Acute exercise causes mitochondrial DNA deletion in rat skeletal muscle

Sakai, Yasutomo; Iwamura, Yukio; Hayashi, Jun‐Ichi; Yamamoto, Nao; Ohkoshi, Norio; Nagata, Hiroshi

doi:10.1002/(sici)1097-4598(199902)22:2<258::aid-mus15>3.0.co;2-1

Cited by 19 publications

(19 citation statements)

References 20 publications

(22 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Exercise has been shown to cause a mtDNA deletion in rat skeletal muscle [30]. In the present study, the subjects recruited as athletes were national class athletes and have been engaged in endurance training for several years.…”

Section: Resultsmentioning

confidence: 99%

The Effects of Cytoplasmic Transfer of mtDNA in Relation to Whole-Body Endurance Performance.

Soma¹,

Murakami²,

Hayashi³

et al. 2001

JJP

Self Cite

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 99%

The Effects of Cytoplasmic Transfer of mtDNA in Relation to Whole-Body Endurance Performance.

Soma¹,

Murakami²,

Hayashi³

et al. 2001

JJP

Self Cite

View full text Add to dashboard Cite

“…There is little information on the association between mtDNA common deletion and exhaustive exercise-induced tissue injury. In an study with adult rats after acute exercise (a running speed of 40 m/min for 20 min), the mtDNA 380-bp deletion was increased in skeletal muscle compared to sedentary controls (Sakai et al 1999). The present exercise training had signiWcant impact on changes in myocardial mtDNA 4834 deletion.…”

Section: Discussionmentioning

confidence: 99%

Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats

et al. 2009

View full text Add to dashboard Cite

Even though exhaustive exercise-induced oxidative stress increases the risk of tissue damage, regular endurance training is widely assumed to improve cardiac function and protects against heart disease. We tested the hypothesis that an endurance training program prevents exhaustive exercise-induced increases in cardiac dysfunction and apoptosis in left ventricle (LV). Thirty-two male Sprague-Dawley rats were randomly divided into four groups: sedentary control (C), trained (T), exhaustively exercised (E), and trained plus exhaustively exercised (TE). Rats in T and TE groups ran on a motorized treadmill for 12 weeks. Rats in groups E and TE performed an exhaustive running test on a treadmill. The main effects of training were indicated by increased running time to exhaustion (80 +/- 5 and 151 +/- 13 min for groups E and TE, respectively, P = 0.0001), myocardial hypertrophy (0.38% and 0.47% for untrained and trained rats, respectively, P = 0.0002), decreased LV ejection fraction (88% and 71% for untrained and trained rats, respectively, P < 0.0001), accelerated mitochondrial DNA 4834-bp large deletion (mtDNA4834 deletion), and up-regulated protein levels of heat shock protein-70, cytochrome C, cleaved capsase-3, and cleaved PARP in LV following a bout of exhaustive exercise. Contrary to our hypothesis, these results suggest that endurance training induced significant impairment of regional systolic and diastolic LV myocardial function and ejection fraction in rats. Our findings show that endurance training accelerates exhaustive exercise-induced mtDNA4834 deletion and apoptosis in the LV.

show abstract

“…Polyunsaturated fatty acids (e.g., in membrane phospholipids) are very sensitive to lipid peroxidation [7]. Acute exercise may also cause large-scale deletion of mitochondrial DNA and ultrastructural mitochondrial changes in the soleus muscle [8].…”

Section: Introductionmentioning

confidence: 99%

Free radical changes in rat muscle tissue after exercise

et al. 2001

View full text Add to dashboard Cite

Intense exercise accompanied by a manifold increase in oxygen utilization over resting conditions has been shown to elevate the probability of the appearance of free radicals. One of the effects of free radicals appears to be the peroxidation of cell membrane lipids resulting in malondialdehyde formation, which is detrimental to cell function. A common method for the measurement of malondialdehyde involves a reaction with thiobarbituric acid. The aim of this study was to evaluate the influence of exercise on concentrations of thiobarbituric acid-reactive substances (TBARS) in the gastrocnemius and soleus muscles of rats. Thirty male rats were used in this study. Soleus and gastrocnemius muscle biopsies were performed and TBARS levels were studied in these two muscles. The rats were randomly assigned to three groups of ten each. Group A was the control group and did not perform exercise. In group B, gastrocnemius and soleus muscle biopsies were performed immediately after exercise, and in group C muscle biopsies were performed on the 2nd postexercise day. The exercise resulted in a significant increase in TBARS in the gastrocnemius muscle. In the soleus, TBARS also increased, but this was not statistically significant. In conclusion, exercise-induced free radical changes may depend on the muscle type studied.

show abstract

Acute exercise causes mitochondrial DNA deletion in rat skeletal muscle

Cited by 19 publications

References 20 publications

The Effects of Cytoplasmic Transfer of mtDNA in Relation to Whole-Body Endurance Performance.

The Effects of Cytoplasmic Transfer of mtDNA in Relation to Whole-Body Endurance Performance.

Endurance training accelerates exhaustive exercise-induced mitochondrial DNA deletion and apoptosis of left ventricle myocardium in rats

Free radical changes in rat muscle tissue after exercise

Contact Info

Product

Resources

About