Human femoral artery and estimated muscle capillary blood flow kinetics following the onset of exercise

Harper, Allison J.; Ferreira, Leonardo F.; Lutjemeier, Barbara J.; Townsend, Dana K.; Barstow, Thomas J.

doi:10.1113/expphysiol.2005.032904

Cited by 86 publications

(87 citation statements)

References 49 publications

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“…Qm responses were calculated using the measured [HHb] as a surrogate of muscle oxygen extraction and the phase 2 response of pulmonary V O 2 kinetics (e.g., representing muscle V O 2 kinetics, V O 2muscle [22,23]) as described previously (16,17):…”

Section: Discussionmentioning

confidence: 99%

“…However, this method has been previously compared and contrasted with that of conduit artery blood flow with qualitative agreement (17). The kinetics of Qm were then evaluated using the two-component exponential model.…”

Section: Discussionmentioning

confidence: 99%

“…Prior studies have demonstrated NIRS to be highly sensitive to muscle changes due to exercise, hypoxemia, and aging (13)(14)(15), and, thus, NIRS [HHb] provides a noninvasive surrogate of muscle oxygen extraction. Moreover, the measurement of [HHb] in parallel with V O 2 during exercise can provide useful inferences regarding regional blood flow and allows for the estimation of the increase in muscle microvascular blood flow (Qm) via the Fick principle (16,17).…”

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Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes

et al. 2007

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OBJECTIVE -People with type 2 diabetes have impaired exercise responses even in the absence of cardiovascular complications. One key factor associated with the exercise intolerance is abnormally slowed oxygen uptake (V O 2 ) kinetics during submaximal exercise. The mechanisms of this delayed adaptation during exercise are unclear but probably relate to impairments in skeletal muscle blood flow. This study was conducted to compare skeletal muscle deoxygenation (deoxygenated hemoglobin/myoglobin [HHb]) responses and estimated microvascular blood flow (Qm) kinetics in type 2 diabetic and healthy subjects after the onset of moderate exercise. CONCLUSIONS -Type 2 diabetic skeletal muscle demonstrates a transient imbalance of muscle O 2 delivery relative to O 2 uptake after onset of exercise, suggesting a slowed Qm increase in type 2 diabetic muscle. Impaired vasodilatation due to vascular dysfunction in type 2 diabetes during exercise may contribute to this observation. Further study of the mechanisms leading to impaired muscle oxygen delivery may help explain the abnormal exercise responses in type 2 diabetes. RESEARCH DESIGN AND METHODS -Pulmonary Diabetes Care 30:2880-2885, 2007E xercise is highly recommended as a cornerstone of treatment for people with type 2 diabetes. However, reduced peak exercise tolerance is common in type 2 diabetes (1-3) and is linked to mortality in individuals with type 2 diabetes as well as healthy individuals (4). Submaximal exercise responses are also affected in individuals with type 2 diabetes, as demonstrated by an abnormally slowed increase of oxygen uptake (V O 2 kinetics) after the onset of exercise, and seem to possibly be related to abnormal cardiovascular responses (1,2). Clinically, these findings observed during submaximal exercise testing are significant because they indicate a greater perturbation of intramuscular homeostasis in response to any exercise challenge, with the potential to contribute to the premature muscular fatigue (5) and hence the reduced exercise tolerance in type 2 diabetic individuals (1,2). However, the mechanisms of impaired muscle oxygen delivery and/or oxidative metabolism responsible for the abnormal exercise responses in type 2 diabetes remain unclear.Recent work in rodent models of type 2 diabetes has demonstrated impaired skeletal muscle capillary hemodynamics (6) and abnormal capillary PO 2 responses during exercise (7). These findings demonstrated a transient impairment of oxygen delivery relative to muscle oxygen uptake after the onset of exercise that may limit oxygen transfer and utilization (7,8). It is not known whether a similar defect exists in individuals with type 2 diabetes. Such an impairment of microvascular oxygen delivery and exchange in human skeletal muscle could similarly contribute to the observed limitation of V O 2 and exercise performance in type 2 diabetes. Indeed, reductions in exercising leg blood flow (9) and baseline metabolic defects (10,11) are known to occur in human type 2 diabetic skeletal muscle. Given that ske...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes

et al. 2007

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“…However, this method does not reflect microvascular blood flow as derived from the Fick equation. In this regard, an estimation of capillary blood flow (Q cap ) has been proposed (7,10). When this method is used, [HHb] is substituted directly into the Fick equation in place of the arterio-venous O 2 difference (avO 2diff ), and kinetic profiles of muscle V O 2 (V O 2m ) are derived using the parameters of pulmonary V O 2 (V O 2p ).…”

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confidence: 99%

Noninvasive estimation of microvascular O₂ provision during exercise on-transients in healthy young males

Murias

Spencer

Pogliaghi

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

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(V O 2p ). An obvious limitation to this methodology is that, even though [HHb] reflects the balance between O 2 delivery and O 2 utilization, and thus, it is used as a proxy for O 2 extraction, neither the actual O 2 content in the arterial nor venous circulations is precisely known, and then, its use for replacing a-vO 2diff in the Fick equation is questionable. As such, the Q cap can only potentially reflect the time course of the adjustment in microvascular blood flow but provides no information on the actual changes in its magnitude.In recent years, our group has provided evidence that improved microvascular delivery of O 2 , as reflected by a smaller normalized [HHb]/V O 2 ratio throughout the exercise on-transient, plays an important role in the control of the rate of adjustment of oxidative phosphorylation (14 -16, 18, 22). These studies collectively showed that, although intracellular mechanisms are likely the principal putative factors controlling the adjustment of V O 2 kinetics during the initial response to a step increment in power output, for pulmonary V O 2p time constant (V O 2p ) values greater than ϳ20 s, the rate of adjustment of phase II V O 2p is also constrained by the matching of local O 2 delivery to muscle V O 2 . More specifically, we have shown recently that a significant reduction in the phase II V O 2p when moderate-intensity exercise is preceded by a bout of heavy-intensity (i.e., supra-lactate threshold) "priming" exercise was related to improvements in the matching of O 2 delivery to O 2 utilization, as reflected by reductions in the [HHb]/V O 2 ratio (16,22). Using a somewhat similar approach, Buchheit et al. (4) indicated that a smaller V O 2p during the second bout of moderate-intensity running in those participants in whom the first bout showed a rather slow rate of adjustment for phase II V O 2p was related to improvements in O 2 provision, as reflected by a faster adjustment of Q cap [i.e., Q cap mean response time (MRT)]. Although the proposed mechanisms explaining the smaller V O 2 in these two studies using a similar intervention were the same, the association between changes in the rate of adjustment of V O 2 and changes in the [HHb]/V O 2 ratio or, alternatively, the Q cap remain to be elucidated.Thus, the goal of this study was to compare two different and established methods for estimation of the changes in microvascular O 2 delivery during the on-transient of exercise and to evaluate the two approaches in determining the role of the adjustment of the estimated microvascular O 2 delivery in the speeding of V O 2 kinetics during moderate-intensity exercise preceded by a bout of heavy-intensity "priming" exercise. We hypothesized that 1) with priming exercise, faster moder-

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“…This effect was not correlated with alterations in the pV O2 response during subsequent heavy exercise. near-infrared spectroscopy; spatial heterogeneity; oxygen uptake kinetics; muscle oxygen delivery THE BALANCE BETWEEN MUSCLE O 2 uptake (mV O 2 ) and muscle O 2 delivery (mQ O 2 ) by capillary blood flow, i.e., the ratio mV O 2 / mQ O 2 , is reflected by the level of muscle oxygenation (14,19,25,27,32). Thus the profile of muscle oxygenation can provide important information concerning the adequacy of the vascular response and the O 2 pressures essential for driving bloodmuscle O 2 flux.…”

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confidence: 99%

Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise

Saitoh

Ferreira²,

Barstow³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Saitoh T, Ferreira LF, Barstow TJ, Poole DC, Ooue A, Kondo N, Koga S. Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise. Am J Physiol Regul Integr Comp Physiol 297: R615-R621, 2009. First published June 17, 2009 doi:10.1152/ajpregu.00048.2009.-We investigated the effects of prior heavy exercise on the spatial heterogeneity of muscle deoxygenation kinetics and the relationship to the pulmonary O2 uptake (pV O2) 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 (⌬de-oxy-[HbϩMb]) 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 pV O2, whereas it reduced the amplitude of the slow component (SC). ⌬Deoxy-[HbϩMb] across all 10 sites for bout 2 displayed a shorter time delay (mean and SD for subjects: 13.5 Ϯ 1.3 vs. 9.3 Ϯ 1.4 s; P Ͻ 0.01) and slower primary component time constant (: 9.3 Ϯ 1.3 vs. 17.8 Ϯ 1.0 s; P Ͻ 0.01) compared with bout 1. Prior exercise significantly reduced both the intersite coefficient of variation (CV) of the of ⌬deoxy- [HbϩMb] (26.6 Ϯ 11.8 vs. 13.7 Ϯ 5.6%; P Ͻ 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 nor RMSE of ⌬deoxy-[HbϩMb] correlated with the reduction in the SC in pV O2 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 pV O2 response during subsequent heavy exercise. near-infrared spectroscopy; spatial heterogeneity; oxygen uptake kinetics; muscle oxygen delivery THE BALANCE BETWEEN MUSCLE O 2 uptake (mV O 2 ) and muscle O 2 delivery (mQ O 2 ) by capillary blood flow, i.e., the ratio mV O 2 / mQ O 2 , is reflected by the level of muscle oxygenation (14,19,25,27,32). Thus the profile of muscle oxygenation can provide important information concerning the adequacy of the vascular response and the O 2 pressures essential for driving bloodmuscle O 2 flux.Prior heavy exercise has been used as an experimental intervention to alter mQ O 2 and elucidate the mechanisms of the mV O 2 kinetics following the onset of exercise (3, 7-11, 15, 16, 22-24, 30 -33, 39, 42, 44, 47, 51-53, 55). Collectively, previous studies reported that prior exercise in the upright position does not alter the phase II time constant of pulmonary O 2 uptake (pV O 2 ) response in the subsequent bout of heavy exercise (3, 7-11, 22, 30, 32, 44, 47, 52), with a few exceptions (16,46,53). The net amplitude of phase II is unaltered in some studies using 6-to 8-min recovery between heavy exercise bouts (7, 10, 44, 52) and incre...

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Human femoral artery and estimated muscle capillary blood flow kinetics following the onset of exercise

Cited by 86 publications

References 49 publications

Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes

Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes

Noninvasive estimation of microvascular O₂ provision during exercise on-transients in healthy young males

Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise

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Human femoral artery and estimated muscle capillary blood flow kinetics following the onset of exercise

Cited by 86 publications

References 49 publications

Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes

Skeletal Muscle Deoxygenation After the Onset of Moderate Exercise Suggests Slowed Microvascular Blood Flow Kinetics in Type 2 Diabetes

Noninvasive estimation of microvascular O2 provision during exercise on-transients in healthy young males

Effects of prior heavy exercise on heterogeneity of muscle deoxygenation kinetics during subsequent heavy exercise

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Noninvasive estimation of microvascular O₂ provision during exercise on-transients in healthy young males