The purpose of this study was to examine the validity of the quantitative measurement of muscle oxidative metabolism in exercise by near-infrared continuous-wave spectroscopy (NIRcws). Twelve male subjects performed two bouts of dynamic handgrip exercise, once for the NIRcws measurement and once for the (31)P-magnetic resonance spectroscopy (MRS) measurement as a standard measure. The resting muscle metabolic rate (RMRmus) was independently measured by (31)P-MRS during 15 min of arterial occlusion at rest. During the first exercise bout, the quantitative value of muscle oxidative metabolic rate at 30 s postexercise was evaluated from the ratio of the rate of oxyhemoglobin/myoglobin decline measured by NIRcws during arterial occlusion 30 s after exercise and the rate at rest. Therefore, the absolute values of muscle oxidative metabolic rate at 30 s after exercise [VO(2NIR(30))] was calculated from this ratio multiplied by RMRmus. During the second exercise bout, creatine phosphate (PCr) resynthesis rate was measured by (31)P-MRS at 30 s postexercise [Q((30))] under the same conditions but without arterial occlusion postexercise. To determine the validity of NIRcws, VO(2NIR(30)) was compared with Q((30)). There was a significant correlation between VO(2NIR(30)), which ranged between 0.018 and 0. 187 mM ATP/s, and Q((30)), which ranged between 0.041 and 0.209 mM ATP/s (r = 0.965, P < 0.001). This result supports the application of NIRcws to quantitatively evaluate muscle oxidative metabolic rate in exercise.

The purpose of this study was to quantify muscle deoxygenation in human skeletal muscles using near infrared time-resolved spectroscopy (NIRTRS) and compare NIRTRS indicators and blood saturation. The forearm muscles of five healthy males (aged 27-32 yrs.) were monitored for changes in hemoglobin saturation (SO2) during 12 min of arterial occlusion and recovery. SO2 was determined by measuring the temporal profile of photon diffusion at 780 and 830 nm using NIRTRS, and was defined as SO2-TRS. Venous blood samples were also obtained for measurements of SvO2, and PvO2. Interstitial PO2(PintO2) was monitored by placing an O2 electrode directly into the muscle tissue. Upon the initiation of occlusion, all parameters fell progressively until reaching a plateau in the latter half of occlusion. It was observed at the end of occlusion that SO2-TRS (24.1 +/- 5.6%) agreed with SvO2 (26.2 +/- 6.4) and that PintO2 (14.7 +/- 1.0 Torr) agreed with PvO2 (17.3 +/- 2.2 Torr). The resting O2 store (oxygenated hemoglobin) and O2 consumption rate were 290 microM and 0.82 microM s-1, respectively, values which reasonably agree with the reported results. These results indicate that there was no O2 gradient between vessels and interstisium at the end of occlusion.

The purposes of this study were to compare the deoxygenation patterns of the vastus lateralis (VL) and the lateral head of gastrocnemius (GL) and examine the relationship between the muscle oxygenation level and pulmonary oxygen uptake (VO(2)) during graded treadmill exercise. Changes in oxygenation in each muscle were measured using near infrared spectroscopy (NIRS). Eight healthy male subjects participated in this study. Two NIRS probes were placed on VL and GL, and thereafter the leg arteries were occluded in all subjects to enable normalization of the NIR signals. The subjects then walked at 4 km x h(-1) and 6 km x h(-1), and then ran continuously at speeds ranging from 8 km x h(-1) to 16 km x h(-1). The muscle oxygenation level was defined as being 100% at rest and 0% at its lowest value during occlusion. Pulmonary VO(2) was measured using indirect calorimetry. After the subjects had started walking, the muscle oxygenation in VL increased and exceeded the level at rest. Thereafter, the muscle oxygenation in both muscles decreased in relation to the increase in speed (P < 0.001). A significant difference in the level of muscle oxygenation between VL and GL was found at speeds of 10 km x h(-1) and 12 km x h(-1) (P < 0.05). The muscle oxygenation level at 16 km x h(-1) was [mean (SEM)] 51.9 (4.6)% in VL and 52.8 (3.6)% in GL. There was a negative relationship between pulmonary VO(2) and the muscle oxygenation level (VL: r=-0.803 to -0.986; GL: r=-0.848 to -0.963, P < 0.05). We concluded that the pattern of deoxygenation between VL and GL was somewhat different and that the muscle oxygenation level was associated with pulmonary VO(2).

Post-exercise related time course of muscle oxygenation during recovery provides valuable information on peripheral vascular disease. The purpose of the present study was to examine post-exercise hyperemia (forearm blood flow; FBF, Doppler ultrasound) assessed by peak FBF, excess FBF and the time constant for FBF (FBF Tc ) following isometric handgrip exercise (IHE). Post-exercise hyperemia was assessed in an ischemic and non-ischemic state at different exercise intensities and durations. Peak FBF and excess FBF were defined as the maximum FBF during recovery, and the total amount of FBF volume, respectively. FBF Tc represents the time to reach approximately 37% of the change in FBF between peak FBF and resting FBF (delta peak FBF). Ten subjects performed IHE at "10% and 30% maximum voluntary contraction (MVC)" for 2 min with or without arterial occlusion (AO), followed by 2 min of AO alone (Study I). In Study II, six subjects performed 30%MVC-IHE with AO for "100%, 66%, 33% and 10% of the exhausted exercise duration" (time to exhaustion). In Study I, although peak FBF and excess FBF were significantly higher in ischemic than non-ischemic IHE for both 10% and 30%MVC (pϽ0.05), FBF Tc was similar in the ischemic and non-ischemic conditions. The peak FBF, excess FBF and FBF Tc were all significantly higher at 30% than at 10%MVC (pϽ0.05). In Study II, the peak FBF and excess FBF increased linearly compared to the absolute and relative exercise durations for ischemic IHE. FBF Tc increased exponentially when compared to the absolute and relative exercise durations. These data suggest the ischemic exercise has a larger hyperemic response compared to the non-ischemic exercise. In conclusion, the peak FBF, excess FBF and FBF Tc seen during post-exercise hyperemia are closely correlated with exercise intensity and duration, not only in non-ischemic, but also in the ischemic exercise. In combination with the ischemic exercise, these parameters could potentially prove to be valuable indicators of peripheral vascular disease.

We hypothesized that after maximal short-term isometric exercise, when O(2) demand is still high and O(2) supply is not fully activated, higher oxidative capacity muscle may exhibit slower muscle reoxygenation after the exercise than low oxidative capacity muscle. Seven healthy male subjects performed a maximal voluntary isometric handgrip exercise for 10 s. The reoxygenation rate after the exercise (Reoxy-rate) in the finger flexor muscle was determined by near infrared continuous wave spectroscopy (NIRcws) while phosphocreatine (PCr) was measured simultaneously by (31)P magnetic resonance spectroscopy. Muscle oxygen consumption (muscle VO(2)) and muscle oxidative capacity were evaluated using the rate of PCr resynthesis post-exercise. The forearm blood flow (FBF) index at the end of exercise was measured using NIRcws. There was a significant positive correlation between the Reoxy-rate, which ranged between 0.53% s(-1) and 12.47% s(-1), and the time constant for PCr resynthesis, which ranged between 17.8 s and 38.3 s (r(2)=0.939, P<0.001). At the end of the exercise, muscle VO(2) exceeded the resting level by approximately 25-fold, while the FBF index exceeded the resting level by only 3-fold on average. The Reoxy-rate closely correlated with muscle VO(2) (r(2)=0.727, P<0.05), but not with the FBF index. Also, the estimated O(2) balance (muscle VO(2) index/FBF index) was negatively correlated with the Reoxy-rate (r(2)=0.820, P<0.001). These results support our hypothesis that higher oxidative capacity muscle shows slower muscle reoxygenation after maximal short-term isometric exercise because the Reoxy-rate after this type of exercise may be influenced more by muscle VO(2) than by O(2) supply.