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- Laaksonen, Marko, 1975-, et al.
(författare)
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Left-ventricular hypertrophy associates to impaired maximal myocardial perfusion in endurance-trained men
- 2009
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Konferensbidrag (refereegranskat)abstract
- Long-term endurance training induces morphological adaptations in heart, such as left-ventricular (LV) hypertrophy caused by wall thickening and cavity enlargement. Interestingly, these anatomical changes in the heart are strikingly similar to certain pathophysiological changes (Pellicia 2000). Previous studies have shown that the perfusion response in myocardium during dipyridamole- or adenosine infusion is decreased in several pathophysiological states with LV hypertrophy (e.g. Stolen et al. 2004). However, studies in endurance athletes with LV hypertrophy have shown contradictory results on myocardial perfusion response ranging from reduced to increased myocardial perfusion during dipyridamole- or adenosine-induced vasodilation compared to untrained men (Kjaer et al. 2005; Kalliokoski et al. 2002). The degree of hypertrophy could explain the discrepant findings in studies in athletes, but it has not been thoroughly investigated. Thus, we examined totally 31 endurance athletes (ET) and 25 untrained (UT) men in order to study the association between myocardial functional and anatomical parameters measured with echocardiography, and myocardial perfusion (at rest and during maximal vasodilation induced by iv adenosine) measured with Positron Emission Tomography. Both VO2max (60+-5 vs 42+-8 ml/kg/min, p<0.001) and LVmass index (169+-27 vs 102+-15 g/m2, p<0.001) were markedly higher in ET. Resting myocardial perfusion was similar between the groups (ET 0.7+-0.2 vs UT 0.8+-0.2 ml/g/min, p=0.22) whereas adenosine-stimulated perfusion was lower in ET (2.9+-1.0 vs 3.7+-1.0 ml/g/min, p<0.01). VO2max correlated inversely with adenosine-stimulated perfusion in ET (r=-0.39, p=0.03) and with resting perfusion in UT (-0.49, p=0.01). Forward LV work correlated linearly with resting perfusion in both groups (ET r=0.54, p<0.01; UT r=0.50, p=0.01). ET group was further divided into three subgroups according to LVmass index (ET1: LVmass index <150g/m2, n=9; ET2 LVmass index 150-180 g/m2, n=12; ET3 LVmass index >180 gm2, n=10). Adenosine-induced myocardial perfusion decreased gradually when LVmass increased (UT 3.7+-1.+0 vs ET1 3.3+-0.9 vs ET2 2.7+-1.4 vs ET3 2.6+-0.5 mL g-1 min-1, p=0.008). LVmass index was also inversely related to adenosine-induced perfusion in entire study population (r=-0.46, p<0.01). Therefore, these results suggest that endurance training-induced severe cardiac hypertrophy impairs myocardial perfusion capacity. Kalliokoski K et al. (2002) Med Sci Sports Exerc 34:948-53 Kjaer A et al. (2005) Am J Cardiol 96:1692-98 Pellicia A (2000) Curr Cardiol Rep 2(2):166-71 Stolen KQ et al (2004) 10(2):132-40
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| 2. |
- Laaksonen, Marko S, 1975-, et al.
(författare)
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VO2peak, myocardial hypertrophy, and myocardial blood flow in endurance-trained men
- 2014
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Ingår i: Medicine and science in sports and exercise. - 1530-0315. ; 46:8, s. 1498-1505
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Tidskriftsartikel (refereegranskat)abstract
- INTRODUCTION: Endurance training induces cardiovascular and metabolic adaptations, leading to enhanced endurance capacity and exercise performance. Previous human studies have shown contradictory results in functional myocardial vascular adaptations to exercise training, and we hypothesized that this may be related to different degrees of hypertrophy in the trained heart. METHODS: We studied the interrelationships between peak aerobic power (V̇O2peak), myocardial blood flow (MBF) at rest and during adenosine-induced vasodilation, and parameters of myocardial hypertrophy in endurance-trained (ET, n = 31) and untrained (n = 17) subjects. MBF and myocardial hypertrophy were studied using positron emission tomography and echocardiography, respectively. RESULTS: Both V̇O2peak (P < 0.001) and left ventricular (LV) mass index (P < 0.001) were higher in the ET group. Basal MBF was similar between the groups. MBF during adenosine was significantly lower in the ET group (2.88 ± 1.01 vs 3.64 ± 1.11 mLg-1min-1, P < 0.05) but not when the difference in LV mass was taken into account. V̇O2peak correlated negatively with adenosine-stimulated MBF, but when LV mass was taken into account as a partial correlate, this correlation disappeared. CONCLUSIONS: The present results show that increased LV mass in ET subjects explains the reduced hyperemic myocardial perfusion in this subject population and suggests that excessive LV hypertrophy has negative effect on cardiac blood flow capacity.
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