1.
Molecular Regulators of Muscle Mass and Mitochondrial Remodeling Are Not Influenced by Testosterone Administration in Young Women.
Horwath, O, Moberg, M, Hirschberg, AL, Ekblom, B, Apró, W
Frontiers in endocrinology. 2022;13:874748
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Testosterone is a sex hormone normally found in higher amounts in adult males than females. Testosterone plays a number of important roles, including influencing muscle size and strength. Treatment with testosterone has been shown to increase lean mass and muscle strength in women as well as men. However, female-only studies are limited, and the precise mechanisms underlying these changes are not well understood. This randomised control trial examined the effect of testosterone administration on regulators of muscle protein turnover and mitochondrial function in muscle samples collected from young women. 48 healthy, pre-menopausal women were assigned to receive either 10mg of transdermal testosterone gel per day, or a placebo, for 10 weeks. Muscle samples were collected via biopsy before and after the intervention. Testosterone administration did not appear to have a significant effect on androgen receptors, 5-alpha reductase, anabolic signalling, or mitochondrial remodelling in muscle tissue. The researchers concluded that improvements in muscle size and oxidative capacity following testosterone administration cannot be explained by changes in protein expression related to muscle protein turnover or mitochondrial remodelling. The authors went on to suggest that the small sample size in this study may have reduced the ability to detect small but biologically relevant changes in protein levels. Within the research, there is large variability among studies in terms of sex, age, route of administration and length of treatment, which makes putting these findings into context of the wider literature difficult.
Abstract
Testosterone (T) administration has previously been shown to improve muscle size and oxidative capacity. However, the molecular mechanisms underlying these adaptations in human skeletal muscle remain to be determined. Here, we examined the effect of moderate-dose T administration on molecular regulators of muscle protein turnover and mitochondrial remodeling in muscle samples collected from young women. Forty-eight healthy, physically active, young women (28 ± 4 years) were assigned in a random double-blind fashion to receive either T (10 mg/day) or placebo for 10-weeks. Muscle biopsies collected before and after the intervention period were divided into sub-cellular fractions and total protein levels of molecular regulators of muscle protein turnover and mitochondrial remodeling were analyzed using Western blotting. T administration had no effect on androgen receptor or 5α-reductase levels, nor on proteins involved in the mTORC1-signaling pathway (mTOR, S6K1, eEF2 and RPS6). Neither did it affect the abundance of proteins associated with proteasomal protein degradation (MAFbx, MuRF-1 and UBR5) and autophagy-lysosomal degradation (AMPK, ULK1 and p62). T administration also had no effect on proteins in the mitochondria enriched fraction regulating mitophagy (Beclin, BNIP3, LC3B-I, LC3B-II and LC3B-II/I ratio) and morphology (Mitofilin), and it did not alter the expression of mitochondrial fission- (FIS1 and DRP1) or fusion factors (OPA1 and MFN2). In summary, these data indicate that improvements in muscle size and oxidative capacity in young women in response to moderate-dose T administration cannot be explained by alterations in total expression of molecular factors known to regulate muscle protein turnover or mitochondrial remodeling.
2.
Effect of ubiquinol supplementation on biochemical and oxidative stress indexes after intense exercise in young athletes.
Orlando, P, Silvestri, S, Galeazzi, R, Antonicelli, R, Marcheggiani, F, Cirilli, I, Bacchetti, T, Tiano, L
Redox report : communications in free radical research. 2018;23(1):136-145
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Strenuous exercise or overtraining increases the production of reactive oxygen species (ROS), especially in mitochondria. ROS production in excess leads to oxidative stress, cellular dysfunction, and oxidation of molecules such as DNA, polyunsaturated fatty acids, amino acids, and proteins. Previous research has shown that antioxidant supplementation might lead to the downregulation of ROS production. Coenzyme Q10 is an antioxidant believed to be effective in downregulating the effects of oxidative stress and preventing cellular damage. However, most previous studies have used ubiquinone, an oxidised form of Coenzyme Q10. Ubiquinol, a reduced form of Coenzyme Q10, is highly bioavailable, stable and in a form that the body can readily use. This randomised, double-blinded, crossover-controlled trial investigated ubiquinol's antioxidant and anti-inflammatory effects on biochemical and oxidative stress indexes after an intense bout of exercise in trained athletes. Twenty-one male athletes in constant training were randomly taking 200 mg/day of ubiquinol for a month. After a single bout of intense aerobic and endurance exercise, the participants showed a rapid and significant reduction in ubiquinol levels, especially lipoprotein CoQ10 and increased muscle damage markers such as Creatine kinase (CK) and Myoglobin (Mb). Ubiquinol supplementation prevented exercise-induced CoQ10 scarcity and reduced the activity of paraoxonase, an anti-inflammatory and antioxidant enzyme protective against oxidative stress in lipoprotein and circulating cells. Ubiquinol supplementation was associated with a significant decrease in cytosolic ROS in peripheral blood mononuclear cells. Ubiquinol supplementation enhanced plasma and cellular antioxidant levels. Healthcare professionals can use the results of this study to understand the antioxidant effects of ubiquinol supplementation and its buffering effect on plasma CoQ10 balances and exercise-induced CoQ10 depletion. However, further robust studies are required to evaluate the therapeutic potential of ubiquinol supplementation in sports nutrition.
Abstract
OBJECTIVES Physical exercise significantly impacts the biochemistry of the organism. Ubiquinone is a key component of the mitochondrial respiratory chain and ubiquinol, its reduced and active form, is an emerging molecule in sport nutrition. The aim of this study was to evaluate the effect of ubiquinol supplementation on biochemical and oxidative stress indexes after an intense bout of exercise. METHODS 21 male young athletes (26 + 5 years of age) were randomized in two groups according to a double blind cross-over study, either supplemented with ubiquinol (200 mg/day) or placebo for 1 month. Blood was withdrawn before and after a single bout of intense exercise (40 min run at 85% maxHR). Physical performance, hematochemical parameters, ubiquinone/ubiquinol plasma content, intracellular reactive oxygen species (ROS) level, mitochondrial membrane depolarization, paraoxonase activity and oxidative DNA damage were analyzed. RESULTS A single bout of intense exercise produced a significant increase in most hematochemical indexes, in particular CK and Mb while, on the contrary, normalized coenzyme Q10 plasma content decreased significantly in all subjects. Ubiquinol supplementation prevented exercise-induced CoQ deprivation and decrease in paraoxonase activity. Moreover at a cellular level, in peripheral blood mononuclear cells, ubiquinol supplementation was associated with a significant decrease in cytosolic ROS while mitochondrial membrane potential and oxidative DNA damage remained unchanged. DISCUSSION Data highlights a very rapid dynamic of CoQ depletion following intense exercise underlying an increased demand by the organism. Ubiquinol supplementation minimized exercise-induced depletion and enhanced plasma and cellular antioxidant levels but it was not able to improve physical performance indexes or markers of muscular damage.