No abstract

The results confirm that spatially resolved near-infrared spectroscopy detects cerebral deoxygenation with systemic hypoxic exposure and hyperventilation. However, a commonly used vasopressor norepinephrine disturbs skin oxygen saturation to an extent that influences scO2.

Neurovascular coupling provides the basis for many functional neuroimaging techniques. Nitric oxide (NO), adenosine, cyclooxygenase, CYP450 epoxygenase, and potassium are involved in dilating arterioles during neuronal activation. We combined inhibition of NO synthase, cyclooxygenase, adenosine receptors, CYP450 epoxygenase, and inward rectifier potassium (Kir) channels to test whether these pathways could explain the blood flow response to neuronal activation. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO(2)) of the somatosensory cortex were measured during forepaw stimulation in 24 rats using a laser Doppler/spectroscopy probe through a cranial window. Combined inhibition reduced CBF responses by two-thirds, somatosensory evoked potentials and activation-induced CMRO(2) increases remained unchanged, and deoxy-hemoglobin (deoxy-Hb) response was abrogated. This shows that in the rat somatosensory cortex, one-third of the physiological blood flow increase is sufficient to prevent microcirculatory increase of deoxy-Hb concentration during neuronal activity. The large physiological CBF response is not necessary to support small changes in CMRO(2). We speculate that the CBF response safeguards substrate delivery during functional activation with a considerable 'safety factor'. Reduction of the CBF response in pathological states may abolish the BOLD-fMRI signal, without affecting underlying neuronal activity.

No abstract

Recently, a universal, simple, and fail-safe mechanism has been proposed by which cerebral blood flow (CBF) might be coupled to oxygen metabolism during neuronal activation without the need for any tissue-based mechanism. According to this concept, vasodilation occurs by local erythrocytic release of nitric oxide or ATP wherever and whenever hemoglobin is deoxygenated, directly matching oxygen demand and supply in every tissue. For neurovascular coupling in the brain, we present experimental evidence challenging this view by applying an experimental regime operating without deoxy-hemoglobin. Hyperbaric hyperoxygenation (HBO) allowed us to prevent hemoglobin deoxygenation, as the oxygen that was physically dissolved in the tissue was sufficient to support oxidative metabolism. Regional CBF and regional cerebral blood oxygenation were measured using a cranial window preparation in anesthetized rats. Hemodynamic and neuronal responses to electrical forepaw stimulation or cortical spreading depression (CSD) were analyzed under normobaric normoxia and during HBO up to 4 ATA (standard atmospheres absolute). Inconsistent with the proposed mechanism, during HBO, CBF responses to functional activation or CSD were unchanged. Our results show that activation-induced CBF regulation in the brain does not operate through the release of vasoactive mediators on hemoglobin deoxygenation or through a tissue-based oxygen-sensing mechanism.

BackgroundThis study examined the effects of different levels of compression (0, 20 and 40 mmHg) produced by leg garments on selected psycho-physiological measures of performance while exposed to passive vibration (60 Hz, amplitude 4-6 mm) and performing 3-min of alpine skiing tuck position.MethodsPrior to, during and following the experiment the electromygraphic (EMG) activity of different muscles, cardio-respiratory data, changes in total hemoglobin, tissue oxygenation and oscillatory movement of m. vastus lateralis, blood lactate and perceptual data of 12 highly trained alpine skiers were recorded. Maximal isometric knee extension and flexion strength, balance, and jumping performance were assessed before and after the experiment.ResultsThe knee angle (−10°) and oscillatory movement (−20-25.5%) were lower with compression (P < 0.05 in all cases). The EMG activities of the tibialis anterior (20.2-28.9%), gastrocnemius medialis (4.9-15.1%), rectus femoris (9.6-23.5%), and vastus medialis (13.1-13.7%) muscles were all elevated by compression (P < 0.05 in all cases). Total hemoglobin was maintained during the 3-min period of simulated skiing with 20 or 40 mmHg compression, but the tissue saturation index was lower (P < 0.05) than with no compression. No differences in respiratory parameters, heart rate or blood lactate concentration were observed with or maximal isometric knee extension and flexion strength, balance, and jumping performance following simulated skiing for 3 min in the downhill tuck position were the same as in the absence of compression.ConclusionsThese findings demonstrate that with leg compression, alpine skiers could maintain a deeper tuck position with less perceived exertion and greater deoxygenation of the vastus lateralis muscle, with no differences in whole-body oxygen consumption or blood lactate concentration. These changes occurred without compromising maximal leg strength, jumping performance or balance. Accordingly, our results indicate that the use of lower leg compression in the range of 20-40 mmHg may improve alpine skiing performance by allowing a deeper tuck position and lowering perceived exertion.

No abstract

No abstract