Skeletal muscle mass has been attributed to important functions such as an individual’s metabolic rate, functional movement, posture, power output, etc. The need for skeletal muscle is universal and the decline of skeletal muscle as individuals age is also universal. This week’s discussion article delves into the use of phosphatidic acid as an enhancer of mTOR signaling. mTOR is a protein kinase that’s considered a key regulator of skeletal muscle growth. Currently the exact mechanism by which phosphatidic acid stimulates mTOR is not confirmed. However, several different stimuli can trigger different pathways that induce mTOR signaling. Mechanical stimuli can cause an increase in the intracellular levels of phosphatidic acid. The resulting increase contributes to the activation of mTOR-dependent signaling events. Exogenous sources are also capable of increasing PA in the system. The activation of LPA receptors, passive stretching of skeletal muscles, and the addition of PA to fibroblasts all result in the activation of mTOR signaling.

The purpose of the study was to determine the most effective mechanism of activating mTOR signaling. Further, to see the extent to which phosphalidic acid influenced skeletal muscle hypertrophy, strength, and power output. The relationship between mTOR and PA signaling has been studied based on the intake of certain food groups. Egg derived PA has been shown to increase mTOR signaling. Further, soy products that contain one saturated fatty acid are ideal for this activation. The soy product generally contains greater amounts of fat, and this could explain the observed efficiency of soy products as a catalyst for mTOR signaling. Maximal mTOR activation in response to PA occurs at the twenty-minute mark according to the study, although there needs to be more research to make this timeframe definitive. The mechanical stress of resistance training has been well-documented as a stimulus for skeletal muscle hypertrophy. However, the conversion from a mechanical stimulus to a chemical signal which leads to skeletal muscle growth has been only recently explained. The cell’s PA content increases following eccentric contractions and this would explain why the eccentric contraction is emphasized in many resistance training protocols, beyond the necessary control of the weight.

Phosphatidic acid appears to be related to skeletal muscle hypertrophy, as well as increases in strength. The training regimen was not designed for power adaptations so the measurements in power were insignificant. Oral supplementation of PA appears to promote the anabolic effects of resistance training. Phosphatidic acid has several interesting and beneficial applications. Supplementation of PA could prove to result in skeletal muscle hypertrophy despite the absence of resistance training. PA could also be used as a fat loss agent since skeletal muscle is a prime motivator for metabolic rate and increases in skeletal muscle would in turn lead to fat oxidation.

The strength of the article is that the findings are backed by reputable sources and knowledge that’s been well established. Linking PA to the different adaptations associated with resistance training is an important landmark in developing more literature on the subject. Since the subject itself has been faintly covered over time, then this is an important focus point to continue to expand. There weren’t considerable weaknesses with the article, as it was well written and veered away from making any dis-credible claims or assumptions about what this PA link means. The future of exercise science, as well as other fields such as physical therapy, can benefit from this knowledge. The oral administration of PA, considering if it did in fact lead to skeletal muscle hypertrophy without resistance training, could be used in bed-ridden patients or for those who cannot exert force through their body enough to stimulate or maintain skeletal muscle.


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