Whether neurogenic vasodilatation contributes to exercise hyperemia is still controversial. Blood flow to noncontracting muscle, however, is chiefly regulated by a neural mechanism. Although vasodilatation in the nonexercising limb was shown at the onset of exercise, it was unclear whether central command or muscle mechanoreflex is responsible for the vasodilatation. To clarify this, using voluntary one-legged cycling with the right leg in humans, we measured the relative changes in concentrations of oxygenated-hemoglobin (Oxy-Hb) of the noncontracting vastus lateralis (VL) muscle with near-infrared spectroscopy as an index of tissue blood flow and femoral blood flow to the nonexercising leg. Oxy-Hb in the noncontracting VL and femoral blood flow increased (P < 0.05) at the start period of voluntary one-legged cycling without accompanying a rise in arterial blood pressure. In contrast, no increases in Oxy-Hb and femoral blood flow were detected at the start period of passive one-legged cycling, suggesting that muscle mechanoreflex cannot explain the initial vasodilatation of the noncontracting muscle during voluntary one-legged cycling. Motor imagery of the voluntary one-legged cycling increased Oxy-Hb of not only the right but also the left VL. Furthermore, an increase in Oxy-Hb of the contracting VL, which was observed at the start period of voluntary one-legged cycling, had the same time course and magnitude as the increase in Oxy-Hb of the noncontracting muscle. Thus it is concluded that the centrally induced vasodilator signal is equally transmitted to the bilateral VL muscles, not only during imagery of exercise but also at the start period of voluntary exercise in humans.
To determine whether output from the forebrain (termed central command) may descend early enough to increase cardiac and renal sympathetic outflows at the onset of voluntary exercise, we examined the changes in regional tissue blood flows of bilateral prefrontal cortices with near-infrared spectroscopy, precisely identifying the onset of voluntary ergometer 30-s exercise at 41 ± 2% of the maximal exercise intensity in humans. Prefrontal oxygenated-hemoglobin (Oxy-Hb) concentration was measured as index of regional blood flow unless deoxygenated-hemoglobin concentration remained unchanged. Prefrontal Oxy-Hb concentration increased significantly ( P < 0.05) 5 s prior to the onset of exercise with arbitrary start, whereas such increase in prefrontal Oxy-Hb was absent before exercise abruptly started by a verbal cue. Furthermore, the increase in prefrontal Oxy-Hb observed at the initial 15-s period of exercise was greater with arbitrary start than cued start. The prefrontal Oxy-Hb, thereafter, decreased during the later period of exercise, irrespective of either arbitrary or cued start. The reduction in prefrontal Oxy-Hb had the same time course and response magnitude as that during motor-driven passive exercise. Cardiac output increased at the initial period of exercise, whereas arterial blood pressure and total peripheral resistance decreased. The depressor response was more pronounced ( P < 0.05) with arbitrary start than cued start. Taken together, it is suggested that the increase in prefrontal Oxy-Hb observed prior to the onset of voluntary exercise may be in association with central command, while the later decrease in the Oxy-Hb during exercise may be in association with feedback stimulated by mechanical limb motion.
Hard X-ray Photoemission spectroscopy (PES) of copper core electronic states, with a probing depth of ∼60Å, is used to show that the Zhang-Rice singlet feature is present in La2CuO4 but is absent in Nd2CuO4. Hole-and electron doping in La2−xSrxCuO4 (LSCO) and Nd2−xCexCuO4 (NCCO) result in new well-screened features which are missing in soft X-ray PES. Impurity Anderson model calculations establish metallic screening as its origin, which is strongly suppressed within 15Å of the surface. Complemented with X-ray absorption spectroscopy, the small chemical-potential shift in core levels (∼ 0.2 eV) are shown to be consistent with modifications of valence and conduction band states spanning the band gap (∼ 1 eV) upon hole-and electron-doping in LSCO and NCCO. [2]. Soft X-ray (SX, hν∼1000-1500 eV) core level photoemission spectroscopy (PES) with a probing depth of ∼10-15Å is valuable in studying valence change, chemical-potential-shift and screening effects in solids [3]. Combination of core level PES with model calculations have been used to describe the parent insulating cuprates La 2 CuO 4 (LCO) and Nd 2 CuO 4 (NCO) as charge-transfer insulators in the Zaanen-SawatzkyAllen classification scheme [4], with the on-site Coulomb energy (≈8 eV), being much larger than the charge transfer energy (≈2 eV) between the O 2p and Cu 3d states [5,6,7,8].La 1.85 Sr 0.15 CuO 4 (LSCO) and Nd 1.85 Ce 0.15 CuO 4 (NCCO) are prototypical of hole-and electron-doped cuprates and exhibit a d x 2 −y 2 superconducting gap. The normal phase resistivity (ρ∝T 2 ) is like a Fermi-liquid for NCCO[9] but non-Fermi-liquid-like (ρ∝T ) for LSCO [10]. The strong correlations lead to special spectral behaviour such as non-local screening effects [11], and anomalous spectral weight transfer upon doping [12]. While valency and chemical potential changes in the high-Tc cuprates can be probed with SX-PES, in spite of several core level and valence band PES studies, there remains a seemingly simple and yet unresolved puzzle about the doping dependent electronic structure of the superconducting cuprates [5,6,7,8,11,12,13,14,15]. The puzzle involves distinguishing between 'mid-gap pinning' or 'crossing the gap' scenario to simultaneously explain changes in core levels and valence bands. The mid-gap pinning scenario [5,6,14,15] involves formation of new states within the band gap on hole-and electron-doping. It explains the small chemical potential shift of -0.2 eV (or +0.2 eV) in O 1s core levels PES of LSCO (or NCCO) compared to undoped LCO (or NCO), but is inconsistent with the large optical gap onset (∼1.0 eV) of the insulating parents [16]. In an alternative picture, the chemical potential moves to the top of the valence band by hole-doping and bottom of the conduction band on electron-doping. Using resonant PES [13], it was shown that electron-and hole-doping leads to a crossing of the gap (∼1.0 eV) from NCCO to LSCO. However, the small chemical potential shift in O 1s core levels cannot be explained by this scenario.While many SX-PES of the Cu 2p core ...
We have recently reported that central command contributes to increased blood flow in both noncontracting and contracting vastus lateralis (VL) muscles at the early period of voluntary one-legged cycling. The purpose of this study was to examine whether sympathetic cholinergic vasodilatation mediates the increases in blood flows of both muscles during one-legged exercise. Following intravenous administration of atropine (10 μg/kg), eight subjects performed voluntary 1-min one-legged cycling (at 35% of maximal voluntary effort) and mental imagery of the exercise. The relative concentrations of oxygenated- and deoxygenated-hemoglobin (Oxy- and Deoxy-Hb) in the bilateral VL were measured as an index of muscle tissue blood flow with near-infrared spectroscopy (NIRS). The Oxy-Hb in both noncontracting and contracting VL increased at the early period of one-legged cycling, whereas the Deoxy-Hb did not alter at that period. Atropine blunted (P < 0.05) the Oxy-Hb responses of both VL muscles but did not affect the Deoxy-Hb responses. The time course and magnitude of the atropine-sensitive component in the Oxy-Hb response were quite similar between the noncontracting and contracting VL muscles. With no changes in the Deoxy-Hb and hemodynamics, imagery of one-legged cycling induced the bilateral increases in the Oxy-Hb, which were completely abolished by atropine. In contrast, imagery of a circle (with no relation to exercise) did not alter the NIRS signals, irrespective of the presence or absence of atropine. It is concluded that central command evokes cholinergic vasodilatation equally in bilateral VL muscles during voluntary one-legged cycling and motor imagery.
Our laboratory has reported that central command blunts the sensitivity of the aortic baroreceptor-heart rate (HR) reflex at the onset of voluntary static exercise in conscious cats and spontaneous contraction in decerebrate cats. The purpose of this study was to examine whether central command attenuates the sensitivity of the carotid sinus baroreceptor-HR reflex at the onset of spontaneous, fictive motor activity in paralyzed, decerebrate cats. We confirmed that aortic nerve (AN)-stimulation-induced bradycardia was markedly blunted to 26 ± 4.4% of the control (21 ± 1.3 beats/min) at the onset of spontaneous motor activity. Although the baroreflex bradycardia by electrical stimulation of the carotid sinus nerve (CSN) was suppressed (P < 0.05) to 86 ± 5.6% of the control (38 ± 1.2 beats/min), the inhibitory effect of spontaneous motor activity was much weaker (P < 0.05) with CSN stimulation than with AN stimulation. The baroreflex bradycardia elicited by brief occlusion of the abdominal aorta was blunted to 36% of the control (36 ± 1.6 beats/min) during spontaneous motor activity, suggesting that central command is able to inhibit the cardiomotor sensitivity of arterial baroreflexes as the net effect. Mechanical stretch of the triceps surae muscle never affected the baroreflex bradycardia elicited by AN or CSN stimulation and by aortic occlusion, suggesting that muscle mechanoreflex did not modify the cardiomotor sensitivity of aortic and carotid sinus baroreflex. Since the inhibitory effect of central command on the carotid baroreflex pathway, associated with spontaneous motor activity, was much weaker compared with the aortic baroreflex pathway, it is concluded that central command does not force a generalized modulation on the whole pathways of arterial baroreflexes but provides selective inhibition for the cardiomotor component of the aortic baroreflex.
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