HYPERTROPHY MECHANISMS REVISITED

Hypertrophy Mechanisms Revisited

By Eric Bugera

Mechanical Tension, Metabolic Stress, and Muscle Damage

• Mechanical tension, metabolic stress, and muscle damage are the three commonly proposed hypertrophy triggers.

• Evidence continues to suggest that of the three, absolute tension is the primary driver with metabolic stress (and possibly muscle damage) serving as surrogate routes to tension.
• Although tension is the main goal, metabolic stress is a useful tool to tailor within programs to achieve said desired tension.

Hypertrophy Mechanisms

Underlying mechanisms serve as the north star in any walk of life – but particularly within the realm of fitness. Whether you’re into German volume training, using bro-splits, or the specialized flavor of the month protocol, your ability to critically appraise a program based upon mechanistic merit can help you make better decisions faster. There are rarely proprietary training strategies that truly break the mold of what your body was already responding to – but, underlying mechanisms help provide clarity as to why.

Mandatory Tension

The three primary triggers of skeletal muscle hypertrophy have been long espoused to be mechanical tension, metabolic stress, and muscle damage. While all three may be associated with muscle hypertrophy, there is currently only one front runner with enough evidence supporting it as an essential component – tension. All training strategies that provide adequate stimulus for growth appear intimately tied to the development of high degrees of tension within the working muscle.

Metabolic stress (the accumulation of metabolic byproducts of energy production) has been closely associated with hypertrophic outcomes, but research has struggled to identify independent or additive means through which metabolic stress provides significant signaling for growth in absence of mechanical tension (or colloquially, tension). While research continues to sift through possible alternative routes – for now, the clear connection is likely due to metabolic stress serving as a proxy for tension. As more metabolic byproducts are generated, the amount of active muscle fibers decreases due to a noxious cellular environment. From there, additional fibers must be recruited for continued action and thus generation of tension when closeness to failure is reached.

Similarly, muscle damage seems to stimulate superficially important pathways such as satellite cell mobilization; however, it also struggles to present unique net-positive growth potential in absence of high degrees of tension. Additionally, too much intentionally damaging activity may actually marshal important resources to specifically repair back to baseline before any new tissue can even be considered for growth. In this sense, muscle damage should likely be left deprioritized outside of its normal occurrence during all exercise.

This brings us back to tension – which is the most supported, easy to replicate and quantify stimulus possible. While metabolic stress and muscle damage may eventually receive higher prioritization if they eventually achieve greater mechanistic validation; currently, tension appears to be the frontrunner to prioritize. Metabolic stress may be a useful proxy to generate high degrees of tension and offer programming options – but underneath it all, likely, tension is the main driver.

Tension Yields Results

High degrees of tension can be inferred by observing an involuntary slowing of repetition speed during a set. While metabolic stress may be a useful tool in pursuit of high degrees of tension, it is just that. A tool. Muscle damage may yet play a role (either additive or redundant) in hypertrophic responses, but when measured against one another – tension is the clear and obvious priority.

• Analyze where your exercise selection, set, and repetitions schemes favor tension, metabolic stress, or muscle damage.
• Refine your choices to better achieve tension with less redundant volume or damaging mechanisms which may undercut recovery.
• When all else fails, pursue closeness to muscle failure.