Sympathetic and hemodynamic responses to exercise and to the activation of the muscle metaboreflex are augmented in postmenopausal women with rheumatoid arthritis (RA), according to study results published in The Journal of Physiology.
Previous studies have suggested abnormal cardiovascular responses to exercise in patients with RA; however, limited data are available on the potential mechanisms. The objective of the current study was to determine the hemodynamic and sympathetic responses to exercise and to the isolated activation of muscle metaboreflex in women with RA.
The study included 33 postmenopausal women with RA (mean age, 61±7 years) and 10 matched control participants. During a protocol of isometric knee extension exercise (3-min, 30% of maximal voluntary contraction), followed by postexercise ischemia, the researchers measured mean arterial pressure, heart rate, and muscle sympathetic nerve activity.
Although no difference was observed between the groups in resting hemodynamic and heart rate variability parameters, the researchers noted increased resting sympathetic activity among patients with RA vs control participants.
During exercise, the increase in mean arterial pressure (16 vs 9 mmHg, P =.03) and muscle sympathetic nerve activity (17 vs 7 bursts/min; P =.04) was greater among women with RA compared with control participants. Similar trends were observed during postexercise ischemia in mean arterial pressure (15 vs 5 mmHg, respectively; P =.001) and muscle sympathetic nerve activity (14 vs 6 bursts/min, P =.04).
There was a significant association (P <.05) between autonomic responses to exercise with proinflammatory (interferon [IFN]-γ, interleukin [IL]-8, monocyte chemoattractant protein 1, and tumor necrosis factor [TNF]-α) and anti-inflammatory (IL-1ra and IL-10) cytokines and pain levels.
The study had several limitations, including the inclusion of a cohort of only postmenopausal women, the potential unmeasured effect of antirheumatic drugs on the autonomic dysregulation in patients with RA, and the lack of available data on metabolite production during the exercise protocol.
“These findings provide mechanistic insights that may explain the abnormal cardiovascular responses to exercise in RA and reinforce the importance of [autonomic nervous system] dysfunction as an important component of the cardiovascular pathophysiology in RA,” the researchers concluded.
Reference
Peçanha T, Meireles K, Pinto AJ, et al. Increased sympathetic and hemodynamic responses to exercise and muscle metaboreflex activation in post-menopausal women with rheumatoid arthritis. J Physiol. Published online November 12, 2020. doi:10.1113/JP280892