PEMF and skeletal muscle development

A recent study published by the QuantumTx group, Yap 2025, demonstrated that some of the PEMF effects in adult mouse skeletal muscle could also be seen in quail embryos. This post asks if the micro and the TRPC1 Ca²⁺ channel are important in chicken embryos. Could QuantumTx technology not only help aging humans as well as chicken embryos? The literature is examined and suggests the preliminary Yap 2025 study deserves further exploration.

Are low kHz EMFs from appliances safe?

Are medium length electromagnetic fields teratogenic? Appliance frequencies are in this “very low” range that is not yet radio frequency but not extremely low.

This was addressed in ferilized chicken eggs. (Nishimura 2009) White Leghorn fertilized eggs (60/group) were either exposed to a 20 kHz, 1.1 mT sinusoidal magnetic field or sham-exposed during the first 2, 7, or 11 days of embryogenesis. Fertilized eggs were also exposed to 0.011 and 0.11 mT for 2 days. The electromagnetic fields tested did not synergize with the established teratogen all trans retinoic acid. In a followup study Nishimura 2013 extended the exposure time to 13 days and added 60 kHz to the initial 20 kHz. No teratogenic effects were observed. Prior to all of this the Pilla group (Sisken 1986) tested their PEMF formula on fertilized Longhorn chicken eggs: 50 msec of 3.8 kHz was repeated at 2 Hz. Specifics of the waveform are available in the publication. Abnormalities were evaluated by a second party at the local university. No developmental abnormalities were observed out of the normal range.

Fast, slow twitch, Wnt4 is involved

The Tanaka 2007 study is presented in this post because the authors sought to better understand the relationship between Wnt4 and myostatin in the developing chicken embryo. UniProt annotation for Gallus gallus (chicken) Wnt 4 suggests it uses the Wnt canonical pathways. Without Wnt binding the frizzled receptor, co-transcription factor β-catenin is degraded. .

Canonical Wnt signalling

Summary of the Tanaka study

Let’s move on to a summary of the chick embryo study of Tanaka 2007

• Wnt isoform expression is specially and temporally regulated in embryonic development.
• Wnt4 cDNA was misexpressed in the presumptive limb fields on the right side of stage 16 chick embryos.
• Muscle development was evaluated at stage 37 with immunohistochemical staining for fast and slow types of the myosin heavy chain (MyHC).
• Overexpression of Wnt4 resulted in up-regulation of Pax7 and MyoD1 expression increasing the muscle mass.
• Wnt4 increased the area for fast MyHC-expressing cells and decreased the area for slow MyHC-expressing cells.
• Tanaka also looked at mammalian C2C12 myoblasts. Wnt4 acted as a stimulator during myogenic proliferation and differentiation,.
• Wnt4 acts against myostatin. 

What does MyoD expression look like in a chick embryo?

We can forgive this gracious student for not posting the age of this chicken embryo in Wikimedia Commons images. We can be grateful for her posting this fine image. At this stage the spinal cord looking structure are “somites” at this stage of development. Judging from this somite map of the chick embryo, From left to right going to the eyeball, the structures along the somites are posterior hind limb bud, anterior limb bud, and heart. MyoD is mentioned in the fat and muscle post. Downfield PEMF decreased the transcripts for MyoD among other proteins. The TRPC1 post goes over features of the TRPC1 channel and ways that long term exposure of cultured myoblasts can increase the expression of MyoD.

Ca²⁺ and Wnt signaling

While the non-canonical Ca²⁺ signaling pathway for Wnt4 does not seem to be favored, it is important in the context of PEMF studies .

PEMF and chicken embryos, Yap 2025

Yap 2025 is a very nice preliminary study. The authors sought to reproduce some of previous work performed in mammalian systems. It is a departure from the company’s focus on healthy aging via myokines and such as that.

The Quantum Tx wave form.

Fig 1, the quail egg protcol

• A. The eggs were exposed to PEMF on five separate occasions starting on day 3 after arrival of the quail fertilized eggs and going to day 13.
• B Eggs were stacked horizontally or apex up. The magnetic field component of the PEMF went down or up with the force of gravity.
• C PEMF, up field or down field, increased the embyronic weight compared to no PEMF provided that the eggs were stacked apex up.
• D. Down field and up field increased the length of the embryos compared to no PEMF.
• E. Embryo survival in percentage in the vertical “apex-up” arrangement. The absolute egg survival-to-dead ratios were 20:5 (0 mT), 22:1 (1.5 mT down), and 22:3 (1.5 mT up).
• F The weight of the eggs decreased over time.

Fig 2 PEMF exposure promotes oxidative red muscle

Oxidative muscle is redder due to myoglobin, more mitochondria, and better vascularization. Chicken leg muscle tends to be darker than white breast muscle because chickens tend to be virtually flightless getting around on their legs. Birds that fly tend to have dark (red before cooking) breast meat.

• A-C Image J is a later generation of software created by the US NIH for image analysis. Panel A shows some actual muscle, red channel. Pixel intensity can be quantified. Unlike other studies showing more results with down field PEMF, up field PEMF resulted in redder muscle.
• PGC-1α mRNA transcript appeared to be increased by 1.5 mT up field and down field PEMF.
• PGC-1α protein levels were also increased by PEMF. Sometimes transcripts of genes never make it to being translated into proteins.
• Sirt1 transcripts were significantly increased by 1.5 mT downfield PEMF.
• Collagen 1A1 was increased by down filed PEMF. ColA1A Gene Ontology include blood vessel and skeletal development as well as response to mechanical stimuli.
• Collagen 3A1 was increased by downfield PEMF. Col3A1 GO lists only extracellular matrix.
• VEGF, PGC-1α is activated by its deacetylation by SIRT1, which, in turn, activates VEGF signaling. Down field PEMF enhanced PGC-1α protein but reduced VEGF expression.  Just looking at images of chicken embryos, it makes sense that vascularization will rise and fall.

This is a very nice preliminary study to determine if QuantumTx muscle related findings in adult mice could be recapitulated in avian embryos. QuantumTx has also shown adult mouse microbiome changes in response to PEMF. Surprisingly, chick embryos have a microbiome. Before diving into this, what are the concerns of back yard chicken farmers in North America?

Problems faced by newly hatched chicks, back yard farmer

• clean drinking water
• warmness Naturally the chicks cannot get too hot or cold. This brings up the heat generating mitochondrial uncoupler protein (UCP).
• vitamins and minerals
• age appropriate feed. In mammals, the mother’s milk helps to establish the right microbiome. How does this occur in non mammalian vertebrates?
• good hygiene Embedded in this category there must be the need to protect the chick from respiratory and gastrointestinal pathogens.

the pre-hatching microbiome?

A previous post has covered microbiome changes in mice exposed to PEMF. The Akinyemi 2020 study used two Chinese breeds of chicken and on used by free range farmers.

We found out that the vitamin metabolism pathway at E3, E12, and E19 was quite similar in its enrichment in the chicken embryo. Together, the findings suggest that most of the crucial functions are performed by the core microbiota regardless of the minute proportion of each. The richness of genetic information processing (translation) pathway at this early stage of development supports previous studies that pointed out that assurance of early development in an animal is on reliance on translation and utilization of the stored mRNA for later development … The abundance of the core microbes in our study specified that chicken gut health is highly correlated to the homeostasis of its gut microbial association. We supposed that the 3 distinct stages of the chicken embryonic growth and development might be a major factor for the dominance of specific genera within the chicken core microbiota

Fig 1 Relative abundance and diversity index stuff. Panel C shows abundance and the genus level at the E3,E16, and E19 days of development. The three strains of chickens appear to be very similar. Ochrobactum, Phyllobacterium, and Amycolatopsis were highly represented with 15-5% of the total.

Fig 2 panel C

• Ochrobactrum (E3 [30.4%], E12 [25.1%], E19 [13.6%])
• Amycolatopsis (E3 [11.5%], E12 [7.4%], E19 [5.6%])
• Phyllobacterium (E3 {3.4%], E12 [1.9%], (E19 [47.9%])

Fig 3 bacteria gene expression profile highlights the symbiotic role of the chick embryo and its microbiota even at this stage of development. Cofactor and vitamin metabolism are on the list. Fig 4 The major the genus were similar in the three breeds of chicken.

What are these three genera doing in a chick? The main source is Wikipedia just to get a handle on the aerotolerance

• Ochrobactrum, now Brucella , is described as a facultatively intracellular pathogen that is associated with Brucellosis in humans.
• Amycolatopsis species are known for their production of antibiotics
• Phyllobacterium is a Gram negative aerobic rod

This is all well and good. It makes sense that aerobes are part of the microbiome. Surely the egg shell must be permeable to oxygen as the avian developing embryo is not getting oxygen from its mother’s blood. What is the microbiome of the adult chicken? Burrows 2025 did a fine job of answering this question along the GI tract from cecum to feces. They also looked at the age of the chicken post hatching as well as the breed. The Lactobacillus genus made a predominate showing. What is in the Amazon probiotics for chickens? Most of these products contain “dried fermentation products” of Lactobacilli, Bifidobacterium, and other species. Most products tend to contain multiple “probiotic” species.

Mouse cecum + feces microbiome changes in response to PEMF were addressed in the PEMF & microbiome post. The species of bacteria that changed are hard to correlate with what was seen in quail eggs. Do the oxygen concentrations compare?

the chick embryo heart beat

There’s the fetal heart beat in humans, why not some sort of propagating action potentials in the embryonic heart? QuantumTx technology is based on mito hormesis that involves opening of TRPC1 channels in response to reactive oxygen species from Crly2 and/or the mitochondria. A PubMed search was performed on “TRPC1 and chick embryo. According to Sabourin 2011 TRPC channels play a key role in the regulation of electromechanical activity of the four day old developing chick heart. The authors mentioned TRPC1 in the pace maker cells called Interstitial Cells of Cajal in their discussion, surely also in skeletal muscle development. This post will keep things at a simple quotation of the abstract.

Introduction It is well established that dysfunction of voltage-dependent ion channels results in arrhythmias and conduction disturbances in the foetal and adult heart. However, the involvement of voltage-insensitive cationic TRPC (transient receptor potential canonical) channels remains unclear. We assessed the hypothesis that TRPC channels play a crucial role in the spontaneous activity of the developing heart.
Methods and Results
TRPC isoforms were investigated in isolated hearts obtained from 4-day-old chick embryos. Using RT-PCR, western blotting and co-immunoprecipitation, we report for the first time that TRPC1, 3, 4, 5, 6, and 7 isoforms are expressed at the mRNA and protein levels and that they can form a macromolecular complex with the a1C subunit of the L-type voltage-gated calcium channel (Cav1.2) in atria and ventricle. Using ex vivo electrocardiograms, electrograms of isolated atria and ventricle and ventricular mechanograms, we found that inhibition of TRPC channels by SKF-96365 leads to negative chrono-, dromo-, and inotropic effects, prolongs the QT interval, and provokes first- and second-degree atrioventricular blocks. Pyr3, a specific antagonist of TRPC3, affected essentially atrioventricular conduction. On the other hand, specific blockade of the L-type calcium channel with nifedipine rapidly stopped ventricular contractile activity without affecting rhythmic electrical activity.
Conclusions These results give new insights into the key role that TRPC channels, via interaction with the Cav1.2 channel, play in regulation of cardiac pacemaking, conduction, ventricular activity, and contractility during cardiogenesis.

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Concluding thoughts

The preliminary quail embryo study of Yap 2025 is exciting in that they reproduced some of the same skeletal muscle changes seen in adult mice in avian embryos. Some of the other published findings (TRPC1 Ca²⁺ channel gating and microbiome changes) might be relevant to the poultry industry. Could back yard chicken farmers be recruited as “citizen scientists”? This group might know about developmental abnormalities, ideal “poop” appearances, and how these birds adapt after hatching.

References

• Akinyemi FT, Ding J, Zhou H, Xu K, He C, Han C, Zheng Y, Luo H, Yang K, Gu C, Huang Q, Meng H. Dynamic distribution of gut microbiota during embryonic development in chicken. Poult Sci. 2020 Oct;99(10):5079-5090. .PMC free paper
• Burrows PB, Godoy-Santos F, Lawther K, Richmond A, Corcionivoschi N, Huws SA. Decoding the chicken gastrointestinal microbiome. BMC Microbiol. 2025 Jan 20;25(1):35. PMC free paper
• Nishimura I, Imai S, Negishi T. Lack of chick embryotoxicity after 20 kHz, 1.1 mT magnetic field exposure. Bioelectromagnetics. 2009 Oct;30(7):573-82. PubMed
• Nishimura I, Tanaka K, Negishi T. Intermediate frequency magnetic field and chick embryotoxicity. Congenit Anom (Kyoto). 2013 Sep;53(3):115-21. free paper
• Sabourin J, Robin E, Raddatz E. A key role of TRPC channels in the regulation of electromechanical activity of the developing heart. Cardiovasc Res. 2011 Nov 1;92(2):226-36. Sci-Hub free paper
• Sisken BF, Fowler I, Mayaud C, Ryaby JP, Ryaby J, Pilla AA. 1986. Pulsed electromagnetic fields and normal chick development. J Bioelectricity 5: 25–34. Sci-Hub free paper
• Takata H, Terada K, Oka H, Sunada Y, Moriguchi T, Nohno T. Involvement of Wnt4 signaling during myogenic proliferation and differentiation of skeletal muscle. Dev Dyn. 2007 Oct;236(10):2800-7. free paper
• Yap JLY, Wu KY, Tai YK, Fong CHH, Manazir N, Paul AP, Yeo O, Franco-Obregón A. Brief Weekly Magnetic Field Exposure Enhances Avian Oxidative Muscle Character During Embryonic Development. Int J Mol Sci. 2025 Jun 5;26(11):5423. PMC free paper