Angiotensin-Converting Enzyme Genotype Predicts Cardiac and Autonomic Responses to Prolonged Exercise

Ashley, Euan A.; Kardos, Attila; Jack, E.; Habenbacher, W.; Wheeler, Matthew T.; Kim, Young Beom; Froning, Jeffrey; Myers, Jonathan; Whyte, Gregory; Froelicher, Victor; Douglas, Pamela S.

doi:10.1016/j.jacc.2006.02.071

Cited by 39 publications

(31 citation statements)

References 32 publications

(41 reference statements)

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“…The lower SV is unlikely to be related to reduced filling time, as HRs were still low (Ͻ100 beats/min). Postexercise orthostatic hypotension has also been attributed to, in part, a drop in SV as a result of myocardial dysfunction (2,13). Evidence from the cTnI data would seemingly rule out cardiomyocyte damage and any associated left ventricular dysfunction, in the genesis of hypotension in the present study.…”

Section: Orthostatic Stress Response Across 24-h Exercise Trialmentioning

confidence: 59%

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Mechanisms of orthostatic intolerance following very prolonged exercise

Lucas¹,

Cotter²,

Murrell³

et al. 2008

Journal of Applied Physiology

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Nine men completed a 24-h exercise trial, with physiological testing sessions before (T1, ϳ0630), during (T2, ϳ1640; T3, ϳ0045; T4, ϳ0630), and 48-h afterwards (T5, ϳ0650). Participants cycled and ran/trekked continuously between test sessions. A 24-h sedentary control trial was undertaken in crossover order. Within testing sessions, participants lay supine and then stood for 6 min, while heart rate variability (spectral analysis of ECG), middle cerebral artery perfusion velocity (MCAv), mean arterial pressure (MAP; Finometer), and end-tidal PCO2 (PETCO 2 ) were measured, and venous blood was sampled for cardiac troponin I. During the exercise trial: 1) two, six, and four participants were orthostatically intolerant at T2, T3, and T4, respectively; 2) changes in heart rate variability were only observed at T2; 3) supine MAP (baseline ϭ 81 Ϯ 6 mmHg) was lower (P Ͻ 0.05) by 14% at T3 and 8% at T4, whereas standing MAP (75 Ϯ 7 mmHg) was lower by 16% at T2, 37% at T3, and 15% at T4; 4) PETCO 2 was reduced (P Ͻ 0.05) at all times while supine (Ϫ3-4 Torr) and standing (Ϫ4 -5 Torr) during exercise trial; 5) standing MCAv was reduced (P Ͻ 0.05) by 23% at T3 and 30% at T4 during the exercise trial; 6) changes in MCAv with standing always correlated (P Ͻ 0.01) with changes in PETCO 2 (r ϭ 0.78 -0.93), but only with changes in MAP at T1, T2, and T3 (P Ͻ 0.05; r ϭ 0.62-0.84); and 7) only two individuals showed minor elevations in cardiac troponin I. Recovery was complete within 48 h. During prolonged exercise, posturalinduced hypotension and hypocapnia exacerbate cerebral hypoperfusion and facilitate syncope.

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Section: Orthostatic Stress Response Across 24-h Exercise Trialmentioning

confidence: 59%

“…INCREASED SYMPATHETIC ACTIVITY and reduced vagal activity following prolonged exercise have been observed in athletes competing in events ranging from 4 to Ͼ100 h (2,4,16,29). Despite elevations in sympathetic activity, low arterial blood pressure (BP) (hypotension) is also observed during recovery (16,29).…”

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confidence: 99%

Mechanisms of orthostatic intolerance following very prolonged exercise

Lucas¹,

Cotter²,

Murrell³

et al. 2008

Journal of Applied Physiology

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“…Although it is logical to conclude that EETrelated pressure/volume challenge, which results in LV hypertrophy, also leads to enhanced resting LV systolic function, this speculation deserves further attention. The cellular response to such stimuli is an area of active interest, and the roles of gene polymorphism and growth factor activation in pathological and EET-induced cardiac hypertrophy have been recently shown (2,16,19,26,29). Furthermore, recent animal data demonstrate an upregulation of several genes with established relevance to cardiac contraction in response to ventricular pressure and volume overload (7,27,28,40).…”

Section: Discussionmentioning

confidence: 99%

The impact of endurance exercise training on left ventricular systolic mechanics

Baggish¹,

Yared²,

Wang³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

117

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Although exercise training-induced changes in left ventricular (LV) structure are well characterized, adaptive functional changes are incompletely understood. Detailed echocardiographic assessment of LV systolic function was performed on 20 competitive rowers (10 males and 10 females) before and after endurance exercise training (EET; 90 days, 10.7 Ϯ 1.1 h/wk). Structural changes included LV dilation (end-diastolic volume ϭ 128 Ϯ 25 vs. 144 Ϯ 28 ml, P Ͻ 0.001), right ventricular (RV) dilation (end-diastolic area ϭ 2,850 Ϯ 550 vs. 3,260 Ϯ 530 mm 2 , P Ͻ 0.001), and LV hypertrophy (mass ϭ 227 Ϯ 51 vs. 256 Ϯ 56 g, P Ͻ 0.001). Although LV ejection fraction was unchanged (62 Ϯ 3% vs. 60 Ϯ 3%, P ϭ not significant), all direct measures of LV systolic function were altered. Peak systolic tissue velocities increased significantly (basal lateral SЈ⌬ ϭ 0.9 Ϯ 0.6 cm/s, P ϭ 0.004; and basal septal SЈ⌬ ϭ 0.8 Ϯ 0.4 cm/s, P ϭ 0.008). Radial strain increased similarly in all segments, whereas longitudinal strain increased with a base-to-apex gradient. In contrast, circumferential strain (CS) increased in the LV free wall but decreased in regions adjacent to the RV. Reductions in septal CS correlated strongly with changes in RV structure (⌬RV end-diastolic area vs. ⌬LV septal CS; r 2 ϭ 0.898, P Ͻ 0.001) and function (⌬peak RV systolic velocity vs. ⌬LV septal CS, r 2 ϭ 0.697, P Ͻ 0.001). EET leads to significant changes in LV systolic function with regional heterogeneity that may be secondary to concomitant RV adaptation. These changes are not detected by conventional measurements such as ejection fraction.athlete's heart; left ventricle; strain; ventricular interdependence LEFT VENTRICULAR (LV) structural adaptation in response to aerobic endurance exercise training (EET) has been well characterized. Increases in LV chamber dimensions, wall thickness, and mass have been documented among individuals who participate in EET, and it is these structural attributes that underlie the concept of the "athlete's heart" (8,38,41). At the present time, the impact of EET on LV functional mechanics is less clear.Several reports demonstrate that EET results in enhanced LV diastolic function (3,23,31). In contrast, existing data suggest that LV systolic function is unchanged by EET (9,15,39). Previous studies examining the impact of EET on LV systolic function have relied on indexes such as ejection fraction or fractional area change that may lack the sensitivity to detect regional changes in myocardial function. Novel imaging techniques such as two-dimensional strain and tissueDoppler echocardiography are direct, more sensitive methods of assessing myocardial systolic function (13,14). To date, a prospective and longitudinal assessment of the impact of EET on LV systolic function using these techniques has not been conducted.We hypothesized that EET would result in enhanced resting LV contractility but that this adaptation would be underrepresented by conventional indexes of systolic function. To address this hypothesis, we performed a focused ...

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“…This integrated system includes a six-channel electrocardiogram (ECG) and allows continuous measurement of beat-to-beat blood pressure (BP) using the vascular uploading technique on the finger [1,8]. These BP values are automatically and continuously corrected to oscillometric BP values obtained on the contralateral arm.…”

Section: Cardiovascular Quantitative Autonomic Testingmentioning

confidence: 99%

Quantitative autonomic testing in the management of botulism

Topakian¹,

Heibl

Stieglbauer³

et al. 2009

J Neurol

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Even with mild neurological signs, patients with botulism frequently complain of autonomic symptoms. This study aimed at the evaluation of sudomotor and cardiovascular reflex functions by quantitative autonomic testing (QAT), which may identify patients with autonomic involvement but otherwise benign clinical presentation. Five patients with food-borne botulism were subjected to a structured questionnaire on autonomic symptoms, cardiac and neurological examination, and QAT after a median of 2 weeks (baseline) and 12 weeks (follow-up) post intoxication. For calculation of haemodynamic and cardiovascular autonomic parameters, we used the Task Force((R)) Monitor (Version 2.1, CNSystems, Graz, Austria). Cardiovagal function was assessed by Ewing's test battery. Autonomic complaints were more pronounced than neurological symptoms. Baseline tests revealed widely abnormal sudomotor function and marked impairment of heart rate variation and blood pressure response to standing. Prominent features of cardiovascular failure were high resting heart rate, supine hypertension, orthostatic hypotension, and impaired baroreflex function. Three patients reported inability to keep up with their routine amount of physical work. Based on the baseline QAT results, these three patients were instructed to engage in physical activity but avoid physical strain until there was considerable improvement. On follow-up, fatigue was the most frequent residual complaint, sympathetic skin responses were present, and cardiovascular QAT results were significantly improved and did not differ from those of ten control subjects. QAT identified autonomic involvement in botulism patients with otherwise benign neurological presentation. Comprehensive evaluation of autonomic failure may provide useful information for the management of botulism.

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Angiotensin-Converting Enzyme Genotype Predicts Cardiac and Autonomic Responses to Prolonged Exercise

Abstract: The ACE genotype predicts the extent of reversible subclinical LV dysfunction after prolonged exercise and is associated with a differential postactivity augmentation of sympathetic nervous system function that may explain it.

Cited by 39 publications

References 32 publications

Mechanisms of orthostatic intolerance following very prolonged exercise

Mechanisms of orthostatic intolerance following very prolonged exercise

The impact of endurance exercise training on left ventricular systolic mechanics

Quantitative autonomic testing in the management of botulism

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