profiles. In a preliminary examination, utilizing a single channel time-resolved NIRS method (38, 39, 41), we found that assuming constant optical path lengths (PL) of the NIR light (the CW-NIRS method) in the transition from unloaded baseline to exercise did not significantly affect the kinetics of muscle oxygenation (S. Koga, unpublished observations). Previous studies (e.g., 12) reported that PL changed 10% at maximum and did not influence the NIRS profiles. Consistent with this, the present study suggests that the multifiber CW-NIRS is a useful method to study muscle deoxygenation kinetics following exercise onset.
Conclusions
Our data show that the dynamics of muscle microvascular oxygenation is heterogeneous within the quadriceps muscles of healthy young subjects. This suggests that at some sites the increase in O2 occurs faster than O2 in some regions, while others display profiles of oxygenation consistent with O2 and O2 increasing in concert such that, following the onset of exercise, muscle deoxygenation (Hb + Mb) remains constant for 7–10 s. The degree of dynamic heterogeneity in muscle deoxygenation (O2/O2) did not predict the muscle O2 (phase 2 O2) kinetics at the onset of moderate or heavy cycling exercise. The results presented herein support that multichannel NIRS is a powerful noninvasive tool to investigate the spatial and temporal profiles of muscle deoxygenation during exercise.
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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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REFERENCES |
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O2 during repeated bouts of heavy knee extension exercise in humans. Exp Physiol 89: 243–253, 2004.O2 on-kinetics in canine muscle contracting at peak O2. J Appl Physiol 89: 1293–1301, 2000.O2 kinetics during moderate-intensity exercise in young adults. J Appl Physiol 98: 1371–1378, 2005.O2 kinetics during high-intensity cycling exercise is situated at the additional slow component. Int J Sports Med 22: 21–26, 2001.[CrossRef][Web of Science][Medline]O2 kinetics and limb blood flow. J Appl Physiol 99: 1462–1470, 2005.This article has been cited by other articles:
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  P. A. Sperandio, A. Borghi-Silva, A. Barroco, L. E. Nery, D. R. Almeida, and J. A. Neder Microvascular oxygen delivery-to-utilization mismatch at the onset of heavy-intensity exercise in optimally treated patients with CHF Am J Physiol Heart Circ Physiol, November 1, 2009; 297(5): H1720 - H1728. [Abstract] [Full Text] [PDF]
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 T. Saitoh, L. F. Ferreira, T. J. Barstow, D. C. Poole, A. Ooue, N. Kondo, and S. Koga Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2009; 297(3): R615 - R621. [Abstract] [Full Text] [PDF]
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 N. Lai, H. Zhou, G. M. Saidel, M. Wolf, K. McCully, L. B. Gladden, and M. E. Cabrera Modeling oxygenation in venous blood and skeletal muscle in response to exercise using near-infrared spectroscopy J Appl Physiol, June 1, 2009; 106(6): 1858 - 1874. [Abstract] [Full Text] [PDF]
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A. Faisal, K. R. Beavers, A. D. Robertson, and R. L. Hughson Prior moderate and heavy exercise accelerate oxygen uptake and cardiac output kinetics in endurance athletes J Appl Physiol, May 1, 2009; 106(5): 1553 - 1563. [Abstract] [Full Text] [PDF]
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F. J. DiMenna, D. P. Wilkerson, M. Burnley, S. J. Bailey, and A. M. Jones Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise at extreme pedal rates J Appl Physiol, February 1, 2009; 106(2): 432 - 442. [Abstract] [Full Text] [PDF]
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R. C. Davies, R. G. Eston, D. C. Poole, A. V. Rowlands, F. DiMenna, D. P. Wilkerson, C. Twist, and A. M. Jones Effect of eccentric exercise-induced muscle damage on the dynamics of muscle oxygenation and pulmonary oxygen uptake J Appl Physiol, November 1, 2008; 105(5): 1413 - 1421. [Abstract] [Full Text] [PDF]
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G. R. Chiappa, A. Borghi-Silva, L. F. Ferreira, C. Carrascosa, C. C. Oliveira, J. Maia, A. C. Gimenes, F. Queiroga Jr, D. Berton, E. M. V. Ferreira, et al. Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics J Appl Physiol, May 1, 2008; 104(5): 1341 - 1350. [Abstract] [Full Text] [PDF]
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