Abstract
The promotion of ketone body (KB) metabolism via ketosis has been suggested as a strategy to increase exercise performance. However, studies in humans and animals have yielded inconsistent results. The purpose of the current study was to examine the effects of ketosis, achieved via fasting or a short-term ketogenic diet (KD), on endurance exercise performance in female mice. After 8 h of fasting, serum KB significantly increased and serum glucose significantly decreased in fasted compared to fed mice. When subjected to an endurance exercise capacity (EEC) test on a motorized treadmill, both fed and fasted mice showed similar EEC performance. A 5-week KD (90% calories from fat) significantly increased serum KB but did not increase EEC times compared to chow-fed mice. KD mice gained significantly more weight than chow-fed mice and had greater adipose tissue mass. Biochemical tissue analysis showed that KD led to significant increases in triglyceride content in the heart and liver and significant decreases in glycogen content in the muscle and liver. Furthermore, KD downregulated genes involved in glucose and KB oxidation and upregulated genes involved in lipid metabolism in the heart. These findings suggest that a short-term KD is not an effective strategy to enhance exercise performance and may lead to increased adiposity, abnormal endogenous tissue storage, and cardiometabolic remodeling.
Highlights
Ketosis is a physiological metabolic state of elevated serum ketone bodies that may occur in situations of fasting/starvation [1], exercise [2], or diabetes [3,4]
The lipid metabolism genes Cd36, Pparα, and Hadhb, and the ketogenic gene Hmgcs1 were downregulated in the liver in response to the ketogenic diet (KD) (Figure 6C). These findings suggest that a shortterm KD has profound effects on the expression of genes involved in cardiac glucose, lipid, and ketone body metabolism, with relatively minor changes in the skeletal m7uosfc1l4e and liver
The KD may result in metabolic remodeling in the heart by downregulating genes involved in glucose and ketone body oxidative pathways and upregulating lipid utilization pathways
Summary
Ketosis is a physiological metabolic state of elevated serum ketone bodies that may occur in situations of fasting/starvation [1], exercise [2], or diabetes [3,4] In these situations, the serum ketone body concentrations in both humans and rodents rise from ~0.2 mM to above 3.0 mM and can rise to even higher levels in the pathological condition of ketoacidosis [5]. Once inside the peripheral cell, β-OHB (the most highly concentrated ketone body) is rapidly oxidized via the enzymes Bdh, succinyl-CoA:3-oxoacid-CoA transferase (Scot, encoded by Oxct1), and Acat into acetyl CoA for subsequent entry into the tricarboxylic acid (TCA) cycle, providing reducing equivalents for the electron transport chain
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