Enhanced Acidotic Myocardial Ca2+ Responsiveness with Training in Hypertension

Renna, Brian F.; Kubo, Hajime; MacDonnell, Scott M.; Crabbe, Deborah L.; Reger, Patricia O.; Houser, Steven R.; Libonati, Joseph R.

doi:10.1249/01.mss.0000218133.89584.a6

Cited by 21 publications

(32 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Recently, specific signaling cascades have been associated with concentric and eccentric hypertrophic phenotypes, i.e., IGF and calcineurin (26,27). While compensatory concentric hypertrophy is often regarded as an adaptation to normalize wall stress in hypertension, it is frequently manifest with abnormal cardiac function (17,24,34,35). While recent reports have questioned the necessity of wall stress normalization (10), the mechanisms associated with the dichotomous adaptive and maladaptive aspects of myocardial hypertrophy are important to understand.…”

Section: Discussionmentioning

confidence: 99%

“…While the control mechanisms for the induction of cardiomyocyte proliferation remain unclear, one theory purports the involvement of a resident population of cardiac progenitor cells (1, 30), which have been shown to increase their activity in stress-induced pathological conditions (1,28,31). In the hypertensive heart, cardiomyocyte proliferation may counteract apoptosis, thus reducing the progressive loss of cardiomyocytes.Recent studies from our laboratory, as well as others, have shown an overall phenotypical improvement for the myocardium with exercise training in hypertension (3,17,24,34,35,42). However, the precise putative mechanisms associated with the observed adaptations with exercise training remain unclear.…”

mentioning

confidence: 93%

“…Recent studies from our laboratory, as well as others, have shown an overall phenotypical improvement for the myocardium with exercise training in hypertension (3,17,24,34,35,42). However, the precise putative mechanisms associated with the observed adaptations with exercise training remain unclear.…”

mentioning

confidence: 93%

See 2 more Smart Citations

Left ventricular remodeling with exercise in hypertension

Kolwicz

MacDonnell

Renna

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

.-We investigated how exercise training superimposed on chronic hypertension impacted left ventricular remodeling. Cardiomyocyte hypertrophy, apoptosis, and proliferation in hearts from female spontaneously hypertensive rats (SHRs) were examined. Four-month-old SHR animals were placed into a sedentary group (SHR-SED; n ϭ 18) or a treadmill running group (SHR-TRD, 20 m/min, 1 h/day, 5 days/wk, 12 wk; n ϭ 18). Age-matched, sedentary Wistar Kyoto (WKY) rats were controls (n ϭ 18). Heart weight was greater in SHR-TRD vs. both WKY (P Ͻ 0.01) and SHR-SED (P Ͻ 0.05). Morphometricderived left ventricular anterior, posterior, and septal wall thickness were increased in SHR-SED relative to WKY and augmented in SHR-TRD. Cardiomyocyte surface area, length, and width were increased in SHR-SED relative to WKY and further increased in SHR-TRD. Calcineurin abundance was increased in SHR-SED vs. WKY (P Ͻ 0.001) and attenuated in SHR-TRD relative to SHR-SED (P Ͻ 0.05). Protein abundance and mRNA of Akt was not different among groups. The rate of apoptosis was increased in SHR-SED relative to WKY and mitigated in SHR-TRD. The abundance of Ki-67 ϩ cells across groups was not statistically different across groups. The abundance of cardiac progenitor cells (c-Kit ϩ cells) was increased in SHR-TRD relative to WKY. These data suggest that exercise training superimposed on hypertension augmented cardiomyocyte hypertrophy, despite attenuating calcineurin abundance. Exercise training also mitigated apoptosis in hypertension and showed a tendency to enhance the abundance of cardiac progenitor cells, resulting in a more favorable cardiomyocyte number in the exercise-trained hypertensive heart. hypertrophy; myocytes; apoptosis; proliferation CHRONIC HYPERTENSION INDUCES overall cardiac enlargement, which is, in part, due to cardiomyocyte hypertrophy. This is a significant health issue, since pathological cardiac enlargement increases the risk for the development of congestive heart failure (4). Increased apoptosis has also been noted in the hypertensive heart, which may be an integral substrate in overall remodeling and progression to heart failure (33).Several studies have reported that cardiac myocytes are capable of mitotic division and proliferation (13,14). While the control mechanisms for the induction of cardiomyocyte proliferation remain unclear, one theory purports the involvement of a resident population of cardiac progenitor cells (1, 30), which have been shown to increase their activity in stress-induced pathological conditions (1,28,31). In the hypertensive heart, cardiomyocyte proliferation may counteract apoptosis, thus reducing the progressive loss of cardiomyocytes.Recent studies from our laboratory, as well as others, have shown an overall phenotypical improvement for the myocardium with exercise training in hypertension (3,17,24,34,35,42). However, the precise putative mechanisms associated with the observed adaptations with exercise training remain unclear. Our present hypothesis is that exercise training in hypertension ...

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 93%

See 1 more Smart Citation

Left ventricular remodeling with exercise in hypertension

Kolwicz

MacDonnell

Renna

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…us one of the major bene�ts of exercise training in hypertension is the preservation of cardiomyocyte cell number. Despite the potential for exercise training to increase myocardial mass in pressure overload, most studies have reported an improved phenotype aer training [25,30,46,61,[80][81][82][83][84][85][86][87]. One of the most proli�c bene�ts of exercise training is its improvement on adrenergic signaling.…”

Section: Cardiac Remodelingmentioning

confidence: 99%

Cardiac Effects of Exercise Training in Hypertension

Libonati

2013

ISRN Hypertension

Self Cite

View full text Add to dashboard Cite

Hypertension is a signi�cant health concern. Hypertension leads to compensatory pathologic hypertrophy and impaired cardiac function. Lifestyle modi�cations 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. �ne of the hallmark bene�cial effects of exercise in hypertension is an improvement in myocardial adrenergic responsiveness. e focus of this paper is to discuss how exercise training impacts cardiac remodeling and function in the hypertensive heart with speci�c reference to adrenergic signaling.

show abstract

“…As a consequence, maximal levels of the aerobic exercise test can create a response of significant lactic acidosis [4], left ventricular contractility and function in healthy adolescent subjects may be altered. Namely, exercise may induce a myocardial phenotype that reduces Ca +2 responsiveness during acidosis [5].…”

Section: Introductionmentioning

confidence: 99%

Are there Differences between Adolescent Males and Females for Maintaining the Metabolic Cost at Maximal Oxygen Uptake?

Saghiv¹,

Sherve²,

Sira³

et al. 2017

J Clin Exp Cardiolog

View full text Add to dashboard Cite

Purpose: The present study looked at gender difference in oxygen delivery-extraction at maximal oxygen uptake in healthy adolescents.Methods: 36 adolescent males (14.9 ± 1.1 years) and 33 adolescent females (15.0 ± 1.1 years) underwent a maximal oxygen uptake test and a two dimensional direct m-mode echocardiography performed on a bicycle ergometry. Arteriovenous oxygen difference was defined by utilizing the Fick equation.Results: At rest, males compared to females had significantly (p<0.05) higher oxygen extraction (38.8 ± 1.4 and 31.8 ± 1.2 mL.kg -1 . min -1 respectively), systolic blood pressure, and mean arterial blood pressure. At peak exercise test, males compared to females demonstrated significant (P<0.05) higher values for cardiac output (16.6 ± 0.7 and 15.4 ± 0.6 L•min -1 respectively), stroke volume (83.9 ± 5.1 and 78.5 ± 4.6 mL respectively), oxygen uptake (47.3 ± 3.7 and 39.6 ± 1.1 mL•kg -1 •min -1 , respectively), while oxygen extraction was significantly higher in females compared to males (123.6 ± 7.6 and 115.5 ± 5.4 mL • L -1 respectively). Conclusions:This study suggests that normal adolescents; male and females respond to the maximal oxygen uptake test by increased their left ventricular systolic function, however, it was less augmented in the females due to gender and energy metabolism differences. Consequently, females increased their oxygen extraction more than the males as a compensation for the lower cardiac output and hence, lower oxygen delivery.

show abstract

Enhanced Acidotic Myocardial Ca2+ Responsiveness with Training in Hypertension

Abstract: Myocardial tolerance to acidosis is improved during the adaptive phase of compensatory hypertrophy. Furthermore, exercise training in SHR induced a myocardial phenotype that preserved Ca(2+) responsiveness during acidosis.

Cited by 21 publications

References 30 publications

Left ventricular remodeling with exercise in hypertension

Left ventricular remodeling with exercise in hypertension

Cardiac Effects of Exercise Training in Hypertension

Are there Differences between Adolescent Males and Females for Maintaining the Metabolic Cost at Maximal Oxygen Uptake?

Contact Info

Product

Resources

About