Preamble

In the previous blog post I asked what really matters in terms of strength and conditioning knowledge that physiotherapists need to know? I proposed that it was not about periodisation, specificity, overload, progression, sets, reps, etc., I believed it to be more fundamental than that and I proposed that if I could give physiotherapists any gifts of knowledge to enhance understanding and practice around the strengthening of muscle, I would take two foci initially: 1) a tissue perspective; and, 2) a mechanical loading perspective. These perspectives look at the structures and drivers of tissue remodelling and subsequent adaptation. If you understand this then most things strength and conditioning will make a lot of sense. So, let’s unpack this mechanical loading perspective.

Mechanical loading or lack of, drives adaptation. Let’s look at this initially with a disuse, inactivity, injury or immobilisation lens. What happens when we can’t get stress (force)or strain (deformation) into a tissue. Lots! Muscle atrophy particularly in the antigravity muscles, loss of tensile strength, fibre type changes, decreased function, etc. What happens when you immobilise muscles at long muscle lengths i.e. introducing strain into the tissues?  In many cases the atrophy is mitigated. Take home here is when you don’t get mechanical loading into the neuromuscular system, tissue remodelling occurs and usually not in a manner that is beneficial for movement.

Okay let’s flip this train of thought. What drives increased metabolic, neural, hormonal, respiratory, and cardiovascular activity? Mechanical load! The magnitude of that mechanical load typically correlates to increase in activity of those systems. For example, a sit to stand is in essence a body weight squat. Do that 10 times with and without 50 kg (mechanical load/stress - force) on your back and you will see very different systemic responses.  

So where am I going with all this? Mechanical loading drives adaptation. Most of you want to understand how to optimise tissue remodelling and adaptation for better client outcomes. Therefore the logical first step is to understand the nuances of mechanical loading, via a process called mechanotransduction and thereafter two important mechanical relationships that are so important for understanding and driving changes in human movement.

Mechanotransduction

Mechanotransduction is a process that converts the mechanical loading placed upon a tissue (bone, ligament, tendon, muscle, connective tissue, etc.) into cellular signalling, which promotes structural change via some sort of tissue remodelling.  

It begins with mechanocoupling where multi-planar stresses (shear, compressive, or tensile forces) and strains (deformation in multiple directions) cause a wide range of internal stresses in the muscle that cause a perturbation in various elements of the muscle cell. Many signalling pathways are initiated depending on the nature of the stress and strain (e.g. active and passive stretch), which then increases muscle protein synthesis, activate satellite cells or release growth factors, ultimately causing some sort of tissue remodelling, repair and adaptation.

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I am not going to go much deeper than that, other than to reiterate that mechanical loading initiates this process. So what is really important to understand is mechanical loading and there happens to be two relationships that are fit for purpose here, the force-length and the force-velocity relationship. Improve your understanding around the mechanics and physiology of these two relationships, and your assessment, programming and overall practice will improve no end.

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Force-Length Relationship (isometrics)

Simply put the force that a muscle can produce is related to its length or more specifically the actin and myosin overlap. In Figure 2 the black line denotes the force length relationship at a sarcomere level. You can see the plateau region is where there is optimal myosin crossbridge overlap with the actin filament occurs, this optimal length/overlap corresponds to the zone of maximal force. Each side of the plateau region force decreases because of too much or too little overlap. Note that at a whole muscle level (see Figure 2 teal curve) you don’t have that plateau region as many sarcomeres/muscle fibres are modelled, the many fibres resulting in the plateau region being offset.

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When the muscle extends past resting length, active force decreases, however, the contribution of passive forces via the parallel elastic component (e.g. mysial tissues, titin) increases (see Figure 2 grey line). This is a design parameter of the muscle to provide structural integrity and tensile strength, when active muscle is weak. So the quality (specific tension) and quantity of the PEC connective tissue is important.

Furthermore the dashed curve that you see in the diagram is a muscle-tendon force-length curve and not a muscle force-length curve as indicated by a rightward shift of the curve. The size of this rightward shift depends on two things, the compliance of the tendon itself and the length of the tendon. Longer and /or compliant tendons mean less sarcomere lengthening, which in turn results in greater sarcomere overlap and hence better length tension and force-velocity relationships.

So in terms of isometric training can you cause different signalling responses, therefore leading to different adaptations, such as increase in muscle fibre length vs increase in transverse CSA. Or can you mechanically load to promote sarcomeric contractile component strengthening as compared to mechanical loading to promote strengthening of the passive titin and mysial tissues? What about mechanical loading for tendon compliance or stiffness? There are multiple ways to isometrically train muscle – I mention the iso-hold, iso-push, iso-catch and iso-swicth in my resources. Also ramped vs ballistic isometric contractions? Isometrics at long muscle lengths vs short muscle lengths? High intensity-short duration vs low intensity-short duration isometrics? What about mixing active isometrics and and passive stretching e.g. PNF?  

Conclusion

Loading muscles differently causes different muscle shape changes and internal stresses, and as a consequence different molecular signalling and tissue remodelling such as protein resynthesis. I feel that this is the strength and conditioning knowledge that really matters to a physiotherapist. Understand mechanical loading (force and length in this example) then you can apply this across the entire body, understanding that if you modify X exercise in a certain way you will get Y adaptation.

Hopefully from this brief treatise you can see the importance of mechanical loading.  A good read in this area is a short article by Khan and Scott (2009), “Mechanotherapy: how physical therapists’ prescription of exercise promotes tissue repair.” A comment that I found interesting was,“mechanotransduction was not being taught as an important biological principle in physical therapy programmes… This is a major failing of medical education when physical inactivity is the major public health problem of the 21st century.” I don’t know whether that is still the case but I leave you with that comment and this question? How good is your understanding mechanical loading, mechanotransduction and/or mechanotherapy. Unpacking the importance of the force-velocity relationship to come.

If you want to grow your knowledge in this area, be sure to check out my online block course designed for physiotherapists with a special focus on mechanotherapy and mechanotransduction.

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Reference

Khan, K.M. &Scott , A. (2009). Mechanotherapy: how physical therapists’ prescription of exercise promotes tissue repair. Br J Sports Med. 43:247-251

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