Forpurposes of data analysis and data interpretation, it is important tohave uniform representation of hue derived from the Hunter L,a, b color space. Using the standard calculation for hue [Arc tan(b/a)], positive signed results are generated for the first quadrant [+a, +b] only. l2e other quadrants should be handled so that a 360" representation is accommodated and results are expressed as positive signed numbers. Second quadrant [-a, +b] and third quadrant [-a, -bJ calculations should be: hue = I80+Arc tan(b/a). Fourth quadrant [+a, -b] calculations should be: hue = 360+Arc tan(b/a). Furthermore when planning statistical analysis of data which transverse the IV and I quadrant, vanformations of the data will continue increasing in hue angle from 361 " on up as high as appropriate. A spreadsheet macro for achieving these results can be easily derived.

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).

These results suggest that the attenuation of muscle deoxygenation near VO2peak is related to and precedes changes in neuromuscular activity under normoxic and hypoxic conditions.

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.

The purpose of this study was to measure O2 consumption of nonexercising skeletal muscles (VO2nonex) at rest and after aerobic exercise and to investigate the stimulant factors of O2 consumption. In experiment 1, we measured the resting metabolic rate of the finger flexor muscles in seven healthy males by 31P-magnetic resonance spectroscopy during a 15 min arterial occlusion. In experiment 2, the VO2nonex of the finger flexor muscles was measured using near infrared continuous wave spectroscopy at rest, immediate postexercise, and 3, 5, 10, 15, and 20 min following a cycling exercise at a workload corresponding to 50% of peak pulmonary O2 uptake for 20 min. We also monitored deep tissue temperature in the VO2nonex measurement area and determined catecholamines and lactate concentrations in the blood at rest and immediate postexercise. VO2nonex at rest was 1.1 +/- 0.1 microM O2/S (mean +/- standard error) and VO2nonex after exercise increased 59.6 +/- 7.2% (p< 0.001) from the resting values. There were significant correlations between the increase in VO2nonex and the increase in epinephrine concentration (p < 0.01), and between the increase in VO2nonex and the increase in lactate concentration (p < 0.05). These results suggest that epinephrine and lactate concentrations are important VO2nonex stimulant factors.

The results of this study suggest that T1/2reoxy time was prolonged with aging, regardless of habitual physical activity levels. However, habitual physical activity may prevent the age-related prolongation in T1/2reoxy time after CycEXmax. VO2peak appears to be one of the major factors determining T1/2reoxy time, not age.

The purpose of this study was to examine the effect of low- vs. high-intensity resistance exercise on lipid peroxidation. In addition, the role of muscle oxygenation on plasma malondialdehyde (MDA) concentrations was explored. Eleven experienced resistance trained male athletes (age: 20.8 +/- 1.3 years; weight: 96.2 +/- 14.4 kg; height: 182.4 +/- 7.3 cm) performed 4 sets of the squat exercise using either a low-intensity, high-volume (LI; 15 repetitions at 60% 1 repetition maximum [1RM]) or high-intensity, low-volume (HI; 4 repetitions at 90% 1RM load). Venous blood samples were obtained before the exercise (PRE), immediately following the exercise (IP), and 20 (20P) and 40 minutes (40P) postexercise. Continuous wave near-infrared spectroscopy was used to measure muscle deoxygenation in the vastus lateralis during exercise. Deoxygenated Hb/Mb change was used to determine reoxygenation rate during recovery. No difference in MDA concentrations was seen between LI and HI at any time. Significant correlations were observed between plasma MDA concentrations at IP and the half-time recovery (T1/2 recovery) of muscle reoxygenation (r = 0.45) and between T1/2 recovery and the area under the curve for MDA concentrations (r = 0.44). Results suggest that increases in MDA occur independently of exercise intensity, but tissue acidosis may have a larger influence on MDA formation.