The purpose of this study was to examine how oxygen uptake (V.o2) in decrement-load exercise (DLE) is affected by changing rate of decrease in power output. DLE was performed at three different rates of decrease in power output (10, 20 and 30 watts ・min-1: DLE10, DLE20 and DLE30, respectively) from power output corresponding to 90 % of peak V.o2. V.o2 exponentially increased and then decreased, and the rate of its decrease was reduced at low power output. The values of V.o2 in the three DLE tests were not different for the first 2 min despite the difference in power output. The relationship between V.o2 and power output below 50 watts was obtained as a slope to estimate excessive V.o2 (ex-V.o2) above 50 watts. The slopes were 10.0±0.9 for DLE10, 9.9±0.7 for DLE20 and 10.2±1.0 ml ・min-1 ・ watt-1 for DLE30. The difference between V.o2 estimated from the slope and measured V.o2 was defined as ex-V.o2. The peak value of ex-V.o2 for DLE10 (189±116 ml ・min-1) was significantly greater than those for DLE20 and for DLE30 (93±97 and 88±34 ml ・min-1). The difference between V.o2 in DLE and that in incremental-load exercise (ILE) below 50 watts (ΔV.o2) was greater in DLE 30 and smallest in DLE10. There were significant differences in ΔV.o2 among the three DLE tests. The values of ΔV.o2 at 30 watts were 283±152 for DLE10, 413±136 for DLE20 and 483±187 ml ・min-1 for DLE30. Thus, a faster rate of decrease in power output resulted in no change of V.o2 at the onset of DLE, smaller ex-V.o2 and greater ΔV.o2. These results suggest that V.o2 is disposed in parallel in each motor unit released from power output or recruited in DLE., T. Yano, T. Yunoki, R. Matsuura, T. Arimitsu, T. Kimura., and Obsahuje bibliografii a bibliografické odkazy
The aim of this study was to determine whether excessive oxygen uptake (V.o2) occurs not only during exercise but also during recovery after heavy exercise. After previous exercise at zero watts for 4 min, the main exercise was performed for 10 min. Then recovery exercise at zero watts was performed for 10 min. The main exercises were moderate and heavy exercises at exercise intensities of 40 % and 70 % of peak V.o2, respectively. V.o2 kinetics above zero watts was obtained by subtracting V.o2 at zero watts of previous exercise (ΔV.o2). ΔV.o2 in moderate exercise was multiplied by the ratio of power output performed in moderate and heavy exercises so as to estimate the ΔV.o2 applicable to heavy exercise. The difference between ΔV.o2 in heavy exercise and ΔV.o2 estimated from the value of moderate exercise was obtained. The obtained V.o2 was defined as excessive V.o2. The time constant of excessive V.o2 during exercise (1.88±0.70 min) was significantly shorter than that during recovery (9.61±6.92 min). Thus, there was excessive V.o2 during recovery from heavy exercise, suggesting that O2/ATP ratio becomes high after a time delay in heavy exercise and the high ratio continues until recovery., T. Zano, T. Yunoki, R. Matsuura, T. Arimitsu, T. Kimura., and Obsahuje bibliografii a bibliografické odkazy
Galanin (GAL) is suggested to be a neuropeptide involved in pain transmission. In this study we tried to determine, whether the increase of GAL concentration in brain cells affects impulse transmission between the motor centers localized in the vicinity of the third and fourth cerebral ventricles. The experiments were carried out on rats under chloralose anesthesia. The study objectives were realized using the method allowing to record the amplitude of evoked tongue jerks (ETJ) in response to noxious tooth pulp stimulation during the perfusion of the cerebral ventricles with solutions containing tested compounds. Perfusion of the cerebral ventricles with GAL concentration-dependently inhibited the ETJ amplitude. The antinociceptive effect of GAL was blocked by a galanin receptor antagonist, galantide (GLT) and by opioid antagonists: non-selective naloxone (Nal) and μ-selective β-funaltrexamine (β-FNA). In contrast, a δ-opioid receptor antagonist, naltrindole (NTI) or the κ-opioid receptor antagonist, nor-binaltrophimine (nor-BNI) did not inhibit the effect of GAL. The antinociceptive effect of GAL was more pronounced when GAL was perfused in combination with other neuropeptides/neurohormones, such as endomorphin-2 (EM-2), vasopressin (AVP) and oxytocin (OT). The present results demonstrate that in the orofacial area analgesic activity is modulated by GAL, OT and AVP and that EM-2-induced antinociception involves GAL., M. Zubrzycka, A. Janecka., and Obsahuje bibliografii a bibliografické odkazy