Mechanisms underlying exaggerated metaboreflex activation in prehypertensive men

Kyung Ae Kim, Charles L Stebbins, Hyun Min Choi, Hosung Nho, Jong Kyung Kim

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Purpose: Previously, we found that the pressor response to muscle metaboreflex activation is enhanced in prehypertension and associated with peripheral vasoconstriction. However, mechanisms underlying this exaggerated response are not clear. Therefore, we tested the hypothesis that activation of this reflex is augmented owing to increased production of muscle metabolites (i.e., lactate, K<sup>+</sup>, and H<sup>+</sup>). Methods: Twenty-two men (11 normotensive and 11 prehypertensive) were studied. Changes in cardiac output (Q), mean arterial pressure (MAP), and total peripheral resistance (TPR) were compared between the two groups during static exercise (SE) and postexercise muscular ischemia (PEMI). Subjects completed 2 min of SE at 50% of maximal voluntary contraction (MVC) followed by 2 min of PEMI. Venous blood samples for determination of metabolites and hormones (catecholamines, vasopressin, and plasma renin activity) were taken from the exercising and nonexercising arm, respectively. Results: Mean arterial pressure responses to SE (39 ± 3 vs 31 ± 2 mm Hg) and PEMI (24 ± 3 vs 19 ± 3 mm Hg) were significantly higher in the prehypertensive group. Increases in lactate and decreases in pH during PEMI were seen in both groups. However, changes in these variables were greater in the prehypertensive group (lactate, 50.1 ± 6.2 vs 32.8 ± 7.6 mg·dL<sup>-1</sup>; pH, -0.06 ± 0.02 vs -0.01 ± 0.01) (P <0.05). Postexercise muscular ischemia did not evoke increases in hormones in either group. Conclusions: Compared to the normotensive group, the augmented pressor response to the metaboreflex in the prehypertensive group was associated with greater production of muscle metabolites that activate its afferent arm. The augmented response was not associated with activation of the vasopressin and renin-angiotensin systems and greater activation of the sympathetic nervous system was not apparent. Consequently, additional factors specific to prehypertension, such as arterial stiffness, may have been involved.

Original languageEnglish (US)
Pages (from-to)1605-1612
Number of pages8
JournalMedicine and Science in Sports and Exercise
Volume47
Issue number8
DOIs
StatePublished - 2015

Fingerprint

Ischemia
Prehypertension
Lactic Acid
Exercise
Vasopressins
Muscles
Arterial Pressure
Hormones
Vascular Stiffness
Sympathetic Nervous System
Renin-Angiotensin System
Vasoconstriction
Renin
Cardiac Output
Vascular Resistance
Catecholamines
Reflex

Keywords

  • Catecholamines
  • Exercise pressor reflex
  • Postexercise muscular ischemia
  • Total peripheral resistance

ASJC Scopus subject areas

  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Mechanisms underlying exaggerated metaboreflex activation in prehypertensive men. / Kim, Kyung Ae; Stebbins, Charles L; Choi, Hyun Min; Nho, Hosung; Kim, Jong Kyung.

In: Medicine and Science in Sports and Exercise, Vol. 47, No. 8, 2015, p. 1605-1612.

Research output: Contribution to journalArticle

Kim, Kyung Ae ; Stebbins, Charles L ; Choi, Hyun Min ; Nho, Hosung ; Kim, Jong Kyung. / Mechanisms underlying exaggerated metaboreflex activation in prehypertensive men. In: Medicine and Science in Sports and Exercise. 2015 ; Vol. 47, No. 8. pp. 1605-1612.
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abstract = "Purpose: Previously, we found that the pressor response to muscle metaboreflex activation is enhanced in prehypertension and associated with peripheral vasoconstriction. However, mechanisms underlying this exaggerated response are not clear. Therefore, we tested the hypothesis that activation of this reflex is augmented owing to increased production of muscle metabolites (i.e., lactate, K+, and H+). Methods: Twenty-two men (11 normotensive and 11 prehypertensive) were studied. Changes in cardiac output (Q), mean arterial pressure (MAP), and total peripheral resistance (TPR) were compared between the two groups during static exercise (SE) and postexercise muscular ischemia (PEMI). Subjects completed 2 min of SE at 50{\%} of maximal voluntary contraction (MVC) followed by 2 min of PEMI. Venous blood samples for determination of metabolites and hormones (catecholamines, vasopressin, and plasma renin activity) were taken from the exercising and nonexercising arm, respectively. Results: Mean arterial pressure responses to SE (39 ± 3 vs 31 ± 2 mm Hg) and PEMI (24 ± 3 vs 19 ± 3 mm Hg) were significantly higher in the prehypertensive group. Increases in lactate and decreases in pH during PEMI were seen in both groups. However, changes in these variables were greater in the prehypertensive group (lactate, 50.1 ± 6.2 vs 32.8 ± 7.6 mg·dL-1; pH, -0.06 ± 0.02 vs -0.01 ± 0.01) (P <0.05). Postexercise muscular ischemia did not evoke increases in hormones in either group. Conclusions: Compared to the normotensive group, the augmented pressor response to the metaboreflex in the prehypertensive group was associated with greater production of muscle metabolites that activate its afferent arm. The augmented response was not associated with activation of the vasopressin and renin-angiotensin systems and greater activation of the sympathetic nervous system was not apparent. Consequently, additional factors specific to prehypertension, such as arterial stiffness, may have been involved.",
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T1 - Mechanisms underlying exaggerated metaboreflex activation in prehypertensive men

AU - Kim, Kyung Ae

AU - Stebbins, Charles L

AU - Choi, Hyun Min

AU - Nho, Hosung

AU - Kim, Jong Kyung

PY - 2015

Y1 - 2015

N2 - Purpose: Previously, we found that the pressor response to muscle metaboreflex activation is enhanced in prehypertension and associated with peripheral vasoconstriction. However, mechanisms underlying this exaggerated response are not clear. Therefore, we tested the hypothesis that activation of this reflex is augmented owing to increased production of muscle metabolites (i.e., lactate, K+, and H+). Methods: Twenty-two men (11 normotensive and 11 prehypertensive) were studied. Changes in cardiac output (Q), mean arterial pressure (MAP), and total peripheral resistance (TPR) were compared between the two groups during static exercise (SE) and postexercise muscular ischemia (PEMI). Subjects completed 2 min of SE at 50% of maximal voluntary contraction (MVC) followed by 2 min of PEMI. Venous blood samples for determination of metabolites and hormones (catecholamines, vasopressin, and plasma renin activity) were taken from the exercising and nonexercising arm, respectively. Results: Mean arterial pressure responses to SE (39 ± 3 vs 31 ± 2 mm Hg) and PEMI (24 ± 3 vs 19 ± 3 mm Hg) were significantly higher in the prehypertensive group. Increases in lactate and decreases in pH during PEMI were seen in both groups. However, changes in these variables were greater in the prehypertensive group (lactate, 50.1 ± 6.2 vs 32.8 ± 7.6 mg·dL-1; pH, -0.06 ± 0.02 vs -0.01 ± 0.01) (P <0.05). Postexercise muscular ischemia did not evoke increases in hormones in either group. Conclusions: Compared to the normotensive group, the augmented pressor response to the metaboreflex in the prehypertensive group was associated with greater production of muscle metabolites that activate its afferent arm. The augmented response was not associated with activation of the vasopressin and renin-angiotensin systems and greater activation of the sympathetic nervous system was not apparent. Consequently, additional factors specific to prehypertension, such as arterial stiffness, may have been involved.

AB - Purpose: Previously, we found that the pressor response to muscle metaboreflex activation is enhanced in prehypertension and associated with peripheral vasoconstriction. However, mechanisms underlying this exaggerated response are not clear. Therefore, we tested the hypothesis that activation of this reflex is augmented owing to increased production of muscle metabolites (i.e., lactate, K+, and H+). Methods: Twenty-two men (11 normotensive and 11 prehypertensive) were studied. Changes in cardiac output (Q), mean arterial pressure (MAP), and total peripheral resistance (TPR) were compared between the two groups during static exercise (SE) and postexercise muscular ischemia (PEMI). Subjects completed 2 min of SE at 50% of maximal voluntary contraction (MVC) followed by 2 min of PEMI. Venous blood samples for determination of metabolites and hormones (catecholamines, vasopressin, and plasma renin activity) were taken from the exercising and nonexercising arm, respectively. Results: Mean arterial pressure responses to SE (39 ± 3 vs 31 ± 2 mm Hg) and PEMI (24 ± 3 vs 19 ± 3 mm Hg) were significantly higher in the prehypertensive group. Increases in lactate and decreases in pH during PEMI were seen in both groups. However, changes in these variables were greater in the prehypertensive group (lactate, 50.1 ± 6.2 vs 32.8 ± 7.6 mg·dL-1; pH, -0.06 ± 0.02 vs -0.01 ± 0.01) (P <0.05). Postexercise muscular ischemia did not evoke increases in hormones in either group. Conclusions: Compared to the normotensive group, the augmented pressor response to the metaboreflex in the prehypertensive group was associated with greater production of muscle metabolites that activate its afferent arm. The augmented response was not associated with activation of the vasopressin and renin-angiotensin systems and greater activation of the sympathetic nervous system was not apparent. Consequently, additional factors specific to prehypertension, such as arterial stiffness, may have been involved.

KW - Catecholamines

KW - Exercise pressor reflex

KW - Postexercise muscular ischemia

KW - Total peripheral resistance

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