Hypertension is a significant health concern. Hypertension leads to compensatory pathologic hypertrophy and impaired cardiac function. Lifestyle modifications such as exercise are encouraged for hypertensive patients. Some studies have shown that exercise training can reverse pathological hypertrophy. Conversely, studies on animal models of hypertension have shown increased cardiac growth with exercise training. Despite the further induction of hypertrophy, exercise training seems protective against cell death and may increase cardiomyocyte proliferation, leading to a putative phenotype. One of the hallmark beneficial effects of exercise in hypertension is an improvement in myocardial
Hypertension is a significant health concern, as it afflicts over 65 million individuals in the United States [
The effects of chronic exercise training on blood pressure have been well studied. In normotensive subjects, there is an approximate 3-4 mmHg reduction in resting systolic and diastolic blood pressure following training [
Chronic hypertension negatively impacts both myocardial structure and function by serving as a substrate for the induction of pathological, concentric hypertrophy (Figure
Compensatory pathologic hypertrophy induces cardiac remodeling. Concentric cardiomyocyte hypertrophy via increased calcineurin signaling, increased cell death per cardiomyocyte proliferation, increased fibrosis, impaired cardiac function, and decreased
With compensated myocardial hypertrophy, the heart remodels by the parallel addition of sarcomeres that characteristically increases cardiomyocyte area and width [
The development of compensated hypertrophy is regulated by mechanical loading factors in concert with the activation of endocrine, paracrine, and autocrine growth factors. These factors activate cardiomyocyte hypertrophic growth by signaling through specific G-protein coupled ligand receptors [
Compensatory cardiac remodeling with pressure overload is also influenced by the number of functioning cardiomyocytes. Thus understanding the balance between cardiomyocyte proliferation and apoptosis in pressure-induced hypertrophy is important [
One molecule that is centrally involved in cell survival is protein kinase B or Akt. Akt-mediated phosphorylation of Bad promotes sustained activation of prosurvival factors that induce cell survival by decreasing mitochondrial membrane destabilization and cytochrome c release [
Of significance, compensatory hypertrophy secondary to pressure overload is associated with a reduction in
The
Overstimulation of
Chronic exercise training causes a beneficial adaptive response of the cardiovascular system, that is, decreased resting and submaximal heart rates and increased LV filling time, venous return, and stroke volume [
Exercise training induces physiologic, eccentric cardiomyocyte hypertrophy where cardiomyocytes increase in cell length by approximately 7% [
The effects of exercise training on cardiac remodeling in hypertensive human subjects have been reviewed elsewhere [
In hypertensive animal studies, exercise training has been shown to reduce or delay the development of hypertension [
However, even though chronic exercise training reduces heart rate and blood pressure, it has been shown to increase hypertrophy at both the whole heart and cellular level in laboratory animals [
Our studies have also found that training mitigated calcineurin gene and protein expression in hypertension [
Studies in both normotensive and hypertensive humans and animals have shown that exercise training enhances
While treadmill running is typically used as the exercise modality, swimming has also been shown to be effective in increasing
In general, cardiac
Our work in SHR animals has shown that despite the induction of hypertrophy with treadmill running, exercise improved
Beyond improved
Compensated left ventricular hypertrophy in hypertension involves cardiomyocyte hypertrophy, apoptosis, and proliferation of cardiomyocytes. Exercise affects each of these pathways, but the contributory role of specific signaling pathways is not clear. Calcineurin expression is attenuated with exercise training, but in animal studies, exercise instead increases cardiomyocyte hypertrophy while decreasing apoptosis and fibrosis. High volume/intensity exercise in hypertension, however, may be deleterious to the heart by increasing apoptosis and cardiac dysfunction. In humans, exercise training shows equivocal morphometric results, with some studies showing a reduction in LV mass and others no change. In both humans and animals, exercise improves the overall phenotype of the heart. This effect appears to be independent of the blood pressure lowering effects of exercise. One of the hallmark phenotypical shifts with hypertension is a downregulation of the