I went to this talk hoping to uncover some secrets to altering my body composition or decreasing inflammation in RA patients through physical exercise. Unfortunately, it was not a practical kind of talk. It was mostly basic science that I will do my best to summarize below.
Dr. Jon T. Giles reviewed research on adiposity and inflammation in patients with RA versus age-matched controls. Adipose tissue contributes to systemic inflammation in RA but we are unclear about whether it contributes to articular inflammation.
The immunophenotype of adipose tissue in RA patients appears to be characterized by a greater macrophage infiltrate and more "crown- like" structures. These are correlated with disease characteristics and can be lowered with some treatments, whereas others have no effect. Additional longitudinal studies are needed to identify any causality.
Lastly, Dr. Giles showed that despite higher systemic levels of inflammation and its downstream consequences, adiposity may have a protective effect on erosive damage in RA. Whether mediated by adipose suppression of joint-damaging adiponectin or by other mechanisms remains unclear.
This talk by Dr. Kim Huffman was about sarcopenic obesity. This is a situation in which a person shows an increase in fat mass and a reduction in lean mass. Her hypothesis was that in RA there is an increase in inflammatory cytokines, causing increased inactivity, which then causes an increase in fatty acid delivery to the adipose tissue and a decrease of fatty acid use by skeletal muscle. The end result is a disruption in insulin-mediated signaling, intramuscular lipid imbalance and mitochondrial dysfunction, which creates skeletal muscle insulin resistance and cardiovascular disease, reduced mobility and poor quality of life. However, absolute differences in muscle insulin resistance are relatively small.
Prednisone, even in small doses (<5 mg/day), is not benign when it comes to insulin resistance.
Finally, traditional risk factors, especially adiposity and physical inactivity, are important in our rheumatic patients.
Dr. Karyn Esser discussed her research on circadian rhythms, which are physical, mental and behavioural changes that roughly follow a 24-hour cycle and are modulated by an endogenous circadian clock. She found that molecular clocks function in skeletal muscle to transcriptionally regulate large numbers of genes. For example, loss of Bmal 1 in skeletal muscle is sufficient to induce weakness and changes in tendon and bone.
Time of exercise serves as a cue to set internal clocks across many peripheral tissues, including skeletal muscle. Research in this area is in its infancy, but her data suggest that time of exercise may have under-appreciated benefits that serve to improve the robustness of clock rhythms and thereby improve overall health outcomes.