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Nine untrained men (22-29 yr) performed 45 min of downhill running (16% incline, 70% of maximum heart rate). Needle biopsies of the vastus lateralis were performed before, 45 min after, and 5 days after exercise. Immunohistochemical staining of muscle cross sections revealed a 135% increase in muscle interleukin-1 beta (IL-1 beta) immediately after and a 250% increase (P < 0.03) 5 days after exercise. Using a rating scale (0-3) for the presence of neutrophils, light microscopic examination showed a significant accumulation of neutrophils in muscle biopsies taken 45 min after and 5 days after exercise [before: 0.5 +/- 0.2, 45 min after: 1.5 +/- 0.3 (P < 0.01), and 5 days after: 1.2 +/- 0.2 (P < 0.04)]. In addition, electron microscopic analysis showed an increase in the percentage of damaged Z-bands relative to total Z-bands [before: 4.8 +/- 3.5%, 45 min after: 32.5 +/- 8.6% (P < 0.05), and 5 days after: 14.1 +/- 3.2%]. Neutrophil accumulation was positively correlated to intracellular Z-band damage (rho = 0.66, P < 0.001). Immunohistochemical staining for IL-1 beta was related to neutrophil accumulation in muscle (rho = 0.38, P < 0.06) and to plasma creatine kinase levels (rho = 0.416, P < 0.04). These data indicate that after eccentric exercise ultrastructural damage to skeletal muscle is associated with neutrophil infiltration and muscle IL-1 beta accumulation.

A decline in insulin sensitivity is associated with aging, inactivity, and obesity. The effects of exercise training on glucose homeostasis independent of weight loss in older glucose-intolerant individuals are not well established. We examined the effects of exercise training on oral glucose tolerance, insulin action, and concentration of the GLUT-4 glucose transporters in skeletal muscle. Exercise training at 50 and 75% of heart rate reserve was performed for 12 wk in 18 individuals (age = 64 +/- 2, body fat = 37.0 +/- 1.5%). Peripheral insulin action was determined 96 h after the last exercise bout using a two-step hyperinsulinemic-euglycemic glucose clamp (insulin = 192 and 708 pmol/l). Percent body fat and fat-free mass (FFM) were unchanged with training. Diet composition, assessed by diet record, did not change over the 12 wk. Improved oral glucose tolerance was observed, as exhibited by lower plasma glucose concentrations after training (P < 0.05), whereas plasma insulin response remained unchanged. The rate of glucose disposal was unchanged during the low insulin concentration but increased 11.0% at the high insulin concentration (P < 0.05) after training (54.4 +/- 4.4 vs. 60.4 +/- 5.5 mumol.kg FFM-1.min-1). Skeletal muscle glycogen and GLUT-4 concentration increased 24 and 60%, respectively, with training. There was no direct relationship between the change in GLUT-4 protein and the change in glucose disposal rate. These findings demonstrate that chronic exercise training without changes in body composition improves peripheral insulin action in subjects with impaired glucose tolerance.(ABSTRACT TRUNCATED AT 250 WORDS)

Interleukin 1 beta (IL-1 beta) is a protein released from blood monocytes and related cells in response to infectious or inflammatory stimuli. Although IL-1 beta is elevated in the circulation for only a few hours after an acute inflammatory challenge or exercise, it has been proposed to mediate anabolic and catabolic processes that can last for several days. In this report, eccentric exercise was used as a noninfectious inflammatory stimulus. IL-1 beta was found in muscle tissue up to 5 days after exercise using specific immunohistochemical tissue staining. Increased IL-1 beta immunoreactivity was observed in muscle tissue from four human subjects who performed the exercise, but not in tissue obtained at the same time intervals from two subjects who did not exercise. Little immunohistochemical evidence of interleukin-1 alpha or tumor necrosis factor alpha was observed before or after exercise. These results implicate IL-1 beta in the metabolic adaptations of muscle tissue, which occur in response to noninfectious stresses.

Based on prior observations that both beta-endorphin and exercise stimulate natural killer (NK) cell activity, we have examined the hypothesis that the release of endogenous opioids during the stress of acute exercise may mediate this NK cell augmentation. Eight healthy young women underwent a maximal bicycle ergometer exercise test with prior in vivo administration of a placebo and an opioid antagonist, naloxone (100 micrograms/kg), in a randomized, blind protocol. Exercise after the placebo injection was accompanied by a dramatic rise in NK activity, as well as an increase in the percentage of lymphocytes bearing the NK cell surface markers Leu 11a and Leu 19. Significant stimulation of NK activity was observed with beta-endorphin in vitro before exercise, but after exercise, beta-endorphin had a nonsignificant inhibitory effect. When these experiments were carried out in the presence of naloxone in vivo, the rise in NK activity after exercise was no longer significant. Naloxone did not significantly alter the rise in Leu 11a+ or Leu 19+ cell after exercise, as compared with the placebo. Finally, when naloxone was given to the subjects beforehand, exercise no longer completely blocked the in vitro beta-endorphin stimulation of NK cells. In conclusion, our observations that the exercise-induced augmentation of NK activity and the lack of effect of beta-endorphin in vitro on NK activity after exercise are both significantly attenuated by prior administration of naloxone suggest that the opioid system may play a major role in the modulation of NK cells during physiologic stress.

Alterations in immune function have been commonly reported in elderly persons. We have examined the effect of age on the responsiveness of natural killer (NK) cells to in vitro stimulation with recombinant interleukin-2 (rIL-2) and in vivo stimulation with exercise in 17 healthy subjects (8 young and 9 old). The old subjects were found to have NK cell numbers and function that were not significantly different from the young subjects at baseline. They also responded as well as the young subjects to rIL-2 stimulation of NK cells in vitro. In response to maximal bicycle ergometry exercise, there was a marked rise in NK activity in the old (7.52 +/- 1.71 LU/10(6) pre-exercise vs 15.20 +/- 3.27 LU/10(6) post-exercise, p less than .03) and the young (6.29 +/- .48 LU 10(6) vs 14.56 +/- 1.86 LU 10(6), p less than .005) subjects. Lymphocytes bearing the NK marker Leu 11a also rose significantly post-exercise in both old and young subjects. We conclude that healthy elderly subjects increase their NK activity in response to the acute stressor, exercise, at least as effectively as do young subjects.