DOMS og rygning

[pingtoft]

Efter at jeg er faldet i og er vbegyndt at ryge igen, synes jeg at DOMS'en kommer oftere og værre, end da jeg ikke røg. jeg har ikke ændret på træningen.

er der nogen, der har erfaringer, viden og/eller teorier?

~pingtoft

[incognito]

rygning gør man ting man kan forestille sig vil påvirke restitutionen, men jeg kender ikke nogen studier, hvor man har forsøgt at vise det.....

[clayman]

Jeg mener selv at have oplevet fænomenet DOMS i lungerne efter en heftig bytur med +20 Kings

[Zoater]

Rygning nedsætter blodcirkulationen..... hvilket da også må have betydning for rest. , da musklerne ikke før tilførte den samme mængde næringsstoffer som hvis man ikke ryger.

[incognito]

restitution består af meget, meget mere end bare tilgængeligheden af næringsstoffer.... Nikotin er så vidt jeg husker også en smule antiinflammatorisk, hvorfor man kunne argumentere for at det hæmmer DOMS. Men der er rigtigt mange ting idet. Det ville være forkert at drage en enkelt ting ud og så lave konklusioner på baggrund af den.

[laush]

Det her studie fortæller lidt om at nikotin faktisk er anti-inflammatorisk som incognito skriver:

TNF alpha er en af de primære cytokiner i inflammationskaskaden og nikotin ser ud til at hæmme denne.

ulcerative colitis = inflammatorisk tarmsygdom.

Immunopharmacology 1996 Oct;35(1):47-51

Nicotine inhibits the in vitro production of interleukin 2 and tumour necrosis factor-alpha by human mononuclear cells.

Madretsma GS, Donze GJ, van Dijk AP, Tak CJ, Wilson JH, Zijlstra FJ.

Dept. of Pharmacology, Erasmus University, Rotterdam, The Netherlands.

Smoking protects against ulcerative colitis (UC), and treatment with nicotine patches has a beneficial symptomatic effect in patients with UC. To find an explanation for this response to nicotine in UC, we assessed the effects of nicotine on cytokine production by mononuclear cells (MNC). MNC were isolated from peripheral blood from healthy volunteers. Non-adherent MNC were preincubated with varying concentrations of nicotine or prednisolone for 24 h followed by addition of phytohemagglutinin (10 micrograms/ml). The concentrations of interleukin 2 (IL-2) and tumour necrosis factor-alpha (TNF alpha) in the supernatants were determined by ELISA. Nicotine as well as prednisolone caused a significant inhibition of IL-2 and TNF alpha production. The maximum inhibition caused by nicotine was about 50% of that caused by prednisolone and was reached at concentrations equivalent to nicotine levels measured in plasma of smokers. These results indicate that nicotine exerts its immunoregulatory role through modulation of the cytokine production by non-adherent mononuclear cells.