Pileggi 2016 Abstract MitoFit Science Camp 2016

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Voluntary exercise prevents high fat diet-induced cardiac mitochondrial dysfunction in male rats.

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Chantal Pileggi

Pileggi C, Hedges CP, Vickers MH, McGlashan SR, Hickey AJR, Cameron-Smith D, Firth EC, Gray C (2016)

Event: MitoFit Science Camp 2016 Kuehtai AT

Obesity, hyperlipidemia and hypertension are all major risk factors for the development of cardiovascular diseases. Of the multiple cardiac aetiologies, cardiac mitochondrial dysfunction is a critical factor in the progression of heart disease. Exercise provides many beneficial health effects and is recommended for the prevention and management of cardiovascular disease. Therefore, this study aimed to determine the impact of voluntary exercise on rats fed a high-fat diet on mitochondrial metabolism of carbohydrate- and lipid-based substrates in cardiac tissue.

Weanling Sprague-Dawley male rats (aged 21 days (D21)) were allocated to receive either a standard chow diet(CD) or a high fat (HF) diet (45% kcal as fat) and fed ad-libitum and then further subdivided into sedentary (cage only exercise) (CD, HFD) or voluntary exercise groups (CDEX, HFEX) from days 64-120. Mitochondrial oxygen (O2) consumption was measured in permeabilized myofibers prepared from samples of the right atrial appendage. Cardiac tissue from the HFD sedentary rats displayed a 1.3-fold decrease in Complex I (CI) and Complex II (CII) oxidation of pyruvate and succinate, an effect that was reversed with exercise in the HFEX rats (p<0.05). Moreover, hearts from HFD and HFEX rats exhibited decreased mitochondrial oxidation of palmitoyl carnitine, malate, and succinate (p<0.05). Cardiac tissue from CDEX rats maintained similar respiratory levels as CD sedentary rats. Furthermore, expression of the mitochondrial transcription factor proliferator-activated receptor γ coacitvator α (PGC1α) was downregulated in sedentary HFD rats, but normalised in HFEX rats (p<0.05), suggesting that voluntary exercise may protect cardiac mitochondria during HFD.

These data show that HFD-induced mitochondrial dysfunction results in specific impairments in CI + CII maximal capacity to oxidize pyruvate and succinate as substrates in cardiac tissue, which is prevented by the introduction of exercise. We also provide evidence of altered mitochondrial transcription factor expression which may be one component of the adaptive responses within cardiac muscle facilitating an increased mitochondrial oxidative capacity.


O2k-Network Lab: NZ Auckland Hickey AJ


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style  Pathology: Cardiovascular  Stress:Mitochondrial disease  Organism: Rat  Tissue;cell: Heart  Preparation: Permeabilized tissue 


Pathway: F, N, NS 

Event: D2  MitoFit Science Camp 2016 

Affiliations

1-Liggins Inst, Univ Auckland; 2-College Sport Exercise Sc, Victoria Univ, Australia; 3-Applied Surgery Metabolism Lab, School Biol Sc, Univ of Auckland; 4-Dept Anatomy with Radiology, Univ Auckland, New Zealand; 5-Dept Paediatrics Child Health, Wellington. Univ Otago; New Zealand. - c.pileggi@auckland.ac.nz