Differential effects of metaboreceptor and chemoreceptor activation on sympathetic and cardiac baroreflex control following exercise in hypoxia in human

Abstract

Muscle metaboreceptors and peripheral chemoreceptors exert differential effects on the cardiorespiratory and autonomic responses following hypoxic exercise. Whether these effects are accompanied by specific changes in sympathetic and cardiac baroreflex control is not known. Sympathetic and cardiac baroreflex functions were assessed by intravenous nitroprusside and phenylephrine boluses in 15 young male subjects. Recordings were performed in random order, under locally circulatory arrested conditions, during: (1) rest and normoxia (no metaboreflex and no chemoreflex activation); (2) normoxic post-handgrip exercise at 30% of maximum voluntary contraction (metaboreflex activation without chemoreflex activation); (3) hypoxia without handgrip (10% O 2 in N 2 , chemoreflex activation without metaboreflex activation); and (4) post-handgrip exercise in hypoxia (chemoreflex and metaboreflex activation). When compared with normoxic rest (−42 ± 7% muscle sympathetic nerve activity (MSNA) mmHg −1 ), sympathetic baroreflex sensitivity did not change during normoxic post-exercise ischaemia (PEI; −53 ± 9% MSNA mmHg −1 , P = 0.5) and increased during resting hypoxia (−68 ± 5% MSNA mmHg −1 , P < 0.01). Sympathetic baroreflex sensitivity decreased during PEI in hypoxia (−35 ± 6% MSNA mmHg −1 , P < 0.001 versus hypoxia without exercise; P = 0.16 versus normoxic PEI). Conversely, when compared with normoxic rest (11.1 ± 1.7 ms mmHg −1 ), cardiac baroreflex sensitivity did not change during normoxic PEI (8.3 ± 1.3 ms mmHg −1 , P = 0.09), but decreased during resting hypoxia (7.3 ± 0.8 ms mmHg −1 , P < 0.05). Cardiac baroreflex sensitivity was lowest during PEI in hypoxia (4.3 ± 1 ms mmHg −1 , P < 0.01 versus hypoxia without exercise; P < 0.001 versus normoxic exercise). The metaboreceptors and chemoreceptors exert differential effects on sympathetic and cardiac baroreflex function. Metaboreceptor activation is the major determinant of sympathetic baroreflex sensitivity, when these receptors are stimulated in the presence of hypoxia.

Activation of the carotid chemoreflex secondary to muscle metaboreflex stimulation in men

“…We hypothesized that 1) the carotid chemoreceptor would be sensitized with activation of the metaboreflex, 2) suppression of the carotid chemoreceptor during metaboreflex activation would attenuate sympathetic nerve activity, 3) activation of the carotid chemoreceptor during activation of the metaboreflex would augment sympathetic nerve activity, and 4) similar to the results of Gujic et al (13), activation of the carotid chemoreceptor with hypoxia would decrease cardiovagal baroreceptor sensitivity (thus increasing heart rate via vagal withdrawal) and that there would be a greater decrease of cardiovagal baroreceptor sensitivity upon concurrent activation of the carotid chemoreceptor and metaboreflex.…”

“…Previous investigations have examined interactions between the metaboreflex and the chemoreflex (13,15,17), yet hypoxia/ hyperoxia was administered before or during exercise rather than during the circulatory occlusion period only. Since sympathetic responses to exercise can be altered with inspired oxygen level (19), these previous findings could have been confounded by interactions with other autonomic reflexes beyond the metaboreflex and chemoreflex (i.e., the mechanoreflex and/or central command).…”

“…Aggarwal et al (1) suggest that even though the interactions were not consistently seen in animals, they may still be present in humans. Indeed, species differences in autonomic cardiovascular control are known to exist (20,21).Previous human studies have investigated interactions between the metaboreflex and the chemoreflex during exercise (13,15,17). These studies found that metaboreceptors, chemoreceptors, and baroreceptors all play a role in the sympathetic response to hypoxic exercise.…”

“…Previous human studies have investigated interactions between the metaboreflex and the chemoreflex during exercise (13,15,17). These studies found that metaboreceptors, chemoreceptors, and baroreceptors all play a role in the sympathetic response to hypoxic exercise.…”

Comparison of the Effects of Hydration with Water or Isotonic Solution on the Recovery of Cardiac Autonomic Modulation

“…In addition, after exercise, metabolites produced by muscle contraction, such as lactate and hydrogen, are removed; there is a reduction in circulating catecholamines, blood pH returns to baseline, and the temperature normalizes (Buchheit et al, 2007;Coote, 2010). Regulation of these factors allows for decreased activity of chemoreceptors, muscle metaboreceptors and thermoreceptors (Coote, 2010;Gujic et al, 2007;Niemela et al, 2008), producing a slow, steady decline in heart rate mediated by vagal reactivation and sympathetic withdrawal (Coote, 2010). These aspects explain the gradual increase in the rMSSD index throughout recovery.…”