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

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


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.


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

MeSH Terms

Body Weight
Diet, High-Fat
Endoplasmic Reticulum Stress*
Endoplasmic Reticulum*
Energy Intake
Intra-Abdominal Fat
Organelle Biogenesis*
Rats, Sprague-Dawley


  • 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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