Does inadequate oxygen delivery trigger pressor response to muscle hypoperfusion during exercise?

Sheriff, Don D.; Wyss, C R; Rowell, L. B.; Scher, Allen M.

doi:10.1152/ajpheart.1987.253.5.h1199

Cited by 71 publications

(67 citation statements)

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“…In anesthetized animals, lactic acid has been shown to stimulate muscle afferents (22,23) and reflexly increase arterial pressure (24). In conscious dogs, the pressor response to progressive muscle ischemia during treadmill exercise was strongly correlated to venous effluent pH (25). In normal humans, we previously found a close temporal relationship between decreases in forearm muscle cell pH and increases in peroneal MSNA during static handgrip (12), an observation that we now have replicated in the present experiments.…”

Section: Resultssupporting

confidence: 81%

Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease).

Pryor¹,

Lewis²,

Haller³

et al. 1990

J. Clin. Invest.

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Section: Resultssupporting

confidence: 81%

Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease).

Pryor¹,

Lewis²,

Haller³

et al. 1990

J. Clin. Invest.

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“…In conscious dogs, the arterial pressure response to progressive muscle ischemia during exercise was highly correlated with venous effluent pH (20). Taken finding because previous observations had suggested that chemosensitive muscle afferents might be activated by some ofthe same metabolites that stimulate mitochondrial respiration (21).…”

Section: Discussionsupporting

confidence: 57%

Sympathetic nerve discharge is coupled to muscle cell pH during exercise in humans.

Victor¹,

Bertocci²,

Pryor³

et al. 1988

J. Clin. Invest.

323

269

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We used phosphorus nuclear magnetic resonance spectroscopy (31P-NMR) to probe the cellular events in contracting muscle that initiate the reflex stimulation of sympathetic outflow during exercise. In conscious humans, we performed 3"P-NMR on exercising forearm muscle and simultaneously recorded muscle sympathetic nerve activity (MSNA) with microelectrodes in the peroneal nerve to determine if the activation of MSNA is coupled to muscle pH, an index of glycolysis, or to the concentrations (0) of inorganic phosphate (Pi) and adenosine diphosphate (ADP) which are modulators of mitochondrial respiration. During both static and rhythmic handgrip, the onset of sympathetic activation in resting muscle coincided with the development of cellular acidification in active muscle. Furthermore, increases in MSNA were correlated closely with decreases in intracellular pH but dissociated from changes in phosphocreatine (IPCrI), [Pi], and [ADPI. The principal new conclusion is that activation of muscle sympathetic outflow during exercise in humans is coupled to the cellular accumulation of protons in contracting muscle.

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“…This suggests that humans rely on local vasodilator mechanisms, and not a reflex increase in pressure, to restore blood flow to hypoperfused contracting muscle. In contrast, there is overwhelming evidence that suggests a pressor response is essential in the restoration of blood flow to underperfused hindlimbs of exercising dogs (12,22,23,30,35). The discrepant findings between our series of studies in humans and those performed in dogs may simply be related to species differences.…”

Section: Restoration Of Flow Via Local Vasodilator Mechanismscontrasting

confidence: 58%

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

Casey

Joyner

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Casey DP, Joyner MJ. Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle. Am J Physiol Heart Circ Physiol 301: H261-H268, 2011. First published May 2, 2011; doi:10.1152/ajpheart.00222.2011.-We tested the hypothesis that 1) prostaglandins (PGs) contribute to compensatory vasodilation in contracting human forearm subjected to acute hypoperfusion, and 2) the combined inhibition of PGs and nitric oxide would attenuate the compensatory vasodilation more than PG inhibition alone. In separate protocols, subjects performed forearm exercise (20% of maximum) during hypoperfusion evoked by intra-arterial balloon inflation. Each trial included baseline, exercise before inflation, exercise with inflation, and exercise after deflation. Forearm blood flow (FBF; ultrasound) and local (brachial artery) and systemic arterial pressure [mean arterial pressure (MAP); Finometer] were measured. In protocol 1 (n ϭ 8), exercise was repeated during cyclooxygenase (COX) inhibition (Ketorolac) alone and during Ke-In protocol 2 (n ϭ 8), exercise was repeated during L-NMMA alone and during L-NMMA-Ketorolac. Forearm vascular conductance (FVC; ml·min Ϫ1 · 100 mmHg Ϫ1 ) was calculated from FBF (ml/min) and local MAP (mmHg). The percent recovery in FVC during inflation was calculated as (steady-state inflation ϩ exercise value Ϫ nadir)/ [steady-state exercise (control) value Ϫ nadir] ϫ 100. In protocol 1, COX inhibition alone did not reduce the %FVC recovery compared with the control (no drug) trial (92 Ϯ 11 vs. 100 Ϯ 10%, P ϭ 0.83). However, combined COX-nitric oxide synthase (NOS) inhibition caused a substantial reduction in %FVC recovery (54 Ϯ 8%, P Ͻ 0.05 vs. Ketorolac alone). In protocol 2, the percent recovery in FVC was attenuated with NOS inhibition alone (69 Ϯ 9 vs. 107 Ϯ 10%, P Ͻ 0.01) but not attenuated further during combined NOS-COX inhibition (62 Ϯ 10%, P ϭ 0.74 vs. L-NMMA alone). Our data indicate that PGs are not obligatory to the compensatory dilation observed during forearm exercise with hypoperfusion.prostaglandins; blood flow; nitric oxide; vasodilation; exercise; hypoperfusion DURING ACUTE EXPERIMENTAL hypoperfusion, skeletal muscle blood flow is partially restored in the exercising forearm through local dilator mechanisms and/or a myogenic response (4, 5). Along these lines, nitric oxide synthase (NOS) inhibition blunts the magnitude of restoration of forearm blood flow (FBF) and vascular conductance (FVC) during exercise with acute hypoperfusion by 10 -20% (4). The fact that a substantial flow restoration still occurs despite NOS inhibition suggests that additional vasodilator signals are likely involved in this response.In general, prostaglandins (PGs) do not appear to contribute significantly to the exercise hyperemic response to dynamic contractions (9,16,20,29,31). These findings are based on little to no change in muscle blood flow following PG synthesis inhibition. However, PGs have been reported to be involved in the regulation of skeletal muscle ...

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Does inadequate oxygen delivery trigger pressor response to muscle hypoperfusion during exercise?

Cited by 71 publications

References 0 publications

Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease).

Impairment of sympathetic activation during static exercise in patients with muscle phosphorylase deficiency (McArdle's disease).

Sympathetic nerve discharge is coupled to muscle cell pH during exercise in humans.

Prostaglandins do not contribute to the nitric oxide-mediated compensatory vasodilation in hypoperfused exercising muscle

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