Dynamic Carotid Baroreflex Function at the Onset of Leg Cycling
Authors: Barbosa Thales , Vianna Lauro , Hashimoto Takeshi , Petersen Lonnie , Olesen Niels , Tsukamoto Hayato , Sørensen Henrik , Ogoh Shigehiko , Nobrega Antonio , Secher Niels 
Published: November 2023

Carotid baroreflex (CBR) controls blood pressure (BP) by altering heart rate (HR), cardiac output (CO) and total vascular conductance (TVC) on a beat‐to‐beat basis at rest and during exercise. However, functional changes in CBR are known to occur during exercise. For example, the decrease in HR during CBR stimulation with neck suction (NS) is attenuated in the first 5 s of static handgrip exercise. In contrast, BP decrease by NS in the first 5 s of static handgrip exercise is similar to that obtained in resting conditions, and the decrease in both HR and BP by NS are similar to rest after 40 s of static handgrip exercise, evidencing a dynamic modulation of CBR control of HR at the onset of handgrip and a differential CBR control of HR and BP. Considering that regulatory mechanisms and physiological responses to exercise are affected by muscle mass, type and intensity of muscle contraction, we investigated whether CBR function is dynamically modulated during 45‐s leg cycling. Fifteen male healthy subjects (age: 24 ± 1 years (mean ± SEM); height: 182 ± 2 cm; weight: 74 ± 3 kg) were screened for CBR responsiveness at rest, using an adjustable collar around the anterior portion of the neck for application of 5‐s NS pulses at −60 mmHg. In addition, workloads for steady‐state low‐ (90 heart beats/min; LI) and moderate‐intensity (130 heart beats/min; MI) exercise at 60 rpm were determined by 3‐min cycling bouts. These workloads were used in a second visit, when subjects performed 45‐s LI and MI leg cycling bouts, without (CTRL) or with NS application during 0–5 s (NS 0–5), 10–15 s (NS 10–15) or 30–35 s (NS 30–35) after the onset of cycling. NS was applied at the end of a normal expiration. Each combination of exercise intensity and NS application was repeated for three exercise bouts and data were averaged for individual responses. Resting CBR was also assessed during a breath hold. Beat‐to‐beat HR (ECG) and BP (Finometer) were measured, stroke volume (SV) was obtained by Modelflow, CO and TVC were calculated (CO = HR SV; TVC = CO/BP), and the respiratory movements were monitored (Pneumobelt). Compared to CTRL cycling, reflex bradycardia was obtained at all exercising NS applications (P < 0.05). The reflex response was small at NS 0–5 in both cycling intensities, as compared to resting NS (LI and MI: −7 ± 1 vs. Rest: −9 ± 1 beats/min; P < 0.05). NS 10–15 and NS 30–35 in both cycling intensities resulted in bradycardia similar to resting NS (P > 0.05). Transient BP decrease was observed at all exercising NS applications (P < 0.05), compared to CTRL cycling. The NS‐induced BP decrease at NS 0–5 (LI and MI: −9 ± 1 mmHg) and NS 10–15 (LI and MI: −8 ± 1 mmHg) was significantly greater than at rest (−5 ± 1 mmHg; P < 0.05 vs. NS 0–5 and NS 10–15). NS 30–35 in both cycling intensities resulted in BP decrease similar to resting NS (P > 0.05). The NS‐induced exaggerated BP decrease during cycling was accompanied by a greater increase of TVC at NS 0–5 (LI: +13 ± 4; MI: +15 ± 3 mL/min/mmHg) and at NS 10–15 of MI cycling (+12 ± 2 mL/min/mmHg) than that obtained at rest (+3 ± 2 mL/min/mmHg; P < 0.05), while the decrease in CO during NS was similar to rest (P > 0.05). Cardiovascular responses to NS were similar between exercise intensities (P > 0.05). A differential dynamic CBR control of HR and BP was detected in the transition from rest to cycling, i.e., CBR control of HR was blunted in the first 5 s, while CBR control of BP was exaggerated in the first 15 s cycling.

Support or Funding Information

CAPES Foundation, Science without Borders Program, Brazil; Ehrenreich Fond, Denmark.