Zachary J White, Keshari H Sudasinghe, David C Poole, Stephanie E Hall
{"title":"Exercise promotes cognition and hippocampal mitochondrial complex II expression in female rats.","authors":"Zachary J White, Keshari H Sudasinghe, David C Poole, Stephanie E Hall","doi":"10.1113/EP092533","DOIUrl":null,"url":null,"abstract":"<p><p>Evidence supports that exercise defends against age-associated declines in brain health and protects against neurodegenerative disease. To help understand the molecular basis for the neuroprotection, we examined the impact of training on mitochondrial protein expression within the exercise-brain axis. Thirty-two F344 rats (50% male/female) were assigned randomly to 10-week treadmill training or sedentary groups. Grip strength, Morris water maze and rotarod were used to assess muscular strength, spatial learning and motor coordination, respectively. Jess automated western blotting was used to quantify mitochondrial complex expression in hippocampus and soleus skeletal muscle samples. Values are means and standard deviation. Exercised females had better spatial memory (9.16 ± 8.70 vs. 32.7 ± 22.7 s, P = 0.043) and motor coordination (69.0 ± 16.1 vs. 47.5 ± 15.6 s, P = 0.042) as well as increased soleus mass (0.043 ± 0.003 vs. 0.039 ± 0.002% body mass, P = 0.039), hippocampal mitochondrial complex II expression (1.96 ± 0.38 vs. 1.11 ± 0.33 a.u., P = 0.007), and soleus mitochondrial complex III expression (6.68 ± 1.40 vs. 4.65 ± 1.26 a.u., P = 0.025) in comparison to sedentary females. Cognitive performance and hippocampal metabolic enzyme expression were concordantly increased following the 10-week exercise intervention in females but not males. These results provide novel support for the putative involvement of cerebral mitochondrial function in the beneficial relationship between exercise and brain health.</p>","PeriodicalId":12092,"journal":{"name":"Experimental Physiology","volume":" ","pages":""},"PeriodicalIF":2.6000,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental Physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1113/EP092533","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Evidence supports that exercise defends against age-associated declines in brain health and protects against neurodegenerative disease. To help understand the molecular basis for the neuroprotection, we examined the impact of training on mitochondrial protein expression within the exercise-brain axis. Thirty-two F344 rats (50% male/female) were assigned randomly to 10-week treadmill training or sedentary groups. Grip strength, Morris water maze and rotarod were used to assess muscular strength, spatial learning and motor coordination, respectively. Jess automated western blotting was used to quantify mitochondrial complex expression in hippocampus and soleus skeletal muscle samples. Values are means and standard deviation. Exercised females had better spatial memory (9.16 ± 8.70 vs. 32.7 ± 22.7 s, P = 0.043) and motor coordination (69.0 ± 16.1 vs. 47.5 ± 15.6 s, P = 0.042) as well as increased soleus mass (0.043 ± 0.003 vs. 0.039 ± 0.002% body mass, P = 0.039), hippocampal mitochondrial complex II expression (1.96 ± 0.38 vs. 1.11 ± 0.33 a.u., P = 0.007), and soleus mitochondrial complex III expression (6.68 ± 1.40 vs. 4.65 ± 1.26 a.u., P = 0.025) in comparison to sedentary females. Cognitive performance and hippocampal metabolic enzyme expression were concordantly increased following the 10-week exercise intervention in females but not males. These results provide novel support for the putative involvement of cerebral mitochondrial function in the beneficial relationship between exercise and brain health.
期刊介绍:
Experimental Physiology publishes research papers that report novel insights into homeostatic and adaptive responses in health, as well as those that further our understanding of pathophysiological mechanisms in disease. We encourage papers that embrace the journal’s orientation of translation and integration, including studies of the adaptive responses to exercise, acute and chronic environmental stressors, growth and aging, and diseases where integrative homeostatic mechanisms play a key role in the response to and evolution of the disease process. Examples of such diseases include hypertension, heart failure, hypoxic lung disease, endocrine and neurological disorders. We are also keen to publish research that has a translational aspect or clinical application. Comparative physiology work that can be applied to aid the understanding human physiology is also encouraged.
Manuscripts that report the use of bioinformatic, genomic, molecular, proteomic and cellular techniques to provide novel insights into integrative physiological and pathophysiological mechanisms are welcomed.