Published online before print November 1, 2001, doi: 10.1161/hh2301.100982
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
© 2001 American Heart Association, Inc.
Clinical Research |
Increased Cardiac Sympathetic Activity and Insulin-Like Growth Factor-I Formation Are Associated With Physiological Hypertrophy in Athletes
From the Clinica Medica Generale e Cardiologia, University of Florence, Italy.
Correspondence to Prof Gian Gastone Neri Serneri, MD, Clinica Medica Generale e Cardiologia, University of Florence, Viale Morgagni 85, 50134 Florence, Italy. E-mail gg.neriserneri{at}dfc.unifi.it
Physiological hypertrophy represents the adaptive changes of the heart required for supporting the increased hemodynamic load in regularly trained healthy subjects. Mechanisms responsible for the athlete’s hypertrophy still remain unknown. In 15 trained competitive soccer players and in 15 healthy men not engaged in sporting activities (sedentary control subjects) of equivalent age, we investigated the relationship among cardiac growth factor formation, cardiac sympathetic activity, and left ventricular morphology and function. Cardiac formation of insulin-like growth factor (IGF)-I, endothelin (ET)-1, big ET-1, and angiotensin (Ang) II was investigated at rest by measuring artery-coronary sinus concentration gradients. Cardiac sympathetic activity was studied by [3H]norepinephrine (NE) kinetics. Cardiac IGF-I, but not ET-1, big ET-1, and Ang II, formation was higher in athletes than in control subjects (P<0.01). NE levels in arterial and peripheral venous blood did not differ between groups. In contrast, coronary sinus NE concentration was higher in athletes than in control subjects (P<0.01). Cardiac, but not total systemic, NE spillover was also increased in athletes (P<0.01), whereas cardiac [3H]NE reuptake and clearance were not different. Echocardiographic modifications indicated a volume overload-induced hypertrophy associated with increased myocardial contractility. Multivariate stepwise analysis selected left ventricular mass index as the most predictive independent variable for cardiac IGF-I formation and velocity of circumferential fiber shortening for cardiac NE spillover. In conclusion, increased cardiac IGF-I formation and enhanced sympathetic activity selectively confined to the heart appear to be responsible for the physiological hypertrophy in athletes performing predominantly isotonic exercise.
Key Words: insulin-like growth factor-I • norepinephrine • sympathetic nervous system • exercise • hypertrophy, left ventricular
This article has been cited by other articles:
 |
|
 |
|
  J. R. McMullen, F. Amirahmadi, E. A. Woodcock, M. Schinke-Braun, R. D. Bouwman, K. A. Hewitt, J. P. Mollica, L. Zhang, Y. Zhang, T. Shioi, et al. Protective effects of exercise and phosphoinositide 3-kinase(p110{alpha}) signaling in dilated and hypertrophic cardiomyopathy PNAS, January 9, 2007; 104(2): 612 - 617. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Mancia, M. Bombelli, G. Corrao, R. Facchetti, F. Madotto, C. Giannattasio, F. Q. Trevano, G. Grassi, A. Zanchetti, and R. Sega Metabolic Syndrome in the Pressioni Arteriose Monitorate E Loro Associazioni (PAMELA) Study: Daily Life Blood Pressure, Cardiac Damage, and Prognosis Hypertension, January 1, 2007; 49(1): 40 - 47. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. Shiojima and K. Walsh Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway Genes & Dev., December 15, 2006; 20(24): 3347 - 3365. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. DeBosch, N. Sambandam, C. Weinheimer, M. Courtois, and A. J. Muslin Akt2 Regulates Cardiac Metabolism and Cardiomyocyte Survival J. Biol. Chem., October 27, 2006; 281(43): 32841 - 32851. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. Abe, T. Matsunaga, K. Kameda, H. Tomita, T. Fujiwara, H. Ishizaka, H. Hanada, K. Fukui, I. Fukuda, T. Osanai, et al. Increased Level of Pericardial Insulin-Like Growth Factor-1 in Patients With Left Ventricular Dysfunction and Advanced Heart Failure J. Am. Coll. Cardiol., October 3, 2006; 48(7): 1387 - 1395. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Lang, M. Bierig, R. B. Devereux, F. A. Flachskampf, E. Foster, P. A. Pellikka, M. H. Picard, M. J. Roman, J. Seward, J. Shanewise, et al. Recommendations for chamber quantification Eur J Echocardiogr, March 1, 2006; 7(2): 79 - 108. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. R. Barton, L. E. Felkin, E. J. Birks, M. E. Cullen, N. R. Banner, S. Grindle, J. L. Hall, L. W. Miller, and M. H. Yacoub Myocardial Insulin-Like Growth Factor-I Gene Expression During Recovery From Heart Failure After Combined Left Ventricular Assist Device and Clenbuterol Therapy Circulation, August 30, 2005; 112(9_suppl): I-46 - I-50. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. P. Konhilas, U. Widegren, D. L. Allen, A. C. Paul, A. Cleary, and L. A. Leinwand Loaded wheel running and muscle adaptation in the mouse Am J Physiol Heart Circ Physiol, July 1, 2005; 289(1): H455 - H465. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Merkus, A. K. Brzezinska, C. Zhang, S. Saito, and W. M. Chilian Cardiac myocytes control release of endothelin-1 in coronary vasculature Am J Physiol Heart Circ Physiol, May 1, 2005; 288(5): H2088 - H2092. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. P. Konhilas, A. H. Maass, S. W. Luckey, B. L. Stauffer, E. N. Olson, and L. A. Leinwand Sex modifies exercise and cardiac adaptation in mice Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2768 - H2776. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. McMullen, T. Shioi, L. Zhang, O. Tarnavski, M. C. Sherwood, A. L. Dorfman, S. Longnus, M. Pende, K. A. Martin, J. Blenis, et al. Deletion of Ribosomal S6 Kinases Does Not Attenuate Pathological, Physiological, or Insulin-Like Growth Factor 1 Receptor-Phosphoinositide 3-Kinase-Induced Cardiac Hypertrophy Mol. Cell. Biol., July 15, 2004; 24(14): 6231 - 6240. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. McMullen, T. Shioi, W.-Y. Huang, L. Zhang, O. Tarnavski, E. Bisping, M. Schinke, S. Kong, M. C. Sherwood, J. Brown, et al. The Insulin-like Growth Factor 1 Receptor Induces Physiological Heart Growth via the Phosphoinositide 3-Kinase(p110{alpha}) Pathway J. Biol. Chem., February 6, 2004; 279(6): 4782 - 4793. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. J. Wilkins, Y.-S. Dai, O. F. Bueno, S. A. Parsons, J. Xu, D. M. Plank, F. Jones, T. R. Kimball, and J. D. Molkentin Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy Circ. Res., January 9, 2004; 94(1): 110 - 118. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Modesti, S. Vanni, I. Bertolozzi, I. Cecioni, C. Lumachi, A. M. Perna, M. Boddi, and G. F. Gensini Different Growth Factor Activation in the Right and Left Ventricles in Experimental Volume Overload Hypertension, January 1, 2004; 43(1): 101 - 108. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. R. McMullen, T. Shioi, L. Zhang, O. Tarnavski, M. C. Sherwood, P. M. Kang, and S. Izumo Phosphoinositide 3-kinase(p110{alpha}) plays a critical role for the induction of physiological, but not pathological, cardiac hypertrophy PNAS, October 14, 2003; 100(21): 12355 - 12360. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. P. Schlaich, D. M. Kaye, E. Lambert, M. Sommerville, F. Socratous, and M. D. Esler Relation Between Cardiac Sympathetic Activity and Hypertensive Left Ventricular Hypertrophy Circulation, August 5, 2003; 108(5): 560 - 565. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. G.F Bronzwaer, C. Zeitz, C. A Visser, and W. J Paulus Endomyocardial nitric oxide synthase and the hemodynamic phenotypes of human dilated cardiomyopathy and of athlete's heart Cardiovasc Res, August 1, 2002; 55(2): 270 - 278. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Zoccali, F. Mallamaci, G. Tripepi, S. Parlongo, S. Cutrupi, F. A. Benedetto, A. Cataliotti, and L. S. Malatino Norepinephrine and Concentric Hypertrophy in Patients With End-Stage Renal Disease Hypertension, July 1, 2002; 40(1): 41 - 46. [Abstract] [Full Text] [PDF]
|
|