Triathlete Ainhoa Murua. (Photo: Inigo Mujika)

Last weekend I lectured at a professional masters degree on high performance in team sports in Barcelona. In my lectures, I spoke about training, recovery and detraining. Many of the changes that take place in the body of athletes as a result of these processes occur at the skeletal muscle level. Indeed, skeletal muscle adapts to the training performed by athletes during periods of intensive work, and also adapts to the lack of training during periods of inactivity, whether voluntary or forced by injury or illness. But is that all skeletal muscle does, adapt to varying levels of physical and mechanical demands?

During the train ride back from Barcelona I read an excellent paper by Bente K. Pedersen and Mark A. Febbraio that has recently been published in Nat. Rev. Endocrinol., indicating that skeletal muscle is much more than a contractile tissue. In the words of these authors, “During the past decade, skeletal muscle has been identified as a secretory organ. Accordingly, we have suggested that cytokines and other peptides that are produced, expressed and released by muscle fibres and exert either autocrine, paracrine or endocrine effects should be classified as myokines. The finding that the muscle secretome consists of several hundred secreted peptides provides a conceptual basis and a whole new paradigm for understanding how muscles communicate with other organs, such as adipose tissue, liver, pancreas, bones and brain. However, some myokines exert their effects within the muscle itself.”

According to this new paradigm, and given that many myokines produced by skeletal muscle depend on contraction, “physical inactivity probably leads to an altered myokine response, which could provide a potential mechanism for the association between sedentary behaviour and many chronic diseases.”

In their article, Pedersen and Febbraio present two wonderfully clear figures summarizing the links between physical inactivity and disease development on the one hand, and the molecular mechanisms that link physical activity to protection against premature mortality on the other. I can’t reproduce these figures without permission, but here is an alternative:

Figure 3. Physical inactivity leads to a loss of muscle mass and abdominal adiposity; the latter stimulates macrophage infiltration of adipose tissue, inducing chronic systemic inflammation; inflammation promotes insulin resistance, atherosclerosis, neurodegeneration, tumour growth, impaired bone formation and a myriad of chronic diseases.

Figure 4. Physical activity, on the contrary, induces the release of myokines from skeletal muscle; these myokines are the signals stimulating muscle growth and hypertrophy, adipose tissue oxidation, insulin sensitivity, osteogenesis, anti-inflammation, anti-tumour defence, páncreas function and browning of fat, thus decreasing the risk of chronic diseases and premature mortality.

Reference

Pedersen, B.K., Febbraio M.A. Muscles, exercise and obesity: Skeletal muscle as a secretory organ. Nat. Rev. Endocrinol. advance online publication 3 April 2012; doi:10.1038/nrendo.2012.49