Spatial heterogeneity of quadriceps muscle deoxygenation kinetics during cycle exercise

2007 ◽  
Vol 103 (6) ◽  
pp. 2049-2056 ◽  
Author(s):  
Shunsaku Koga ◽  
David C. Poole ◽  
Leonard F. Ferreira ◽  
Brian J. Whipp ◽  
Narihiko Kondo ◽  
...  

To test the hypothesis that, during exercise, substantial heterogeneity of muscle hemoglobin and myoglobin deoxygenation [deoxy(Hb + Mb)] dynamics exists and to determine whether such heterogeneity is associated with the speed of pulmonary O2 uptake (pV̇o2) 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, 2∼21% for >GET]. The primary component kinetics (time constant) of muscle deoxy(Hb + Mb) reflecting increased O2 extraction were also spatially inhomogeneous (intersite CV, 6∼48% for <GET, 7∼47% for >GET) and faster (P < 0.05) than those of phase 2 pV̇o2. However, the degree of dynamic intersite heterogeneity in muscle deoxygenation did not correlate significantly with phase 2 pV̇o2 kinetics. In conclusion, the dynamics of quadriceps microvascular oxygenation demonstrates substantial spatial heterogeneity that must arise from disparities in the relative kinetics of V̇o2 and O2 delivery increase across the regions sampled.

2011 ◽  
Vol 301 (2) ◽  
pp. R534-R541 ◽  
Author(s):  
Shunsaku Koga ◽  
David C. Poole ◽  
Yoshiyuki Fukuoka ◽  
Leonardo F. Ferreira ◽  
Narihiko Kondo ◽  
...  

The conventional continuous wave near-infrared spectroscopy (CW-NIRS) has enabled identification of regional differences in muscle deoxygenation following onset of exercise. However, assumptions of constant optical factors (e.g., path length) used to convert the relative changes in CW-NIRS signal intensity to values of relative concentration, bring the validity of such measurements into question. Furthermore, to justify comparisons among sites and subjects, it is essential to correct the amplitude of deoxygenated hemoglobin plus myoglobin [deoxy(Hb+Mb)] for the adipose tissue thickness (ATT). We used two time-resolved NIRS systems to measure the distribution of the optical factors directly, thereby enabling the determination of the absolute concentrations of deoxy(Hb+Mb) simultaneously at the distal and proximal sites within the vastus lateralis (VL) and the rectus femoris muscles. Eight subjects performed cycle exercise transitions from unloaded to heavy work rates (>gas exchange threshold). Following exercise onset, the ATT-corrected amplitudes (Ap), time delay (TDp), and time constant (τp) of the primary component kinetics in muscle deoxy(Hb + Mb) were spatially heterogeneous (intersite coefficient of variation range for the subjects: 10–50 for Ap, 16–58 for TDp, 14–108% for τp). The absolute and relative amplitudes of the deoxy(Hb+Mb) responses were highly dependent on ATT, both within subjects and between measurement sites. The present results suggest that regional heterogeneity in the magnitude and temporal profile of muscle deoxygenation is a consequence of differential matching of O2 delivery and O2 utilization, not an artifact caused by changes in optical properties of the tissue during exercise or variability in the overlying adipose tissue.


2009 ◽  
Vol 297 (3) ◽  
pp. R615-R621 ◽  
Author(s):  
Tadashi Saitoh ◽  
Leonardo F. Ferreira ◽  
Thomas J. Barstow ◽  
David C. Poole ◽  
Anna Ooue ◽  
...  

We investigated the effects of prior heavy exercise on the spatial heterogeneity of muscle deoxygenation kinetics and the relationship to the pulmonary O2 uptake (pV̇o2) kinetics during subsequent heavy exercise. Seven healthy men completed two 6-min bouts of heavy work rate cycling exercise, separated by 6 min of unloaded exercise. The changes in the concentration of deoxyhemoglobin/myoglobin (Δdeoxy-[Hb+Mb]) were assessed simultaneously at 10 different sites on the rectus femoris muscle using multichannel near-infrared spectroscopy. Prior exercise had no effect on either the time constant or the amplitude of the primary component pV̇o2, whereas it reduced the amplitude of the slow component (SC). ΔDeoxy-[Hb+Mb] across all 10 sites for bout 2 displayed a shorter time delay (mean and SD for subjects: 13.5 ± 1.3 vs. 9.3 ± 1.4 s; P < 0.01) and slower primary component time constant (τ: 9.3 ± 1.3 vs. 17.8 ± 1.0 s; P < 0.01) compared with bout 1. Prior exercise significantly reduced both the intersite coefficient of variation (CV) of the τ of Δdeoxy-[Hb+Mb] (26.6 ± 11.8 vs. 13.7 ± 5.6%; P < 0.01) and the point-by-point heterogeneity [root mean square error (RMSE)] during the primary component in the second bout. However, neither the change in the CV for τ nor RMSE of Δdeoxy-[Hb+Mb] correlated with the reduction in the SC in pV̇o2 kinetics during subsequent heavy exercise. In conclusion, prior exercise reduced the spatial heterogeneity of the primary component of muscle deoxygenation kinetics. This effect was not correlated with alterations in the pV̇o2 response during subsequent heavy exercise.


2003 ◽  
Vol 95 (1) ◽  
pp. 113-120 ◽  
Author(s):  
Darren S. DeLorey ◽  
John M. Kowalchuk ◽  
Donald H. Paterson

The temporal relationship between the kinetics of phase 2 pulmonary O2 uptake (V̇o2p) and deoxygenation of the vastus lateralis muscle was examined during moderate-intensity leg-cycling exercise. Young adults (5 men, 6 women; 23 ± 3 yr; mean ± SD) performed repeated transitions on 3 separate days from 20 W to a constant work rate corresponding to 80% of lactate threshold. Breath-by-breath V̇o2p was measured by mass spectrometer and volume turbine. Deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin and myoglobin were sampled each second by near-infrared spectroscopy (Hamamatsu NIRO-300). V̇o2p data were filtered, interpolated to 1 s, and averaged to 5-s bins; HHb data were averaged to 5-s bins. Phase 2 V̇o2p data were fit with a monoexponential model. For HHb, a time delay (TDHHb) from exercise onset to an increase in HHb was determined, and thereafter data were fit with a monoexponential model. The time constant for V̇o2p (30 ± 8 s) was slower ( P < 0.01) than that for HHb (10 ± 3 s). The TDHHb before an increase in HHb was 13 ± 2 s. The possible mechanisms of the TDHHb are discussed with reference to metabolic activation and matching of local muscle O2 delivery and O2 utilization. After this initial TDHHb, the kinetics of local muscle deoxygenation were faster than those of phase 2 V̇o2p (and presumably muscle O2 consumption), reflecting increased O2 extraction and a mismatch between local muscle O2 consumption and perfusion.


2005 ◽  
Vol 98 (5) ◽  
pp. 1697-1704 ◽  
Author(s):  
Darren S. DeLorey ◽  
John M. Kowalchuk ◽  
Donald H. Paterson

The purpose was to examine the adaptation of pulmonary O2 uptake (V̇o2p) and deoxygenation of the vastus lateralis muscle at the onset of heavy-intensity, constant-load cycling exercise in young (Y; 24 ± 4 yr; mean ± SD; n = 5) and older (O; 68 ± 3 yr; n = 6) adults. Subjects performed repeated transitions on 4 separate days from 20 W to a work rate corresponding to heavy-intensity exercise. V̇o2p was measured breath by breath. The concentration changes in oxyhemoglobin, deoxyhemoglobin (HHb), and total hemoglobin/myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). V̇o2p data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb-near-infrared spectroscopy data were filtered and averaged to 5-s bins. A monoexponential model was used to fit V̇o2p [phase 2, time constant (τ) of V̇o2p] and HHb [following the time delay (TD) from exercise onset to the start of an increase in HHb] data. The τV̇o2p was slower ( P < 0.001) in O (49 ± 8 s) than Y (29 ± 4 s). The HHb TD was similar in O (8 ± 3 s) and Y (7 ± 1 s); however, the τ HHb following TD was faster ( P < 0.05) in O (8 ± 2 s) than Y (14 ± 2 s). The slower V̇o2p kinetics and faster muscle deoxygenation in O compared with Y during heavy-intensity exercise imply that the kinetics of muscle perfusion are slowed relatively more than those of V̇o2p in O. This suggests that the slowed V̇o2p kinetics in O may be a consequence of a slower adaptation of local muscle blood flow relative to that in Y.


2004 ◽  
Vol 97 (4) ◽  
pp. 1227-1236 ◽  
Author(s):  
Daryl P. Wilkerson ◽  
Katrien Koppo ◽  
Thomas J. Barstow ◽  
Andrew M. Jones

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (V̇o2) kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to V̇o2 kinetics in the control (i.e., no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to ∼105% of the predetermined V̇o2 peak, separated by 3 × 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means ± SD: MAX1: 1.3 ± 0.4 mM vs. MAX2: 7.7 ± 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e., phase II) increase in V̇o2 was not significantly different between the two conditions (MAX1: 33.8 ± 5.5 s vs. MAX2: 33.2 ± 7.7 s). Rather, the asymptotic “gain” of the primary V̇o2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 ± 0.9 ml·min−1·W−1 vs. MAX2: 9.0 ± 0.7 ml·min−1·W−1; P < 0.05), such that V̇o2 was projecting to a higher “steady-state” amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component V̇o2 response but does increase the amplitude to which V̇o2 may rise following the onset of perimaximal-intensity cycle exercise.


2007 ◽  
Vol 103 (3) ◽  
pp. 771-778 ◽  
Author(s):  
Darren S. DeLorey ◽  
John M. Kowalchuk ◽  
Aaron P. Heenan ◽  
Gregory R. duManoir ◽  
Donald H. Paterson

The effect of prior exercise on pulmonary O2 uptake (V̇o2p), leg blood flow (LBF), and muscle deoxygenation at the onset of heavy-intensity alternate-leg knee-extension (KE) exercise was examined. Seven subjects [27 ( 5 ) yr; mean (SD)] performed step transitions ( n = 3; 8 min) from passive KE following no warm-up (HVY 1) and heavy-intensity (Δ50%, 8 min; HVY 2) KE exercise. V̇o2p was measured breath-by-breath; LBF was measured by Doppler ultrasound at the femoral artery; and oxy (O2Hb)-, deoxy (HHb)-, and total (Hbtot) hemoglobin/myoglobin of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS; Hamamatsu NIRO-300). Phase 2 V̇o2p, LBF, and HHb data were fit with a monoexponential model. The time delay (TD) from exercise onset to an increase in HHb was also determined and an HHb effective time constant (HHb − MRT = TD + τ) was calculated. Prior heavy-intensity exercise resulted in a speeding ( P < 0.05) of phase 2 V̇o2p kinetics [HVY 1: 42 s ( 6 ); HVY 2: 37 s ( 8 )], with no change in the phase 2 amplitude [HVY 1: 1.43 l/min (0.21); HVY 2: 1.48 l/min (0.21)] or amplitude of the V̇o2p slow component [HVY 1: 0.18 l/min (0.08); HVY 2: 0.18 l/min (0.09)]. O2Hb and Hbtot were elevated throughout the on-transient following prior heavy-intensity exercise. The τLBF [HVY 1: 39 s ( 7 ); HVY 2: 47 s ( 21 ); P = 0.48] and HHb-MRT [HVY 1: 23 s ( 4 ); HVY 2: 21 s ( 7 ); P = 0.63] were unaffected by prior exercise. However, the increase in HHb [HVY 1: 21 μM ( 10 ); HVY 2: 25 μM ( 10 ); P < 0.001] and the HHb-to-V̇o2p ratio [(HHb/V̇o2p) HVY 1: 14 μM·l−1·min−1 ( 6 ); HVY 2: 17 μM·l−1·min−1 ( 5 ); P < 0.05] were greater following prior heavy-intensity exercise. These results suggest that the speeding of phase 2 τV̇o2p was the result of both elevated local O2 availability and greater O2 extraction evidenced by the greater HHb amplitude and HHb/V̇o2p ratio following prior heavy-intensity exercise.


2004 ◽  
Vol 97 (1) ◽  
pp. 165-172 ◽  
Author(s):  
Darren S. DeLorey ◽  
John M. Kowalchuk ◽  
Donald H. Paterson

Phase 2 pulmonary O2 uptake (V̇o2p) kinetics are slowed with aging. To examine the effect of aging on the adaptation of V̇o2p and deoxygenation of the vastus lateralis muscle at the onset of moderate-intensity constant-load cycling exercise, young (Y) ( n = 6; 25 ± 3 yr) and older (O) ( n = 6; 68 ± 3 yr) adults performed repeated transitions from 20 W to work rates corresponding to moderate-intensity (80% estimated lactate threshold) exercise. Breath-by-breath V̇o2p was measured by mass spectrometer and volume turbine. Deoxy (HHb)-, oxy-, and total Hb and/or myoglobin were determined by near-infrared spectroscopy (Hamamatsu NIRO-300). V̇o2p data were filtered, interpolated to 1 s, and averaged to 5-s bins. HHb data were filtered and averaged to 5-s bins. V̇o2p data were fit with a monoexponential model for phase 2, and HHb data were analyzed to determine the time delay from exercise onset to the start of an increase in HHb and thereafter were fit with a single-component exponential model. The phase 2 time constant for V̇o2p was slower ( P < 0.01) in O (Y: 26 ± 7 s; O: 42 ± 9 s), whereas the delay before an increase in HHb (Y: 12 ± 2 s; O: 11 ± 1 s) and the time constant for HHb after the time delay (Y: 13 ± 10 s; O: 9 ± 3 s) were similar in Y and O. However, the increase in HHb for a given increase in V̇o2p (Y: 7 ± 2 μM·l−1·min−1; O: 13 ± 4 μM·l−1·min−1) was greater ( P < 0.01) in O compared with Y. The slower V̇o2p kinetics in O compared with Y adults was accompanied by a slower increase of local muscle blood flow and O2 delivery discerned from a faster and greater muscle deoxygenation relative to V̇o2p in O.


2011 ◽  
Vol 16 (9) ◽  
pp. 097007 ◽  
Author(s):  
Ylenia Santoro ◽  
Anaïs Leproux ◽  
Albert Cerussi ◽  
Bruce Tromberg ◽  
Enrico Gratton

2012 ◽  
Vol 112 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Shunsaku Koga ◽  
Yutaka Kano ◽  
Thomas J. Barstow ◽  
Leonardo F. Ferreira ◽  
Etsuko Ohmae ◽  
...  

The overarching presumption with near-infrared spectroscopy measurement of muscle deoxygenation is that the signal reflects predominantly the intramuscular microcirculatory compartment rather than intramyocyte myoglobin (Mb). To test this hypothesis, we compared the kinetics profile of muscle deoxygenation using visible light spectroscopy (suitable for the superficial fiber layers) with that for microvascular O2 partial pressure (i.e., PmvO2, phosphorescence quenching) within the same muscle region (0.5∼1 mm depth) during transitions from rest to electrically stimulated contractions in the gastrocnemius of male Wistar rats ( n = 14). Both responses could be modeled by a time delay (TD), followed by a close-to-exponential change to the new steady level. However, the TD for the muscle deoxygenation profile was significantly longer compared with that for the phosphorescence-quenching PmvO2 [8.6 ± 1.4 and 2.7 ± 0.6 s (means ± SE) for the deoxygenation and PmvO2, respectively; P < 0.05]. The time constants (τ) of the responses were not different (8.8 ± 4.7 and 11.2 ± 1.8 s for the deoxygenation and PmvO2, respectively). These disparate (TD) responses suggest that the deoxygenation characteristics of Mb extend the TD, thereby increasing the duration (number of contractions) before the onset of muscle deoxygenation. However, this effect was insufficient to increase the mean response time. Somewhat differently, the muscle deoxygenation response measured using near-infrared spectroscopy in the deeper regions (∼5 mm depth) (∼50% type I Mb-rich, highly oxidative fibers) was slower (τ = 42.3 ± 6.6 s; P < 0.05) than the corresponding value for superficial muscle measured using visible light spectroscopy or PmvO2 and can be explained on the basis of known fiber-type differences in PmvO2 kinetics. These data suggest that, within the superficial and also deeper muscle regions, the τ of the deoxygenation signal may represent a useful index of local O2 extraction kinetics during exercise transients.


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