The effect of prior heavy exercise on the parameters of the power-duration curve for cycle ergometry.

The tolerable duration (t) of high-intensity cycle ergometry is well characterized by a hyperbolic function of power output (P) with an asymptote (termed the critical power (CP)) and a curvature constant (denoted W'). The purpose of this study was to investigate the effect of prior heavy exercise (W-up) that specifically engenders an acidosis on CP and W'. Eight healthy subjects performed 2 sets of 4 high-intensity square-wave exercise bouts on a bicycle ergometer to estimate CP and W', with (W-up) and without (control) prior exercise, respectively. Exercise intensities of the 4 main bouts were selected in the range of 90% to 135% peak oxygen uptake so as to reach the limit of tolerance between approximately 1.5 and 10 min. The W-up bout was preceded by 6 min cycling at a work rate halfway between the lactate threshold and peak oxygen uptake (mean +/- SD of 153.8 +/- 29.8 W) starting 12 min before the main bout. Blood lactate levels ([La]b) just before the main exercise bouts in W-up conditions were significantly higher than those of the control (4.7 +/- 1.1 and 1.4 +/- 0.4 mEq.L(-1), respectively; p < 0.05). However, there were no significant differences in end-exercise [La]b. W-up increased significantly the tolerable duration at every work rate compared with the control, which was attributable exclusively to increased CP (176.5 +/- 34.3 and 168.7 +/- 31.3 W, respectively; p < 0.05), without any significant change in W' (11.0 +/- 3.2 and 11.0 +/- 3.1 kJ, respectively). It is concluded that the prior heavy exercise improved performance mainly because of an enhanced aerobic component of exercise energetics, as indicated by a higher CP and lower increment in the [La]b.

Effects of posture on peripheral vascular responses to lower body positive pressure.

We tested the hypothesis that peripheral vascular responses (in the lower and upper limbs) to application of lower body positive pressure (LBPP) are dependent on the posture of the subjects. We measured heart rate, stroke volume, mean arterial pressure, leg and forearm blood flow (using the Doppler ultrasound technique), and leg (LVC) and forearm (FVC) vascular conductance in 11 subjects (9 men, 2 women) without and with LBPP (25 and 50 mmHg) in supine and upright postures. Mean arterial pressure increased in proportion to increases in LBPP and was greater in supine than in upright subjects. Heart rate was unchanged when LBPP was applied to supine subjects but was reduced in upright ones. Leg blood flow and LVC were both reduced by LBPP in supine subjects [LVC: 4.8 (SD 4.0), 3.6 (SD 3.5), and 1.4 (SD 1.8) ml.min(-1).mmHg(-1) before LBPP and during 25 and 50 mmHg LBPP, respectively; P < 0.05] but were increased in upright ones [LVC: 2.0 (SD 1.2), 3.4 (SD 3.4), and 3.0 (SD 2.0) ml.min(-1).mmHg(-1), respectively; P < 0.05]. Forearm blood flow and FVC both declined when LBPP was applied to supine subjects [FVC: 1.3 (SD 0.6), 1.0 (SD 0.4), and 0.9 (SD 0.6) ml. min(-1).mmHg(-1), respectively; P < 0.05] but remained unchanged in upright ones [FVC: 0.7 (SD 0.4), 0.7 (SD 0.4), and 0.6 (SD 0.5) ml.min(-1).mmHg(-1), respectively]. Together, these findings indicate that the leg vascular response to application of LBPP is posture dependent and that the response differs in the lower and upper limbs when subjects assume an upright posture.

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.

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].

Effects of wheelchair training on VO2 kinetics in the participants with spinal-cord injury.

PURPOSE: We tested the hypothesis that, in eight participants (seven males, one female; 46.5 +/- 8.3 years) with spinal-cord injury (complete lesions, T7-L1), the effects of exercise training on pulmonary O2 uptake (VO2) on- and off-kinetics would appear early in this pilot study. METHODS: The subjects underwent the wheelchair-training program (3 day/w, 30 min/day, and 50% HRreserve), and were evaluated before training ("time 0", T0), and after 7 (T7), 15 (T15), 30 (T30), and 60 (T60) days of training. Breath-by-breath peak VO2 was determined during the incremental exercise until their exhaustion. At another day following the incremental exercise, the subjects performed three repetitions of a constant exercise at 50% peak VO2 workload so that VO2 could be determined for both on- and off-kinetics. RESULTS AND CONCLUSION: Peak VO2 showed a tendency to increase with training; the increases became significant at T30. The time constants (tau 2) during "phase II" of the VO2 on-kinetics were 62.4 +/- 13.0 (s) (T0), 51.2 +/- 8.7 (T7), 46.1 +/- 7.4 (T15), 45.0 +/- 7.2 (T30), and 43.4 +/- 6.4 (T60); a significant difference compared to T0 was observed from T7 onward. The same pattern of change as a function of training was described for the VO2 off-kinetics. It is concluded that in SCI participants, the acceleration of VO2 kinetics at the onset of exercise was observed over a short term.

Comparison of cardiovascular responses between lower body negative pressure and head-up tilt.

To investigate local blood-flow regulation during orthostatic maneuvers, 10 healthy subjects were exposed to -20 and -40 mmHg lower body negative pressure (LBNP; each for 3 min) and to 60 degrees head-up tilt (HUT; for 5 min). Measurements were made of blood flow in the brachial (BF(brachial)) and femoral arteries (BF(femoral)) (both by the ultrasound Doppler method), heart rate (HR), mean arterial pressure (MAP), cardiac stroke volume (SV; by echocardiography), and left ventricular end-diastolic volume (LVEDV; by echocardiography). Comparable central cardiovascular responses (changes in LVEDV, SV, and MAP) were seen during LBNP and HUT. During -20 mmHg LBNP, -40 mmHg LBNP, and HUT, the following results were observed: 1) BF(brachial) decreased by 51, 57, and 41%, and BF(femoral) decreased by 40, 53, and 62%, respectively, 2) vascular resistance increased in the upper limb by 110, 147, and 85%, and in the lower limb by 76, 153, and 250%, respectively. The increases in vascular resistance were not different between the upper and lower limbs during LBNP. However, during HUT, the increase in the lower limb was much greater than that in the upper limb. These results suggest that, during orthostatic stimulation, the vascular responses in the limbs due to the cardiopulmonary and arterial baroreflexes can be strongly modulated by local mechanisms (presumably induced by gravitational effects).

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.

Modulation of arterial baroreflex dynamic response during mild orthostatic stress in humans.

We tested the hypothesis that in humans, carotid-baroreflex dynamic responses (evaluated by examining the time course of the carotid-baroreflex-induced alterations in muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) would be altered during mild orthostatic stress in ways that serve to limit orthostatic hypotension. In 12 healthy subjects (10 male, 2 female), 5-s periods of neck pressure (NP) (50 mmHg) and neck suction (NS) (-60 mmHg) were used to evaluate carotid baroreflex function at rest (CON) and during lower body negative pressure (LBNP) (-15 mmHg). During LBNP (as compared with CON) (a) the augmentations in MSNA and MAP elicited by NP were greater, (b) the NS-induced period of MSNA suppression was, if anything, shorter, (c) the peak decrement in MAP elicited by NS, although not different in amplitude, occurred earlier and recovered to its initial level more quickly after NS, and (d) the HR responses to NP and NS were greater. These results suggest that during mild orthostatic stress, carotid-baroreflex dynamic responses are modulated in ways that should help maintain blood pressure and limit orthostatic hypotension.

Modulation of arterial baroreflex control of muscle sympathetic nerve activity by muscle metaboreflex in humans.

We aimed to investigate the interaction [with respect to the regulation of muscle sympathetic nerve activity (MSNA) and blood pressure] between the arterial baroreflex and muscle metaboreflex in humans. In 10 healthy subjects who performed a 1-min sustained handgrip exercise at 50% maximal voluntary contraction followed by forearm occlusion, arterial baroreflex control of MSNA (burst incidence and strength and total activity) was evaluated by analyzing the relationship between beat-by-beat spontaneous variations in diastolic arterial blood pressure (DAP) and MSNA both during supine rest (control) and during postexercise muscle ischemia (PEMI). During PEMI (vs. control), 1) the linear relationship between burst incidence and DAP was shifted rightward with no alteration in sensitivity, 2) the linear relationship between burst strength and DAP was shifted rightward and upward with no change in sensitivity, and 3) the linear relationship between total activity and DAP was shifted to a higher blood pressure and its sensitivity was increased. The modification of the control of total activity that occurs in PEMI could be a consequence of alterations in the baroreflex control of both MSNA burst incidence and burst strength. These results suggest that the arterial baroreflex and muscle metaboreflex interact to control both the occurrence and strength of MSNA bursts.

Modulation of arterial baroreflex dynamic response during muscle metaboreflex activation in humans.

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflexes (as reflected by alterations in the dynamic responses shown by muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) in humans. In nine healthy subjects (eight male, one female) who performed a sustained 1 min handgrip exercise at 50 % maximal voluntary contraction followed by forearm occlusion, a 5 s period of neck pressure (NP) (30 and 50 mmHg) or neck suction (NS)(-30 and -60 mmHg) was used to evaluate carotid baroreflex function at rest (CON) and during post-exercise muscle ischaemia (PEMI). In PEMI (as compared with CON): (a) the augmentations in MSNA and MAP elicited by 50 mmHg NP were both greater; (b) MSNA seemed to be suppressed by NS for a shorter period, (c) the decrease in MAP elicited by NS was smaller, and (d) MAP recovered to its initial level more quickly after NS. However, the HR responses to NS and NP were not different between PEMI and CON. These results suggest that during muscle metaboreflex activation, the dynamic arterial baroreflex response is modulated, as exemplified by the augmentation of the MSNA response to arterial baroreflex unloading (i.e. NP) and the reduction in the suppression of MSNA induced by baroreceptor stimulation (i.e. NS).