Left ventricular volumes and hemodynamic responses to postexercise ischemia in healthy humans

Bastos, Bianca Gouvêa; Williamson, Jon W.; Harrelson, Tom; Nóbrega, Antônio Cláudio Lucas da

doi:10.1097/00005768-200006000-00012

Cited by 45 publications

(54 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Therefore, it is possible that the experimental model of Farquhar and colleagues is one that is driven by peripheral vasoconstriction and not CO. Indeed, previous studies both support (8, 16 -18, 44, 48, 55, 60) and refute (6,18,44) any role for CO in mediating the pressor response during PEMI. As such, we would not expect the pressor response to fall during PEMI in HTN as in our model.…”

Section: Discussionmentioning

confidence: 88%

See 1 more Smart Citation

Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension

Spranger

Kaur

Sala‐Mercado

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

DS. Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension. Am J Physiol Regul Integr Comp Physiol 308: R650 -R658, 2015. First published January 28, 2015 doi:10.1152/ajpregu.00464.2014.-During dynamic exercise, muscle metaboreflex activation (MMA; induced via partial hindlimb ischemia) markedly increases mean arterial pressure (MAP), and MAP is sustained when the ischemia is maintained following the cessation of exercise (postexercise muscle ischemia, PEMI). We previously reported that the sustained pressor response during PEMI in normal individuals is driven by a sustained increase in cardiac output (CO) with no peripheral vasoconstriction. However, we have recently shown that the rise in CO with MMA is significantly blunted in hypertension (HTN). The mechanisms sustaining the pressor response during PEMI in HTN are unknown. In six chronically instrumented canines, hemodynamic responses were observed during rest, mild exercise (3.2 km/h), MMA, and PEMI in the same animals before and after the induction of HTN [Goldblatt two kidney, one clip (2K1C)]. In controls, MAP, CO and HR increased with MMA (ϩ52 Ϯ 6 mmHg, ϩ2.1 Ϯ 0.3 l/min, and ϩ37 Ϯ 7 beats per minute). After induction of HTN, MAP at rest increased from 97 Ϯ 3 to 130 Ϯ 4 mmHg, and the metaboreflex responses were markedly attenuated (ϩ32 Ϯ 5 mmHg, ϩ0.6 Ϯ 0.2 l/min, and ϩ11 Ϯ 3 bpm). During PEMI in HTN, HR and CO were not sustained, and MAP fell to normal recovery levels. We conclude that the attenuated metaboreflex-induced HR, CO, and MAP responses are not sustained during PEMI in HTN.exercise pressor reflex; postexercise circulatory occlusion; peripheral resistance; hypertension THE MUSCLE METABOREFLEX IS a very powerful blood pressureraising reflex (1,3,12,22,42,48,51,65). Metabolically sensitive afferents of this reflex (group III/IV) are stimulated by metabolites (e.g., protons, lactate, potassium, and diprotonated phosphate), which accumulate within underperfused active skeletal muscle (10, 19, 30, 32, 35, 46, 47, 56 -58, 61). Muscle metaboreflex activation results in a reflex increase in sympathetic outflow (9, 28 -30, 36 -38, 62). During submaximal dynamic exercise, metaboreflex activation markedly increases heart rate (HR), cardiac output (CO) and left ventricular dP/dt max , with little effect on the peripheral vasculature (5,16,17,26,27,55,60,65). Therefore, the substantial metaboreflex-mediated pressor response observed during mild dynamic exercise is virtually solely the result of the increase in CO.In contrast, when metaboreflex activation is maintained following the cessation of submaximal dynamic exercise (postexercise muscle ischemia, PEMI) in normal subjects, the pressor response is sustained despite a decrease in HR toward resting levels with a time course similar to normal recovery from exercise (1,2,21,44,49,50,(62)(63)(64). The fall in HR during PEMI led some investigators to question the role of CO in mediating the sustained pressor response during PEMI (21,49,50,63)....

show abstract

Section: Discussionmentioning

confidence: 88%

“…In contrast, other investigators have concluded that elevated arterial pressure stems from peripheral vasoconstriction, not CO (6,18,44). Several factors could account for these disparate conclusions, including differences in species, age, type, and intensity of exercise performed and experimental methodology.…”

Section: Perspectives and Significancementioning

confidence: 93%

Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension

Spranger

Kaur

Sala‐Mercado

et al. 2015

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…From recent and early findings, it appears that the capacity to centralize blood volume and to increase venous return plays a pivotal role during the metaboreflex, and altered hemodynamic responses have been described where this capacity is impaired (4,13,33,53). In the present investigation, VFR was used to investigate venous return.…”

Section: Discussionmentioning

confidence: 93%

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Milia

Velluzzi

Roberto

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Patients suffering from obesity and metabolic syndrome (OMS) manifest a dysregulation in hemodynamic response during exercise, with an exaggerated systemic vascular increase. However, it is not clear whether this is the consequence of metabolic syndrome per se or whether it is due to concomitant obesity. The aim of the present investigation was to discover whether OMS and noncomplicated obesity resulted in different hemodynamic responses during the metaboreflex. Twelve metabolically healthy but obese subjects (MHO; 7 women), 13 OMS patients (5 women), and 12 normal age-matched controls (CTL; 6 women) took part in this study. All participants underwent a postexercise muscle ischemia protocol to evaluate the metaboreflex activity. Central hemodynamics were evaluated by impedance cardiography. The main result shows an exaggerated increase in systemic vascular resistance from baseline during the metaboreflex in the OMS patients as compared with the other groups (481.6 ± 180.3, -0.52 ± 177.6, and -60.5 ± 58.6 dynes·s(-1)·cm(-5) for the OMS, the MHO, and the CTL groups, respectively; P < 0.05). Moreover, the MHO subjects and the CTL group showed an increase in cardiac output during the metaboreflex (288.7 ± 325.8 and 703.8 ± 276.2 ml/m increase with respect to baseline), whereas this parameter tended to decrease in the OMS group (-350 ± 236.5 ml/m). However, the blood pressure response, which tended to be higher in the OMS patients, was not statistically different between groups. The results of the present investigation suggest that OMS patients have an exaggerated vasoconstriction in response to metaboreflex activation and that this fact is not due to obesity per se

show abstract

“…Recent physiological studies, with the quantification of some of the cardiorespiratory responses to predominantly static exercises using small and different muscle groups and with different percentages of maximal voluntary strength, have contributed to a better understanding of the mechanisms associated with IHT and similar exercises 14,15,[33][34][35][36][37] . Nevertheless, when these physiological data, respecting the methodological differences and small samples involved, are compared with our results, one can identify a 13 .…”

Section: Discussionmentioning

confidence: 99%

Respostas hemodinâmicas a um protocolo de treinamento isométrico de preensão manual

Araújo¹,

Duarte

Gonçalves

et al. 2011

Arq. Bras. Cardiol.

View full text Add to dashboard Cite

show abstract

Left ventricular volumes and hemodynamic responses to postexercise ischemia in healthy humans

Abstract: Activation of muscle metaboreceptors during OCCL increased MAP by elevating TPR. Despite the higher afterload and increased ESV, CO and SV were kept similar to resting values because EDV also increased, implying the involvement of the Frank-Starling mechanism.

Cited by 45 publications

References 9 publications

Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension

Attenuated muscle metaboreflex-induced pressor response during postexercise muscle ischemia in renovascular hypertension

Differences in hemodynamic response to metaboreflex activation between obese patients with metabolic syndrome and healthy subjects with obese phenotype

Respostas hemodinâmicas a um protocolo de treinamento isométrico de preensão manual

Contact Info

Product

Resources

About