VO2peak, Hypertrophy, and Blood Flow in Endurance Training
VO2peak, Hypertrophy, and Blood Flow in Endurance Training
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 mL·g·min, 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.
Chronic endurance training induces several morphological and functional cardiac adaptations, which have generally been considered physiological and beneficial for health and especially for fitness. One of the most prominent cardiac adaptations in a chronically trained heart is the increase in heart size, especially the left ventricular (LV) hypertrophy caused by wall thickening and cavity enlargement, the so-called athlete's heart.
Exercise training also causes changes in vascular function. Although studies in different patient groups with impaired vascular function show that endurance-type exercise training has the potential to improve peripheral and cardiovascular function, healthy endurance-trained (ET) subjects seem not to have supranormal vascular function. For example, some studies have demonstrated reduced flow-mediated dilation in an athlete's peripheral artery despite systemic remodeling. This apparent "athlete paradox", documented largely in peripheral arteries in humans to date, is explained by vascular remodeling that follows from repetitive short-term changes in arterial blood flow due to exercise training sessions. Cross-sectional studies in humans also generally suggest that cardiovascular function is normal in endurance athletes. Studies using positron emission tomography (PET) and [O]H2O to measure myocardial perfusion capacity show large variation in the results from reduced to unchanged and even increased myocardial blood flow (MBF) during dipyridamole- or adenosine-induced vasodilation in ET subjects.
In addition to human studies, experiments performed in animals also show highly discrepant findings regarding exercise training and coronary blood flow capacity, as recently extensively reviewed by Laughlin et al.. Differences in results are likely to be explained by several factors such as differences in species, age, and sex, as well as duration, intensity, and type of exercise training. Interestingly, however, in animal studies that have reported increased cardiac blood flow capacity and in those where the used animal model most closely resembles the human heart, exercise training did not cause cardiac hypertrophy in dogs. In swine, higher LV-to-body mass ratio was documented, but this was due to the lower body weights and not absolutely higher LV mass. Although even fairly long-term (6 months) exercise interventions in previously untrained (UT) humans do not increase LV mass substantially, high LV mass is, however, one of the paramount features of highly trained endurance athletes. Importantly, in those swine studies where strenuous and long-term training produced substantial cardiac hypertrophy, cardiac capillary density was found to be reduced.
Along these lines, we hypothesized that large variation in previous human studies in relation to endurance training and myocardial vascular function might be related to the extent of LV hypertrophy. Accordingly, we investigated the interrelationships between peak aerobic power (V̇O2peak), MBF, and parameters of myocardial hypertrophy in ET and UT men. It was hypothesized on the basis of the animal studies that, because relative capillary density might be decreased in ET men with substantial cardiac hypertrophy, myocardial perfusion would also be reduced along the increments in LV hypertrophy.
Abstract and Introduction
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 mL·g·min, 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.
Introduction
Chronic endurance training induces several morphological and functional cardiac adaptations, which have generally been considered physiological and beneficial for health and especially for fitness. One of the most prominent cardiac adaptations in a chronically trained heart is the increase in heart size, especially the left ventricular (LV) hypertrophy caused by wall thickening and cavity enlargement, the so-called athlete's heart.
Exercise training also causes changes in vascular function. Although studies in different patient groups with impaired vascular function show that endurance-type exercise training has the potential to improve peripheral and cardiovascular function, healthy endurance-trained (ET) subjects seem not to have supranormal vascular function. For example, some studies have demonstrated reduced flow-mediated dilation in an athlete's peripheral artery despite systemic remodeling. This apparent "athlete paradox", documented largely in peripheral arteries in humans to date, is explained by vascular remodeling that follows from repetitive short-term changes in arterial blood flow due to exercise training sessions. Cross-sectional studies in humans also generally suggest that cardiovascular function is normal in endurance athletes. Studies using positron emission tomography (PET) and [O]H2O to measure myocardial perfusion capacity show large variation in the results from reduced to unchanged and even increased myocardial blood flow (MBF) during dipyridamole- or adenosine-induced vasodilation in ET subjects.
In addition to human studies, experiments performed in animals also show highly discrepant findings regarding exercise training and coronary blood flow capacity, as recently extensively reviewed by Laughlin et al.. Differences in results are likely to be explained by several factors such as differences in species, age, and sex, as well as duration, intensity, and type of exercise training. Interestingly, however, in animal studies that have reported increased cardiac blood flow capacity and in those where the used animal model most closely resembles the human heart, exercise training did not cause cardiac hypertrophy in dogs. In swine, higher LV-to-body mass ratio was documented, but this was due to the lower body weights and not absolutely higher LV mass. Although even fairly long-term (6 months) exercise interventions in previously untrained (UT) humans do not increase LV mass substantially, high LV mass is, however, one of the paramount features of highly trained endurance athletes. Importantly, in those swine studies where strenuous and long-term training produced substantial cardiac hypertrophy, cardiac capillary density was found to be reduced.
Along these lines, we hypothesized that large variation in previous human studies in relation to endurance training and myocardial vascular function might be related to the extent of LV hypertrophy. Accordingly, we investigated the interrelationships between peak aerobic power (V̇O2peak), MBF, and parameters of myocardial hypertrophy in ET and UT men. It was hypothesized on the basis of the animal studies that, because relative capillary density might be decreased in ET men with substantial cardiac hypertrophy, myocardial perfusion would also be reduced along the increments in LV hypertrophy.
