Role of cardiac output in the pressor responses to graded muscle ischemia in man

Bonde-Petersen, F; Rowell, L. B.; Murray, R. G.; Blomqvist, G. G.; White, R. T.; Karlsson, E.; Campbell, William; Mitchell, Jere H.

doi:10.1152/jappl.1978.45.4.574

Cited by 51 publications

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“…The conflicting results of the present study and those from Farquhar and colleagues is potentially due to differences in exercise intensity and the muscle group, in which the reflex was evoked. For example, CO responses are often seen during PEMI following more intense exercise with a large muscle group, whereas with PEMI following lower-intensity exercise with smaller muscle groups, the pressor response usually occurs primarily via peripheral vasoconstriction (8,16,18,55). In our model, we robustly activated the metaboreflex by inducing hindlimb ischemia in an exercise workload, wherein hindlimb blood flow constitutes about 10% of cardiac output, whereas Farquhar and colleagues (20,25) elicited the reflex from one arm after 30 -40% MVC static contractions.…”

Section: Discussionmentioning

confidence: 99%

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

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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)....

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Section: Discussionmentioning

confidence: 99%

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

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“…This additional test aimed at verifying whether or not this condition "per se" could affect hemodynamics in heart failure patients, even though we as well as others (5,11,12) have demonstrated that, in normal individuals, RCO that was not preceded by exercise was incapable of eliciting any substantial hemodynamic modifications. On a day following the PEMI and CER tests, a RCO session consisting of 12 min (i.e., the same duration as the PEMI and CER tests) was applied: after 6 min of resting, 3 min of regional circulatory occlusion of the arm was applied followed by 3 more min of rest.…”

Section: Methodsmentioning

confidence: 99%

Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

Crisafulli¹,

Salis²,

Tocco³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

106

156

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“…The muscle ''metaboreflex'', a reflex evoked by those afferent nerve endings sensitive to accumulation of muscle metabolic end-products, is attracting growing interest in the scientific community because it is thought to contribute significantly to cardiovascular regulation during exercise by providing continuous feedback to the cardiovascular control areas about the metabolic status of contracting muscles [4,26,30,31,35,36].…”

Section: Introductionmentioning

confidence: 99%

Role of heart rate and stroke volume during muscle metaboreflex-induced cardiac output increase: differences between activation during and after exercise

et al. 2011

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We hypothesized that the role of stroke volume (SV) in the metaboreflex-induced cardiac output (CO) increase was blunted when the metaboreflex was stimulated by exercise muscle ischemia (EMI) compared with post-exercise muscle ischemia (PEMI), because during EMI heart rate (HR) increases and limits diastolic filling. Twelve healthy volunteers were recruited and their hemodynamic responses to the metaboreflex evoked by EMI, PEMI, and by a control dynamic exercise were assessed. The main finding was that the blood pressure increment was very similar in the EMI and PEMI settings. In both conditions the main mechanism used to raise blood pressure was a CO elevation. However, during the EMI test CO was increased as a result of HR elevation whereas during the PEMI test CO was increased as a result of an increase in SV. These results were explainable on the basis of the different HR behavior between the two settings, which in turn led to different diastolic time and myocardial performance.

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Role of cardiac output in the pressor responses to graded muscle ischemia in man

Cited by 51 publications

References 0 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

Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

Role of heart rate and stroke volume during muscle metaboreflex-induced cardiac output increase: differences between activation during and after exercise

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