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Cardiopulmonary afferents modulate sympathetically‐mediated heart rate responses to muscle metaboreflex activation in humans
Author(s) -
Souza Mayara C.,
Teixeira Andre L.,
Nunes Diego,
Lopes Paulo M.,
Gomes Mauricio D.,
Fisher James P.,
Vianna Lauro C.
Publication year - 2016
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.30.1_supplement.1286.7
Subject(s) - heart rate , supine position , microneurography , medicine , blood pressure , reflex , cardiology , baroreflex , baroreceptor , anesthesia
The sensory component of the exercise pressor reflex is comprised of group III and IV skeletal muscle afferents that respond to both mechanical (i.e., muscle mechanoreflex) and metabolic (i.e., muscle metaboreflex) stimuli. In humans, isolated muscle metaboreflex activation with post‐exercise ischemia (PEI) has a major effect on increasing sympathetic nerve activity. This can cause peripheral vasoconstriction and partially maintain the exercise‐induced increase in blood pressure. A smaller heart rate response is evoked, which can be blocked by antagonism of b‐1 receptor. The loading of cardiopulmonary baroreceptors, associated with the supine posture, also provides neuromodulatory signals to the brainstem and elicits cardiac sympathoinhibition. Here, we aimed to test the hypothesis that the sympathetically‐mediated heart rate response to muscle metaboreflex activation is blunted by cardiopulmonary loading in men. Nineteen healthy male subjects participated in the study (20 ± 2 years). Beat‐to‐beat blood pressure and heart rate were continuously measured by finger photoplethysmography (ML282B1‐X, AdInstruments). After a rest period a 90‐s static handgrip at 40% maximum voluntary contraction was performed followed by PEI. Trials were conducted with concurrent cardiopulmonary loading (supine posture) or unloading (seated posture). In a subset of subjects (n=5) trials were repeated after b‐1 adrenergic blockade (Atenolol 25 mg). At rest, the shift from supine to seated posture increased heart rate from 64±2 to 69±2 beats.min −1 (P<0.05), whereas blood pressure decreased from 90±2 to 84±2 mmHg (P<0.05). PEI provoked a robust increase in blood pressure from rest (Δ36±3 mmHg, P<0.05), which was not affected by body posture. During upright PEI, heart rate was elevated from rest (Δ10±2 beats.min −1 , P<0.05), but blunted with cardiopulmonary loading (Δ2±2 beats.min −1 , P>0.05 vs. rest). Following b‐1 adrenergic blockade, the heart rate response to upright PEI was significantly reduced (Δ5±3 beats.min −1 , P<0.05), whereas the heart rate response to supine PEI was unaffected (Δ3±2 beats.min −1 ). In summary, the current study demonstrates that the heart rate response to isolated muscle metaboreflex activation is elevated by cardiopulmonary baroreceptor unloading due to a b‐1 adrenergic mechanism. Support or Funding Information CAPES ‐ Coordination for the Improvement of Higher Education PersonnelCNPq ‐ National Council for Scientific and Technological Development