Angiotensin-Converting Enzyme Genotype Predicts Cardiac and Autonomic Responses to Prolonged Exercise
Euan A. Ashley, MRCP, DPhil*,*,
Attila Kardos, MD, PhD, FESC ,
Ewan S. Jack, MB, ChB, FRCA ,
Walter Habenbacher, PhD ,
Mathew Wheeler, MD, PhD||,
Young M. Kim, BS¶,
Jeffrey Froning, MA#,
Jonathan Myers, PhD*,
Gregory Whyte, PhD, FACSM**,
Victor Froelicher, MD* and
Pamela Douglas, MD, FACC, FASE
* Division of Cardiology
|| Division of Medicine, Stanford University, Stanford, California
Department of Cardiovascular Medicine, University of Oxford, Oxford, United Kingdom
Department of Anaesthetics, University of Glasgow, Glasgow, Scotland
CNSystems, Graz, Austria
¶ Department of Cardiovascular Medicine, University of Toronto, Toronto, Canada
# Sunnyside Biomedical, Los Altos, California
** Director of Science and Research, English Institute of Sport, Manchester, United Kingdom
Ursula Geller Professor of Research in Cardiovascular Diseases and Cardiology Division, Duke University Medical Center, Durham, North Carolina
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Figure 1 Echocardiographic and hemodynamic variables. Echocardiographic and hemodynamic variables (n = 48) before and after the race (mean ± SE) (A) Preload represented by left ventricular end diastolic diameter was unchanged (p = 0.19). (B) Ejection fraction decreased significantly after the race (p < 0.001). (C) Heart rate increased significantly after the race (p = 0.05). (D) Afterload represented by mean arterial pressure did not change (p = 0.52). (E) Continuous heart rate tracing from lead competitor. bpm = beats/minute; EF = ejection fraction; HR = heart rate; LVED = left ventricular end-diastolic diameter; MAP = mean arterial pressure.
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Figure 2 Changes in fractional shortening. (A) Four competitors were rescanned at 24 and 48 h after the race. Partial recovery of systolic function was demonstrated. (B) Decline in fractional shortening plotted against length of race as reported for key studies. In the current study, the exercise challenge and drop in fractional shortening were greater than previously reported. FS = fractional shortening.
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Figure 3 Effect of angiotensin-converting enzyme (ACE) genotype. There was a differential decline in systolic function according to ACE genotype (A, p = 0.017, n = 22 [ID], 11 [II], 15 [DD]). Individuals homozygous for the insertion allele exhibited greater declines in systolic function than those homozygous for the deletion allele. Heterozygous individuals exhibited an intermediate phenotype. In contrast, ACE genotype did not predict athletic hypertrophy (B, p = 0.8). LV = left ventricular.
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Figure 4 Heart rate and blood pressure (BP) variability. There was a differential effect of angiotensin-converting enzyme genotype on both the low- and high-frequency (units normalized to overall power; LFnu, HFnu) components of BP variability (A and B) and an overall significant enhancement of the sympathovagal balance in participants homozygous for the deletion allele. (C) In addition, there was a more dramatic increase (from a lower initial value) in these individuals in the baroreceptor effectiveness index (BEI). (D) Shown are raw tracings for one competitor (heart rate variability [HRV] is signified by upper tracings, blood pressure variability [BPV] by lower tracings) illustrating the strongest overall signals (decrease in very low frequency component of BPV, increase in low- and high-frequency; increase in very low frequency component of HRV). dBP = diastolic blood pressure; RRI = R-R interval.
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