Abstract
Short-term consumption of a high-fat diet impairs exercise capacity in both rats and humans, and increases expression of the mitochondrial uncoupling protein, UCP3, in rodent cardiac and skeletal muscle via activation of the transcription factor, peroxisome proliferator-activated receptor α (PPARα). Unlike long-chain fatty acids however, medium-chain fatty acids do not activate PPARα and do not increase muscle UCP3 expression. We therefore investigated exercise performance and cardiac mitochondrial function in rats fed a chow diet (7.5% kcal from fat), a long-chain triglyceride (LCT) rich diet (46% kcal from LCTs) or a medium-chain triglyceride (MCT) rich diet (46% kcal from MCTs). Rats fed the LCT-rich diet for 15 days ran 55% less far than they did at baseline, whereas rats fed the chow or MCT-rich diets neither improved nor worsened in their exercise capacities. Moreover, consumption of an LCT-rich diet increased cardiac UCP3 expression by 35% and decreased oxidative phosphorylation efficiency, whereas consumption of the MCT-rich diet altered neither UCP3 expression nor oxidative phosphorylation efficiency. Our results suggest that the negative effects of short-term high-fat feeding on exercise performance are predominantly mediated by long-chain rather than medium-chain fatty acids, possibly via PPARα-dependent upregulation of UCP3.
Highlights
Metabolic efficiency is a major determinant of endurance performance, determining the speed or power that can be generated for a given level of oxygen consumption [1]
We demonstrated that consumption of a high fat diet for 9 days impaired exercise capacity in rats [2] and in similar studies, found that short-term high fat feeding impaired exercise efficiency [3] and cardiac energetics [4] in men, interestingly the detrimental effects on exercise performance were not seen in highly-trained individuals [5]
Unlike long-chain fatty acids medium-chain fatty acids do not activate peroxisome proliferator-activated receptor a (PPARa) [12], and in this study we investigated the effects of short-term high-fat feeding on exercise capacity and cardiac mitochondrial function using diets rich in long-chain triglyceride (LCT) and medium-chain triglyceride (MCT)
Summary
Metabolic efficiency is a major determinant of endurance performance, determining the speed or power that can be generated for a given level of oxygen consumption [1]. We demonstrated that consumption of a high fat diet for 9 days impaired exercise capacity in rats [2] and in similar studies, found that short-term high fat feeding impaired exercise efficiency [3] and cardiac energetics [4] in men, interestingly the detrimental effects on exercise performance were not seen in highly-trained individuals [5]. PPARa activation, upregulates levels of the mitochondrial uncoupling protein UCP3 [9,10]. We found that short-term high fat feeding increased cardiac and skeletal muscle UCP3 levels, and uncoupled skeletal muscle mitochondria [2]. A similar regime of high-fat feeding in rats increased mitochondrial fatty acid oxidation and uncoupling, resulting in decreasing cardiac efficiency [11]
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