Skin: if you don't use it, you lose it

“TL;DR: Collagen cells respond to physical activity by producing more collagen and elastin. When physical activity is lacking skin becomes weaker.

You can re-firm your skin slowly by exercising a lot and by having deep-acting, high-power radiofrequency, the strongest SAFE skin tightening technology known today.”

Skin: just like muscle - and bone - if you do't use it, you lose it

• The importance of physical activity in the maintenance of muscle and bone

• The importance of physical activity in the maintenance of skin firmness

• Why do we lose skin firmness when we stay inactive?

• From human movement to fat/cellulite reduction and skin tightening

• From intense deep heat with radiofrequency to fat/cellulite reduction and skin tightening

• The science of mechanotransduction in connective tissue - including skin

• How do fibroblasts translate mechanical signals into changes in extracellular matrix production?

• Gene regulation by mechanotransduction in fibroblasts

• From mechanotransduction to extracellular matrix gene expression in fibroblasts

• Mechanoregulation of gene expression in fibroblasts

• Have a skin tightening/cellulite treatment in London with the experts

• Advanced, infrared / blue / red light therapy treatments in London at LipoTherapeia

• The Cellulite School™: Get advanced training in cellulite reduction and skin tightening

The importance of physical activity in the maintenance of muscle and bone

We usually say that for muscle mass: “if you don’t use it, you lose it”.

If we don’t walk, play sports or do weights, we will gradually lose our muscle. This is especially true when we recover from injury or a long-lasting health condition, where we find ourselves with much less muscle, especially on the legs.

You may also be aware that if we do not do weights or at least walk, i.e. if we somehow do not stay physically active, we lose bone mass, especially after menopause or after about 50 years of age, for both sexes.

The reason why we lose muscle or bone if we don’t use them is because nature has to be very frugal. Whatever is not used much in the human body it tends to gradually atrophy to save precious body resources. Hence we must use our muscles and bones to give signals to the body to maintain them.

The importance of physical activity in the maintenance of skin firmness

However, the motto “if you don’t use it, you lose it” does not just apply to muscle and bone mass, it also applies to skin - and it applies at any age, not just after the 50s.

At the clinic have seen many clients who, due to either a fracture, a health condition or in some cases extremely sedentary work for months on end, they lost a lost of skin firmness and skin thickness too, with their skin ending up appearing thin and loose, and cellulite also looking worse.

Why do we lose skin firmness when we stay inactive?

But why is that? Why do we lose skin if we don’t move? After all, we don’t use skin to walk, like we use muscles, which enable us to walk. And we don’t bear any weight on skin, like we do on bone.

The explanation is simple: the body takes cues on whether it should maintain a certain level of collagen and elastin on the skin by sensing vibration and micro-stretching. Every time we take a step, our fibroblasts (collagen and elastin producing cells in the skin, fascia, ligaments and tendons) sense some micro-stretching on the tissues resulting from vibration from the contact with the ground

The more the vibration, the more cues fibroblasts get that they have to up their game and produce more collagen (and elastin) to maintain the integrity of the connective tissue in our body. The more we move, the more our connective tissues (including the skin) need to stay firm and elastic to keep the body in place. So the more we move, the more we build tissue to keep our body in place, including, fascia, tendons, ligaments and skin.

This is how anything in your body, from your face to your bum, stays firm and lifted.

From human movement to fat/cellulite reduction and skin firming

This process of converting vibration cues to collagen and elastin synthesis is called mechanotransduction. The sensing of vibration is called mechanosensitivity. The vibration that itself is called connective tissue mechanical deformation.

Mechanotransduction does not just work on fibroblasts. It also works on adipocyte (fat cells), inhibiting adipocyte formation and expansion and leading to adipocyte shrinkage and early adipocyte death.

Mechanotransduction is how vibration plate works, which, for connective tissues, such as bone, muscle, skin, fasciae, ligaments and tendonds, is like concentrated walking.

Mechanotransduction is also, partially, how ultrasound works, which results in lipolysis and apoptosis (in addition to heat and in addition physical breakage of a percentage of fat cells in adipose tissue).

From intense deep heat with radiofrequency to fat/cellulite reduction and skin tightening

In addition to mechanotransduction, there are other types of transduction, including heat transduction, which is how radiofrequency works. This also results in lipolysis (fat release from fat cells), as well as adipocyte apoptosis (early fat cell death).

Deep-acting, high-power radiofrequency and deep-acting, high-power ultrasound cavitation are the two techniques at the clinic to safely and affectively reduce cellulite and tighten skin.

In fact, strong, deep tissue, radiofrequency is the best technology to stimulate collagen syntheses - and collagen contraction fast, i.e. within days and weeks.

Of course, exercise and physical activity are absolutely essential and do the exact same thing, but much more slowly, i.e. within months and years, and less effectively.

The science of mechanotransduction in connective tissue - including skin

As you understand, this is not some vague theory that someone made up to explain things, this is established science regarding the function of connective tissue and fibroblasts, known to scientists for a couple of decades, but a science that no-one in the shallow beauty industry talks about. But we do.

Below we present four studies (out of hundreds of similar studies) which explain the mechanics of conversion of mechanical stimuli received by fibroblast into collagen production, in case you would like to delve deeper.

Enjoy :)

How do fibroblasts translate mechanical signals into changes in extracellular matrix production?

• Research paper link: https://pubmed.ncbi.nlm.nih.gov/12714044/

• Abstract: Mechanical forces are important regulators of connective tissue homeostasis. Our recent experiments in vivo indicate that externally applied mechanical load can lead to the rapid and sequential induction of distinct extracellular matrix (ECM) components in fibroblasts, rather than to a generalized hypertrophic response. Thus, ECM composition seems to be adapted specifically to changes in load. Mechanical stress can regulate the production of ECM proteins indirectly, by stimulating the release of a paracrine growth factor, or directly, by triggering an intracellular signalling pathway that activates the gene. We have evidence that tenascin-C is an ECM component directly regulated by mechanical stress: induction of its mRNA in stretched fibroblasts is rapid both in vivo and in vitro, does not depend on prior protein synthesis, and is not mediated by factors released into the medium. Fibroblasts sense force-induced deformations (strains) in their ECM. Findings by other researchers indicate that integrins within cell-matrix adhesions can act as 'strain gauges', triggering MAPK and NF-kappaB pathways in response to changes in mechanical stress. Our results indicate that cytoskeletal 'pre-stress' is important for mechanotransduction to work: relaxation of the cytoskeleton (e.g. by inhibiting Rho-dependent kinase) suppresses induction of the tenascin-C gene by cyclic stretch, and hence desensitizes the fibroblasts to mechanical signals. On the level of the ECM genes, we identified related enhancer sequences that respond to static stretch in both the tenascin-C and the collagen XII promoter. In the case of the tenascin-C gene, different promoter elements might be involved in induction by cyclic stretch. Thus, different mechanical signals seem to regulate distinct ECM genes in complex ways.

Gene regulation by mechanotransduction in fibroblasts

• Research paper link: https://pubmed.ncbi.nlm.nih.gov/18059623/

• Abstract: Mechanical forces are important for connective tissue homeostasis. How do fibroblasts sense mechanical stress and how do they translate this information into an adaptive remodeling of the extracellular matrix (ECM)? Tenascin-C is rapidly induced in vivo by loading muscles and in vitro by stretching fibroblasts. Regulation of tenascin-C expression by mechanical signals occurs at the transcriptional level. Integrin receptors physically link the ECM to the cytoskeleton and act as force transducers: intracellular signals are triggered when integrins engage with ECM, and later when forces are applied. We found that cyclic strain does not induce tenascin-C messenger ribonucleic acid (mRNA) in fibroblasts lacking the beta1-integrin chain. An important link in integrin-dependent mechanotransduction is the small guanosine 5'-triphosphatase. RhoA and its target kinase, ROCK. In fibroblasts, cyclic strain activates RhoA and thereby induces ROCK-dependent actin assembly. Interestingly, tenascin-C mRNA induction by cyclic strain was suppressed by relaxing the cytoskeleton with a ROCK inhibitor or by actin depolymerization. Conversely, chemical activators of RhoA enhanced the effect of strain both on actin dynamics and on tenascin-C expression. Thus, RhoA/ROCK-controlled actin dynamics are required for the induction of specific ECM genes by mechanical stress. These findings have implications for the understanding of regeneration and for tissue engineering.

From mechanotransduction to extracellular matrix gene expression in fibroblasts

• Research paper link: https://pubmed.ncbi.nlm.nih.gov/19339214/

• Abstract: Tissue mechanics provide an important context for tissue growth, maintenance and function. On the level of organs, external mechanical forces largely influence the control of tissue homeostasis by endo- and paracrine factors. On the cellular level, it is well known that most normal cell types depend on physical interactions with their extracellular matrix in order to respond efficiently to growth factors. Fibroblasts and other adherent cells sense changes in physical parameters in their extracellular matrix environment, transduce mechanical into chemical information, and integrate these signals with growth factor derived stimuli to achieve specific changes in gene expression. For connective tissue cells, production of the extracellular matrix is a prominent response to changes in mechanical load. We will review the evidence that integrin-containing cell-matrix adhesion contacts are essential for force transmission from the extracellular matrix to the cytoskeleton, and describe novel experiments indicating that mechanotransduction in fibroblasts depends on focal adhesion adaptor proteins that might function as molecular springs. We will stress the importance of the contractile actin cytoskeleton in balancing external with internal forces, and describe new results linking force-controlled actin dynamics directly to the expression of specific genes, among them the extracellular matrix protein tenascin-C. As assembly lines for diverse signaling pathways, matrix adhesion contacts are now recognized as the major sites of crosstalk between mechanical and chemical stimuli, with important consequences for cell growth and differentiation.

Mechanoregulation of gene expression in fibroblasts

• Research paper link: https://pubmed.ncbi.nlm.nih.gov/17331678/

• Abstract: Mechanical loads placed on connective tissues alter gene expression in fibroblasts through mechanotransduction mechanisms by which cells convert mechanical signals into cellular biological events, such as gene expression of extracellular matrix components (e.g., collagen). This mechanical regulation of ECM gene expression affords maintenance of connective tissue homeostasis. However, mechanical loads can also interfere with homeostatic cellular gene expression and consequently cause the pathogenesis of connective tissue diseases such as tendinopathy and osteoarthritis. Therefore, the regulation of gene expression by mechanical loads is closely related to connective tissue physiology and pathology. This article reviews the effects of various mechanical loading conditions on gene regulation in fibroblasts and discusses several mechanotransduction mechanisms. Future research directions in mechanoregulation of gene expression are also suggested.

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