We concluded that blood flow to the nonworking limbs increases markedly in proportion to the work intensity. These results suggest that the conduit arteries in the nonworking limbs are exposed to increases in blood flow and shear stress during exercise.

We estimated a blood flow index, O2 supply index, and O2 consumption index from near-infrared (NIR) signals during venous occlusion imposed at rest and immediately after handgrip exercise with loads equal to 5, 10, 15, 20, 25, and 30% of the maximum voluntary contraction. We also estimated forearm blood flow (BFfa) by strain-gauge plethysmography and forearm O2 consumption (VO2fa) by the invasive method. There was a significant correlation between the rate of increase in total hemoglobin during venous occlusion obtained from NIR signals and BFfa in each subject (r = 0.853 approximately 0.981, P < 0.001). There was also a significant correlation (r = 0.854 approximately 0.944, P < 0.001) between the O2 consumption index estimated from NIR signals and VO2fa. The mean values for O2 supply index in five subjects increased with exercise intensity, while the O2 consumption index showed no further increase about 25% of maximum voluntary contraction. We found significant positive correlations between the O2 supply index and BFfa (r = 0.986, P < 0.001) and the O2 consumption index and VO2fa (r = 0.976, P < 0.001) during exercise at 5-30% of maximum voluntary contraction. These results demonstrate that analysis of NIR signals during venous occlusion provides an advantageous method of estimation of O2 supply and consumption in working muscles during exercise of varying intensity.

The aim of this study was to clarify the influence of subcutaneous adipose tissue (AT) thickness on nearinfrared (NIR) optical density and the penetration depth of light in muscle tissue in vivo. The thickness of adipose tissue in the leg was measured using ultrasonography in 12 young subjects. Optical densities (OD) at 775, 807, and 827 nm were measured when the distance between the light source and the detector was increased from 20 to 100 mm in 10 mm steps. Ultrasonography showed that AT thickness ranged from 4 to 10 mm. The OD increased with increasing distance between the light source and the detector in all subjects. At the same distance between the light source and the detector (30 mm), the OD values correlated negatively with AT thickness (r ϭ Ϫ0.79, −0.82, and −0.79 at 775, 807, and 827 nm, respectively). Ultrasonography also showed that only the extensor hallucis longus muscle (EHL), which is under the extensor digitrum longus muscle (EDL), was activated during the flexion of the big toe. In order to evaluate the penetration depth of NIR light, the depth of EHL was measured and the OD observed before and during flexion. When the distance between the light source and detector was set at 30 mm, the OD values before exercise ranged from 0.36 to 3.18 at 775 nm, from 0.19 to 2.43 at 807 nm, and from 0.15 to 1.60 at 827 nm. Changes in OD during exercise were detectable for all subjects, and the EHLs of the subjects were located 10.0 to 20.2 mm under the detector. However, when the light source-detector distance was set at 20 mm, changes in OD during exercise were detectable for only 2 subjects, whose AT thicknesses were 4.0 or 5.0 mm, and the EHLs of the subjects were 10.0 or 11.7 mm deep. At a distance of 40 mm, 9 out of 12 subjects showed changes in OD, and their AT thicknesses and EHL locations ranged from 6.4 to 10.0 mm and from 11.4 to 20.4 mm deep, respectively. However, at this distance, OD reached our instrumental limit (4.82) and no OD change could be detected in three subjects with small AT values (4.0, 4.0, and 5.3 mm). These findings suggested that the thinner the AT, the higher the OD when the light source and detector are set a certain distance apart, and that NIR light penetrates the muscle tissue at least deep enough to reach half the distance between the light source and the detector when the AT thickness ranges from 4 to 10 mm.

The purpose of this study was to determine forearm blood flow changes during static handgrip exercise at different intensities in relation to heart rate and blood pressure. Seven active women performed static handgrip exercise at intensities of 10, 30, 50 and 70% maximum voluntary contraction (MVC) in a supine position for 1 min. During exercise at different intensities, the brachial arterial blood flow (Doppler ultrasound method), calculated from vessel diameter, flow velocity and heart rate (measured by ECG), increased to a similar level (137.3 +/- 20.2-160.9 +/- 26.1 mL min-1) from pre-exercise control value (87.5 +/- 14.1 mL min-1). These increases at the lower intensities were attributable to increased in-flow during one cardiac cycle, whereas at the higher intensities, they were due to increased heart rate. Both systolic and diastolic blood pressure (Finapres) changes increased from 10% MVC (16.1 +/- 3.4, 9.0 +/- 1.7 mmHg) up to 50% MVC (33.8 +/- 6.7, 25.0 +/- 4.9 mmHg), but were disproportionately more elevated at 70% MVC (46.1 +/- 7.9, 42.9 +/- 8.9 mmHg), suggesting neural vasoconstriction had occurred. Immediate post-exercise hyperaemia, used as an indicator of poor blood supply, became greater as the exercise intensity increased. These results suggest that the brachial arterial blood flow was maintained at a similar level during 60-s static handgrip exercise at different intensities by elevating the blood pressure and heart rate, which probably counteracted the increased intramuscular pressure and neural vasoconstriction occurring at the higher exercise intensity. The magnitude of the post-exercise hyperemic response increased as exercise level increased despite increased blood-flow to the arm during-exercise. This suggests a worsening imbalance in oxygen delivery in forearm muscles at higher levels of exercise.

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