BASES conference at UCLAN; signal transduction theory of adaptation

I am just back from the BASES conference which was held at the University of Central Lancashire from the 3-5th of September. The conference was very enjoyable because it was organised very well by Steve Atkins, his team & BASES and also I met a lot of former colleagues and students. My talk was entitled 'Molecular Exercise Physiology. Using molecular biology to answer key questions in sport and exercise science'. As the audience was broad (physiologists, psychologists, biomechanists, practioners) I tried to avoid the jargon and pathway diagramme trap and instead tried to explain the relevance, practical applications and focus on eye opening results and it seemed to work.

One of my topics was to make a case for the signal transduction theory of adaptation. It is illustrated in Figure 1 and explained below.

Figure 1. Schematical drawing depicting a general model that explains adaptation to exercise.

'How do we adapt to exercise?' is a key question for all exercise physiologists. The continental European sport science school has for a long time used the Yakovlev 'supercompensation' or 'overcompensation' hypothesis not only to describe the time course of the glycogen concentration before, during and after exercise (yes, it overshoots) but also tried to use it as a general explanation for adaptation to exercise. However, the latter has many flaws and its use to generally explain adaptation to exercise is not supported by experimental data. In contrast, UK-based training scientists and practicioners frequently use the principles of training as pseudo-mechanisms but I frequently find them trivial (who would have thought that organs need to be overloaded to trigger adaptations?) and struggle to see practical applications.

So for these reasons I argue that we should teach the signal transduction hypothesis of adaptation as illustrated in Figure 1. It is supported by a large amount of experimental data and helps students, coaches and athletes to understand how exercise changes cells and organs. Here is how it works (see Figure 1). (1) Sensor proteins (SE) sense, similar to our eyes, ears and muscle spindles, signals associate with exercise. Such signals in muscle fibres are calcium (sensed by calmodulin), oxygen (sensed by the HIF-system), AMP (sensed by AMPK), glycogen (sensed by AMPK) and mechanical signals (sensed by an unknown sensor and activates mTOR). These signals are then computed by signalling proteins (SP) which for signal transduction pathways or networks. These networks are comparable to the brain. The signalling proteins frequently phosphorylate or dephosphorylate each other but there are many other forms of signalling. (2) Downstream are effector proteins which regulate cellular changes that together are the adaptation. Transcription factors (TF) are an important class of effector proteins as they regulate the switching on and off of genes (transcription). (3) Especially after resistance exercise translation/protein synthesis is activated by translational regulators. Other effector proteins regulate the cell cycle or cell death.

Of the many talks of BASES I have most enjoyed the talk by James Morton, Liverpool John Moores. James has shown that training with low glycogen can increase adaptation and he has linked this to AMPK. His research bridges from molecular mechanisms (e.g. the glycogen binding domain of AMPK) to practical applications and this is a very good example of how effective Molecular Exercise Physiology can be.

Finally, if you are interested in the slides of the BASES presentation then just e-mail me (h.wackerhage@abdn.ac.uk).
HW