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- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Duration and mechanisms of the increased natural cytotoxicity seen after chronic voluntary exercise in rats.
- 1997
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 160:4, s. 333-9
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Tidskriftsartikel (refereegranskat)abstract
- We have recently shown that in vivo natural cytotoxicity is enhanced after chronic exercise in spontaneously hypertensive rats (SHRs). In the present report, we have studied the duration of this augmentation and some possible mechanisms involved. Exercise consisted of voluntary running for 4-5 weeks, with the running distance ranging from 2.7-15.6 km day(-1) during the last week of running. In vivo cytotoxicity was measured as clearance of injected 51Cr-labelled YAC-1 lymphoma cells from the lungs. The in vivo natural cytotoxicity was increased in running SHRs, and also in SHRs that had their running wheel locked for 24 and 48 h prior to the experiment, and was still present after 96 h. The enhancement of in vivo cytotoxicity after 5 weeks of exercise was abolished after an acute injection of the beta-adrenergic receptor antagonist timolol (0.5 mg kg(-1) i.v.), indicating that catecholamines are involved in this augmentation. Interestingly, 24 h after the last exercise bout, the increased natural cytotoxicity could be blocked by timolol. The opioid receptor antagonist naloxone given subcutaneously for 7 days by osmotic pumps (6 mg kg(-1) h(-1)) could not reverse the increased in vivo cytotoxicity seen in the running SHRs, suggesting that opioid receptor mechanisms are not involved, or at least not the naloxone-sensitive mu-receptor. Natural immunity was not influenced by the histamine H2 receptor antagonist ranitidine, either in controls or in runners, indicating that the natural killer cell-regulatory effect of histamine is not present in SHRs and does not seem to be involved in the exercise-induced changes in natural immune function. We conclude that the augmentation of in vivo natural cytotoxicity after voluntary chronic exercise in rats is long-lasting and that the augmentation is partly mediated by beta-adrenergic receptors.
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- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Physical exercise, endogenous opioids and immune function.
- 1997
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Ingår i: Acta physiologica Scandinavica. Supplementum. - 0302-2994. ; 640, s. 47-50
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Forskningsöversikt (refereegranskat)abstract
- The experimental data available today strongly indicate that various types of physiological stressors, including physical exercise and emotional stress, can influence immune function. Natural immunity represents a first line of defence in viral infections and cytotoxicity to a variety of tumour cells. Natural immunity is strongly influenced by chronic exercise and this regulation includes interaction between the nervous, endocrine and immune systems. Central mechanisms including the endogenous opioids are of great interest. Chronic activation of endogenous opioid systems augments natural cytotoxicity and the possible involvement the opioids in the exercise-induced enhancement of natural immunity is discussed. Also, catecholamines seem to play an important role in the regulation of immune function, both after chronic exercise and emotional stress. The physiological significance of the reported changes in natural cytotoxicity after exercise-training is as yet unclear.
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- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Acute mental stress but not enforced muscle activity transiently increases natural cytotoxicity in spontaneously hypertensive rats.
- 1996
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 157:4, s. 443-9
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Tidskriftsartikel (refereegranskat)abstract
- The influence of acute mental stress and the effect of electrically induced skeletal muscle contractions on natural cytotoxicity in vivo was investigated in spontaneously hypertensive rats Natural cytotoxicity in vivo was measured as the clearance of injected 51Cr-labelled YAC-1 lymphoma cells from the lungs, which are specifically lysed by natural killer cells. The mental stress consisted of an air jet directed towards the animals in their cage for 25 min. During the mental stress there was a significant increase in natural cytotoxicity. Thus, retained radioactivity in the lungs was decreased to 74 +/- 6% of the control levels which was set to 100% (P < 0.01). This augmentation of YAC-1-cell clearance could be blocked with the beta-adrenergic receptor antagonist Timolol. Two hours after termination of the air stress, in vivo cytotoxicity had returned to control levels. In contrast, acute physical stress, consisting of electrically induced muscle contractions for 60 min, had no significant effects on in vivo cytotoxicity, either during the stimulation or 1, 2 or 24 h after the stimulation. Further, significantly increased plasma levels of adrenaline were seen after the air jet stress, but not after muscle stimulation. There were no significant changes in plasma noradrenaline levels either after air stress or muscle stimulation. These results indicate that changes in in vivo cytotoxicity after mild mental stress are dependent on increased plasma catecholamine levels while acute physical stress without changes in catecholamine levels, does not influence in vivo cytotoxicity.
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- Jonsdottir, Ingibjörg H, 1966, et al.
(författare)
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Increase in nitric oxide formation after chronic voluntary exercise in spontaneously hypertensive rats.
- 1998
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Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 162:2, s. 149-53
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Tidskriftsartikel (refereegranskat)abstract
- The effect of chronic voluntary exercise on the plasma level of nitrate, a major stable metabolite of nitric oxide (NO) was studied in spontaneously hypertensive rats (SHR). Exercise consisted of spontaneous running in wheels for 3-35 days. Blood samples were collected after 3, 7, 14, 21 and 35 days of exercise and all samples were drawn after the running wheel had been locked during the preceding 12 h. The plasma nitrate level was significantly (P < 0.05) elevated in SHR after 35 days of exercise. Surprisingly after 7 days of exercise a significant (P < 0.001) decrease in the nitrate level in plasma was noted. Further research is needed to elucidate this biphasic change in nitrate seen in this study. The elevated level of plasma nitrate seen after 35 days of voluntary exercise was still present up to 36 h after termination of exercise. We conclude that exercise training in SHR elicits an enhanced formation of NO.
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