Autophagy And Exercise Cardioprotection: The Role Of Mitochondrial And Sarcolemmal KATP Channels

Quindry, John C.; Schreiber, Lindsey; McGinnis, Graham R.; Nanayakkara, Gayani; Amin, Rajesh

doi:10.1249/01.mss.0000389632.92682.05

Cited by 1 publication

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“…This idea, although speculative, is supported by reports showing that endurance exercise training is accompanied by terminal deoxynucleotidyl-dUTP nick end labelingpositive nuclei and activation of apoptotic mediators (Bax, cytochrome c, cleaved caspase-3, and cleaved PARP) in LV cardiomyocytes (18) as well as enhanced abundance of cardiac progenitor cells (21). In addition, cardiac autophagy has been recently associated with exercise training, with some data pointing to its involvement in exercise-induced cardioprotection (4,40). However, the role of apoptosis and autophagy in the exercised heart is still under debate, and further data are needed to clarify this issue.…”

Section: Discussionmentioning

confidence: 95%

Moderate exercise training provides left ventricular tolerance to acute pressure overload

Moreira-Gonçalves

Henriques‐Coelho²,

Fonseca

et al. 2011

American Journal of Physiology-Heart and Circulatory Physiology

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The present study evaluated the impact of moderate exercise training on the cardiac tolerance to acute pressure overload. Male Wistar rats were randomly submitted to exercise training or sedentary lifestyle for 14 wk. At the end of this period, the animals were anaesthetized, mechanically ventilated, and submitted to hemodynamic evaluation with biventricular tip pressure manometers. Acute pressure overload was induced by banding the descending aorta to induce a 60% increase of peak systolic left ventricular pressure during 120 min. This resulted in the following experimental groups: 1) sedentary without banding (SED + Sham), 2) sedentary with banding (SED + Band), and 3) exercise trained with banding (EX + Band). In response to aortic banding, SED + Band animals could not sustain the 60% increase of peak systolic pressure for 120 min, even with additional narrowing of the banding. This was accompanied by a reduction of dP/d tmax and dP/d tmin and a prolongation of the time constant tau, indicating impaired systolic and diastolic function. This impairment was not observed in EX + Band ( P < 0.05 vs. SED + Band). Additionally, compared with SED + Band, EX + Band presented less myocardial damage, exhibited attenuated protein expression of active caspase-3 and NF-κB ( P < 0.016), and showed less protein carbonylation and nitration ( P < 0.05). These findings support our hypothesis that exercise training has a protective role in the modulation of the early cardiac response to pressure overload.

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