Acute intensive interval training and Tlymphocyte function

Autor: FRY, ROD W., MORTON, ALAN R., KEAST, DAVID
Zdroj: Medicine & Science in Sports & Exercise; March 1992, Vol. 24 Issue: 3 p339-345, 7p
Abstrakt: FRY, R. W., A. R. MORTON, and D. KEAST. Acute intensive interval training and T-lymphocyte function. Med. Sci. Sports Exerc., Vol. 24, No. 3, pp. 339–345, 1992. Immune suppression has been suggested to occur as a result of acute exercise although results of previous studies are variable, possibly due to the failure of some researchers to control exercise intensity and duration. Most of the studies so far have investigated immediate effects after bouts of exercise mainly in subjects undertaking lower body exercise (running or cycling), and the time course of recovery has rarely been determined. We chose two groups of athletes for our studies. One group represented subjects of a range of fitness levels from recreational runners to high-performance runners. The second group represented kayakists with a similar range of fitness levels. Following interval training designed to stress either the lower or upper body anaerobically, we have now shown that upper body exercise (kayaking) induces similar in vitroresponses to those described for lower body exercise. There were no differences between the responses of low-fitness versus high-fitness subjects. In addition we have studied the in vitroresponses of leukocytes following acute anaerobic exercise over a 24-h recovery period. The results showed that the reduced lymphocyte proliferative response, in vitro, to the T-cell mitogen CONA experienced immediately after exercise returned to normal levels within 2 h of recovery time. This suggests that the reduction in lymphocyte proliferative response is a short transient one. The addition of interleukin-2 (IL-2) or indomethacin to the mitogen-stimulated cultures of preexercise and postexercise cells demonstrated that the postexercise suppression in 3H-DNA synthesis of the leukocytes could not be accounted for by either an inability of the T-cells to produce IL-2 or the inhibitory action of prostaglandin production.
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