146 research outputs found
The effect of exercise training on transverse tubules in normal, remodeled, and reverse remodeled hearts
No full textThe response of transverse (T)-tubules to exercise training in health and disease remains unclear. Therefore, we studied the effect of exercise training on the density and spacing of left ventricle cardiomyocyte T-tubules in normal and remodeled hearts that associate with detubulation, by confocal laser scanning microscopy. First, exercise training in normal rats increased cardiomyocyte volume by 16% (P < 0.01), with preserved T-tubule density. Thus, the T-tubules adapted to the physiologic hypertrophy. Next, we studied T-tubules in a rat model of metabolic syndrome with pressure overload-induced concentric left ventricle hypertrophy, evidenced by 15% (P < 0.01) increased cardiomyocyte size. These rats had only 85% (P < 0.01) of the T-tubule density of control rats. Exercise training further increased cardiomyocyte volume by 8% (P < 0.01); half to that in control rats, but the T-tubule density remained unchanged. Finally, post-myocardial infarction heart failure induced severe cardiac pathology, with a 70% (P < 0.01) increased cardiomyocyte volume that included both eccentric and concentric hypertrophy and 55% (P < 0.01) reduced T-tubule density. Exercise training reversed 50% (P < 0.01) of the pathologic hypertrophy, whereas the T-tubule density increased by 40% (P < 0.05) compared to sedentary heart failure, but remained at 60% of normal hearts (P < 0.01). Physiologic hypertrophy associated with conserved T-tubule spacing (similar to 1.8-1.9 mu m), whereas in pathologic hypertrophy, T-tubules appeared disorganized without regular spacing. In conclusion, cardiomyocytes maintain the relative T-tubule density during physiologic hypertrophy and after mild concentric pathologic hypertrophy, whereas after severe pathologic remodeling with a substantial loss of T-tubules; exercise training reverses the remodeling and partly corrects the T-tubule density
Longitudinal study of the effect of a 5-year exercise intervention on structural brain complexity in older adults. A Generation 100 substudy
No full textPhysical inactivity has been identified as an important risk factor for dementia. High levels of cardiorespiratory fitness (CRF) have been shown to reduce the risk of dementia. However, the mechanism by which exercise affects brain health is still debated. Fractal dimension (FD) is an index that quantifies the structural complexity of the brain. The purpose of this study was to investigate the effects of a 5-year exercise intervention on the structural complexity of the brain, measured through the FD, in a subset of 105 healthy older adults participating in the randomized controlled trial Generation 100 Study. The subjects were randomized into control, moderate intensity continuous training, and high intensity interval training groups. Both brain MRI and CRF were acquired at baseline and at 1-, 3- and 5-years follow-ups. Cortical thickness and volume data were extracted with FreeSurfer, and FD of the cortical lobes, cerebral and cerebellar gray and white matter were computed. CRF was measured as peak oxygen uptake (VO2peak) using ergospirometry during graded maximal exercise testing. Linear mixed models were used to investigate exercise group differences and possible CRF effects on the brain's structural complexity. Associations between change over time in CRF and FD were performed if there was a significant association between CRF and FD. There were no effects of group membership on the structural complexity. However, we found a positive association between CRF and the cerebral gray matter FD (p < 0.001) and the temporal lobe gray matter FD (p < 0.001). This effect was not present for cortical thickness, suggesting that FD is a more sensitive index of structural changes. The change over time in CRF was associated with the change in temporal lobe gray matter FD from baseline to 5-year follow-up (p < 0.05). No association of the change was found between CRF and cerebral gray matter FD. These results demonstrated that entering old age with high and preserved CRF levels protected against loss of structural complexity in areas sensitive to aging and age-related pathology
Exercise training corrects control of spontaneous calcium waves in hearts from myocardial infarction heart failure rats
No full textImpaired cardiac control of intracellular diastolic Ca<sup>2+</sup> gives rise to arrhythmias. Whereas exercise training corrects abnormal cyclic Ca<sup>2+</sup> handling in heart failure, the effect on diastolic Ca<sup>2+</sup> remains unstudied. Here, we studied the effect of exercise training on the generation and propagation of spontaneous diastolic Ca<sup>2+</sup> waves in failing cardiomyocytes. Post-myocardial infarction heart failure was induced in Sprague–Dawley rats by coronary artery ligation. Echocardiography confirmed left ventricular infarctions of 40 ± 5%, whereas heart failure was indicated by increased left ventricular end-diastolic pressures, decreased contraction-relaxation rates, and pathological hypertrophy. Spontaneous Ca<sup>2+</sup> waves were imaged by laser linescanning confocal microscopy (488 nm excitation/505–530 nm emission) in 2 μM Fluo-3-loaded cardiomyocytes at 37°C and extracellular Ca<sup>2+</sup> of 1.2 and 5.0 mM. These studies showed that spontaneous Ca<sup>2+</sup> wave frequency was higher at 5.0 mM than 1.2 mM extracellular Ca<sup>2+</sup> in all rats, but failing cardiomyocytes generated 50% (P < 0.01) more waves compared to sham-operated controls at Ca<sup>2+</sup> 1.2 and 5.0 mM. Exercise training reduced the frequency of spontaneous waves at both 1.2 and 5.0 mM Ca2+ (P< 0.05), although complete normalization was not achieved. Exercise training also increased the aborted/completed ratio of waves at 1.2 mM Ca<sup>2+</sup> (P < 0.01), but not 5.0 mM. Finally, we repeated these studies after inhibiting the nitric oxide synthase with L-NAME. No differential effects were found; thus, mediation did not involve the nitric oxide synthase. In conclusion, exercise training improved the cardiomyocyte control of diastolic Ca<sup>2+</sup> by reducing the Ca<sup>2+</sup> wave frequency and by improving the ability to abort spontaneous Ca<sup>2+</sup> waves after their generation, but before cell-wide propagation
Interval training confers greater gains than continuous training in people with heart failure
No full textSummary of: Wisloff U et al (2007) Superior cardiovascular effect of aerobic interval training versus moderate continuous training in heart failure patients: a randomized study. Circulation 115: 3086–3094. [Prepared by Kylie Hill, CAP Editor.
Individual patient meta-analysis of exercise training effects on systemic brain natriuretic peptide expression in heart failure.
No full textMechanisms of exercise-induced improvements in the contractile apparatus of the mammalian myocardium
No full textOne of the main outcomes of aerobic endurance exercise training is the improved maximal oxygen uptake, and this is pivotal to the improved work capacity that follows the exercise training. Improved maximal oxygen uptake in turn is at least partly achieved because exercise training increases the ability of the myocardium to produce a greater cardiac output. In healthy subjects, this has been demonstrated repeatedly over many decades. It has recently emerged that this scenario may also be true under conditions of an initial myocardial dysfunction. For instance, myocardial improvements may still be observed after exercise training in post-myocardial infarction heart failure. In both health and disease, it is the changes that occur in the individual cardiomyocytes with respect to their ability to contract that by and large drive the exercise training-induced adaptation to the heart. Here, we review the evidence and the mechanisms by which exercise training induces beneficial changes in the mammalian myocardium, as obtained by means of experimental and clinical studies, and argue that these changes ultimately alter the function of the whole heart and contribute to the changes in whole-body function
Individual patient meta-analysis of exercise training effects on systemic brainnatriuretic peptide expression in heart failure
No full textBackground: Brain natriuretic peptide (BNP) predicts exercise performance and
exercise training may modulate BNP and its N-terminal portion (NT-pro-BNP), we
therefore conducted an individual patient analysis of exercise training effects
on BNP and NT-pro-BNP. Aims: To use an individual patient meta-analysis to relate
changes in BNP, NT-pro-BNP, and peak VO(2); to link these changes to volume
parameters of exercise training programmes (intensity etc.); and to identify
patient characteristics likely to lead to greater improvements in BNP,
NT-pro-BNP, and peak VO(2). Design: Individual patient meta-analysis. Methods: A
systematic search was conducted of Medline (Ovid), Embase.com, Cochrane Central
Register of Controlled Trials, and CINAHL (until July 2008) to identify
randomized controlled trials of aerobic and/or resistance exercise training in
systolic heart failure patients measuring BNP and/or NT-pro-BNP. Primary outcome
measures were change in BNP, NT-pro-BNP, and peak VO2. Subanalyses were conducted
to identify (1) patient groups that benefit most and (2) exercise programme
parameters enhancing favourable changes in primary outcome measures. Results: Ten
randomized controlled studies measuring BNP or NT-pro-BNP met eligibility
criteria, authors provided individual patient data for 565 patients (313 exercise
and 252 controls). Exercise training had favourable effects on BNP (-28.3%, p <
0.0001), NT-pro-BNP (-37.4%, p = < 0.0001), and peak VO(2) (17.8%, p < 0.0001).
The analysis showed a significant change in primary outcome measures; moreover,
change in BNP (r = -0.31, p < 0.0001) and NT-pro-BNP (r = -0.22, p < 0.0001) were
correlated with peak VO(2) change. Conclusion: Exercise training has favourable
effects on BNP, NT-pro-BNP, and peak VO(2) in heart failure patients and
BNP/NT-pro-BNP changes were correlated with peak VO(2) changes
The Effects of Exercise Training on Systemic Brain Natriuretic Peptide (BNP) and N-terminal BNP Expression in Heart Failure Patients: An Individual Patient Meta-analysis
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