Dietary long-chain, but not medium-chain, triglycerides impair exercise performance and uncouple cardiac mitochondria in rats

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.

Novel ketone diet enhances physical and cognitive performance

“…Performance was elevated both above baseline running performance and above that of rats that were pair fed isocaloric diets with ketone ester replaced with fat or carbohydrate. In previous studies, using this protocol, we have found that provision of a high‐fat diet (55% of kcal from fat) worsened running performance in rats (15), as did a diet in which long‐chain triglycerides (46% kcal) were provided, although rats that consumed medium‐chain triglycerides (46% kcal; associated with increased ketone body production) were not affected to the same extent (42). Researchers have proposed the use of the ketogenic diet as a training aid because of its effects in elevating muscle fatty acid oxidation rates (43).…”

Potential Role of Leptin in Cardiac Steatosis Induced by Highly Saturated Fat Intake during Adolescence

“…In regard to the role that FAs might have on both UCP2 and UCP3 regulation, it has to be noted that oleic acid has been suggested to stimulate the activity of the promoter regions of UCP2 and UCP3 genes and the FA responsive regions . Another study has reported that medium‐chain fatty acids, such as lauric acid contained in SOLF, are less efficient that long‐chain fatty acids in triggering cardiac mitochondrial uncoupling; therefore, the difference between SOLF and UOLF adolescent mice could be due in part to the elevated lauric acid content in in SOLF.…”

A Ketogenic Diet in Rodents Elicits Improved Mitochondrial Adaptations in Response to Resistance Exercise Training Compared to an Isocaloric Western Diet

“…The putative KD utilized in the current study contained fat sources primarily from medium chain triglycerides (i.e., MCTs, canola oil, and flaxseed oil). Interestingly, it has been reported that long-chain triglycerides, but not medium-chain triglycerides, can result in uncoupling of mitochondrial respiration along with increased uncoupling protein expression (Murray et al, 2011). This observation would explain the increased uncoupling protein expression and respiration rates described in previous studies, while our current findings may be explained by long-chain triglycerides in the WD-fed animals causing an uncoupling stimulus in complex II and lack of this stimulus in KD-fed animals.…”