Key result
HIIT fails to change inflammatory markers in stable CAD patients despite acute exercise spikes.
Why the study?
Persistent low-grade inflammation contributes to coronary artery disease, but how acute vigorous exercise and structured training affect systemic inflammatory biomarkers in stable CAD remains unclear.
Does 12 weeks of high-intensity interval training reduce systemic inflammatory biomarkers in optimally treated patients with stable coronary artery disease?
Does 12 weeks of high-intensity interval training reduce systemic inflammatory biomarkers in optimally treated patients with stable coronary artery disease?
In optimally treated patients with stable coronary artery disease, regular high-intensity interval training does not produce a sustained anti-inflammatory effect, though acute vigorous exercise triggers short-term inflammatory activation.
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HIIT yields no sustained anti-inflammatory benefit in stable CAD; confirms acute exercise triggers transient marker rises without chronic modulation.
Background Persistent low‐grade inflammation contributes to coronary artery disease (CAD), but how acute vigorous exercise and structured training affect systemic inflammatory biomarkers in stable CAD remains unclear. We evaluated the acute response to a single vigorous bout and the effects of a 12‐week high‐intensity interval training program on systemic inflammation in patients with stable CAD. Methods In 168 patients with stable CAD, blood samples were collected before, immediately after, and 2 hours after a maximal incremental cycling test. Participants were then randomized to 12 weeks of high‐intensity interval training or standard care; 142 completed follow‐ups. High‐sensitivity CRP (C‐reactive protein), leukocytes, interleukin‐2, interleukin‐6, interleukin‐10, interferon‐γ, and tumor necrosis factor‐α were measured at baseline, week 6, and week 12. Results Acute exercise elevated CRP by 7.7% [95% CI, 5.5–10.0] and leukocytes by 50.5% [95% CI, 48.2–52.8]; CRP returned to baseline by 2 hours, whereas leukocytes remained elevated. Interferon‐γ increased by 13.1% [95% CI, 9.2–17.3] following exercise but fell below baseline after 2 hours. Tumor necrosis factor‐α (12.9% [95% CI, 8.4–17.4]), interleukin‐2 (22.8% [95% CI, 17.5–28.5]), and interleukin‐6 (42.4% [95% CI, 36.5–48.5]) also increased following acute exercise and stayed elevated after 2 hours, while interleukin‐10 decreased by 9.2% [95% CI, −14.1 to –4.0] and returned to baseline after 2 hours. Over 12 weeks, high‐intensity interval training did not significantly alter these inflammatory markers compared with standard care. Conclusions Acute strenuous exercise induces transient increases in inflammatory markers in stable CAD, which begin to resolve within 2 hours. In this optimally treated cohort, regular high‐intensity interval training did not produce a sustained anti‐inflammatory effect. Registration URL: https://clinicaltrials.gov ; Unique identifier: NCT04268992.
Kristiansen et al. (2026) studied this question. Acute exercise elevated CRP by 7.7% and leukocytes by 50.5% in stable CAD patients, but 12 weeks of high-intensity interval training did not significantly change inflammatory markers.
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