Left ventricular hemodynamics during exercise recovery

1990 ◽  
Vol 69 (1) ◽  
pp. 104-111 ◽  
Author(s):  
E. C. Johnson ◽  
T. L. Hudson ◽  
E. R. Greene

The directional response of human left ventricular stroke volume during exercise recovery is unclear. Stroke volume has been reported to increase and decrease over exercise values during early recovery. The confounding variable may be posture. With the use of pulsed Doppler ultrasound, we tested the hypothesis that there is a significant difference between seated and supine stroke index (SI) during passive recovery from seated ergometer exercise. Thirteen subjects aged 26 +/- 2 yr performed two seated cycle ergometer exercise tests to 70% of predicted maximum heart rate (HR). Recovery was supine on one test and seated on the other. Cardiac index (CI), HR, and SI were calculated during rest, exercise, and 10 min of recovery. At rest, SI and CI were significantly (P less than 0.01) less and HR significantly (P less than 0.01) greater when the subjects were seated than when they were supine. At the last exercise work load, no significant differences were found in any measured variable between tests. During recovery, supine SI was maximal 180 s postexercise (99 +/- 14 ml/m2) and exceeded (P less than 0.01) resting supine (81 +/- 14 ml/m2) and peak exercise (77 +/- 14 ml/m2) SI by 22 and 29%, respectively. Seated SI was constant at peak exercise levels for 2 min. Seated and supine recovery CI never exceeded exercise values. Systolic and diastolic blood pressure recovery curves were similar in the two postures. We conclude that posture significantly affects SI during recovery from submaximal seated exercise. These results have implications for choice of recovery posture after stress testing in cardiac patients where it is desirable to minimize ventricular loading.

1997 ◽  
Vol 83 (3) ◽  
pp. 948-957 ◽  
Author(s):  
Kenneth R. Turley ◽  
Jack H. Wilmore

Turley, Kenneth R., and Jack H. Wilmore. Cardiovascular responses to treadmill and cycle ergometer exercise in children and adults. J. Appl. Physiol. 83(3): 948–957, 1997.—This study was conducted to determine whether submaximal cardiovascular responses at a given rate of work are different in children and adults, and, if different, what mechanisms are involved and whether the differences are exercise-modality dependent. A total of 24 children, 7 to 9 yr old, and 24 adults, 18 to 26 yr old (12 males and 12 females in each group), participated in both submaximal and maximal exercise tests on both the treadmill and cycle ergometer. With the use of regression analysis, it was determined that cardiac output (Q˙) was significantly lower ( P ≤ 0.05) at a given O2 consumption level (V˙o 2, l/min) in boys vs. men and in girls vs. women on both the treadmill and cycle ergometer. The lower Q˙ in the children was compensated for by a significantly higher ( P ≤ 0.05) arterial-mixed venous O2difference to achieve the same or similarV˙o 2. Furthermore, heart rate and total peripheral resistance were higher and stroke volume was lower in the children vs. in the adult groups on both exercise modalities. Stroke volume at a given rate of work was closely related to left ventricular mass, with correlation coefficients ranging from r = 0.89–0.92 and r = 0.88–0.93 in the males and females, respectively. It was concluded that submaximal cardiovascular responses are different in children and adults and that these differences are related to smaller hearts and a smaller absolute amount of muscle doing a given rate of work in the children. The differences were not exercise-modality dependent.


1998 ◽  
Vol 85 (2) ◽  
pp. 484-489 ◽  
Author(s):  
James M. Hagberg ◽  
Andrew P. Goldberg ◽  
Loretta Lakatta ◽  
Frances C. O’Connor ◽  
Lewis C. Becker ◽  
...  

To determine whether expanded intravascular volumes contribute to the older athlete’s higher exercise stroke volume and maximal oxygen consumption (V˙o 2 max), we measured peak upright cycle ergometry cardiac volumes (99mTc ventriculography) and plasma (125I-labeled albumin) and red cell (NaCr51) volumes in 7 endurance-trained and 12 age-matched lean sedentary men. The athletes had ∼40% higherV˙o 2 max values than did the sedentary men and larger relative plasma (46 vs. 38 ml/kg), red cell (30 vs. 26 ml/kg), and total blood volumes (76 vs. 64 ml/kg) (all P < 0.05). Athletes had larger peak cycle ergometer exercise stroke volume indexes (75 vs. 57 ml/m2, P < 0.05) and 17% larger end-diastolic volume indexes. In the total group,V˙o 2 maxcorrelated with plasma, red cell, and total blood volumes ( r = 0.61–0.70, P < 0.01). Peak exercise stroke volume was correlated directly with the blood volume variables ( r = 0.59–0.67, P < 0.01). Multiple regression analyses showed that fat-free mass and plasma or total blood volume, but not red cell volume, were independent determinants ofV˙o 2 max and peak exercise stroke volume. Plasma and total blood volumes correlated with the stroke volume and end-diastolic volume changes from rest to peak exercise. This suggests that expanded intravascular volumes, particularly plasma and total blood volumes, contribute to the higher peak exercise left ventricular end-diastolic volume, stroke volume, and cardiac output and hence the higherV˙o 2 max in master athletes by eliciting both chronic volume overload and increased utilization of the Frank-Starling effect during exercise.


1986 ◽  
Vol 251 (6) ◽  
pp. H1101-H1105 ◽  
Author(s):  
G. D. Plotnick ◽  
L. C. Becker ◽  
M. L. Fisher ◽  
G. Gerstenblith ◽  
D. G. Renlund ◽  
...  

To evaluate the extent to which the Frank-Starling mechanism is utilized during successive stages of vigorous upright exercise, absolute left ventricular end-diastolic volume and ejection fraction were determined by gated blood pool scintigraphy at rest and during multilevel maximal upright bicycle exercise in 30 normal males aged 26-50 yr, who were able to exercise to 125 W or greater. Left ventricular end-systolic volume, stroke volume, and cardiac output were calculated at rest and during each successive 3-min stage of exercise [25, 50, 75, 100, and 125–225 W (peak)]. During early exercise (25 W), end-diastolic and stroke volumes increased (+17 +/- 1 and +31 +/- 4%, respectively), with no change in end-systolic volume. With further exercise (50–75 W) end-diastolic volume remained unchanged as end-systolic volume decreased (-12 +/- 4 and -24 + 5%, respectively). At peak exercise end-diastolic volume decreased to resting level, stroke volume remained at a plateau, and end-systolic volume further decreased (-48 +/- 7%). Thus the Frank-Starling mechanism is used early in exercise, perhaps because of a delay in sympathetic mobilization, and does not appear to play a role in the later stages of vigorous exercise.


1991 ◽  
Vol 69 (2) ◽  
pp. 254-261 ◽  
Author(s):  
R. S. McKelvie ◽  
N. L. Jones ◽  
G. I. F. Heigenhauser

β-Adrenoceptor blockers are widely used clinically and can be classified as nonselective (β1 and β2) or selective (β1). Impairment of exercise performance is a well-known side effect of this group of drugs. This paper reviews mechanisms that could potentially be responsible for this impairment. In addition to cardiovascular and metabolic effects, β -blockade inhibits Na+–K+ ATPase pumps controlling ion movement between muscle and plasma and thus may contribute to muscle fatigue through this mechanism. To investigate the relationship between the change in plasma [K+] and exercise performance, we studied healthy male subjects taking propranolol. Eight subjects performed maximal incremental cycle ergometer exercise tests during control (no drug), low dose (LD) (40 mg daily), and high dose (HD) (265 ± 4.3 (SE) mg daily) of propranolol. The control plasma [K+] (5.8 ± 0.12 mequiv./L) during exercise was significantly lower than either the LD (6.4 ± 0.05 mequiv./L) or HD (6.1 ± 0.16 mequiv./L) values. There was no significant difference between plasma [K+] for the LD and HD of propranolol. However, maximum oxygen uptake was reduced only while taking the HD of propranolol. Six of the subjects also performed three 30-s bouts of high intensity exercise on an isokinetic cycle ergometer while taking the LD and HD of propranolol. There was no significant difference between doses for the increase in plasma [K+] (LD, 7.8 ± 0.35 mequiv./L vs. HD, 7.6 ± 0.36 mequiv./L) during exercise. However, exercise performance was significantly reduced during HD compared with LD. These results suggest that the increases in plasma [K+] with propranolol did not play a direct significant role in the reduced performance observed during the HD.Key words: exercise, potassium, performance, lactate.


1997 ◽  
Vol 83 (3) ◽  
pp. 712-717 ◽  
Author(s):  
Antonio C. L. Nóbrega ◽  
Jon W. Williamson ◽  
Jorge A. Garcia ◽  
Jere H. Mitchell

Nóbrega, Antonio C. L., Jon W. Williamson, Jorge A. Garcia, and Jere H. Mitchell. Mechanisms for increasing stroke volume during static exercise with fixed heart rate in humans. J. Appl. Physiol. 83(3): 712–717, 1997.—Ten patients with preserved inotropic function having a dual-chamber (right atrium and right ventricle) pacemaker placed for complete heart block were studied. They performed static one-legged knee extension at 20% of their maximal voluntary contraction for 5 min during three conditions: 1) atrioventricular sensing and pacing mode [normal increase in heart rate (HR; DDD)], 2) HR fixed at the resting value (DOO-Rest; 73 ± 3 beats/min), and 3) HR fixed at peak exercise rate (DOO-Ex; 107 ± 4 beats/min). During control exercise (DDD mode), mean arterial pressure (MAP) increased by 25 mmHg with no change in stroke volume (SV) or systemic vascular resistance. During DOO-Rest and DOO-Ex, MAP increased (+25 and +29 mmHg, respectively) because of a SV-dependent increase in cardiac output (+1.3 and +1.8 l/min, respectively). The increase in SV during DOO-Rest utilized a combination of increased contractility and the Frank-Starling mechanism (end-diastolic volume 118–136 ml). However, during DOO-Ex, a greater left ventricular contractility (end-systolic volume 55–38 ml) mediated the increase in SV.


1993 ◽  
Vol 75 (5) ◽  
pp. 1989-1995 ◽  
Author(s):  
M. U. Brandao ◽  
M. Wajngarten ◽  
E. Rondon ◽  
M. C. Giorgi ◽  
F. Hironaka ◽  
...  

The influence of exercise training on left ventricular function at rest (R), at anaerobic threshold (AT), and during peak exercise (PE) was evaluated in 12 healthy untrained and 13 trained (T) subjects who underwent Doppler echocardiography at R and radionuclide ventriculography at R and during exercise. The end-diastolic volume and stroke volume were significantly higher in the T group than in the untrained group at R. The ejection fraction rose significantly from R to AT and from AT to PE (80.0 +/- 0.84 vs. 83.6 +/- 0.91%), but no significant difference was observed between groups. The peak diastolic filling rate rose significantly during exercise, with a further significant increase observed in the T group (AT, 6.38 +/- 0.40 vs. 5.01 +/- 0.16 end-diastolic counts/s; PE, 8.24 +/- 0.42 vs. 7.15 +/- 0.35 end-diastolic counts/s). The percent variation of minimal systolic counts fell significantly at AT and PE in relation to R. Our data demonstrate that exercise training produces a significant increase in peak diastolic filling rate but no change in systolic function during exercise and that metabolic acidosis caused by exercise does not limit systolic function.


Heart ◽  
2020 ◽  
pp. heartjnl-2020-317550 ◽  
Author(s):  
Clément Karsenty ◽  
Diala Khraiche ◽  
Jean Philippe Jais ◽  
Francesca Raimondi ◽  
Magalie Ladouceur ◽  
...  

Background and objectivesChronic pulmonic regurgitation (PR) following repair of congenital heart disease (CHD) impairs right ventricular function that impacts peak exercise cardiac index (pCI). We aimed to estimate in a non-invasive way pCI and peak oxygen consumption (pVO2) and to evaluate predictors of low pCI in patients with significant residual pulmonic regurgitation after CHD repair.MethodWe included 82 patients (median age 19 years (range 10–54 years)) with residual pulmonic regurgitation fraction >40%. All underwent cardiac MRI and cardiopulmonary testing with measurement of pCI by thoracic impedancemetry. Low pCI was defined <7 L/min/m2.ResultsLow pCI was found in 18/82 patients. Peak indexed stroke volume (pSVi) tended to compensate chronotropic insufficiency only in patients with normal pCI (r=−0.31, p=0.01). Below 20 years of age, only 5/45 patients had low pCI but near-normal (≥6.5 L/min/m2). pVO2 (mL/kg/min) was correlated with pCI (r=0.58, p=0.0002) only in patients aged >20 years. Left ventricular stroke volume in MRI correlated with pSVi only in the group of patients with low pCI (r=0.54, p=0.02). No MRI measurements predicted low pCI. In multivariable analysis, only age predicted a low pCI (OR=1.082, 95% CI 1.035 to 1.131, p=0.001) with continuous increase of risk with age.ConclusionsIn patients with severe PR, pVO2 is a partial reflection of pCI. Risk of low pCI increases with age. No resting MRI measurement predicts low haemodynamic response to exercise. Probably more suitable to detect ventricular dysfunction, pCI measurement could be an additional parameter to take into account when considering pulmonic valve replacement.


2020 ◽  
Vol 42 (01) ◽  
pp. 56-65
Author(s):  
Xavier Woorons ◽  
Frederic Lemaitre ◽  
Guido Claessen ◽  
Cloé Woorons ◽  
Henri Vandewalle

AbstractEight well-trained male cyclists participated in two testing sessions each including two sets of 10 cycle exercise bouts at 150% of maximal aerobic power. In the first session, subjects performed the exercise bouts with end-expiratory breath holding (EEBH) of maximal duration. Each exercise bout started at the onset of EEBH and ended at its release (mean duration: 9.6±0.9 s; range: 8.6–11.1 s). At the second testing session, subjects performed the exercise bouts (same duration as in the first session) with normal breathing. Heart rate, left ventricular stroke volume (LVSV), and cardiac output were continuously measured through bio-impedancemetry. Data were analysed for the 4 s preceding and following the end of each exercise bout. LVSV (peak values: 163±33 vs. 124±17 mL, p<0.01) was higher and heart rate lower both in the end phase and in the early recovery of the exercise bouts with EEBH as compared with exercise with normal breathing. Cardiac output was generally not different between exercise conditions. This study showed that performing maximal EEBH during high-intensity exercise led to a large increase in LVSV. This phenomenon is likely explained by greater left ventricular filling as a result of an augmented filling time and decreased right ventricular volume at peak EEBH.


2004 ◽  
pp. 757-762 ◽  
Author(s):  
EA Palmieri ◽  
S Fazio ◽  
V Palmieri ◽  
G Lombardi ◽  
B Biondi

OBJECTIVES: To ascertain whether myocardial contractility and total arterial stiffness are significantly altered in human thyrotoxicosis, and to what extent they are affected by acute beta(1)-adrenergic blockade. METHODS: Doppler-echocardiography was used to assess left ventricular (LV) structure and function, hemodynamics and total arterial stiffness in untreated overt hyperthyroid patients before and 2 h after 5 mg bisoprolol given orally compared with age- and sex-matched healthy euthyroid controls. RESULTS: Compared with controls, untreated patients (n=20) had a higher heart rate (HR) and LV stroke index (SI), which were associated with higher pulse pressure (PP), larger LV end-diastolic volume index (EDVI, an index of preload,+11%, P<0.05), marginally increased stress-corrected LV midwall fractional shortening (MWS, an index of myocardial contractility,+5%; P=0.066), and shorter isovolumic relaxation time (IVRT). These changes resulted in a higher cardiac index (CI) and a lower systemic vascular resistance (SVR), which were associated with fairly normal mean blood pressure (BP) but higher PP/stroke volume (an index of total arterial stiffness,+29%; P<0.01). After bisoprolol, compared with controls, the randomly treated patients (n=10) had comparable HR but additionally increased SI; PP remained enhanced, EDVI was further enlarged (+26%, P<0.001), stress-corrected MWS was substantially unchanged, and IVRT remained shorter. Overall, these effects attenuated the high-output state, which was associated with normalization of PP/stroke volume without changes of mean BP. CONCLUSIONS: In human overt hyperthyroidism, myocardial contractility does not play a major role in increasing LV performance, which is instead predominantly sustained by increased preload with enhanced LV diastolic function. In addition, human thyrotoxicosis is associated with increased total arterial stiffness despite fairly normal mean BP. In this scenario, acute beta(1)-adrenergic blockade blunts the cardiovascular hyperkinesia predominantly by slowing HR - a process that is associated with normalization of total arterial stiffness.


2000 ◽  
Vol 98 (5) ◽  
pp. 545-551 ◽  
Author(s):  
Pier Giuseppe AGOSTONI ◽  
Karlman WASSERMAN ◽  
Giovanni B. PEREGO ◽  
Marco GUAZZI ◽  
Gaia CATTADORI ◽  
...  

The objective of the present study was to determine the variability of the arterio–venous O2 concentration difference [C(a–v)O2] at anaerobic threshold and at peak oxygen uptake (VO2) during a progressively increasing cycle ergometer exercise test, with the purpose of assessing the possible error in estimating stroke volume from measurements of VO2 alone. We sampled mixed venous and systemic arterial blood every 1 min during a progressively increasing cycle ergometer exercise test and measured, in each blood sample, haemoglobin concentration and blood gas data. Ventilation, VO2 and CO2 uptake were also measured continuously. We studied 40 patients with normal haemoglobin concentrations and with stable heart failure due to ischaemic or idiopathic cardiomyopathy. Mean values (±S.D.) for C(a–v)O2 were 7.8±2.6, 13.0±2.4 and 15.0±2.7 ml/100 ml at rest, anaerobic threshold and peak VO2 respectively. The patients with heart failure were divided into classes according to their peak VO2. Classes A, B and C contained patients with peak VO2 values of > 20, 15–20 and 10–15 ml·min-1·kg-1 respectively. At anaerobic threshold, C(a–v)O2 was 12.3±1.3, 13.1±2.7 and 13.5±2.6 ml/100 ml for classes A, B and C respectively (class A significantly different from classes B and C; P < 0.05). At peak exercise C(a–v)O2 was 13.6±1.4, 15.6±2.5 and 15.4±3.2 ml/100 ml for classes A, B and C respectively (class A significantly different from classes B and C; P < 0.05). Stroke volume was estimated for each subject using the mean values of the measured C(a–v)O2 in each functional class and individual values of VO2 and heart rate using the Fick formulation. The average difference between the stroke volume estimated from mean C(a–v)O2 and that obtained using the patient's actual C(a–v)O2 value was 9.2±9.7, 1.0±8.8 and -0.2±6.1 ml at anaerobic threshold, and -1.9±11.3, 0.9±10.0 and -2.3±8.5 ml at peak exercise, in classes A, B and C respectively. Among the various classes, the most precise estimation of stroke volume was observed for class C patients. We conclude that stroke volume during exercise can be estimated with the accuracy needed for most purposes from measurement of VO2 at the anaerobic threshold and at peak exercise, and from population-estimated mean values for C(a–v)O2 in heart failure patients.


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