NIRS‐derived Microvascular Oxygen Saturation Kinetics Related to Skeletal Muscle Metabolic Rate

Abstract

IntroductionSkeletal muscle tissue oxygen hemoglobin/myoglobin saturation (STO2) measured during post occlusive reactive hyperemia (PORH) provides a kinetic parameter (STO2 upslope (%/time)) that has increasingly been used as a measure of microvascular responsiveness. The magnitude of the oxygen saturation prior to cuff release (STO2 min) often correlates to STO2 upslope but the physiological variable associated with variability in STO2 min is most likely muscle metabolic rate (MR). This physiologic variable likely influences the rate of reperfusion after cuff release. The purpose of this study, therefore, was to isolate variables contributing to differences in STO2 upslope through their influence on STO2 min. Our hypothesis was that MR would significantly affect STO2 upslope.MethodsThe anterior antebrachium of twenty‐two (11 male, 11 female), 18–26 years, normoglycemic subjects was monitored continuously by near infrared spectroscopy during three upper limb PORH tests. Tissue oxygenation variables were determined prior to, during the cuff and for 2.5 min. post‐cuff release. MR was calculated in ml O2/100 g lean tissue/min and used both corrected and uncorrected for ATT (MRC). Body fat and abdominal adiposity (%) were quantified by dual energy‐ray absorptiometry. Forearm adipose tissue thickness (ATT) (3.32 + 1.43 mm, range 2.8–6.7 mm) was measured by ultrasound.ResultsSTO2 min and STO2 upslope were significantly negatively correlated (r=−0.47, P= 0.03) and both were significantly negatively correlated with MR (r = −0.75, P = <0.001 and r = −0.52, P = 0.01, respectively). In a multiple, forward step‐wise regression analysis with a dependent variable of STO2 upslope and independent variables of ATT, MR or MRC, STO2min, and total body fat, only ATT entered the equation (R squared 0.334, P= 0.006); no other variable statistically added any independent predictive power to the regression equation.ConclusionsTo our knowledge, this is the first study to assess the effects of MR on NIRS STO2 upslope. In contrast to our hypothesis, MR did not affect STO2 upslope but ATT did. This finding suggests that ATT must be taken into account when assuming differences in STO2 upslope reflect differences in microvascular reactivity even in largely lean subjects.Support or Funding InformationAmerican Heart Association, Grant/Award Number: 0151183ZWheaton College Alumni Summer Research Support