Immune and inflammation responses to a 3-day period of intensified running versus cycling
Participants
n=35: 13 trained long-distance runners (age 34.4 ± 2.4 yr) + 22 trained cyclists (age 36.6 ± 1.7 yr; P=0.452 for age)
Protocol
Key Results
| Parameter | Runners vs Cyclists (post 3-day block) |
|---|---|
| Creatine kinase (CK) | 133% higher in runners |
| Myoglobin (MYO) | 404% higher in runners |
| C-reactive protein (CRP) | 87% higher in runners |
| Interleukin-6 (IL-6) | 256% higher in runners |
| IL-8 | 61% higher in runners |
| IL-10 | 32% higher in runners |
| MCP (monocyte chemoattractant protein) | 29% higher in runners |
| DOMS (delayed onset muscle soreness) | 87% higher in runners |
| Granulocyte/monocyte phagocytosis | Significant downturns by 14 h and 38 h recovery, pattern not different between groups |
| Granulocyte/monocyte oxidative burst | Significant downturns by 14 h and 38 h recovery, pattern not different between groups |
| 12-week URTI severity | No difference (runners 18.3 ± 5.6 vs cyclists 16.6 ± 4.0, P=0.803) |
| 12-week URTI symptom score | No difference (runners 33.4 ± 12.6 vs cyclists 24.7 ± 5.8, P=0.477) |
Mechanism
Inference, not tested in this study: running's ground-impact (eccentric) loading is the usual explanation for the far greater muscle damage and the larger systemic inflammatory response (CK, MYO, IL-6, CRP), while cycling is predominantly concentric. What the data do show: the innate-immune downturn (phagocytosis, oxidative burst) and the 12-week URTI symptomatology were the same in both groups, so the immune cost of the 3-day block did not track the muscle damage.
Practical Application
Limitations
Unequal group sizes (n=13 vs n=22) and allocation by sport, not randomization; trained but not elite athletes; single intensity (70% VO2max) — responses may differ at threshold or supra-threshold; no dietary standardization reported in the abstract; running group inherently self-selected for eccentric tolerance.