Muscular work and the release of prostaglandin-like substances

Herbaczyńska-Cedro, K; Staszewska-Barczak, Janina; Janczewska, H

doi:10.1093/cvr/10.4.413

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“…The activation of group III afferents occurs mainly due to mechanical deformation of the receptive fields, whereas group IV afferents are activated by metabolic by-products of muscle contraction (19). One important group of metabolites noted in several prior animal reports are the prostaglandins (17,39,49,51). These reports suggest that cyclooxygenase products of arachidonic acid metabolism (e.g., prostaglandin) can sensitize group III afferents during muscle contraction (16,40), and hence muscle mechanoreflexes may be sensitized by prostaglandins.…”

Section: Discussionmentioning

confidence: 99%

Local prostaglandin blockade attenuates muscle mechanoreflex-mediated renal vasoconstriction during muscle stretch in humans

Momen¹,

Cui²,

McQuillan³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Momen A, Cui J, McQuillan P, Sinoway LI. Local prostaglandin blockade attenuates muscle mechanoreflex-mediated renal vasoconstriction during muscle stretch in humans. Am J Physiol Heart Circ Physiol 294: H2184-H2190, 2008. First published March 7, 2008 doi:10.1152/ajpheart.00948.2007.-During exercise, muscle mechanoreflex-mediated sympathoexcitation evokes renal vasoconstriction. Animal studies suggest that prostaglandins generated within the contracting muscle sensitize muscle mechanoreflexes. Thus we hypothesized that local prostaglandin blockade would attenuate renal vasoconstriction during ischemic muscle stretch. Eleven healthy subjects performed static handgrip before and after local prostaglandin blockade (6 mg ketorolac tromethamine infused into the exercising forearm) via Bier block. Renal blood flow velocity (RBV; Duplex Ultrasound), mean arterial pressure (MAP; Finapres), and heart rate (HR; ECG) were obtained during handgrip, post-handgrip muscle ischemia (PHGMI) followed by PHGMI with passive forearm muscle stretch (PHGMI ϩ stretch). Renal vascular resistance (RVR, calculated as MAP/RBV) was increased from baseline during all paradigms except during PHGMI ϩ stretch after the ketorolac Bier block trial where RVR did not change from baseline. Before Bier block, RVR rose more during PHGMI ϩ stretch than during PHGMI alone (P Ͻ .01). Similar results were found after a saline Bier block trial (⌬53 Ϯ 13% vs. ⌬35 Ϯ 10%; P Ͻ 0.01). However, after ketorolac Bier block, RVR was not greater during PHGMI ϩ stretch than during PHGMI alone [⌬39 Ϯ 8% vs. ⌬40 Ϯ 12%; P ϭ not significant (NS)]. HR and MAP responses were similar during PHGMI and PHGMI ϩ stretch (P ϭ NS). Passive muscle stretch during ischemia augments renal vasoconstriction, suggesting that ischemia sensitizes mechanically sensitive afferents. Inhibition of prostaglandin synthesis eliminates this mechanoreceptor sensitization-mediated constrictor responses. Thus mechanoreceptor sensitization in humans is linked to the production of prostaglandins. kidney; exercise; nervous system; sympathetic; muscle metabolite EXERCISE ACTIVATES THE sympathetic nervous system (SNS) that contributes to increases in heart rate (HR), blood pressure, ventilation, and peripheral vascular resistance. These adjustments are essential for adequate perfusion of vital organs, e.g., skeletal muscle, heart, and brain (31). Work by Alam and Smirk (1) more than half a century ago suggested that during exercise, muscle metabolites accumulate in active skeletal muscle and that when these metabolites are trapped in the muscle during a period of postexercise circulatory arrest, a pressor reflex is evoked, presumably by direct stimulation of metabolite sensitive afferents in the muscle. This response has been termed the "muscle metaboreflex" (3,23,32,38,43). It has been further demonstrated that stimulation of mechanically sensitive afferents during muscle contraction activates the SNS (18, 19, 52) and evokes vasoconstriction. This response has been termed the "muscle mechanoreflex." O...

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Section: Discussionmentioning

confidence: 99%

Local prostaglandin blockade attenuates muscle mechanoreflex-mediated renal vasoconstriction during muscle stretch in humans

Momen¹,

Cui²,

McQuillan³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Additionally, the doses we used were similar or slightly greater than those used previously to abolish the release of prostaglandins from contracting skeletal muscle of the dog. 28 Finally, it is known that a reduction in renal PGE 2 synthesis caused by indomethacin injections results in a reduction in renal blood flow. 29 Examination of our regional blood flow data (Table 1) shows that administration of 2-5 mg/kg of indomethacin caused a decrease in renal blood flow of about 50%.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction.

Stebbins¹,

Maruoka

Longhurst

1986

Circulation Research

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The purpose of this study was to determine the contribution of prostaglandins to the reflex cardiovascular responses induced by static contraction of the hind limb in cats, i.e., the exercise reflex. To accomplish this, the cardiovascular responses to hind limb contraction induced by electrical stimulation of spinal cord ventral roots L^ and S, were compared before and after inhibition of prostaglandin synthesis (indomethacin, 2-6 mg/kg i.v., n = 5, or sodium meclofenamate, 2-6 mg/kg i.v., n = 5) or after injection of prostaglandin E 2 into the hind limb arterial blood supply. Treatment with indomethacin attenuated the contraction-induced increase in mean arterial pressure and left ventricular dP/dt by 76% and 86%, respectively. Heart rate and average developed triceps surae muscle tension were unchanged. After administering sodium meclofenamate, the reflex response was attenuated to a similar degree. In the indomethacin-treated animals, injection of exogenous prostaglandin E 2 (PGE 2 ) partially restored the pressor and myocardial contractile responses. In 6 animals, treatment with exogenous PGE 2 without prior inhibition of prostaglandin synthesis did not significantly augment the contraction-induced cardiovascular response. Using the radioactive microsphere technique, we measured skeletal muscle blood flow during contraction before and after treatment with indomethacin (n = 6) to determine if an indomethacin-induced alteration in blood flow could account for the attenuated contraction-induced cardiovascular response. Blood flow during static muscle contraction was not significantly altered by indomethacin. We conclude that prostaglandins contribute to the exercise reflex through an action on afferent nerve endings rather than through a regional vascular effect. (Circulation Research 1986;59:645-654)

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“…The first studies of PG production and release by skeletal muscle in response to muscular work were published by Herbaczynska-Cedro and colleagues (41)(42)(43)47) in 1974 and 1976 (Table 1). These studies were focused on identifying muscle-produced vasodilators and blood flow regulation during simulated exercise in dogs and showed that more than one PG was produced by exercising skeletal muscle (suggested as at least PGE 2 and PGF 2␣ ), which could be eliminated by the COX inhibitor indomethacin.…”

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confidence: 99%

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

Trappe

Liu

2013

Journal of Applied Physiology

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Trappe TA, Liu SZ. Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise. J Appl Physiol 115: 909 -919, 2013. First published March 28, 2013 doi:10.1152/japplphysiol.00061.2013.-It has been ϳ40 yr since the discovery that PGs are produced by exercising skeletal muscle and since the discovery that inhibition of PG synthesis is the mechanism of action of what are now known as cyclooxygenase (COX)-inhibiting drugs. Since that time, it has been established that PGs are made during and after aerobic and resistance exercise and have a potent paracrine and autocrine effect on muscle metabolism. Consequently, it has also been determined that orally consumed doses of COX inhibitors can profoundly influence muscle PG synthesis, muscle protein metabolism, and numerous other cellular processes that regulate muscle adaptations to exercise loading. Although data from acute human exercise studies, as well as animal and cell-culture data, would predict that regular consumption of a COX inhibitor during exercise training would dampen the typical muscle adaptations, the chronic data do not support this conjecture. From the studies in young and older individuals, lasting from 1.5 to 4 mo, no interfering effects of COX inhibitors on muscle adaptations to resistance-exercise training have been noted. In fact, in older individuals, a substantial enhancement of muscle mass and strength has been observed. The collective findings of the PG/COX-pathway regulation of skeletal muscle responses and adaptations to exercise are compelling. Considering the discoveries in other areas of COX regulation of health and disease, there is certainly an interesting future of investigation in this re-emerging area, especially as it pertains to older individuals and the condition of sarcopenia, as well as exercise training and performance of individuals of all ages. PGE 2; PGF2␣; acetaminophen; ibuprofen; sarcopenia PGS PRODUCED BY the cyclooxygenase (COX) enzyme are ubiquitous in human physiology and regulate numerous processes (105, 108), including muscle protein metabolism (78,93,106,126,128). As a result, PGs regulate adaptations to muscular exercise, and COX-inhibiting drugs can alter the acute and chronic responses to exercise. Because of the continuum of acute responses and chronic adaptations that exists from lowerintensity, longer-duration exercise to higher-intensity, shorterduration exercise, it is difficult to adopt a "one-mechanismfits-all" approach to PG and COX involvement in skeletal muscle exercise adaptations. This is also true when distinguishing between muscle injury and muscular exercise for health and performance.COX-inhibiting drugs are one of the most commonly consumed classes of drugs in the world. In the United States, the COX inhibitors, acetaminophen, ibuprofen, and aspirin, are the top three consumed drugs of young, middle-aged, and older individuals, with ϳ50 million individuals using each of these drugs during any given week (52, 129). Interestingly, two of these drugs (acetaminophen...

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Muscular work and the release of prostaglandin-like substances

Cited by 50 publications

References 0 publications

Local prostaglandin blockade attenuates muscle mechanoreflex-mediated renal vasoconstriction during muscle stretch in humans

Local prostaglandin blockade attenuates muscle mechanoreflex-mediated renal vasoconstriction during muscle stretch in humans

Prostaglandins contribute to cardiovascular reflexes evoked by static muscular contraction.

Effects of prostaglandins and COX-inhibiting drugs on skeletal muscle adaptations to exercise

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