Abstract: Maintenance of mitochondrial health, which is supported in part by dietary antioxidants such as selenium (Se) and vitamin E (vitE), is pertinent to optimizing athletic performance. Deficiencies in Se and vitE negatively impact muscle health but mitochondrial adaptations to various levels of dietary Se and vitE are poorly understood. Young Quarter Horses (mean ± SD: 17.6 ± 0.9 mo) undergoing submaximal exercise training were used to test the hypothesis that a proprietary antioxidant blend containing elevated Se yeast (EconomasE, Alltech, Inc., Nicholasville, KY) would improve mitochondrial characteristics compared to Se at current requirements, even with reduced vitE intake. Horses were balanced by age, sex, body weight (BW), and farm of origin and randomly assigned to one of three custom-formulated concentrates fed at 1% BW (dry matter, DM basis) for 12 wk: 1) 100 IU vitE/kg DM and 0.1 mg Se/kg DM (CON, n = 6); 2) no added vitE plus EconomasE to provide 0.1 mg Se/kg DM (ESe1, n = 6); or 3) no added vitE plus EconomasE to provide 0.3 mg Se/kg DM (ESe3, n = 6). Samples collected at week 0 and 12 were analyzed for serum Se and middle gluteal glutathione peroxidase (GPx) and mitochondrial enzyme activities by kinetic colorimetry and mitochondrial capacities by high-resolution respirometry. Data were analyzed using mixed linear models in SAS v9.4 with repeated measures (time) and fixed effects of time, diet, and time × diet; horse(diet) served as a random effect. Serum Se tended to increase in all horses by week 12 (P = 0.08) but was unaffected by diet. Muscle GPx activity remained similar among all horses throughout the duration of the study. Mitochondrial volume density (citrate synthase [CS] activity), integrative function (cytochrome c oxidase [CCO] activity per mg protein), and integrative (per mg tissue) oxidative (P) and electron transfer (E) capacities increased from week 0 to 12 in all horses (P ≤ 0.01). Intrinsic (relative to CS) CCO activity decreased in all horses (P = 0.001), while intrinsic P and E capacities decreased only in ESe1 horses from week 0 to 12 (P ≤ 0.002). These results suggest that feeding EconomasE to provide 0.3 mg Se/kg DM may prevent adverse effects of removing 100 IU dietary vitE/kg DM on mitochondria in young horses. More research is needed to determine optimal dietary Se and vitE levels in performance horses to maximize mitochondrial energy production. Mitochondria, colloquially referred to as the powerhouses of the cell, are essential for sustained energy production, which is particularly important for athletic performance. During exercise, reactive oxygen species (ROS) are produced as a normal byproduct of muscle contraction. ROS act as critical signaling molecules and are essential to stimulate adaptation to exercise and other stressors. However, if excess ROS are produced and not sequestered by antioxidants, they may damage cellular components such as lipids, proteins, and DNA. Selenium (Se) and vitamin E (vitE) are two primary dietary antioxidants that aid in quenching excess ROS. To evaluate the impact of Se and vitE on mitochondria, three diets differing in Se and vitE levels were provided to lightly exercising young horses for 12 wk. Skeletal muscle mitochondrial capacity was negatively impacted by the reduction of dietary vitE, which was rescued with elevated dietary Se. The results highlight the importance of determining optimal levels of minerals and vitamins in performance horse diets to ensure proper energy production during exercise.
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The study explores how a selenium-rich diet can counteract the harmful effects on mitochondrial function in young horses caused by reduced intake of vitamin E. This has important implications for optimizing their athletic performance.
Study Design and Participants
The investigation involved young Quarter Horses who underwent submaximal exercise training. These horses were assigned to one of three specially formulated diets for 12 weeks.
The three different diets contained varying amounts of vitamin E and selenium. The first diet had 100 IU vitamin E/kg (dry matter, DM) and 0.1 mg selenium/kg DM, the second had no added vitamin E and 0.1 mg selenium/kg DM, and the third had no added vitamin E and 0.3 mg selenium/kg DM.
The different levels of vitamin E and selenium were achieved by supplementing the horses’ meals with an antioxidant blend (EconomasE) known for its high yeast selenium content.
Data Collection and Analysis
The researchers collected samples at the start and end of the trial. These were analyzed for selenium levels in serum, and the glutathione peroxidase (an enzyme that neutralizes damaging free radicals) and mitochondrial enzyme functions in middle gluteal muscles.
The results were analysed using mixed linear models in SAS v9.4 with repeated measures (time) and fixed effects of time, diet, and the interaction of time and diet; each horse’s diet serve as a random effect.
Key Findings
All horses showed a slight increase in serum selenium levels by the end of the experiment.
There were no significant changes in muscle glutathione peroxidase activity across all horses during the trial.
All horses exhibited significant increases in mitochondrial volume density and function, and oxidative and electron transfer capacities.
Relative to citrate synthase activity, cytochrome c oxidase activity decreased in all horses, while oxidative and electron transfer capacities decreased only in horses fed with lower selenium but with no Vitamin E. This suggests a protective effect of supplemented selenium against the adverse effects of reduced Vitamin E intake.
Results suggest that a diet providing 0.3 mg selenium/kg DM can potentially counteract the negative impacts of removing 100 IU dietary vitamin E/kg DM on mitochondria in young horses.
The researchers highlight the need for further research to determine optimal dietary selenium and vitamin E levels in performance horses to maximize mitochondrial energy production.
Cite This Article
APA
Owen RN, Semanchik PL, Latham CM, Brennan KM, White-Springer SH.
(2022).
Elevated dietary selenium rescues mitochondrial capacity impairment induced by decreased vitamin E intake in young exercising horses.
J Anim Sci, 100(8), skac172.
https://doi.org/10.1093/jas/skac172
Department of Animal Science, Texas A&M University and Texas A&M AgriLife Research, College Station, TX 77843, USA.
Semanchik, Pier L
Department of Animal Science, Texas A&M University and Texas A&M AgriLife Research, College Station, TX 77843, USA.
Latham, Christine M
Department of Animal Science, Texas A&M University and Texas A&M AgriLife Research, College Station, TX 77843, USA.
Brennan, Kristen M
Alltech Inc., Nicholasville, KY 40356, USA.
White-Springer, Sarah H
Department of Animal Science, Texas A&M University and Texas A&M AgriLife Research, College Station, TX 77843, USA.
MeSH Terms
Animals
Antioxidants / metabolism
Body Weight
Dietary Supplements
Horses
Mitochondria / metabolism
Selenium / metabolism
Vitamin E / pharmacology
Grant Funding
Alltech, Inc.
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