The Effects of Fortetropin Supplementation on Body Composition, Strength, and Power in Humans and Mechanism of Action in a Rodent Model
Matthew H. Sharp MS, Ryan P. Lowery MS, C. Brooks Mobley MEd, Carlton D. Fox BS, Eduardo O. de Souza PhD, Kevin A. Shields MS, James C. Healy BS, Ned Q. Arick MS, Richard M. Thompson BS, Michael D. Roberts PhD & Jacob M. Wilson PhD
Journal of the American College of Nutrition, DOI: 10.1080/07315724.2016.1142403
The purpose of this study was to investigate the effects of Fortetropin (Yolked) on skeletal muscle growth and strength in resistance-trained individuals and to investigate the anabolic and catabolic signaling effects using human and rodent models.
In the rodent model, male Wistar rats (250 g) were gavage fed with either 1.2 ml of tap water control (CTL) or 0.26 g Fortetropin for 8 days. Then rats participated in a unilateral plantarflexion exercise bout. Nonexercised and exercised limbs were harvested at 180 minutes following and analyzed for gene and protein expression relative to mammalian target of rapamycin (mTOR) and ubiquitin signaling. For the human model, 45 (of whom 37 completed the study), resistance-trained college-aged males were divided equally into 3 groups receiving a placebo macronutrient matched control, 6.6 or 19.8 g of Fortetropin supplementation during 12 weeks of resistance training. Lean mass, muscle thickness, and lower and upper body strength were measured before and after 12 weeks of training.
The human study results indicated a Group £ Time effect (p 0.05) for lean mass in which the 6.6 g (C1.7 kg) and 19.8 g (C1.68 kg) but not placebo (C0.6 kg) groups increased lean mass. Similarly, there was a Group £ Time effect for muscle thickness (p 0.05), which increased in the experimental groups only. All groups increased equally in bench press and leg press strength. In the rodent model, a main effect for exercise (p 0.05) in which the control plus exercise but not Fortetropin plus exercise increased both ubiquitin monomer protein expression and polyubiquitination. mTOR signaling was elevated to a greater extent in the Fortetropin exercising conditions as indicated by greater phosphorylation status of 4EBP1, rp6, and p70S6K for both exercising conditions.
Fortetropin supplementation increases lean body mass (LBM) and decreases markers of protein breakdown while simultaneously increasing mTOR signaling.
The molecular mechanisms that underpin skeletal muscle hypertrophy are complex and involve the interplay between anabolic and catabolic signaling pathways. One key variable that mediates skeletal muscle anabolism is activation of the mammalian target of rapamycin (mTOR) pathway . Proteolysis in skeletal muscle appears to be mediated by ubiqutin–proteasomal degradation .
Myostatin is a major regulatory protein that impacts both mTOR and ubiquitin signaling . Myostatin, also known as growth differentiation factor-8 (GDF-8), is a member of the transforming growth factor-b (TGF-b) superfamily of growth and differentiation factors . Once myostatin binds to its activin type II receptors, ActRIIA and ActRIIB , it initiates a signaling cascade through the transcription factors, Smad2 and 3, that results in an increase in protein breakdown and subsequent inhibition of protein synthesis.
Myostatin knockout mice have shown a 2- to 3-fold greater muscle mass than their wild-type littermates and accumulate less fat . Moreover, researchers have found that reduction of myostatin was associated with greater skeletal muscle hypertrophy and strength .
Inhibition of myostatin as a modality for preventing loss of skeletal muscle or increasing lean body mass (LBM) is being pursued by both therapeutics and nutrition scientists. One promising nutritional ingredient, which has clinically been shown to lower myostatin levels, is Fortetropin . Fortetropin is an allnatural proteo-lipid complex made from fertilized egg yolk.
Although a previous clinical study showed that Fortetropin substantially reduced serum myostatin levels, its mechanism of action (MOA) and ability to induce skeletal muscle growth have yet to be evaluated . Therefore the purpose of this study was 2-fold. First, we sought to investigate whether plausible mechanisms existed that could support the contention that Fortetropin supplementation could induce hypertrophy. If plausible mechanisms were identified in a preclinical rodent model, our second purpose was to evaluate its effect on skeletal muscle growth. This was conducted in a double-blind placebo-controlled clinical study using resistance-trained individuals.
The present research provided initial insight into plausible mechanisms of action for Fortetropin. Our research demonstrated that Fortetropin supplementation in a rodent model decreased catabolic signaling (ubiquitin proteasome pathway), increased anabolic (mTOR), signaling and reduced mRNA expression of the myostatin receptor ActRIIB. Consistent with these findings, our human clinical trial showed that Fortetropin supplementation resulted in positive changes in muscle thickness and lean body mass in healthy resistance-trained young males. In addition, future research should be focused on further elucidating the underlying mechanism of these outcomes and determining the effect of Fortetropin supplementation on other populations susceptible to accelerated muscle loss (i.e., cachectic or sacropenic individuals).
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