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T Yunoki

Publications and source records attributed to T Yunoki.

At least 19 recordsLinked to original sources
PubMed2006

Effects of rate of decrease in power output in decrement-load exercise on oxygen uptake.

The purpose of this study was to examine how oxygen uptake (Vo2) 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 Vo2. Vo2 exponentially increased and then decreased, and the rate of its decrease was reduced at low power output. The values of Vo2 in the three DLE tests were not different for the first 2 min despite the difference in power output. The relationship between Vo2 and power output below 50 watts was obtained as a slope to estimate excessive Vo2 (ex-Vo2) 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 Vo2 estimated from the slope and measured Vo2 was defined as ex-Vo2. The peak value of ex-Vo2 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 Vo2 in DLE and that in incremental-load exercise (ILE) below 50 watts (DeltaVo2) was greater in DLE30 and smallest in DLE10. There were significant differences in DeltaVo2 among the three DLE tests. The values of DeltaVo2 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 Vo2 at the onset of DLE, smaller ex-Vo2 and greater DeltaVo2. These results suggest that Vo2 is disposed in parallel in each motor unit released from power output or recruited in DLE.

Adult↗
PubMed2006

Actions of ZD0947, a novel ATP-sensitive K+ channel opener, on membrane currents in human detrusor myocytes.

BACKGROUND AND PURPOSE: ATP-sensitive K+ channels (K(ATP) channels) play important roles in regulating the resting membrane potential of detrusor smooth muscle. Actions of ZD0947, a novel KATP channel opener, on both carbachol (CCh)-induced detrusor contractions and membrane currents in human urinary bladder myocytes were investigated. EXPERIMENTAL APPROACH: Tension measurements and patch-clamp techniques were utilized to study the effects of ZD0947 in segments of human urinary bladder. Immunohistochemistry was also performed to detect the expression of the sulphonylurea receptor 1 (SUR1) and the SUR2B antigens in human detrusor muscle. KEY RESULTS: ZD0947 (> or = 0.1 microM) caused a concentration-dependent relaxation of the CCh-induced contraction of human detrusor, which was reversed by glibenclamide. The rank order of the potency to relax the CCh-induced contraction was pinacidil > ZD0947 > diazoxide. In conventional whole-cell configuration, ZD0947 (> or = 1 microM) caused a concentration-dependent inward K+ current which was suppressed by glibenclamide at -60 mV. When 1 mM ATP was included in the pipette solution, application of pinacidil or ZD0947 caused no inward K+ current at -60 mV. Gliclazide (< or =1 microM), a selective SUR1 blocker, inhibited the ZD0947-induced currents (Ki = 4.0 microM) and the diazoxide-induced currents (high-affinity site, Ki1 = 42.4 nM; low-affinity site, Ki2 = 84.5 microM) at -60 mV. Immunohistochemical studies indicated the presence of SUR1 and SUR2B proteins, which are constituents of KATP channels, in the bundles of human detrusor smooth muscle. CONCLUSIONS AND IMPLICATIONS: These results suggest that ZD0947 caused a glibenclamide-sensitive detrusor relaxation through activation of glibenclamide-sensitive KATP channels in human urinary bladder.

ATP-Binding Cassette Transporters↗
PubMed2006

Comparison of oxygen uptake at the onset of decrement-load and constant-load exercise.

The purpose of the present study was to examine whether the level of oxygen uptake (V(.)(O2) at the onset of decrement-load exercise (DLE) is lower than that at the onset of constant-load exercise (CLE), since power output, which is the target of V(.)(O2) response, is decreased in DLE. CLE and DLE were performed under the conditions of moderate and heavy exercise intensities. Before and after these main exercises, previous exercise and post exercise were performed at 20 watts. DEL was started at the same power output as that for CLE and power output was decreased at a rate of 15 watts per min. V(.)(O2) in moderate CLE increased at a fast rate and showed a steady state, while V(.)(O2) in moderate DLE increased and decreased linearly. V(.)(O2) at the increasing phase in DLE was at the same level as that in moderate CLE. V(.)(O2) immediately after moderate DLE was higher than that in the previous exercise by 98+/-77.5 ml/min. V(.)(O2) in heavy CLE increased rapidly at first and then slowly increased, while V(.)(O2) in heavy DLE increased rapidly, showing a temporal convexity change, and decreased linearly. V(.)(O2) at the increasing phase of heavy DLE was the same level as that in heavy CLE. V(.)(O2) immediately after heavy DLE was significantly higher than that in the previous exercise by 156+/-131.8 ml/min. Thus, despite the different modes of exercise, V(.)(O2) at the increasing phase in DLE was at the same level as that in CLE due to the effect of the oxygen debt expressed by the higher level of V(.)(O2) at the end of DLE than that in the previous exercise.

Adult↗
PubMed2006

Relationship between oxygenation in inactive biceps brachii muscle and hyperventilation during leg cycling.

Inactive forearm muscle oxygenation has been reported to begin decreasing from the respiratory compensation point (RCP) during ramp leg cycling. From the RCP, hyperventilation occurs with a decrease in arterial CO2 pressure (PaCO2). The aim of this study was to determine which of these two factors, hyperventilation or decrease in PaCO2, is related to a decrease in inactive biceps brachii muscle oxygenation during leg cycling. Each subject (n = 7) performed a 6-min two-step leg cycling. The exercise intensity in the first step (3 min) was halfway between the ventilatory threshold and RCP (170+/-21 watts), while that in the second step (3 min) was halfway between the RCP and peak oxygen uptake (240+/-28 watts). The amount of hyperventilation and PaCO2 were calculated from gas parameters. The average cross correlation function in seven subjects between inactive muscle oxygenation and amount of hyperventilation showed a negative peak at the time shift of zero (r = -0.72, p<0.001), while that between inactive muscle oxygenation and calculated PaCO2 showed no peak near the time shift of zero. Thus, we concluded that decrease in oxygenation in inactive arm muscle is closely coupled with increase in the amount of hyperventilation.

Adult↗
PubMed2005

Relationship between maximal oxygen uptake and oxygenation level in inactive muscle at exhaustion in incremental exercise in humans.

The aim of the present study was to determine whether the oxygenation level in an inactive muscle during an incremental exercise test, determined by near-infrared spectroscopy, influences the maximal oxygen uptake (Vo2max). The oxygenation level at the onset of incremental exercise was higher than that at rest and started to decrease at a high power output. A minimal level was observed at exhaustion during incremental exercise. Vo2 increased linearly after some delay, and the rate of increase in Vo2 was greater at a higher power output. Heart rate increased linearly after the time delay, and the rate of increase in heart rate did not change. There was a significant correlation between Vo2max and oxygenation level in inactive muscle at exhaustion (r=-0.89). We therefore concluded that the oxygenation level in inactive muscle at exhaustion during incremental exercise is associated with an individual difference in Vo2max.

Adult↗
PubMed2004

Effect of exercise intensity on the slow component of oxygen uptake in decremental work load exercise.

The paper sought to determine the exercise intensity where the slow component of oxygen uptake (Vo(2)) first appears in decremental work load exercise (DLE). Incremental work load exercise (ILE) was performed with an increment rate of 15 watts (W) per minute. In DLE, power outputs were decreased by 15 W per minute, from 120 (DLE(120)), 160 (DLE(160)), 200 (DLE(200)) and 240 (DLE(240)) W, respectively. The slopes of Vo(2) against the power output were obtained in the lower section from 0 to 50 W in all DLEs, and in the upper section from 80 to 120 W in DLE(160) and from 100 to 150 W in DLE(200) and DLE(240). The power output at exhaustion in ILE was 274 +/- 20 W. The power output at the ventilatory threshold (VT) obtained in ILE was 167 +/- 22 W. The initial power output in DLE(160) was near the power output at VT. The slopes obtained in the upper sections were 11.4 +/- 0.9 ml x min(-1) x W(-1)1 in DLE(160), 12.8 +/- 0.8 ml x min(-1) x W(-1) in DLE(200), and 14.8 +/- 1.1 ml x min(-1) x W(-1) in DLE(240). The slope obtained in DLE(120) was 10.9 +/- 0.6 ml x min(-1). There were no differences in slope between the upper and lower sections in DLE(160) but there were significant differences in slopes between the upper and lower sections in DLE(200) and DLE(240). Thus, the slow component, which could be observed as a steeper slope in DLE, began to increase when the initial power output in DLE was near to VT.

Adult↗
PubMed2002

Effect of arm cranking on the NIRS-determined blood volume and oxygenation of human inactive and exercising vastus lateralis muscle.

In this study, the effects of arm cranking on total (HbT) and oxygenated haemoglobin concentrations (HbO2) of inactive and exercising vastus lateralis muscles were investigated using near-infrared spectrometry (NIRS). Four exercise protocols were performed, 6-min arm cranking at intensities of 30% and 50% of peak oxygen uptake (VO2peak, recorded during incremental arm exercise; AE30 and AE50, respectively), and 6 min of combined exercise in which AE30 or AE50 was added to on-going leg cycling at an intensity of 40% VO2peak (LE40: AE30LE40 and AE50LE40, respectively). During AE30 in the inactive vastus lateralis, neither HbT nor HbO2 changed from the control values, whereas they both decreased during AE50. The decrease in HbT was observed from the 1st to the 5th min of exercise, whereas the decrease in HbO2 was observed from the 3rd to the 6th min of exercise. In the exercising vastus lateralis, neither HbT nor HbO2 changed from the control value during AE30LE40. In addition, HbO2 did not change during AE50LE40. During AE50LE40, however, although HbT did not change from the 1st to the 4th min of exercise, it increased from the 4th to the 6th min. These results indicate that although in the inactive vastus lateralis both HbT and HbO2 decrease during moderate arm exercise, these decreases are suppressed in the exercising vastus lateralis muscle.

Adult↗
PubMed2002

Kinetics of CO(2) excessive expiration in constant-load exercise.

BACKGROUND: The purpose of this study was to examine the kinetics of excessively expired CO(2) (VCO(2) excess) in response to an increase in blood lactate (La) during constant-load exercise. METHODS: O(2) uptake (VO(2) ) and CO(2) output (VCO(2) ) were measured at exercise intensities of 55% and 70% of individual peak values of Vo2 obtained in incremental exercise. VCO(2) excess was obtained by multiplying the Vo2 obtained at 55% or 70% peakVoz by the difference between respiratory gas exchange ratios (VCO(2) /Vo(2) ) at 55% or 70% peak VO(2) and at 40% peakVO(2) . RESULTS: In both exercises of 55% and 70% peakVO(2) , VCO(2) excess remained constant for about the first minute, increased until about 2 min after the start of exercise, and then decreased. VCO(2) excess showed positive values even at 10 min after the start of exercise. The La level, on the other hand, increased during the first 5 min of exercise but did not show any significant change during the next 5 min. The values of VCO(2) excess were integrated from the start to the end of 10 min of exercise (CO(2) excess). CO(2) excess was found to be significantly related to the difference between La at 10 min after the start of exercise and at rest (DLa). End tidal CO(2) pressure (PETCO(2)) increased and then decreased in both exercises. The difference between PETCO(2) values at peak and at 10 min after the start of exercise (DPETCO(2) ) was significantly related to CO(2) excess. DPetco2 was also found to be significantly related to the increase in DLa. CONCLUSIONS: The kinetics of estimated VCO2excess is affected first by the increase in La and later by the decrease in PETCO(2) induced by the La increase.

Adult↗
PubMed2001

Dual action of ZD6169, a novel K(+) channel opener, on ATP-sensitive K(+) channels in pig urethral myocytes.

1. The effects of ZD6169, a novel K(+) channel opener, on both membrane and unitary currents in pig urethra were investigated using patch-clamp techniques. Its effect was also examined on currents in inside-out patches of COS7 cells expressing carboxy terminus truncated inwardly rectifying K(+) channel (Kir6.2) subunits (Kir6.2C36) which form ATP-sensitive K(+) channels (K(ATP) channels). 2. In current-clamp mode, ZD6169 (< or = 10 microM) induced a concentration-dependent membrane hyperpolarization. Higher concentrations (> or = 30 microM) caused a transient membrane hyperpolarization, followed by a gradual membrane depolarization. On removal of ZD6169, an after hyperpolarization was observed. 3. In conventional voltage-clamp configuration, at -50 mV in symmetrical 140 mM K(+) conditions, ZD6169 (100 microM) caused a transient inward current which gradually decayed. Removal of ZD6169 evoked a much larger amplitude K(+) current with a similar time course. 4. ZD6169 produced an inward glibenclamide-sensitive K(+) current, demonstrating a bell-shaped concentration-response relationship. 5. In cell-attached configuration in symmetrical 140 mM K(+) conditions, ZD6169 (< or = 30 microM) activated an K(ATP) channel which was reversibly suppressed by application of glibenclamide. In contrast, ZD6169 (100 microM) inhibited the activity of the levcromakalim-induced K(ATP) channels. 6. ZD6169 (100 microM) had no significant effect on the channel activity of Kir6.2C36 in inside-out configuration, although cibenzoline greatly suppressed the channel activity. 7. These results demonstrate that ZD6169 possesses a dual effect on the activity of the K(ATP) channel; activating at low concentration and inhibiting at higher concentration.

Adenosine Triphosphate↗
PubMed2001

The effects of flecainide on ATP-sensitive K(+) channels in pig urethral myocytes.

The effects of the antiarrhythmic drug flecainide on levcromakalim-induced hyperpolarization, macroscopic and unitary K(+) currents in pig urethra were investigated using patch-clamp techniques. The effects of flecainide were also examined on currents in inside-out patches of COS7 cells expressing carboxy terminus truncated inwardly rectifying K(+) channel (Kir6.2) subunits (i.e. Kir6.2DeltaC36) which form ATP-sensitive K(+) channels (K(ATP) channels). In current-clamp mode, application of flecainide (> or =100 microM) caused a significant depolarization after the membrane potential had been hyperpolarized by levcromakalim. In voltage-clamp experiments, the levcromakalim-induced outward current was suppressed by 300 microM flecainide in quasi-physiological K(+) conditions (K(i)=51 microM). In contrast, approximately 20% of the levcromakalim-induced inward current still remained even after application of 300 microM flecainide in symmetrical 140 mM K(+) conditions (K(i)=51 microM). In contrast, approximately 20% of the levcromakalim-induced inwar=126 microM). In cell-attached configuration, the channel activity of the levcromakalim-induced K(ATP) channels was reversibly inhibited by flecainide (> or =30 microM) at -50 mV. Their activity was also suppressed by either disopyramide or cibenzoline. Flecainide reversibly inhibited the channel activity of Kir6.2DeltaC36 expressed in COS7 cells using inside-out configuration. Inhibitory effects of flecainide on the levcromakalim-induced currents became more potent when the value of external pH increased, although this slightly reduced the proportion of drug molecules carrying a positive charge. These results suggest that flecainide inhibits channel activity through blocking the pore site of the K(ATP) channel in pig urethra.

Adenosine Triphosphate↗
PubMed2001

The involvement of L-type Ca(2+) channels in the relaxant effects of the ATP-sensitive K(+) channel opener ZD6169 on pig urethral smooth muscle.

1. The effects of ZD6169, a novel ATP-sensitive K(+) channel (K(ATP) channel) opener, were investigated on membrane currents in isolated myocytes using patch-clamp techniques. Tension measurement was also performed to study the effects of ZD6169 on the resting tone of pig urethral smooth muscle. 2. Levcromakalim was more potent than ZD6169 in lowering the resting urethral tone. Relaxation induced by low concentrations of ZD6169 (< or =3 microM) was completely suppressed by additional application of glibenclamide (1 microM). In contrast, glibenclamide (1-10 microM) only partially inhibited the relaxation induced by higher concentrations of ZD6169 (> or = microM). 3. Bay K8644 (1 microM) reduced the maximum relaxation produced by ZD6169 (> or =10 microM). 4. In whole-cell configuration, ZD6169 suppressed the peak amplitude of voltage-dependent Ba(2+) currents in a concentration- and voltage-dependent manner, and at 100 microM, shifted the steady-state inactivation curve of the voltage-dependent Ba(2+) currents to the left at a holding potential of -90 mV. 5. In cell-attached configuration, open probability of unitary voltage-dependent Ba(2+) channels (27 pS, 90 mM Ba(2+)) was inhibited by 100 microM ZD6169 and by 10 microM nifedipine. 6. Reverse transcriptase-polymerase chain reaction (RT - PCR) analysis revealed the presence of the transcript of the alpha(1C) subunit of L-type Ca(2+) channels in pig urethra. 7. These results demonstrate that ZD6169 causes urethral relaxation through two distinct mechanisms, activation of K(ATP) channels at lower concentrations and inhibition of voltage-dependent Ca(2+) channels at higher concentrations (about 10 microM).

Adenosine Triphosphate↗
PubMed2001

Relationship between the slow component of oxygen uptake and the potential reduction in maximal power output during constant-load exercise.

BACKGROUND: The purpose of the present study was to examine the relationship between the slow component of oxygen uptake (VO2) and muscle fiber fatigue. Maximal power output (MPO) was used as an index of muscle fiber fatigue. METHODS: Two constant exercises were carried out at exercise intensities of 40% and 80% of maximal oxygen uptake (VO2max). Each exercise was repeated three times, once for the measurement for VO2, and the other two times for MPO testing, at 3 and 6 minutes after work output. RESULTS: Reproducibility of MPO at rest was assessed by correlation coefficient. Its value was 0.933. At 40% VO2max, MPO did not significantly decrease from the resting value. At 80% VO2max, MPO significantly decreased by 129+/-77 watts at 3 min and by 178+/-108 watts at 6 min. The VO2 kinetic at 40% VO2 was well described by a monoexponential function with a time constant of 0.432 min. However, at 80% VO2max, a slow component of the form of a linear drift superimposed on a monoexponential function with an essentially equal time constant (0.469 min) was unambiguously detected. This slow component was significantly related to the decrease in MPO (r=0.567). CONCLUSIONS: The present results suggested that the fatigue of muscle fibers may be one of the factors that produce the slow component of VO2 during high intensity exercise.

Adult↗
PubMed2000

The effects of caffeine on ATP-sensitive K(+) channels in smooth muscle cells from pig urethra.

The effects of caffeine on both levcromakalim-induced macroscopic and unitary currents in pig proximal urethra were investigated by the use of patch-clamp techniques (conventional whole-cell configuration and cell-attached configuration). The effects of caffeine were also examined on currents in inside-out patches of COS7 cells expressing carboxy terminus truncated inwardly rectifying K(+) channel (Kir6.2) subunits (i.e. Kir6.2DeltaC36) which form ATP-sensitive K(+) channels (K(ATP) channels). In conventional whole-cell configuration, the levcromakalim (100 microM)-induced inward current (symmetrical 140 mM K(+) conditions) was inhibited by caffeine (> or =1 mM) at a holding potential of -50 mV. In contrast, ryanodine (10 microM) caused no significant inhibitory effect on the gradual decay of the levcromakalim-induced current at -50 mV. The amplitude of the 30 microM levcromakalim-induced current was enhanced by 3-isobutyl-1-methylxanthine (IBMX, 100 microM). In cell-attached configuration, the levcromakalim-induced K(+) channel openings were inhibited by subsequent application of 10 mM caffeine, decreasing the channel open probability at -50 mV. Reverse transcriptase-polymerase chain reaction (RT - PCR) analysis revealed the presence of Kir6.2 transcript in pig urethra. Caffeine (> or =3 mM) inhibited the channel activity of Kir6.2DeltaC36 expressed in COS7 cells (3 mM caffeine, 65+/-6%, n=4; 10 mM caffeine, 29+/-2%, n=4). These results suggest that caffeine can inhibit the activity of K(ATP) channels through a direct blocking effect on the pore-forming Kir subunit.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Excess CO(2) output response during and after short-term intensive exercise in sprinters and long-distance runners.

The purpose of the present study was to examine the response of excess CO(2) output to short-term intensive exercise in sprinters (SPR) and long-distance runners (LDR). End-tidal CO(2) pressure (PETCO(2)) increased up to about 20 s postexercise and then returned to the resting level at about 2-3 min postexercise. Thereafter, PETCO(2) remained below the resting level. VCO(2) excess, defined as the difference between VCO(2) and VO(2) was integrated from the start of exercise until PETCO(2) returned to the resting level. This integrated VCO(2) excess was defined as the first phase of CO(2) excess (1st CO(2) excess). The subsequent integrated VCO(2) excess until 10 min postexercise was defined as the second phase of CO(2) excess (2nd CO(2) excess). The ratio of 1st CO(2) excess to the lactate rise from rest to the peak value was significantly lower in SPR than in LDR, whereas 2nd CO(2) excess was significantly greater in SPR than in LDR. The decrease in PETCO(2) at 10 min postexercise was significantly larger in SPR than in LDR. The 2nd CO(2) excess was closely related to the decrease in PETCO(2). The results in the second phase suggest that the difference in the response of excess CO(2) output is derived from the difference in the respiratory chemosensitivity to lactic acid rise.

Carbon Dioxide↗
PubMed2000

Kinetics of oxygen uptake during decremental ramp exercise.

BACKGROUND: The purpose of the present study was to examine the kinetics of oxygen uptake (VO2) during decremental ramp exercises after incremental ramp exercise above the anaerobic threshold. METHODS: Triangle exercise consisting of incremental and decremental exercises, and trapezoid exercise in which a constant load was inserted between incremental and decremental exercises were carried out. RESULTS: Blood lactate (La) increased in incremental phases during triangle and trapezoid exercises, and showed a further increase at constant work during trapezoid exercise. It significantly decreased during decremental exercise. Initial VO2 level during decremental exercise was significantly higher in trapezoid exercise than in triangle exercise. The VO2 level then exponentially decreased and later showed a linear decrease during both exercises. These VO2 kinetics were expressed by an approximate equation. The time constant expressing the exponential manner was about one minute on average in both exercises. The slope of the linearly decreasing phase of VO2 was significantly related to La at 100 watts during the decremental exercise. CONCLUSIONS: VO2 kinetics during decremental exercise after incremental exercise above the anaerobic threshold consists of at least three components: initial level, exponentially decreasing phase, and linearly decreasing phase.

Adult↗
PubMed1999

Kinetics of excess CO2 output during and after intensive exercise.

In order to clarify the kinetics of excess CO2 output during and after intensive exercise, six male subjects were each instructed to perform 40-, 60- and 80-s cycle ergometer exercises (282 +/- 9 W, 90 rpm). Ventilation and gas exchange parameters were recorded breath-by-breath, and lactate concentration (La) was repeatedly measured with blood samples from a finger tip. The increase in La from the resting value to peak value and the duration of exercise showed a significant linear relationship (r = 0.91, p<0.01) passing through zero, indicating that lactic acid was produced at a constant rate in working muscles from the beginning of exercise. However, in contrast to this increase in La, excess V.CO2, defined as the difference between V.CO2 and V.O2, showed a temporary negative value after the start of exercise. Subsequently, excess V.CO2 became positive, reaching a peak at 60 s post-exercise, and then decreased down to zero at about 9 min after the end of the 80-s exercise. End-tidal CO2 rose above the pre-exercise level during exercise and at about 3 min post-exercise, and thereafter remained below the pre-exercise level. Excess CO2, calculated by the sum of excess V. CO2 from the start of exercise to the 10th min after the end of exercise, was significantly COrrelated with the increase in La from resting to 10 min post-exercise (r = 0.88, p<0.01). These results suggest that although excessive CO2 output (excess CO2) in response to intensive exercise is related to the increase in lactic acid, the time course of excessive CO2 output (excess V.CO2) is delayed, relative to the production of lactic acid, and is affected by hyperventilation.

Adult↗