title: Exercise-induced heart mitochondrial cholesterol depletion influences the inhibition of mitochondrial swelling.
abstract: The significance of the reduction of the cholesterol pool in heart mitochondria after exercise is still unknown. Recently, published data have suggested that cholesterol may influence the components of mitochondrial contact site and affect mitochondrial swelling. Therefore, the aim of this study was to determine whether the decreased cholesterol content in heart mitochondria caused by prolonged swimming may provoke changes in their bioenergetics and result in an increased resistance to calcium chloride-induced mitochondrial swelling. Male Wistar rats were divided into a sedentary control group and an exercise group. The rats exercised for 3 h, burdened with an additional 3% of their body weight. Their hearts were removed immediately after completing the exercise. The left ventricle was divided and used for experiments. Mitochondrial cholesterol content, membrane fluidity and mitochondrial bioenergetics were measured in the control and exercised rat heart mitochondria. To assess whether mitochondrial modifications are linked to disruption of lipid microdomains, methyl-β-cyclodextrin, a well-known lipid microdomain-disrupting agent and cholesterol chelator, was applied to the mitochondria of the control group. Cholesterol depletion, increased membrane fluidity and increased resistance to calcium chloride-induced swelling were observed in postexercise heart crude mitochondrial fraction. Similar results were achieved in control mitochondria treated with 2% methyl-β-cyclodextrin. All of the mitochondrial bioenergetics parameters were similar between the groups. Therefore, the disruption of raft-like microdomains appears to be an adaptive change in the rat heart following exercise.
authors.affiliation: W. Ziolkowski: Department of Biochemistry, Gdansk University of Physical Education and Sport, 1 K. Gorskiego Street, 80-336 Gdansk, Poland. wiech@awf.gda.pl.
authors.forename: Wieslaw
authors.initials: W
authors.lastname: Ziolkowski
authors.forename: Dhivya
authors.initials: D
authors.lastname: Vadhana M S
authors.forename: Jan Jacek
authors.initials: JJ
authors.lastname: Kaczor
authors.forename: Robert Antoni
authors.initials: RA
authors.lastname: Olek
authors.forename: Damian Jozef
authors.initials: DJ
authors.lastname: Flis
authors.forename: Malgorzata
authors.initials: M
authors.lastname: Halon
authors.forename: Michal
authors.initials: M
authors.lastname: Wozniak
authors.forename: Donatella
authors.initials: D
authors.lastname: Fedeli
authors.forename: Manuel
authors.initials: M
authors.lastname: Carloni
authors.forename: Jedrzej
authors.initials: J
authors.lastname: Antosiewicz
authors.forename: Rosita
authors.initials: R
authors.lastname: Gabbianelli
mesh_terms: D000818:Animals; D002122:Calcium Chloride / Q000494:pharmacology; D002784:Cholesterol / Q000378:metabolism*; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008560:Membrane Fluidity; D008929:Mitochondria, Heart / Q000378:metabolism*; D008933:Mitochondrial Swelling / Q000187:drug effects / Q000502:physiology*; D018384:Oxidative Stress; D010805:Physical Conditioning, Animal; D051381:Rats; D017208:Rats, Wistar; D013550:Swimming
chemical_list: D019344:Lactic Acid; D002784:Cholesterol; D002122:Calcium Chloride