Exercise-induced release of pancreatic polypeptide and its inhibition by propranolol: evidence for adrenergic stimulation

To examine the effect of exercise and adrenergic blockade on lymphocyte cytokine production, six men ingested either a placebo (control) or an α- (prazosin hydrochloride) and β-adrenoceptor antagonist (timolol malate) capsule (blockade, or BLK) 2 h before performing 19 ± 1 min of supine bicycle exercise at 78 ± 3% peak pulmonary uptake. Blood was collected before and after exercise, stimulated with phorbol 12-myristate 13-acetate and ionomycin, and surface stained for T (CD3+) and natural killer [NK (CD3−CD56+)] lymphocyte surface antigens. Cells were permeabilized, stained for the intracellular cytokines interleukin (IL)-2 and interferon (IFN)-γ, and analyzed using flow cytometry. BLK had no effect on the resting concentration of stimulated cytokine-positive T and NK lymphocytes or the amount of cytokine they were producing. Exercise resulted in an increase ( P< 0.05) in the concentration of stimulated T and NK lymphocytes producing cytokines in the circulation, but these cells produced less ( P < 0.05) cytokine post- compared with preexercise. BLK attenuated ( P < 0.05) the elevation in the concentration of lymphocytes producing cytokines during exercise; however, BLK did not affect the amount of IL-2 and IFN-γ produced. These results suggest that adrenergic stimulation contributes to the exercise-induced increase in the concentration of lymphocytes in the circulation; however, it does not appear to be responsible for the exercise-induced suppression in cytokine production.

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β 2 ‐Adrenergic stimulation enhances Ca 2+ release and contractile properties of skeletal muscles, and counteracts exercise‐induced reductions in Na + –K + ‐ATPase V max in trained men

The Journal of Physiology ◽

10.1113/jphysiol.2014.277095 ◽

2014 ◽

Vol 592 (24) ◽

pp. 5445-5459 ◽

Cited By ~ 38

Author(s):

M. Hostrup ◽

A. Kalsen ◽

N. Ørtenblad ◽

C. Juel ◽

K. Mørch ◽

...

Keyword(s):

Skeletal Muscles ◽

Contractile Properties ◽

Adrenergic Stimulation ◽

Exercise Induced

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Exercise-induced alterations of hepatic mitochondrial function

Biochemical Journal ◽

10.1042/bj2080695 ◽

1982 ◽

Vol 208 (3) ◽

pp. 695-701 ◽

Cited By ~ 13

Author(s):

C A Tate ◽

P E Wolkowicz ◽

J McMillin-Wood

Keyword(s):

Mitochondrial Function ◽

Exercise Group ◽

Male Rats ◽

Control Group ◽

Adrenergic Stimulation ◽

Assay Medium ◽

Single Bout ◽

The Difference ◽

Exercise Induced

In order to examine the effect of a single bout of exercise on hepatic mitochondrial function, starved untrained male rats swam at 34-35 degrees C with a tail weight (5% of body wt.) for 100 min. The rates of ADP-stimulated and uncoupled respiration were higher in the mitochondria isolated from the exercised rats regardless of the substrate utilized. Succinate-linked Ca2+ uptake was 48% greater in the exercised group; however, Ca2+ efflux was markedly depressed. The inhibition of Ca2+ uptake by Mg2+ was higher in the control group, so that the difference in Ca2+ uptake between the two groups was greater in the presence of Mg2+ than in its absence. The response of phosphorylating respiration and Ca2+ fluxes to exogenous phosphate and the pH of the assay medium differed in the exercise group. These observations with the exercised group were not related to non-specific stress. The exercise-induced mitochondrial-functional alterations are reminiscent of those obtained from mitochondria isolated from glucagon- or catecholamine-treated sedentary rats. Thus, adrenergic stimulation as well as other factors may be operating during exercise, leading to an alteration of mitochondrial function in vitro.

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The RyR2-R2474S Mutation Sensitizes Cardiomyocytes and Hearts to Catecholaminergic Stress-Induced Oxidation of the Mitochondrial Glutathione Pool

Frontiers in Physiology ◽

10.3389/fphys.2021.777770 ◽

2021 ◽

Vol 12 ◽

Author(s):

Jörg W. Wegener ◽

Ahmed Wagdi ◽

Eva Wagner ◽

Dörthe M. Katschinski ◽

Gerd Hasenfuss ◽

...

Keyword(s):

Contractile Activity ◽

Atp Synthesis ◽

Missense Mutations ◽

Mitochondrial Matrix ◽

Adrenergic Stimulation ◽

Fluorescent Biosensor ◽

Ryr2 Channel ◽

Mitochondrial Oxidation ◽

Exercise Induced ◽

Mitochondrial Glutathione

Missense mutations in the cardiac ryanodine receptor type 2 (RyR2) characteristically cause catecholaminergic arrhythmias. Reminiscent of the phenotype in patients, RyR2-R2474S knockin mice develop exercise-induced ventricular tachyarrhythmias. In cardiomyocytes, increased mitochondrial matrix Ca2+ uptake was recently linked to non-linearly enhanced ATP synthesis with important implications for cardiac redox metabolism. We hypothesize that catecholaminergic stimulation and contractile activity amplify mitochondrial oxidation pathologically in RyR2-R2474S cardiomyocytes. To investigate this question, we generated double transgenic RyR2-R2474S mice expressing a mitochondria-restricted fluorescent biosensor to monitor the glutathione redox potential (EGSH). Electrical field pacing-evoked RyR2-WT and RyR2-R2474S cardiomyocyte contractions resulted in a small but significant baseline EGSH increase. Importantly, β-adrenergic stimulation resulted in excessive EGSH oxidization of the mitochondrial matrix in RyR2-R2474S cardiomyocytes compared to baseline and RyR2-WT control. Physiologically β-adrenergic stimulation significantly increased mitochondrial EGSH further in intact beating RyR2-R2474S but not in RyR2-WT control Langendorff perfused hearts. Finally, this catecholaminergic EGSH increase was significantly attenuated following treatment with the RyR2 channel blocker dantrolene. Together, catecholaminergic stimulation and increased diastolic Ca2+ leak induce a strong, but dantrolene-inhibited mitochondrial EGSH oxidization in RyR2-R2474S cardiomyocytes.

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