Left ventricular performance in normal subjects: a comparison of the responses to exercise in the upright and supine positions.

Poliner, L. R.; Dehmer, Gregory J.; Lewis, Samuel E.; Parkey, Robert W.; Blomqvist, C. Gunnar; Willerson, James T.

doi:10.1161/01.cir.62.3.528

Cited by 370 publications

(134 citation statements)

References 44 publications

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“…In a review by Sawka and colleagues (1996), S V augmentation has been attributed to heat-acclimationinduced PV expansion (Hales et al 1996). (Poliner et al 1980). …”

Section: Adaptation To Repeated Heat Stressmentioning

confidence: 99%

Induction and decay of short-term heat acclimation

et al. 2009

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Abstract:Most advice for heat adaptation is to use long-term (>10 d) regimes, in which hydration status is maintained. We tested the hypothesis that short-term (5-day) heat acclimation would confer substantial improvements in physiological strain and exercise tolerance for exercise in the heat, and fluid regulatory strain provides a thermally-independent stimulus for such adaptations. Ten moderately-fit males were heat acclimated using controlled hyperthermia (rectal temperature 38.5°C) for 90 min on five consecutive days (T a = 40°C, 60% RH), on two occasions separated by a five-week washout, in a randomly assigned, cross-over design; one with euhydration (EUH) and one with dehydration (DEH) during acclimation bouts. One week before, then on the 2 nd day after each acclimation regime, a heat stress test (HST) was completed, comprising cycling at 40% peak power output for 90 min (T a = 35°C, 60% RH), before incrementing to exhaustion. Plasma volume (PV) at rest was measured using CO rebreathing. Acclimation exercise-induced response of[aldo] p became more pronounced across DEH (  178 pg . mL -1 ; 95%CI: 33 to 324) but not EUH (  -47 pg . mL -1 : -209 to 115) and this difference was significant (P=0.02).Compared to EUH, permissive DEH during acclimation bouts conferred larger acclimation-induced increases in resting PV (4.1%: -1.5 to 9.8%; P=0.06), F Q  (4.2: 0.7 to 7.8 ml . min -1. 100 ml -1 ; P=0.009), FVC (0.06: 0.02 to 0.10 ml . 100ml Tissue -1. min -1. mmHg -1 ; P=0.006) and decreased end-exercise c f by 17% (19: -29 to 9 b·min-1; P=0.05). In conclusion, short-term (5-day) heat acclimation was effective with several adaptations more pronounced after fluid-regulatory strain from a dehydration acclimation regime.

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“…In a review by Sawka and colleagues (1996), S V augmentation has been attributed to heat-acclimationinduced PV expansion (Hales et al 1996). (Poliner et al 1980). …”

Section: Adaptation To Repeated Heat Stressmentioning

confidence: 99%

Induction and decay of short-term heat acclimation

et al. 2009

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“…All subjects had marked ventricular dilatation at rest, with mean LV end-diastolic volume index approximately twice normal and end-systolic volume index over five times normal (Rackley et al, 1980). Instead of the normally unchanged or decreased end-systolic volume with exercise (Manyari and Kostuk, 1983;Poliner et al, 1980), IDC patients developed progressive end-systolic enlargement. LV end-diastolic volume also increased significantly, a pattern which may be abnormal (Manyari and Kostuk, 1983).…”

Section: Discussionmentioning

confidence: 94%

The exercise response in idiopathic dilated cardiomyopathy

Kirlin

Das

Zijnen

et al. 1984

Clinical Cardiology

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Summary:In order to more clearly define the exercise response of idiopathic dilated cardiomyopathy (IDC), 20 patients in this study with strictly defined IDC were evaluated with radionuclide ventriculography and invasive hemodynamic monitoring. Severe cardiovascular impairment was present at rest, and peak supine exercise produced progressive left ventricular (LV) dilatation in both diastole and systole (meanf SEM from 172 f 14 to 212f22 ml/m2 at end-diastole and from 137f14 to 170 f 22 d / m 2 at end-systole; both p < 0.03). There were marked increases in LV and right ventricular filling pressure (from 17 f 2 to 36 f 3 mmHg and from 7 f 2 to 15 f 2 mmHg, respectively; both p O.8), but individual patients demonstrated substantial variability. Cardiac output rose less than in normals and increases were brought about primarily by subnormal heart rate increases. High resting and exercise systemic and pulmonary vascular resistance were indicative of limited vasodilator reserve. Despite marked hemodynamic abnormalities, 10 of the 20 subjects had well preserved exercise capacity ( 2 12 min exercise duration). These patients as a group had significantly lower resting heart rate and higher exercise cardiac output and lower exercise systemic vascular resistance. However, they did not differ from the other patients with respect to resting LV function. Thus, the exercise response in IDC has specific characteristics that distinguish it from normal and from the exercise response of other causes of LV dysfunction. An interesting subset of patients with IDC has well preserved exercise capacity associated with greater chronotropic and vasodilator reserve. This finding suggests less sympathetic activation in these subjects.

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“…Prolonged hyperglycaemia alters myocardial structure through the accumulation of advanced glycation end-products and, in the case of collagen, by promoting fibrosis and decreased connective tissue flexibility [6]. Because the increment in stroke volume during upright exercise is caused primarily by increases in end-diastolic volume [7], increased myocardial stiffness and/or altered filling characteristics might limit the exercise.…”

Section: Discussionmentioning

confidence: 99%

Impaired stroke volume and aerobic capacity in female adolescents with type 1 and type 2 diabetes mellitus

et al. 2008

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Aim/hypothesis This study was designed to determine whether type 2 diabetic adolescents have reduced aerobic capacity and to investigate the role of cardiac output and arteriovenous oxygen difference (a−vO 2 ) in their exercise response. Methods Female adolescents (age 12-18 years) with type 2 diabetes mellitus (n=8) and type 1 diabetes mellitus (n=12) and obese (n=10) and non-obese (n=10) non-diabetic controls were recruited for this study. Baseline data included maximal aerobic capacity (cycle ergometer) and body composition. Cardiac output and a−vO 2 were determined at rest and during submaximal exercise. Results Diabetic groups had lower aerobic capacity than nondiabetic groups (p<0.05). Adolescents with type 2 diabetes had lower aerobic capacity than the type 1 diabetic group. Maximal heart rate was lower in the type 2 diabetic group (p <0.05). Exercise stroke volume was 30-40% lower at 100 and 120 beats per min in the diabetic than in the nondiabetic groups (p<0.05). The a−vO 2 value was not different in any condition. Conclusions and interpretation Type 2 diabetic adolescents have reduced aerobic capacity and reduced heart rate response to maximal exercise. Furthermore, type 2 and type 1 diabetic adolescent girls have a blunted exercise stroke volume response compared with non-diabetic controls. Central rather than peripheral mechanisms contribute to the reduced aerobic capacity in diabetic adolescents. Although of short duration, type 2 diabetes in adolescence is already affecting cardiovascular function in adolescents.

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Left ventricular performance in normal subjects: a comparison of the responses to exercise in the upright and supine positions.

Cited by 370 publications

References 44 publications

Induction and decay of short-term heat acclimation

Induction and decay of short-term heat acclimation

The exercise response in idiopathic dilated cardiomyopathy

Impaired stroke volume and aerobic capacity in female adolescents with type 1 and type 2 diabetes mellitus

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