Mechanical loading or lack of, drives physiological adaptation. Let’s look at this initially with a disuse, inactivity, injury or immobilisation lens. What happens when you can’t get stress (force) or strain (length) 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 (additional mechanical load/stress - force) on your back and you will see very different systemic responses.

So mechanical loading initiates molecular signalling that drives tissue remodelling (e.g. protein synthesis), this process called mechanotransduction. The two relationships that are central to mechanical loading and hence driving musculotendinous adaptation, are the force-length (isometrics) and force velocity (eccentrics and concentrics) relationships. Click here to unpack these two relationships and take your understanding of exercise and human movement to new levels.