Exercise training inducibility of MnSOD protein expression and activity is retained while reducing prooxidant signaling in the heart of senescent rats

Abstract

While the stress response to heat and exercise is limited in the heart with progressive aging, recent data indicate that acute or short-term exercise upregulates the Mn isoform of superoxide dismutase (MnSOD), which may provide protection against ischemia-reperfusion injury and cell death by reducing oxidative stress. Growing evidence indicates that inducible nitric oxide synthase (iNOS) contributes to age-induced increases in oxidative stress and risk of heart failure. We postulated that oxidative stress and iNOS levels would be related to the ability of the aging heart to upregulate MnSOD in response to long-term exercise training. Six- and twenty-seven-mo-old Fischer-344 rats had been assigned to young sedentary (YS), young exercise (YE), old sedentary (OS), or old exercise (OE) groups. ET groups ran on a treadmill for 60 min/day, 5 days/wk for a total of 12 wk. MnSOD protein expression in the left ventricle was increased (+43%) by 12 wk of exercise training in the old age group, with no changes in Cu,ZnSOD. Exercise training also increased MnSOD activity in left ventricles from old and young rats. HSP70 was inducible by exercise training in hearts exclusively from the young age group. iNOS protein expression increased markedly with aging (+548%), while exercise training decreased iNOS levels by -73% in OE compared with OS. In addition, 4-hydroxynonenal protein adducts in the left ventricle increased by 237% with aging, while 12 wk of exercise training resulted in attenuation (-55%). These data indicate that inducibility of MnSOD is preserved with long-term exercise training in the aging rat heart. Moreover, upregulation of MnSOD in the aging heart was directly associated with attenuated levels of oxidative stress, including iNOS.

Vascular redox imbalance in rats submitted to chronic exercise

“…Moreover, the training was able to attenuate the increase on 4-hydroxynonenal protein adducts with the aging. 29 On arterial level similar results were found by another study, which had played increased SOD activity and no change in CAT activity in female Yucatan miniature pigs that had physical training for 16-19 weeks. It was also seen in this same study an increase in the immunocontent of SOD-1, but no modification in CAT immunocontent.…”

A 6-week training program increased muscle antioxidant system in elderly diabetic fatty rats

“…Previous data have demonstrated that the major antioxidant enzyme, MnSOD, is most consistently upregulated by exercise training. In this respect, a 12-week training program resulted in upregulation of MnSOD in hearts from old rats [23]. The ability of exercise training to upregulate protective MnSOD protein may explain, at least in part, the improvement of total antioxidant status (TAS) that we also found in diabetic exercised rats.…”

Exercise and Cardiac Preconditioning Against Ischemia Reperfusion Injury

“…Neither iNOS nor COX-2 levels were over-expressed in young hearts from exercised animals that exhibited cardioprotection against global IR [54, 58]. Given the obvious link between advancing age and heart disease incidence, cardiac iNOS levels increase with advancing age, though a few weeks of exercise training effectively reverses this effect [103]. Building on this understanding, we also demonstrated that myocardial iNOS and COX-2 levels were not associated with anti-apoptotic effects in aged hearts exposed to IR [54, 58].…”