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Biomedical subjects

B J Whipp

Publications and source records attributed to B J Whipp.

At least 55 records · Page 3Linked to original sources
PubMed1998

Effects of prior arm exercise on pulmonary gas exchange kinetics during high-intensity leg exercise in humans.

For moderate work rates (i.e. below the lactate threshold, theta), oxygen uptake (Vo2) approaches the steady state mono-exponentially. At higher work rates, the Vo2 kinetics are more complex, reflecting the delayed superimposition of an additional, slow component. The mechanisms of this 'slow' component are poorly understood. It has been demonstrated, however, that while a prior bout of supra theta L cycling (with a 6 min recovery) does not significantly affect the V02 time course for a subsequent sub-theta L bout, it significantly speeds the V02 response to a subsequent supra-theta L bout (Gausche, Harmon, Lamarra & Whipp, 1989; Gerbino, Ward & Whipp, 1996). These investigators proposed that this speeding was a result of improved muscle perfusion during the exercise transient, possibly related to the residual metabolic acidaemia still present at the start of the subsequent exercise bout. To determine whether speeding of the V02 kinetics could also be induced by a bout of prior high-intensity exercise performed at a remote site (e.g. the arms), subjects each performed two 6 min bouts of high-intensity cycling (leg exercise: LE) at a work rate equivalent to 50% of lambda le' (the difference between maximum V02,LE and theta L,LE). On one occasion this was preceded by a 6 min period of cycling at 50% lambda LE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50% lambda LE in each case, the work bouts were separated by 6 min of unloaded pedalling. Pulmonary gas exchange variables were derived breath-by-breath. During unloaded pedalling and at minute 6 of each work bout, arterialized venous blood samples were drawn from the dorsum of the heated hand or at the wrist for analysis of PH, lactate, pyruvate, noradrenaline (NAdr), adrenaline (Adr), and potassium (K+). The difference in V02 between minute 6 and 3 of each work bout (lambda V02 ¿6-3] and the 'partial' O2 deficit (O2 Def) provided indices of the slow phase of V02 kinetics. The initial AE and LE bouts resulted in similar degrees of metabolic (lactic) acidaemia; the residual acidaemia at the end of the subsequent 6 min recovery phase was also similar for the two protocols, as were [K+], [Adr¿ and [NAdr]. The subsequent LE bouts were associated with reductions in both lambda V02[6-3] and O2 Def, relative to control, with the effect being more marked when the work was preceded by a prior LE bout than a prior AE bout: lambda V02[6-3] averaging 32 and 56% of control, respectively, and O2 Def 71 and 81%. Consequently, the increase in [lactate] and decrease in PH induced in this second LE bout were smaller when preceded by prior leg exercise than prior arm exercise. It is therefore concluded that while metabolic acidaemia induced at a site remote from the legs is associated with a less prominent slow phase of the V02 kinetics for high-intensity leg exercise, a component specific to the involved contractile units appears to exert the dominant effect. The mechanisms underlying this response are, however, presently uncertain.

Adult↗
PubMed1998

Cardiopulmonary responses to exercise in patients with hypertrophic cardiomyopathy.

OBJECTIVE: To examine the submaximal and maximal indices of the exercise response of patients with hypertrophic cardiomyopathy. DESIGN AND SETTING: Prospective examination of cardiopulmonary responses to ramp exercise test of a consecutive group of patients with hypertrophic cardiomyopathy attending a cardiomyopathy outpatient clinic. METHODS: 50 patients aged 12 to 76 years (mean (SD) 35 (14)) with diagnosis of hypertrophic cardiomyopathy performed incremental cycle ergometry; 22 sedentary volunteers (seven female, 15 male) aged 14 to 58 years (mean (SD) 31 (12)) served as controls. Respiratory gas was continuously sampled from the mouth-piece, and its concentration profile phase aligned to the respired air flow signals. Following analogue to digital conversion, gas exchange variables were computed breath by breath and the data were averaged every 30 seconds for graphic display. A 12 lead ECG was monitored continuously and recorded every three minutes during the exercise. RESULTS: Both the peak oxygen uptake attained on the test (VO2 peak) and anaerobic threshold were reduced in patients with hypertrophic cardiomyopathy compared with the control group (p < 0.0001). In 29 patients (59%) the VO2 peak was less than 60% and only two patients achieved a peak above 80% of their predicted values. The anaerobic threshold was below 60% of the predicted value in 31 patients and above 80% in only three patients. The slope of oxygen uptake/work rate relation (delta VO2/delta WR) was decreased in 16 patients (32%). The maximum oxygen pulse (VO2/HR) was reduced as a percentage of the predicted value, and became flat at high work rates in 32 patients. There was a significant correlation between anaerobic threshold and VO2 peak (p < 0.0001), work efficiency (p < 0.0001), and maximum oxygen pulse (p < 0.0001). The slope of change in ventilation against change in carbon dioxide output (delta VE/delta VCO2) for the subanaerobic threshold range was increased in 36 patients (72%) and was inversely correlated with anaerobic threshold (p < 0.0002). CONCLUSIONS: There were severe abnormalities in maximal and submaximal indices of pulmonary gas exchange in a cohort of hypertrophic cardiomyopathy patients attending a referral cardiovascular clinic. The pattern of the abnormalities suggests that a reduced stroke volume response, ventilation/perfusion mismatch, and abnormal peripheral oxygen utilisation are the possible mechanisms of exercise intolerance.

Adolescent↗
PubMed1996

Changes in gas exchange kinetics with training in patients with spinal cord injury.

We examined the ability of patients with spinal cord injury to undergo adaptations to chronic exercise training (cycle ergometry) invoked by functional electrical stimulation (FES) of the legs. Nine such patients performed incremental and constant work rate exercise before and after exercise training. Exercise sessions averaged 2.1 +/- 0.4/wk, and consisted of 30 min/session of continuous FES recumbent cycling with increasing work rate as tolerated. Peak VO2 and peak work rate significantly improved with training. Peak VO2 was significantly correlated with peak heart rate both before and after training (r = 0.97 pre and 0.85 post, P < 0.01 for both). The time course of the VO2, VCO2 and VE responses to constant-load exercise (unloaded cycling) and in recovery (mean response time MRT) were very long prior to training, and became significantly faster following training. However, there was no correlation between percentage improvement in either MRTon or MRToff for VO2 and the percentage increase in peak VO2. Exercise tolerance in these patients with spinal cord injury appears to be a direct function of the ability to increase heart rate. Further, exercise training can elicit significant improvements in both exercise tolerance and in gas exchange kinetics, even when performed only twice per week. However, these improvements may be accomplished by different mechanisms.

Adaptation, Physiological↗
PubMed1996

Haemodynamic and metabolic responses of the lower limb after high intensity exercise in humans.

This study assessed blood flow in the common femoral, superficial femoral and profunda femoris arteries, the effects of vasodilator metabolites and changes in blood pressure and pulse during recovery after high intensity exercise (Wingate test). Mean common femoral artery flow increased sevenfold in response to the exercise. The subsequent decline in mean common femoral artery flow was mono-exponential with a mean time constant of 19 min. The post-exercise increase in profunda femoris artery flow (ninefold) was significantly greater than the superficial femoral artery flow (fourfold, P < 0.05). Systolic blood pressure and heart rate decreased monotonically throughout recovery. In contrast, diastolic blood pressure showed a significant fall below baseline at 3 min (P < 0.05) with a return to baseline at 60 min. The greatest drop below baseline (approximately 20 mmHg) occurred around 7 min. Lactate reached a maximum of 13.6 +/- 2.3 mmol -1 at 8 min (P < 0.05) and was still significantly above baseline at 60 min. pH remained below 7.2 until 20 min of recovery. The results demonstrate that following high intensity exercise, blood flow to the limbs appears to be controlled by complex interactions of various vaso-active metabolites, each contributing proportionally more at different times during recovery.

Adult↗
PubMed1996

Unaltered oxygen uptake kinetics at exercise onset with lower-body positive pressure in humans.

The purpose of this study was to determine the influence of a reduced skeletal muscle blood flow on oxygen uptake (VO2) kinetics at the onset of cycle ergometer exercise. Seven healthy subjects performed rest-to-exercise transitions with a lower-body positive pressure (LBPP) of 45 Torr. Two work rates were selected for each subject: a moderate intensity (VO2, approximately 1.9 l min-1; delta[lactate], approximately 1 mequiv l-1) below the estimated lactate threshold and a heavy intensity (VO2, approximately 2.6 l min-1; delta[lactate], approximately 3 mequiv l-1) above this threshold. Pulmonary gas exchange variables and ventilatory (VE) responses were computed breath-by-breath from mass spectrometer and turbine volume meter signals, respectively, and mean response times (MRT) calculated. Samples of 'arterialized' venous blood were used for the determination of [lactate], pH and [K+]. While the application of 45 Torr LBPP had no effects on VO2 kinetics during moderate exercise (MRT: 33.5 +/- 1.2 s at 45 Torr vs. 32.8 +/- 1.3 s at 0 Torr; P > 0.05) or on [lactate], pH or [K+], breathing frequency (f) was increased (P < 0.05) and tidal volume (VT) reduced (P < 0.05). The addition of LBPP during heavy exercise did not alter VO2 kinetics (MRT: 35.2 +/- 1.5 s at 45 Torr vs. 34.8 +/- 1.5 s at 0 Torr; P > 0.05), or [lactate], pH or [K+]. Although both the VE (via an increased f) and CO2 output (VCO2) were significantly greater with LBPP by approximately 30 l min-1 and approximately 500 ml min-1, respectively, end-tidal CO2 partial pressure was decreasing, suggesting an additional ventilatory stimulus. These data can be interpreted to suggest that oxygen delivery is not critically dependent upon blood flow to the working muscle at exercise onset, while LBPP-induced increases in VE during suprathreshold exercise may be related to an accumulation of metabolites at the working muscle or the effects of pressure per se.

Adult↗
PubMed1996

Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans.

The effects of prior exercise on O2 uptake (VO2) kinetics during supra-lactate threshold (LT) cycling were assessed in 11 subjects. Protocols consisted of two consecutive 6-min work bouts separated by 0 W (6 min) with 1) both bouts sub-LT, 2) both bouts supra-LT, 3) bout 1 sub-LT and bout 2 supra-LT, and 4) bout 1 supra-LT and bout 2 sub-LT. Sub-LT VO2 kinetics were similar whether the prior bout was supra- or sub-LT. The VO2 kinetics for supra-LT work preceded by a sub-LT "warm-up" were similar to those for supra-LT work that was not preceded by exercise (O-W warm-up): the "partial": O2 deficit averaged 2.64 vs. 2.57 liters, and the "effective" VO2 time constant averaged 56 vs. 65 s. Exercise responses (i.e., the change between O W and minute 6 of exercise) were unaffected for lactate concentration (4.58 vs. 4.50 meq/l), pH (-0.08 vs. -0.10), and CO2 output (VCO2; 2.65 vs. 2.49 l/min). However, when the supra-LT work was preceded by a supra-LT warm-up, VO2 kinetics were appreciably faster (O2 deficit = 1.82 liters, VO2 time constant = 37 s) relative to 0-W warm-up; the lactate (0.69 meq/l), pH (-0.01), and VCO2 (2.08 l/min) responses were smaller; and the effective VCO2 time constant was longer (58 vs. 43 s). The mechanism(s) that underlie this speeding of the VO2 kinetics cannot be firmly established, but we suggest that an improved muscle perfusion during the exercise may be involved consequent to the residual metabolic acidemia from the high-intensity warm-up.

Acidosis↗
PubMed1996

Estimating exercise stroke volume from asymptotic oxygen pulse in humans.

Noninvasive techniques have been devised to estimate cardiac output (Q) during exercise to obviate vascular cannulation. However, although these techniques are noninvasive, they are commonly not nonintrusive to subjects' spontaneous ventilation and gas-exchange responses. We hypothesized that the exercise stroke volume (SV) and, hence, Q might be accurately estimated simply from the response pattern of two standardly determined variables: O2 uptake (VO2) and heart rate (HR). Central to the theory is the demonstration that the product of Q and mixed venous O2 content is virtually constant (k) during steady-state exercise. Thus from the Fick equation, VO2 = Q.CaCO2-k, where CaCO2 is the arterial CO2 content, the O2 pulse (O2-P) equals SV.CaCO2-(k/HR). Because the arterial O2 content (CaO2) is usually relatively constant in normal subjects during exercise, O2-P should change hyperbolically with HR, asymptoting at SV.CaO2. In addition, because the asymptotic O2-P equals the slope (S) of the linear O2-HR relationship, exercise SV may be predicted as S/CaO2. We tested this prediction in 23 normal subjects who underwent a 3-min incremental cycle-ergometer test with direct determination of CaO2 and mixed venous O2 content from indwelling catheters. The predicted SV closely reflected the measured value (r = 0.80). We therefore conclude that, in normal subjects, exercise SV may be estimated simply as five times S of the linear VO2-HR relationship (where 5 is approximately 1/CaO2).

Cardiac Output↗
PubMed1995

Excessive oxygen deficit during low-level exercise in heart failure.

Although peak oxygen consumption is reduced in patients with symptomatic heart failure, the degree of limitation during routine activity often appears greater or lesser than expected from peak capacity. This study was undertaken to determine whether abnormalities could be detected during the initiation of steady-state low-level exercise, approximating routine activity, which were distinct from limitation in peak capacity. We sought to determine whether a delay in the integrated response to the increased metabolic demand caused by exercise, assessed by the oxygen deficit incurred between exercise initiation and the achievement of steady-state oxygen uptake, was present in heart failure. Low-level and symptom-limited maximal exercise tests in 33 ambulatory patients with heart failure were analyzed and compared with 9 tests in control subjects. Oxygen deficit was determined during the 8-minute low-level exercise at 20 W. During maximal exercise, as expected, patients with heart failure had lower peak oxygen uptake (16 +/- 4 vs 31 +/- 6 ml/kg/min) and anaerobic threshold (870 +/- 270 vs 1,180 +/- 370 ml/min) than controls. After 8 minutes of low-level exercise, the oxygen deficit was higher in patients than in controls (550 +/- 230 vs 270 +/- 100 ml, respectively, p < 0.01). Among patients with heart failure, the oxygen deficit did not correlate with peak oxygen uptake or anaerobic threshold. Although the time to steady-state heart rate was later in patients with heart failure, this delay did not correlate with oxygen deficit. The oxygen deficit represents a distinct abnormality of exercise response that may reflect impaired central and peripheral responses to the initiation of exercise.

Adult↗
PubMed1995

Obligatory anaerobiosis resulting from oxygen uptake-to-blood flow ratio dispersion in skeletal muscle: a model.

We constructed a computer model whereby the dispersion of the oxygen uptake-to-blood flow ratio (VO2/Q) in working muscle could be altered around its mean level during simulated exercise. The model incorporated standard values for the cardiac output and whole-body O2 uptake responses to incremental exercise in humans. Dispersion of the VO2/Q ratio was induced by distributing Q in a Gaussian fashion around its appropriate mean value with a standard deviation (sigma). By increasing sigma, more regions of the muscle became "anaerobic" as the corresponding local muscle venous blood O2 content fell to zero; these regions thus required proportionally greater rates of lactate production to sustain the required energy transfer. The model yielded a relatively high mixed-muscle venous partial pressure of O2, suggesting that the latter may not be a sufficient indicator of whether or not there may be diffusional limitation to muscle O2 transfer during exercise or whether or not there may be anaerobic production of lactate in certain regions of exercising muscle.

Anaerobiosis↗
PubMed1995

Vascular distension in muscles contributes to respiratory control in sheep.

It has recently been proposed that afferent fibers from skeletal muscle could sense the state of the microvascular circulation, linking ventilation to the degree of peripheral perfusion or vascular distension (Huszczuk et al., Respir. Physiol., 91:207-226, 1993). Ventilatory and circulatory responses to manipulation of peripheral vascular pressures in the hind limbs of anaesthetized (sodium thiopental) sheep were examined. Inflatable balloons were placed at the caudal ends of the abdominal aorta and the vena cava (Vc). Aortic (Ao) occlusion induced a consistent normocapnic decrease in minute ventilation (VE). In contrast, VE increased significantly during vena cava obstruction, leading to hypocapnia. Small changes in systemic blood pressure were observed (+7 mmHg for Ao occlusion and -12 mmHg during Vc obstruction). Moreover, inflation of the caval balloon superimposed on a previously established Ao occlusion, preventing venous drainage of anastomotic inflow, resulted in a significant rise in distal vascular pressures with trivial changes in systolic blood pressure. This led to a gradual rise of VE, despite further reduction of the CO2 flux to the lungs. The subsequent deflation of the aortic balloon, exposing the hindlimb vasculature to aortic pressure, resulted in an even more profound hypocapnic hyperpnea. The concurrent arterial blood pressure changes were too small to possibly involve the ventilatory component of the arterial baroreflex. We therefore hypothesize, that perfusion-related afferent signals within the muscles could contribute to respiratory homeostasis by maintaining ventilation of the lungs commensurate with the circulatory state of the muscular apparatus.

Afferent Pathways↗
PubMed1995

Gas exchange kinetics during functional electrical stimulation in subjects with spinal cord injury.

We examined the kinetics of VO2, VCO2, and VE following the onset of unloaded leg cycling, and in recovery, in six patients with spinal cord injury (SCI). Exercise was produced by functional electrical stimulation (FES) of the quadriceps, hamstrings, and gluteal muscles. End-exercise VO2 (1.03 +/- 0.16 l.min-1), VCO2 (1.20 +/- 0.22 l.min-1) and VE (41 +/- 10 l.min-1) were elevated compared to values typically seen in healthy ambulatory subjects performing similar unloaded cycling. Mean response times for the on transients (MRTon) were both long and variable across subjects for VO2 (165 +/- 62 s), VCO2 (173 +/- 58 s), and VE (202 +/- 61 s). Recovery kinetics showed much less intersubject variability, and for five of six subjects were faster than the equivalent exercise MRT for all three variables (MRToff for VO2 of 103 +/- 28 s, VCO2 136 +/- 20 s, and VE 144 +/- 34 s), but P > 0.05 for all three. Size of the O2 deficit (1.96 +/- 0.90 l) and end-exercise lactate (7.05 +/- 1.65 mmol.l-1) were similar to values reported for healthy sedentary subjects performing maximal voluntary exercise, but the end-exercise heart rate (102 +/- 16 bpm) was lower than expected for this intensity of exercise. In conclusion, FES-induced unloaded cycling leads to exaggerated responses of pulmonary gas exchange and long time constants in patients with SCI. The delayed kinetics may be due in part to a blunted increase in heart rate in addition to severe deconditioning.

Adult↗
PubMed1994

Dynamic asymmetries of cardiac output transients in response to muscular exercise in man.

1. We determined the kinetics of cardiac output (Q) with respect to oxygen uptake (VO2) at the on- and off-transients of constant-load exercise. Six subjects performed constant-load exercise which consisted of 5 min rest, 5 min one-legged pedalling at 50 W and a 5 min recovery period. 2. The transient responses were characterized by first-order kinetics. There was no significant difference between the time constants for VO2 (tau VO2) at the on- (33.9 +/- 3.5 s, mean +/- S.E.M.) and off-transient (37.2 +/- 2.9 s). The time constant for Q (tau Q, 29.4 +/- 3.2 s) was consistently shorter than tau VO2 at the on-transient. However, tau Q was appreciably longer at the off-transient (44.3 +/- 3.6 s) than the on-transient. 3. The results support the contention that the time constant for the on-transient of Q is appreciably faster than that for VO2 and hence there seems little justification for the notion that the time constants for the kinetics of VO2 are determined by the limitations of blood flow in the transient. The asymmetry of Q kinetics, with the off-transient tau Q being appreciably slower than the on-transient tau Q, serves to maintain a sufficiently high oxygen flow to the muscle during recovery from exercise at a time when the muscle oxygen uptake remains high.

Cardiac Output↗
PubMed1994

Effects of infused epinephrine on slow phase of O2 uptake kinetics during heavy exercise in humans.

We tested the hypothesis that infused epinephrine (Epi) would augment the slow phase of oxygen uptake (VO2) during heavy exercise. Six normal healthy males initially performed a ramp test on a cycle ergometer to estimate the lactate threshold (LT) and determine peak VO2. Each subject then performed two 20-min constant-load tests at a power output calculated to elicit a VO2 equal to estimated LT + 0.2(peak VO2--estimated LT) under control conditions throughout and with an intravenous infusion of Epi from minutes 10 to 20 at a rate of 100 ng.kg-1.min-1. Pulmonary gas exchange variables were determined breath by breath. Arterialized venous blood was repeatedly sampled from the dorsum of the heated hand. Epi infusion elevated (P < 0.05) plasma Epi concentration (i.e., from 420 +/- 130 pg/ml at minute 10 to 2,190 +/- 410 pg/ml at minute 20) but had no effect on plasma norepinephrine or K+ concentrations. Concentrations of blood lactate and pyruvate were increased, pH was decreased, and base excess became more negative by infusion of Epi (P < 0.05). Epi infusion increased (P < 0.05) CO2 production and the respiratory exchange ratio but had no effect on ventilation or VO2. VO2 increased (P < 0.05) to the same extent in both control (3.14 +/- 0.12 l/min at minute 10, 3.28 +/- 0.12 l/min at minute 20) and Epi infusion (3.10 +/- 0.11 l/min at minute 10, 3.25 +/- 0.11 l/min at minute 20) trials. We therefore concluded that neither Epi nor its associated humoral consequences contribute significantly to the slow phase of VO2 kinetics during heavy exercise.

Adult↗