Korean J Physiol Pharmacol.  2017 Nov;21(6):633-641. 10.4196/kjpp.2017.21.6.633.

Effects of intermittent ladder-climbing exercise training on mitochondrial biogenesis and endoplasmic reticulum stress of the cardiac muscle in obese middle-aged rats

Affiliations
  • 1Department of Physical Education, College of Physical Education, Keimyung University, Daegu 42601, Korea. kjk744@kmu.ac.kr

Abstract

The aim of this study is to investigate the effects of intermittent ladder-climbing exercise training on mitochondrial biogenesis and ER stress of the cardiac muscle in high fat diet-induced obese middle-aged rats. We induced obesity over 6 weeks of period in 40 male Sprague-Dawley rats around 50 weeks old, and were randomly divided into four experimental groups: chow, HFD, exercise+HFD, and exercise+chow. The exercising groups underwent high-intensity intermittent training using a ladder-climbing and weight exercise 3 days/week for a total of 8 weeks. High-fat diet and concurrent exercise resulted in no significant reduction in body weight but caused a significant reduction in visceral fat weight (p<0.05). Expression of PPARδ increased in the exercise groups and was significantly increased in the high-fat diet+exercise group (p<0.05). Among the ER stress-related proteins, the expression levels of p-PERK and CHOP, related to cardiac muscle damage, were significantly higher in the cardiac muscle of the high-fat diet group (p<0.05), and were significantly reduced by intermittent ladder-climbing exercise training (p<0.05). Specifically, this reduction was greater when the rats underwent exercise after switching back to the chow diet with a reduced caloric intake. Collectively, these results suggest that the combination of intermittent ladder-climbing exercise training and a reduced caloric intake can decrease the levels of ER stress-related proteins that contribute to cardiac muscle damage in obesity and aging. However, additional validation is required to understand the effects of these changes on mitochondrial biogenesis during exercise.

Keyword

Aging; Cardiac muscle; ER stress; High-fat diet-induced obesity; Ladder climbing exercise; Mitochondrial biogenesis

MeSH Terms

Aging
Animals
Body Weight
Diet
Diet, High-Fat
Endoplasmic Reticulum Stress*
Endoplasmic Reticulum*
Energy Intake
Humans
Intra-Abdominal Fat
Male
Myocardium*
Obesity
Organelle Biogenesis*
Rats*
Rats, Sprague-Dawley

Figure

  • Fig. 1 Body weight and visceral fat weight. (A) Changes in body weight after 8-week intervention. αSignificantly different from CD, CE (p<0.05). (B) Changes of visceral fat weight after 8-week intervention. +significantly different from CD, CE (p<0.05); *Significantly different from CD, CE, FE (p<0.05). CD, normal chow diet; CE, chow diet+exercise; FD, high-fat diet only; FE, high-fat diet+exercise.

  • Fig. 2 Expression levels of mitochondrial enzymes in the cardiac muscles. +Significantly different from CD, FD (p<0.05); *Significantly different from CD, FD, FE (p<0.05). CD, normal chow diet; CE, chow diet+exercise; FD, high-fat diet only; FE, high-fat diet+exercise. SUD, succinate dehydrogenase (A); Cyto C (B), cytochrome C.

  • Fig. 3 Changes in PPARβ (A) and PGC-1α (B) protein expression in the cardiac muscle after 8-week diet and/or exercise intervention. *Significantly different from CD, CE, FD (p<0.05). CD, normal chow diet; CE, chow diet+exercise; FD, high-fat diet only; FE, high-fat diet+exercise.

  • Fig. 4 Changes in (A) p-PERK, and (B) GRP78 (blue) and CHOP (red) protein expression levels in the cardiac muscle after 8 weeks of diet and/or exercise intervention. (A) +Significantly different from CD (p < 0.05); *Significantly different from CD, CE, FE (p<0.05). (B) +Significantly different from CD, FE (p<0.05); *Significantly different from CD, CE, FE (p<0.05). CD, normal chow diet; CE, chow diet+exercise; FD, high-fat diet only; FE, high-fat diet+exercise.

  • Fig. 5 Effect of ladder-climbing exercise training on mitochondrial biogenesis and ER stress of the cardiac muscle. We put forward a hypothesis that the concurrent stimulation from exercise training is more effective through inhibition of PERK and CHOP expression or the activation of PGC-1α and PPARb in protecting the cardiac muscle compared to a weight loss scheme that is entirely dependent on diet and reduced caloric intake. However, we could not suggest the significant relationship between PGC-1α and PPARβ and the activation GRP78 expression.


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