Introduction

The effect of mechanoreflex on central blood pressure (BP) is unclear, although the influence of metaboreflex has been investigated. A relatively small contribution of the mechanoreflex to the pressor response to exercise has been considered in humans because many studies have failed to isolate the mechanoreflex-mediated pressor response. In a recent study, we successfully isolated a mechanoreflex-mediated pressor response using static passive stretching (SPS) in the forearm. Thus, it is possible to isolate the effect of the mechanoreflex on the central BP using this recently developed method. We investigated the effect of muscle mechanoreflex on central BP and compared the changes in the shape of the central BP waveform during mechanoreflex and metaboreflex.

Methods

We measured 12 healthy males (age, 26 ± 2 years; height, 171.1 ± 5.2 cm; body mass, 63.3 ± 10.3 kg; body fat, 16.7% ± 3.9%; means ± standard deviation [SD]) in this study. All participants performed static passive stretching (SPS) of the forearm for 60 s to isolate the muscle mechanoreflex. They also performed 120 s of isometric handgrip (IHG) at 30% maximal voluntary contraction and underwent 180 s of post-exercise ischemia (PEI) to isolate the muscle metaboreflex. The carotid BP (cBP) waveform was obtained from the right common carotid artery as the central BP waveform. We evaluated the first systolic peak (P1) and second systolic peak (P2) from the cBP waveform.

Results

SPS increased cBP with an increase in P1 (p < 0.05), whereas PEI increased cBP with an increase in P2 (p < 0.05). SPS did not alter augmentation pressure (AP) (p > 0.05), whereas PEI increased it (p < 0.05). The relative change from rest (Δ) in P1 during SPS was positively correlated with that in stroke volume (r = 0.68; p < 0.05), and the ΔAP during PEI was positively correlated with that in total peripheral resistance TPR (r = 0.61; p < 0.05).

Conclusion

These results suggest different effects of mechano- and metaboreflex on the change in shape of the central BP waveform; mechanoreflex and metaboreflex deform P1 and P2, respectively.

Cardiovascular responses to diving are characterized by two opposing responses: tachycardia resulting from exercise and bradycardia resulting from the apnea. The convergence of bradycardia and tachycardia may determine the cardiovascular responses to diving. The purpose of this study was to investigate the interaction of breath holding and muscle mechanoreflex on cardiovascular responses in breath-hold divers (BHDs) and non-BHDs. We compared the cardiovascular responses to combined apnea and the mechanoreflex in BHDs and non-BHDs. All participants undertook three trials—apnea, passive leg cycling (PLC), and combined trials—for 30 s after rest. Cardiovascular variables were measured continuously. Nine BHD (male:female, 4:5; [means ± SD] age, 35 ± 6 years; height, 168.6 ± 4.6 cm; body mass, 58.4 ± 5.9 kg) and eight non-BHD (male:female, 4:4; [means ± SD] age, 35 ± 7 years; height, 163.9 ± 9.1 cm; body mass, 55.6 ± 7.2 kg) participants were included. Compared to the resting baseline, heart rate (HR) and cardiac output (CO) significantly decreased during the combined trial in the BHD group, while they significantly increased during the combined trials in the non-BHD group (P < 0.05). Changes in the HR and CO were significantly lower in the BHD group than in the non-BHD group in the combined trial (P < 0.05). These results suggest that bradycardia with apnea in BHDs is prioritized over tachycardia with the mechanoreflex, whereas that in non-BHDs is not. This finding implies that diving training changes the interaction between apnea and the mechanoreflex in cardiovascular control.

The muscle mechanoreflex has been considered to make a small contribution to the cardiovascular response to exercise in healthy humans because no pressor response has been observed during stimulation of mechanosensitive receptors, such as static passive stretching, during many human studies. There is room for rethinking this consideration since the pressor response to upper limb exercise is greater than that to lower limb exercise. We examined whether static passive stretching of the forearm muscles causes a muscle mechanoreflex-induced pressor response in humans. Eighteen healthy men were recruited for this study. After a 15-min rest period in the supine position with a neutral (0◦) wrist joint angle, all participants completed static passive stretching of the forearm for 60 s at four different intensities: minimal painful passive stretching (PPS), moderate-intensity passive stretching (MPS), low-intensity passive stretching (LPS), and no load (NL). During the procedure, beat-to-beat arterial blood pressure was measured using finger photoplethysmography. The force generated between the passively stretched hand and the experimenter’s hands was recorded using a force transducer. Mean arterial pressure (MAP) during PPS and MPS significantly increased from baseline during the last 40 s (P < 0.05). MAP was significantly greater at 50 s and 60 s, depending on the intensity. MPS induced a greater peak response in MAP than lower intensities (P < 0.05). None of the subjects reported pain during the MPS and LPS trials. Static passive stimulation of the forearm is an effective method of isolating the muscle mechanoareflex-induced pressor response in humans.