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Group III/IV muscle afferents contribute to carotid baroreflex resetting during evoked contractions in humans
Author(s) -
Hureau Thomas J,
Weavil Joshua C,
Thurston Taylor S,
Broxterman Ryan M,
Nelson Ashley D,
Bledsoe Amber D,
Jessop Jacob E,
Richardson Russell S,
Wray D Walter,
Amann Markus
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.848.7
Subject(s) - baroreflex , medicine , baroreceptor , blood pressure , anesthesia , heart rate , mean arterial pressure , isometric exercise , carotid sinus , stimulation , cardiology
Background Arterial baroreflexes play an important role in the control and regulation of the cardiovascular response to exercise. In fact, carotid baroreflex control of arterial blood pressure needs to be reset during exercise to tolerate the higher blood pressures associated with physical activities. This resetting of carotid baroreflex control to operate at a higher blood pressure during exercise is thought to be mediated by both feedback and feed forward mechanisms. Purpose To investigate the contribution of group III/IV muscle afferents to the carotid baroreflex control during evoked quadriceps contractions, devoid of feed forward input (i.e. no central command). Methods Eight recreationally active males (29 ± 5 yrs) performed electrically evoked isometric quadriceps contractions for 10 min (femoral nerve stimulation, 40 Hz, 50‐s on, 10‐s off) under control conditions (CTRL) and following lumbar intrathecal fentanyl (FENT) injection to impair feedback from μ‐opioid receptor sensitive lower limb muscle afferents. Carotid baroreflex function was assessed by applying rapid 5‐s pulses of neck pressure (NP, +40 mmHg) or suction (NS, −60 mmHg) via a customized collar. Heart rate (HR) and mean arterial pressure (MAP) were derived from a 12‐lead ECG and a radial arterial catheter, respectively. The carotid baroreflex operating point was determined using the average pre‐stimulus values for HR and MAP. Results Resting HR (~70 bpm) and MAP (~87 mmHg) were similar between CTRL and FENT conditions ( P > 0.4). FENT administration did not alter the cardiac response to NP (+9 ± 3 bpm; P = 0.99) or NS (−24 ± 11 bpm; P = 0.49) at rest. Similarly, FENT did not alter changes in MAP in response to NP (+13 ± 5 mmHg; P = 0.85) or NS (−13 ± 5 mmHg; P = 0.99) at rest. During exercise, FENT attenuated both HR (82 ± 10 bpm vs 93 ± 14 bpm; P < 0.05) and MAP (100 ± 14 mmHg vs 112 ± 14 mmHg; P < 0.05). However, similar to resting responses ( P > 0.4), the cardiac response to NP (+11 ± 4 bpm) or NS (−23 ± 9 bpm) was similar during CTRL and FENT exercise ( P > 0.5). Furthermore, changes in MAP in response to NP (+12 ± 4 mmHg) or NS (−14 ± 5 mmHg) were similar during CTRL and FENT exercise ( P > 0.4). Conclusion Inhibition of group III/IV muscle afferents during evoked muscle contractions reduced the operating point for both HR and MAP, suggesting this feedback pathway is important for carotid baroreflex resetting during exercise. However, carotid baroreflex responsiveness at rest and during exercise was preserved despite muscle afferent blockade, indicating that group III/IV muscle afferents do not govern the carotid baroreflex control of HR and MAP. Support or Funding Information The authors were supported by National Heart, Lung, and Blood Institute grants (HL‐103786 and HL‐116579) and a Veterans Affairs Spire grant (E1572P).