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Key points  Rheumatoid arthritis (RA) patients present exacerbated blood pressure responses to exercise, but little is known regarding the underlying mechanisms involved.  This study assessed autonomic and haemodynamic responses to exercise and to the isolated activation of muscle metaboreflex in post‐menopausal women with RA.  Participants with RA showed augmented pressor and sympathetic responses to exercise and to the activation of muscle metaboreflex. These responses were associated with multiple pro‐ and anti‐inflammatory cytokines and with pain.  The results of the present study support the suggestion that an abnormal reflex control of circulation is an important mechanism underlying the exacerbated cardiovascular response to exercise and increased cardiovascular risk in RA. Abstract Studies have reported abnormal cardiovascular responses to exercise in rheumatoid arthritis (RA) patients, but little is known regarding the underlying mechanisms involved. This study assessed haemodynamic and sympathetic responses to exercise and to the isolated activation of muscle metaboreflex in women diagnosed with RA. Thirty‐three post‐menopausal women diagnosed with RA and 10 matched controls (CON) participated in this study. Mean arterial pressure (MAP), heart rate (HR) and muscle sympathetic nerve activity (MSNA frequency and incidence) were measured during a protocol of isometric knee extension exercise (3 min, 30% of maximal voluntary contraction), followed by post‐exercise ischaemia (PEI). Participants with RA showed greater increases in MAP and MSNA during exercise and PEI than CON (ΔMAPexercise = 16 ± 11 vs. 9 ± 6 mmHg, P = 0.03; ΔMAPPEI = 15 ± 10 vs. 5 ± 5 mmHg, P = 0.001; ΔMSNAexercise = 17 ± 14 vs. 7 ± 9 bursts min–1, P = 0.04; ΔMSNAPEI = 14 ± 10 vs. 6 ± 4 bursts min–1, P = 0.04). Autonomic responses to exercise showed significant (P < 0.05) association with pro‐ (i.e. IFN‐γ, IL‐8, MCP‐1 and TNFα) and anti‐inflammatory (i.e. IL‐1ra and IL‐10) cytokines and with pain. In conclusion, post‐menopausal women with RA showed augmented pressor and sympathetic responses to exercise and to the activation of muscle metaboreflex. These findings provide mechanistic insights that may explain the abnormal cardiovascular responses to exercise in RA.

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