Biomedical subjects

Yoshiyuki Fukuba

Publications and source records attributed to Yoshiyuki Fukuba.

16 recordsLinked to original sources

PubMed2006

Central circulatory and peripheral O2 extraction changes as interactive facilitators of pulmonary O2 uptake during a repeated high-intensity exercise protocol in humans.

It has frequently been demonstrated that prior high-intensity exercise facilitates pulmonary oxygen uptake [Formula: see text] response at the onset of subsequent identical exercise. To clarify the roles of central O(2) delivery and/or peripheral O(2) extraction in determining this phenomenon, we investigated the relative contributions of cardiac output (CO) and arteriovenous O(2) content difference [Formula: see text] to the [Formula: see text] transient during repeated bouts of high-intensity knee extension (KE) exercise. Nine healthy subjects volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate 70-75% of peak power) separated by 6 min of rest. Throughout the protocol, continuous-wave Doppler ultrasound was used to measure beat-by-beat CO (i.e., via simultaneous measurement of stroke volume and the diameter of the arterial aorta). The phase II [Formula: see text] response was significantly faster and the slow component (phase III) was significantly attenuated during the second KE bout compared to the first. This was a result of increased CO during the first 30 s of exercise: CO contributing to 100 and 56% of the [Formula: see text] speeding at 10 and 30 s, respectively. After this, the contribution of [Formula: see text] became increasingly more predominant: being responsible to an estimated 64% of the [Formula: see text] speeding at 90 s, which rose to 100% by 180 s. This suggests that, while both CO and [Formula: see text] clearly interact to determine the [Formula: see text] response, the speeding of [Formula: see text] kinetics by prior high-intensity KE exercise is predominantly attributable to increases in [Formula: see text].

Adaptation, Physiological↗

PubMed2006

Effects of femoral vascular occlusion on ventilatory responses during recovery from exercise in human.

We investigated the effect of occluding of femoral blood flow on the post-exercise ventilatory response of both the sub- and supra-anaerobic threshold (AT) leg cycling in humans. Seven healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of 6 min constant-load upright cycling at either a sub-AT (80% of AT) or supra-AT (midway between AT and VO(2)max) work rate and a subsequent 6 min rest period either with or without femoral blood flow being occluded by a rapid cuff inflation to 250 Torr during the first 2 min of recovery. Blood lactate levels at the cessation of the sub- and supra-AT exercise averaged 1.8+/-0.2 and 4.9+/-0.4 mequiv.l(-1) (mean+/-S.E.M.), respectively. Compared to spontaneous recovery, the circulatory occlusion significantly reduced ventilation irrespective of the intensity of the preceding exercise. The relative contribution of the ventilatory deficit to the total spontaneous ventilation (defined as the difference between the cumulative ventilation with and without cuff inflation during the first 2 min of recovery) was significantly greater supra-AT (18.0+/-3.9%) than sub-AT (9.3+/-2.9%, P<0.05). The subsequent release of occlusion was accompanied by a rapid increase in ventilation that began on the first breath after release. We concluded that the relatively greater speeding of ventilatory decline with occlusion during the first 2 min of recovery from supra-AT exercise argues against a significant role for an intramuscular chemoreflex-induced hyperpnoea. Rather, mechanisms related to the hemodynamic effects of suddenly altered muscle perfusion seem more consistent with this phenomenon.

Adult↗

PubMed2006

Volitional hyperventilation during ramp exercise to exhaustion.

The purpose of this study was to determine whether volitional hyperventilation at 20 L x min(-1) above normal exercise values affected exercise duration while performing ramp exercise to exhaustion. Nine healthy subjects performed a ramp exercise test to exhaustion. On a subsequent test they hyperventilated, with the aid of visual and audio feedback, at 20 L x min(-1) greater than their initial test. Ramp exercise time to exhaustion was substantially reduced from 771.6 +/- 85.2 s to 726.6 +/- 86.6 s (p < 0.002) with the additional hyperventilation. Subjects underwent 2 more ramp exercise tests and performed a 5 s maximum voluntary ventilation or a forced vital capacity test at work rates corresponding to rest, below lactate threshold (LT), above LT, immediately after exercise, and 3 min recovery. Generally, the flow rates were not affected by exercise below LT and were enhanced during above-LT exercise, exhaustion, and recovery. This indicated a change in pulmonary function that is dependent on exercise intensity. In spite of this increased ability to generate high flow rates, exercise performance was diminished when respiratory muscle work was increased volitionally by 20 L x min(-1), indicating a strong coupling between respiratory muscle work and fatigue during ramp exercise in normal subjects.

Adult↗

PubMed2005

Vasoconstriction and blood flow responses in visceral arteries to mental task in humans.

The vascular responses to mental task in visceral arteries in humans have not been elucidated. We observed the responses in the renal (RA) and superior mesenteric (SMA) arteries to mental stress, using simultaneous pulsed and echo Doppler ultrasound flowmetry. Nine healthy females performed a computerized colour word conflict test (CWT) for 3 min. The mean blood velocity (MBV) in the right RA and SMA, heart rate (HR) and blood pressure were measured. The mean arterial pressure (MAP) was divided by the flow velocity to assess the vascular resistance (VR). The CWT significantly increased the MAP, HR and VR in both arteries from the first minute. During the CWT, flow in the RA decreased significantly at the third minute relative to baseline, while flow in the SMA showed no significant change from the first to the third minute. The degree of vasoconstriction in the RA bed was greater than that in the SMA bed. These results suggest that the mental task causes vasoconstriction in visceral arteries, and imply that it induces differential blood flow and vascular responses in visceral arteries.

Adult↗

PubMed2005

Kinetics of pulmonary VO2 and femoral artery blood flow and their relationship during repeated bouts of heavy exercise.

The mechanism that alters the pulmonary VO2 response to heavy-intensity exercise following prior heavy exercise has been frequently ascribed to an improvement in pre-exercise blood flow (BF) or O(2) delivery. Interventions to improve O(2) delivery have rarely resulted in a similar enhancement of VO2. However, the actual limb blood flow and VO2 dynamics in the second bout of repeated exercise remain equivocal. Seven healthy female subjects (21-32 years) performed consecutive 6-min (separated by 6 min of 10 W exercise) bilateral knee extension (KE) exercise in a semisupine position at a work rate halfway between the lactate threshold (LT) and VO2peak. Femoral artery blood flow (FBF) was measured by Doppler ultrasound simultaneously with breath-by-breath VO2 each protocol being repeated at least four times for precise kinetic characterization. The effective time-constant (tau') of the VO2 response was reduced following prior exercise (bout 1: 61.0 +/-10.5 vs. bout 2: 51.6+/-9.0 s; mean +/- SD; P<0.05), which was a result of a reduced slow component (bout 1: 16.0+/-8.0 vs. bout 2: 12.5+/-6.7 %; P<0.05) and an unchanged 'primary' tau. FBF was consistently faster than VO2. However, there was no bout-effect on tau' FBF (bout 1: 28.2+/-12.0 vs. bout 2: 34.2+/-8.5 s). The relationship between the exercise-associated VO2 (i.e., deltaVO2) and Delta FBF was similar between bouts, with a tendency (N.S: P>0.05) for deltaVO2/deltaFBF to be increased during the transition to bout 2 rather than decreased, as hypothesized. The return of VO2 kinetics toward first order, therefore, was associated with an 'appropriate', not enhanced, BF to the working muscles. Whether a relative prior-hyperemia in bout 2 enables a more homogeneous intramuscular distribution of BF and/or metabolic response is unclear, however, these data are consistent with events more proximal to the exercise muscle in mediating the VO2 response during repeated heavy-intensity KE exercise.

Adult↗

PubMed2004

Comparison of oxygen uptake kinetics during knee extension and cycle exercise.

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O(2) uptake (pVo(2)) kinetics and 2) to characterize the muscle blood flow, muscle Vo(2) (mVo(2)), and pVo(2) kinetics during KE to investigate the rate-limiting factor(s) of pVo(2) on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pVo(2) during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mVo(2) at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pVo(2) for both moderate and heavy exercise was higher during KE ( approximately 12 ml.W(-1).min(-1)) compared with CE ( approximately 10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mVo(2) during heavy KE [25.8 +/- 9.0 s (SD)] was not significantly different from that of the phase II pVo(2). Moreover, the slow component of pVo(2) evident for the heavy KE reflected the gradual increase in mVo(2). The initial LBF kinetics after onset of KE were significantly faster than the phase II pVo(2) kinetics (moderate: time constant LBF = 8.0 +/- 3.5 s, pVo(2) = 32.7 +/- 5.6 s, P < 0.05; heavy: LBF = 9.7 +/- 2.0 s, pVo(2) = 29.9 +/- 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pVo(2). These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pVo(2), consistent with an intramuscular limitation to Vo(2) kinetics, i.e., a microvascular O(2) delivery-to-O(2) requirement mismatch or oxidative enzyme inertia.

Adolescent↗

PubMed2004

Dissociation between the time courses of femoral artery blood flow and pulmonary VO2 during repeated bouts of heavy knee extension exercise in humans.

It has frequently been demonstrated that prior heavy cycling exercise facilitates pulmonary O(2) kinetics at the onset of subsequent heavy exercise. This might be due to improved muscle perfusion via acidosis-induced vasodilating effects. However, it is difficult to measure the blood flow (BF) to the working muscles (via the femoral artery) during cycling exercise. We therefore selected supine knee extension (KE) exercise as an alternative, and investigated whether the faster O(2) kinetics in the 2nd bout was matched by proportionally faster BF kinetics to the exercising muscle. Nine healthy subjects (aged 21-44 years) volunteered to participate in this study. The protocol consisted of two consecutive 6-min KE exercise bouts in a supine position (work rate: 70-75% of peak power) separated by a 6-min baseline rest (EX1 to EX2). During the protocol, a pulsed Doppler ultrasound technique was utilized to continuously measure the BF in the right femoral artery. The protocol was repeated at least 6 times to characterize the precise kinetics. In agreement with previous studies using cycling exercise, the O(2) kinetics in the 2nd bout were facilitated compared with that in the 1st bout [mean +/-s.d. of the 'effective' time constant (tau): EX1, 68.6 +/- 15.9, versus EX2, 58.0 +/- 14.4 s. Phase II-tau: EX1, 48.7 +/- 9.0, versus EX2, 41.2 +/- 13.3 s. Empirical index of the slow component (Delta O(2(6-3))): EX1, 78 +/- 44, versus EX2, 57 +/- 36 ml min(-1) (P < 0.05)]. However, no substantial difference was observed for the facilitation of the femoral artery BF response to the 1st and 2nd exercise bouts [i.e. the 'effective'tau of the femoral artery BF: EX1, 40.8 +/- 16.9, versus EX2, 39.0 +/- 17.1 s (P > 0.05)]. It was concluded that the faster pulmonary O(2) kinetics during heavy KE exercise following prior heavy exercise was not associated with a similar modulation in the BF to the working muscles.

Adult↗

PubMed2004

Pressor response to static and dynamic knee extensions at equivalent workload in humans.

Static exercise has been thought to induce greater pressor response than dynamic exercise, but in contrast it has been recently reported that repetitive muscle contraction recruiting small muscles evokes greater response than sustained contraction. It remained unknown whether sustained contraction induces greater pressor response if large muscles were recruited. Nine subjects performed three types of isometric knee extensions recruiting the large muscle group, i.e., 2-min sustained (20% and 40% maximal voluntary contraction [MVC]) and 4-min repetitive (40% MVC, duty cycle = 1:1 s) muscle contractions. Compared under the equivalent TTI and exercising duration (2 min), the changes in femoral arterial blood flow and VO(2) from baseline (Delta BF, Delta VO(2)) were significantly less during sustained contraction than during repetitive contraction (sustained vs. repetitive; Delta BF: +92 +/- 195 vs. +1,174 +/- 269 ml.min(-1), Delta VO(2): +53 +/- 12 vs. +180 +/- 32 ml.min(-1), mean +/- SE, p < 0.05), although the change in mean arterial pressure (Delta MAP) was greater during sustained contraction (+24 +/- 3 vs. +19 +/- 3 mmHg). Compared under the equivalent TTI and peak tension (40% MVC), Delta BF and Delta VO(2) were less and Delta MAP was greater during sustained contraction (Delta BF: -296 +/- 176 vs. +868 +/- 272 ml.min(-1); Delta VO(2): +104 +/- 16 vs. + 212 +/- 46 ml.min(-1); Delta MAP: +37 +/- 8 vs. +20 +/- 4 mmHg). Moreover Delta MAP during postexercise occlusion of the active limb was significantly greater after sustained contraction than after repetitive contraction (+17.0 +/- 2.8 vs. +9.5 +/- 4.4 mmHg). These results demonstrated that pressor response is greater during sustained than during repetitive contraction, recruiting a large muscle group. This finding should be mainly due to the greater accumulation of metabolites in active muscles during sustained contraction.

Adult↗

PubMed2003

Effects of priming exercise intensity on the dynamic linearity of the pulmonary VO(2) response during heavy exercise.

Prior heavy-intensity exercise facilitates the pulmonary oxygen uptake ( VO(2)) response during subsequent exercise, such that its kinetics returns towards first-order. To better understand this "priming" phenomenon, we investigated the effect of priming exercise, over a range of intensities, on the VO(2) response to heavy-intensity cycle ergometry at a work rate of Delta50% [halfway between lactate threshold (LT) and VO(2max)]. Eight subjects performed two consecutive 6-min bouts separated by 6 min at 20 W. The first bout was each of: no warm-up control (CON), sub-lactate threshold (LT) at 80% of LT, and three supra-LT conditions (Delta20%, Delta40%, and Delta60%). The VO(2) response during the subsequent bout was evaluated using the "effective" time constant (tau'), and the VO(2) difference between minutes 3 and 6 (Delta VO(2(6-3))). The goodness-of-fit, indicative of "first-order" kinetics, was determined by the residual profile, and the mean square of errors (MSEr). The heart rate and blood lactate concentration ([La]r) just prior to the second bout were also measured. Compared with CON, tau' and Delta VO(2(6-3)) were significantly reduced following all supra-LT priming bouts, while the goodness-of-fit was significantly improved following Delta40% exercise. Delta VO(2(6-3)) and [La]r were negatively correlated ( P<0.05), unlike HR. In conclusion, prior exercise just above, but not below, LT facilitated the VO(2) response in a threshold-like manner. Supra-LT priming exercise influenced the VO(2) response allowing it to return to within as little as 12% from first-order (compared to approximately 50% in CON). The associated increases in circulating lactate and/or related factors seem to be centrally involved in this phenomenon.

Adaptation, Physiological↗

PubMed2003

Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise.

The mechanism(s) underlying the attenuation of the slow component of pulmonary O2 uptake (Vo2) by prior heavy-intensity exercise is (are) poorly understood but may be ascribed to either an intramuscular-metabolic or a circulatory modification resulting from "priming" exercise. We investigated the effects of altering the circulatory dynamics by delayed vagal withdrawal to the circulation induced by the cold face stimulation (CFS) on the Vo2 kinetics during repeated bouts of heavy-intensity cycling exercise. Five healthy subjects (aged 21-43 yr) volunteered to participate in this study and initially performed two consecutive 6-min leg cycling exercise bouts (work rate: 50% of the difference between lactate threshold and maximal Vo2) separated by 6-min baseline rest without CFS as a control (N1 and N2). CFS was then applied separately, by gel-filled cold compresses to the face for 2-min spanning the rest-exercise transition, to each of the first bout (CFS1) or second bout (CFS2) of repeated heavy-intensity exercise. In the control protocol, Vo2 responses in N2 showed a facilitated adaptation compared with those in N1, mainly attributable to the reduction of slow component. CFS application successfully slowed and delayed the heart rate (HR) kinetics (P < 0.05) on transition to exercise [HR time constant; N1: 55.6 +/- 16.0 (SD) vs. CFS1: 69.0 +/- 12.8 s and N2: 55.5 +/- 11.8 vs. CFS2: 64.0 +/- 17.5 s]; however, it did not affect the "primary" Vo2 kinetics [Vo2 time constant; N1: 23.7 +/- 7.9 (SD) vs. CFS1: 20.9 +/- 3.8 s, and N2: 23.3 +/- 10.3 vs. CFS2: 17.4 +/- 6.3 s]. In conclusion, increased vagal withdrawal delayed and slowed the circulatory response but did not alter the Vo2 kinetics at the onset of supra-lactate threshold cycling exercise. As the facilitation of Vo2 subsequent to prior heavy leg cycling exercise is not attenuated by slowing the central circulation, it seems unlikely that this facilitation is exclusively determined by a blood flow-related mechanism.

Adult↗

PubMed2003

Intensity-dependent tolerance to exercise after attaining V(O2) max in humans.

The tolerable duration of high-intensity, constant-load cycle ergometry is a hyperbolic function of power, with an asymptote termed critical power (CP) and a curvature constant (W') with units of work. It has been suggested that continued exercise after exhaustion may only be performed below CP, where predominantly aerobic energy transfer can occur and W' can be partially replenished. To test this hypothesis, six volunteers each performed cycle-ergometer exercise with breath-by-breath determination of ventilatory and pulmonary gas exchange variables. Initially, four exercise tests to exhaustion were made: 1). a ramp-incremental and 2). three high-intensity constant-load bouts at different work rates, to estimate lactate (theta(L)) and CP thresholds, W', and maximum oxygen uptake (Vo2 max). Subsequently, subjects cycled to the limit of tolerance (for approximately 360 s) on three occasions, each followed by a work rate reduction to 1). 110% CP, 2). 90% CP, and 3). 80% theta(L) for a 20-min target. W' averaged 20.9 +/- 2.35 kJ or 246 +/- 30 J/kg. After initial fatigue, 110% CP was tolerated for only 30 +/- 12 s. Each subject completed 20 min at 80% theta(L), but only two sustained 20 min at 90% CP; the remaining four subjects fatigued at 577 +/- 306 s, with oxygen consumption at 89 +/- 8% Vo2 max. The results support the suggestion that replenishing W' after fatigue necessitates a sub-CP work rate. The variation in subjects' responses during 90% CP was unexpected but consistent with mechanisms such as reduced CP consequent to prior high-intensity exercise, variation in lactate handling, and/or regional depletion of energy substrates, e.g., muscle glycogen.

Adult↗

PubMed2003

The curvature constant parameter of the power-duration curve for varied-power exercise.

INTRODUCTION: The tolerable duration (t) for high-intensity cycle ergometry bears a hyperbolic relationship to the power output (P) with an asymptote termed the critical power (CP), and a curvature constant (W') that is numerically equivalent to an amount of work that can be performed above CP. The physiological nature of W' has received little consideration compared with CP, e.g., whether the total amount of work above CP remains constant when the power actually changes during the high-intensity task. PURPOSE: The purpose of this study was to compare W' derived from the standard estimation method, consisting of several different constant-P tests, and the total amount of work above CP during an exhausting exercise bout using a variable-P protocol. METHODS: Eleven healthy male subjects (age: 21-40 yr) volunteered to participate in this study. Each initially performed four-to-six high-intensity square-wave exercise bouts for estimation of CP [mean (SD); 213.3 (22.4) W] and W' [12.68 (3.08) kJ]. The subjects subsequently performed two variable-P tests to the limit of tolerance. During the first part, P was 117% or 134% of CP for a duration that expended approximately half of W'. The work rate was then abruptly increased to 134% (UP protocol) or decreased to 117% (DOWN protocol) of CP for the second part. RESULTS: There were no significant differences between W' [12.68 (3.08) kJ] and the total amount of work above CP during the UP [12.14 (4.18) kJ] and DOWN [12.72 (4.05) kJ] protocols (P > 0.05). CONCLUSION: We conclude that the work equivalent of W' is not affected by power variations during exhausting cycle ergometry, at least in the P range of 100-134% of CP.

Adult↗

PubMed2002

Relationship between the curvature constant parameter of the power-duration curve and muscle cross-sectional area of the thigh for cycle ergometry in humans.

For high-intensity cycle ergometer exercise, the relationship between power output ( P) and its tolerable duration ( t) has been well characterized by the hyperbolic relationship: ( P- theta;(F)). t=W', where theta;(F) has been termed the "critical power" or "fatigue threshold". The curvature constant (W') reflects a constant amount of work which can be performed above theta;(F), and it may be regarded as a muscle energy store. The relationship of this energy store to muscle mass is not known. Therefore, the purpose of this study was to determine the relationships among W', accumulated peak oxygen deficit (accumulated peak O(2)-deficit), and muscle cross-sectional area (CSA) of the thigh for high-intensity cycle ergometry in humans. A group of 17 healthy male subjects (aged 21-41 years) participated in this study. The theta;(F) and W' of the P- t hyperbolic relationship and the accumulated peak O(2)-deficit was calculated by standard procedures. The CSA of muscle, fat and bone in the right thigh were measured using ultrasonography. The mean (SD) of theta;(F), W', accumulated peak O(2)-deficit, and muscle CSA of the thigh were 200.0 (17.8) W, 12.60 (2.94) kJ, 2.29 (0.41) l, and 185.3 (22.6) cm(2), respectively. The muscle CSA of the thigh was positively correlated with W' ( r=0.59, P<0.01) and with accumulated peak O(2)-deficit ( r=0.54, P<0.05). The relationship between W' and accumulated peak O(2)-deficit also showed a positive correlation ( r=0.63, P<0.005). Our results indicated that W' derived from the P- t hyperbolic curve as anaerobic working capacity is related to the CSA of muscle.

Adult↗

PubMed2002

Effects of ischaemia on subsequent exercise-induced oxygen uptake kinetics in healthy adult humans.

Leg muscles were occluded (33 kPa) prior to exercise to determine whether the induced metabolic changes, and reactive hyperaemia upon occlusion release just prior to the exercise, would accelerate the subsequent oxygen consumption (VO2) response. Eight subjects performed double bouts (6 min duration, 6 min rest in-between) of square wave leg cycle ergometry both below and above their lactate threshold (LT). Prior to exercise, large blood pressure cuffs were put around the upper thighs. Occlusion durations were 0 min (control), 5 min and 10 min. Ischaemia was terminated within 5 s prior to exercise onset. Heart rate, VO2, ventilatory rate (V(E)), electromyogram (EMG) and haemoglobin/myoglobin (Hb/Mb) saturation were recorded continuously. Single exponential modelling demonstrated that, compared to control (time constant = 53.9 +/- 13.9 s), ischaemia quickened the VO2 response (P < 0.05) for the first bout of exercise above LT (time constant = 48.3 +/- 14.5 s) but not to any other exercise bout below or above LT. The 3-6 min integrated EMG (iEMG) slope was correlated to the 3-6 min VO2 slope (r = 0.73). Hb/Mb saturation verified the ischaemia but did not show a consistent relation to the VO2 time course. Reactive hyperaemia induced a faster VO2 response for work rates above LT. The effect, while significant, was not large considering the expected favourable metabolic and circulatory changes induced by ischaemia.

Adult↗

PubMed2002

VO(2) kinetics in heavy exercise is not altered by prior exercise with a different muscle group.

We examined whether lactic acidemia-induced hyperemia at the onset of high-intensity leg exercise contributed to the speeding of pulmonary O(2) uptake (VO(2)) after prior heavy exercise of the same muscle group or a different muscle group (i.e., arm). Six healthy male subjects performed two protocols that consisted of two consecutive 6-min exercise bouts separated by a 6-min baseline at 0 W: 1) both bouts of heavy (work rate: 50% of lactate threshold to maximal VO(2)) leg cycling (L1-ex to L2-ex) and 2) heavy arm cranking followed by identical heavy leg cycling bout (A1-ex to A2-ex). Blood lactate concentrations before L1-ex, L2-ex, and A2-ex averaged 1.7 +/- 0.3, 5.6 +/- 0.9, and 6.7 +/- 1.4 meq/l, respectively. An "effective" time constant (tau) of VO(2) with the use of the monoexponential model in L2-ex (tau: 36.8 +/- 4.3 s) was significantly faster than that in L1-ex (tau: 52.3 +/- 8.2 s). Warm-up arm cranking did not facilitate the VO(2) kinetics for the following A2-ex [tau: 51.7 +/- 9.7 s]. The double-exponential model revealed no significant change of primary tau (phase II) VO(2) kinetics. Instead, the speeding seen in the effective tau during L2-ex was mainly due to a reduction of the VO(2) slow component. Near-infrared spectroscopy indicated that the degree of hyperemia in working leg muscles was significantly higher at the onset of L2-ex than A2-ex. In conclusion, facilitation of VO(2) kinetics during heavy exercise preceded by an intense warm-up exercise was caused principally by a reduction in the slow component, and it appears unlikely that this could be ascribed exclusively to systemic lactic acidosis.

Acidosis, Lactic↗

PubMed2002

Dynamics of the heart rate response to sinusoidal work in humans: influence of physical activity and age.

The purpose of the present study was to define the influence of age and exercise training on the heart rate (HR) dynamic response (i.e. kinetics) to sinusoidal work. A total of 63 healthy subjects (31 men and 32 women; age range 19-69 years) underwent a three-step incremental work test, during which peak oxygen uptake (.V(O)(2peak)) was estimated by the YMCA method. Sinusoidal work varying between 20% and 60% of HR(reserve) was employed for periods of 1, 3, 6, 9 and 12 min. HR was monitored in a beat-by-beat manner with a cardiotachometer. The kinetics of the HR response were analysed by frequency analysis and estimated by a first-order transfer function with time constant (tau) and time delay (TD). Physical training status was estimated as stepping frequency, as measured with a pedometer during the daytime, and averaged over seven consecutive days. The mean response time of HR kinetics (HR(MRT): tau pulse TD) tended to increase gradually with age (0.36 s.year(-1)), and linear regression analysis revealed that the correlation between HR(MRT) and age was significant (r=0.31, P<0.05), although not as highly significant as that between HR(MRT) and physical activity (r=-0.48, P<0.0001). HR(MRT) was not related to the S.D. of HR variation (an indicator of parasympathetic mediation) at rest. In addition, .V(O)(2peak) showed a significantly greater correlation with age (r=-0.60, P<0.0001) than with physical activity (r=-0.14, not significant). In conclusion, these findings suggest that HR dynamics, which may depend on sympathetic nervous activity, are more sensitive to physical activity than to age, but that .V(O)(2peak), as estimated by the age-associated decline in maximum HR, is unrelated to physical training status.

Adult↗