Immune Suppression and Diving
June 8, 2025 · 6 min read
Diving Stresses the Immune System — Even Without DCS
After long, deep, or repetitive dives, some divers report fatigue, mild illness, or an unexplained "off" feeling even when everything went to plan. These symptoms reflect temporary immune disruption and systemic inflammation triggered by mechanisms active on every dive, not just those that produce clinical decompression illness.
The Inflammatory Cascade
Every dive — including safe, shallow, within-limits recreational dives — produces small venous gas emboli during ascent. These are the bubbles detected by precordial Doppler ultrasound. Most are too small to cause clinical DCS but large enough to interact with the vascular endothelium. When bubble microemboli contact the endothelial lining of blood vessels, they activate endothelial cells, triggering the complement cascade and coagulation pathways — the same early-response systems that activate during infection or tissue injury.
Endothelial activation drives the release of inflammatory mediators: IL-6 (Interleukin-6), a pro-inflammatory cytokine that acts on the hypothalamus to induce fatigue, malaise, and the acute-phase response; TNF-alpha (Tumour Necrosis Factor alpha), which amplifies the inflammatory signal, increases vascular permeability, and activates neutrophils; and complement proteins whose activated fragments (C3a, C5a) drive neutrophil recruitment and can increase bubble surface adhesion. These markers have been measured at elevated levels in divers post-dive. They are the same cytokines elevated during illness and heavy exercise, which is why the subjective feeling of post-dive immune stress resembles a mild systemic infection.
Bubble microemboli also directly activate neutrophils. Activated neutrophils adhere to endothelial surfaces and release reactive oxygen species and proteases — their antimicrobial toolkit, which in the context of bubbles rather than infection generates oxidative tissue damage without clearing any pathogen.
Scuba diving additionally involves breathing elevated partial pressures of oxygen, particularly on nitrox or during oxygen-rich decompression stops. Hyperoxia drives production of reactive oxygen and nitrogen species in the lungs and bloodstream. After prolonged or repetitive exposure, this load can exceed the capacity of endogenous antioxidant systems — superoxide dismutase, catalase, glutathione peroxidase — contributing to the overall oxidative burden.
Temporary Immune Suppression
While pro-inflammatory markers rise, certain limbs of the immune system are simultaneously suppressed. Studies of divers post-dive have shown reduced lymphocyte cytotoxic activity, disrupted CD4/CD8 T-cell ratios, and elevated neutrophil-to-lymphocyte ratio — a recognised marker of systemic stress and inflammation. The pattern is consistent with the immunological response to acute physiological stress: innate immunity (inflammation, neutrophil activation) is upregulated while adaptive immunity (lymphocyte-mediated targeted response) is temporarily downregulated. This is why divers may be transiently more susceptible to mild infections in the hours following demanding dives.
A Related Stress Response: The Popa 2022 Hypoxia Study
Popa et al. (2022, Diving and Hyperbaric Medicine) studied hypoxia responses in CCR and open-circuit divers during controlled normobaric hypoxia induction. The study found that gradual-onset hypoxia produced a recognisable cluster including cognitive impairment, psychomotor incoordination, anxiety, dyspnoea, and confusion. Only 25% of subjects performed unprompted bailout in the unblinded condition; 15% were unable to bail out even when prompted.
The relevance to immune stress: acute physiological stress from hypoxia, cold, or heavy workload compounds the inflammatory burden from bubble microemboli. Divers who have pushed their physiological limits — high workload, thermal stress, significant gas switching — carry a larger cumulative stress load than a simple dive profile analysis suggests.
Diving While Acutely Ill
An active infection already drives systemic inflammation — elevated IL-6, TNF-alpha, C-reactive protein, complement activation, and endothelial dysfunction. Diving in this state adds bubble microemboli to an already-primed inflammatory environment. The concern is that the combined state may lower the threshold for symptomatic DCS from a given bubble load. Vascular endothelium already compromised by infection is more vulnerable to the mechanical and chemical effects of bubble contact. Dehydration from fever reduces blood volume and impairs gas transport.
Do not dive during any active febrile illness. Do not dive with respiratory infections — congestion compromises middle-ear and sinus equalisation, and impaired mucociliary clearance increases gas-trapping risk in the airways. Wait for full symptomatic recovery, including resolution of fatigue, before returning to diving. Two inflammatory systems operating simultaneously do not simply add; they interact.
Adaptation vs Overload
Divers who rest adequately between dives and between dive days often show measurable physiological adaptation over a diving career: lower inflammatory responses to comparable dive exposures, more efficient antioxidant defence, and faster recovery of immune parameters. This adaptation requires time. Short surface intervals, sleep deprivation, high cumulative thermal stress, and nutritional deficits impair the recovery cycle. Without adequate recovery, the immune disruption from each dive compounds into the next — gradually accumulating a physiological debt that expresses as persistent fatigue, lower infection resistance, and slower healing.
Supporting Recovery
Rest days after multi-day technical programs are physiological necessities, not optional comfort. Dehydration concentrates inflammatory mediators and reduces lymphatic clearance, so hydration is not a soft recommendation. Antioxidant-rich nutrition — fruits, vegetables, nuts, polyphenols — supports ROS buffering capacity; vitamins C, E, and D and zinc appear frequently in the dive medicine literature. Immune rebalancing, particularly lymphocyte recovery, is primarily sleep-dependent. Alcohol impairs sleep quality, worsens dehydration, and directly suppresses immune cell function — the post-dive celebration culture is at odds with recovery physiology.
Related Reading
References
Popa D, Kutz C, Carlile M, Brett K, Moya EA, Powell F, Witucki P, Sadler R, Sadler C. Hypoxia signatures in closed-circuit rebreather divers. Diving and Hyperbaric Medicine. 2022;52(4):237–244. doi:10.28920/dhm52.4.237-244
Obad A, Palada I, Valic Z, Bhagat A, Dujic Z, Bhatt D. The effects of acute oral antioxidants on diving-induced alterations in human cardiovascular function. Journal of Physiology. 2007;578(3):859–870.
Madden D, Lozo M, Dujic Z, Bhagat A. Exercise after SCUBA diving increases the incidence of arterial gas embolism. Journal of Applied Physiology. 2013;115(3):716–722.
Bosco G, Yang ZJ, Nandi J, Wang J, Chen C, Camporesi EM. Effects of hyperbaric oxygen on glucose, lactate, glycerol and anti-oxidant enzymes in the skeletal muscle of rats during ischaemia and reperfusion. Clinical and Experimental Pharmacology and Physiology. 2007;34(1-2):70–76.
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