This study aims to test the separated and combined effects of mechanoreflex activation and nociception through exercise-induced muscle damage (EIMD) on central and peripheral haemodynamics before and during single passive leg movement (sPLM). Eight healthy young males undertook four experimental sessions, in which a sPLM was performed on the dominant limb while in each specific session the contralateral was: a) in a resting condition (CTRL), b) stretched (ST), c) resting after EIMD called delayed-onset-muscle-soreness (DOMS) condition, or d) stretched after EIMD (DOMS+ST). EIMD was used to induce DOMS in the following 24-48h. Femoral blood flow (FBF) was assessed using doppler ultrasound while central haemodynamics were assessed via finger photoplethysmography. Leg vascular conductance (LVC) was calculated as FBF/MAP. RR-interval were analyzed in the time (RMSSD) and frequency domain (LF/HF). Blood samples were collected before each condition and gene expression analysis showed increased fold changes for P2X4 and IL1β in DOMS and DOMS+ST compared with baseline. Resting FBF and LVC were decreased only in the DOMS+ST condition (-26ml/min and -50ml/mmHg/min respectively) with decreased RMSSD and increased LF/HF ratio. MAP, HR, CO, and SV were increased in ST and DOMS+ST compared with CTRL. Marked decreases of delta peaks and AUC for FBF (∆: -146ml/min and -265ml respectively) and LVC (∆: -8.66ml/mmHg/min and ±1.7ml/mmHg/min respectively) all p<.05. These results suggest that combination of mechanoreflex and nociception resulted in decreased vagal tone and concomitant rise in sympathetic drive that led to increases in resting central hemodynamic with reduce limb blood flow before and during sPLM.

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Previous studies in animal models showed that exercise-induced metabolites accumulation may sensitize the mechanoreflex-induced response. The aim of this study was to assess whether the magnitude of the central hemodynamic and ventilatory adjustments evoked by isolated stimulation of the mechanoreceptors in humans are influenced by the prior accumulation of metabolic byproducts in the muscle. 10 males and 10 females performed two exercise bouts consisting of 5-min of intermittent isometric knee-extensions performed 10% above the previously determined critical force. Post-exercise, the subjects recovered for 5 min either with a suprasystolic circulatory occlusion applied to the exercised quadriceps (PECO) or under freely-perfused conditions (CON). Afterwards, 1-min of continuous passive leg movement was performed. Central hemodynamics, pulmonary data, and electromyography from exercising/passively-moved leg were recorded throughout the trial. Root mean square of successive differences (RMSSD, index of vagal tone) was also calculated. Δpeak responses of heart rate (ΔHR) and ventilation ($$\Delta \dot{V}_{{\text{E}}}$$ Δ V ˙ E ) to passive leg movement were higher in PECO compared to CON (ΔHR: 6 ± 5 vs 2 ± 4 bpm, p = 0.01; 3.9 ± 3.4 vs 1.9 ± 1.7 L min−1, p = 0.02). Δpeak of mean arterial pressure (ΔMAP) was significantly different between conditions (5 ± 3 vs  − 3 ± 3 mmHg, p < 0.01). Changes in RMSSD with passive leg movement were different between PECO and CON (p < 0.01), with a decrease only in the former (39 ± 18 to 32 ± 15 ms, p = 0.04). No difference was found in all the other measured variables between conditions (p > 0.05). These findings suggest that mechanoreflex-mediated increases in HR and $$\dot{V}_{{\text{E}}}$$ V ˙ E are sensitized by metabolites accumulation. These responses were not influenced by biological sex.