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Effect of exercise on complement activity
1Department of Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City.
Insights
Aerobic exercise activates complement pathways, increasing anaphylatoxins C3a and C4a. Asthmatic runners show heightened responses, suggesting a role in exercise-induced asthma.
Area of Science:
- Immunology
- Exercise Physiology
Background:
- The complement system is crucial for immune response.
- Exercise can modulate immune functions, but its effect on complement pathways is not fully understood.
Purpose of the Study:
- To investigate the impact of short-term aerobic exercise on complement system activation in experienced runners.
- To compare complement levels between runners and non-exercisers.
- To explore complement activation in asthmatic runners during exercise.
Main Methods:
- Measurement of complement components (C1, C1q, C2, C3, C4, C5), anaphylatoxins (C3a, C4a, C5a), and hemolytic activity (classical and alternative pathways).
- Analysis of 26 experienced adult runners before and after exercise, compared to age-matched controls.
- Preliminary assessment in three asthmatic runners.
Main Results:
- Running increased C3a and C4a levels and decreased C4 hemolytic activity (C4H).
- Runners exhibited lower baseline C3 and C4H compared to controls.
- Asthmatic runners showed significantly higher resting, post-exercise, and exercise-induced C3a levels.
Conclusions:
- Short-term exercise activates complement C3 and C4, generating C3a and C4a anaphylatoxins.
- Regular aerobic exercise may involve classical complement pathway activation and C3 downregulation.
- Exaggerated C3a generation in asthmatic runners suggests a potential role in exercise-induced asthma.
Abstract:
Complement measurements of C1, C1q, C2, C3, C4, C5; the anaphylatoxins, C3a, C4a, and C5a; and total hemolytic activity of the classical and alternative pathways were made in 26 experienced adult runners before and after shortterm aerobic exercise. The baseline results were compared with those of nonexercising age-matched controls. In most subjects tested, running resulted in nanogram increases in C3a and C4a with corresponding decreases in the hemolytic activity of C4 (C4H). Baseline values of C3 and C4H were decreased significantly in runners when compared with nonexercising controls. Preliminary studies measuring the effect of exercise on C3a levels were also done in three asthmatic runners. Mean resting and postexercise levels, and exercise-induced increases in C3a anaphylatoxin in the asthmatic subjects were significantly higher than in the nonasthmatic subjects. The findings indicate that short-term exercise results in the activation of C3 and C4 and subsequent generation of C3a and C4a anaphylatoxins, and suggest that both activation of the classical pathway of complement and a selective downregulation of C3 production may occur in persons regularly engaged in aerobic exercise. The exaggerated generation of C3a by asthmatic subjects during exercise raises the possibility that anaphylatoxins play an etiologic role in exercise-induced asthma.