In this article I talk about the phenomenon of concurrent training interference (strength+cardio) and why there are training responders and non-responders to training. Here we go!

What is concurrent training?
In recent years, there has been a lot of research and discussion about concurrent training, which basically and in general terms, consists of performing strength and endurance training together, raising questions about whether or not there is negative interference between the two, how much time should there be between them to avoid possible negative interference or, for example, if performed in the same session, in what order it should be done depending on the objective.

There is a lot of conflicting research on certain aspects when it comes to adaptations to combined training and it is certainly an open debate, which I have written and talked about quite a bit myself, especially what happens at the cellular level and explaining the mechanisms that can lead to the phenomenon of crosstalk.

JNK, a cellular protein complex
To date, JNK, a cellular protein complex, has been known as an important regulator of cellular stress and inflammatory responses. However, knowledge of molecular physiology is advancing and this leads to a better understanding of the mechanisms leading to adaptations to training.

Lessard et al 2018, have identified that JNK plays an important role as a regulator of muscle hypertrophy when this is active and conversely, when inactive, it plays an important role in muscle adaptations in endurance sports, ie, that adaptations leading to muscle hypertrophy and those leading to oxidative enhancement typical of endurance sports are regulated in opposite directions by JNK, which leads us to put JNK as a key factor in the possible interferences of concurrent training, i.e. when strength and endurance are trained together. Thus, JNK is activated when strength training and leads to increased muscle hypertrophy and conversely, it is inactivated in aerobic endurance sports, leading to muscle adaptations that lead to smaller, more oxidative muscle fibers and improved aerobic fitness.

JNK is not the only player
While JNK is obviously not the only player in this regard (I’ve written a lot about this), it does seem to represent an important factor in the molecular mechanisms that can lead to the classic interference phenomenon of concurrent training.

While it has long been known that exercise can activate JNK in muscle, the role of JNK activation during exercise and its contribution to training-induced adaptations was not previously understood. It is now shown that in humans, a single exercise session can activate JNK, leading to myostatin inhibition.

How does myostatin act?
Myostatin acts as a molecular brake that prevents muscle hypertrophy, i.e. it is a repressor of muscle growth, while its inhibition allows muscle growth. In addition, animal studies show that myostatin can act as a positive regulator of aerobic endurance capacity.

Aerobic endurance exercise and strength training
Aerobic endurance exercise modalities, therefore, result in low levels of JNK activation, which would allow myostatin to remain active and endurance adaptations to take place. Strength training, on the other hand, strongly activates JNK and will result in inhibition of myostatin and thus a shift towards muscle hypertrophy, through mechanical tension, having mechanosensitive properties.

Why are there training responders and non-responders to training?
In addition, JNK may represent a key factor in the difference between responders and non-responders to exercise. That is, individuals with high JNK activation in response to aerobic endurance exercise may be less responsive to muscle hypertrophy and therefore fail to undergo strength training adaptations.

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