The Health & Performance Signals of Carbon Monoxide (CO): What the Research Actually Shows
Read first: we do not recommend smoking or inhaling carbon monoxide at any time for any reason. This article summarizes research and mechanisms only. It is not medical advice.
Update (July 2024): Media reports note some athletes experimenting with CO inhalation protocols; see this article. You should not do this.
Why talk about CO at all?
CO is best known as a deadly poison. Yet the human body also produces small amounts of CO endogenously via heme oxygenase activity, and these tiny, tightly regulated amounts act as cell signals (a “gasotransmitter”), similar in concept to nitric oxide. See background overviews here: CO research landscape, endogenous CO, and sources in the body.
First principles: CO toxicity is real
CO causes asphyxiation by binding hemoglobin with far greater affinity than oxygen, leading to hypoxia and potential death. Each year, tens of thousands are hospitalized in the U.S. and ~400 die from CO poisoning. See CDC and clinical overviews such as Mayo Clinic.
Then what’s the “good side” researchers study?
At low, controlled, clinically monitored exposures, CO can act as a signaling molecule influencing inflammation, oxidative stress, and cell-death pathways. See research and reviews: anti-inflammatory and cytoprotective signals (Nature Med, Immunity, J Exp Med), and disease-model work in sepsis, sickle cell disease, transplant, lung fibrosis, colitis, cancer, and heart disease (AJP Lung, Am J Hematol, AJP Renal, Am J Pathol, Dig Dis, Cancer Res, JCI). Mechanistically related interest rose alongside nitric oxide’s 1998 Nobel recognition; see the Nobel summary and NO reference (and note the NO context alongside PURECLEAN BEET JUICE).
Is “one cigarette a day” a viable strategy?
No. Historical anecdotes (e.g., cyclists smoking before climbs) are not a justification. Modern cigarettes contain addictive nicotine and a complex mixture of toxic compounds. Even if a single cigarette can transiently raise carboxyhemoglobin modestly (study shows ~4.5 ppm for ~45 minutes), that does not make it safe or advisable. See health-risk summaries: CDC. Environmental sources can also elevate CO (sometimes even in non-smokers: study), and urban particle pollution may carry broader risks than a simplistic “single-cigarette” thought experiment (related post). For context on permissible exposure guidelines, see reference charts like this overview. Again: do not smoke and do not inhale CO.
What about “performance hacks” using CO?
Some research groups explore whether controlled, clinical CO exposure can trigger adaptations resembling altitude (reduced O₂-carrying capacity → compensatory hematological adaptations). For example: Schmidt et al., 2020 reported increased hemoglobin mass and VO₂max after repeated low-dose CO exposure; popular summaries include this article. Ethical, medical, and anti-doping issues remain; ultimately, WADA governs prohibited methods. This is not a recommendation to attempt CO protocols.
Clinical translation: where is the field?
Delivery is the challenge. Inhaled CO requires hospital controls; alternative strategies include CO-releasing molecules (CORMs) or organic pro-drug approaches being studied to target tissues and limit toxicity (see overviews and primary papers in the C&EN feature, including work by Wang and colleagues: J Med Chem, Nat Chem, Org Lett). Company pipelines have started and stalled over the years, and some trials were halted for business reasons rather than efficacy signals. Summary: intriguing biology; translation requires rigorous, regulated clinical paths.
Key context on nitric oxide vs. carbon monoxide
CO is not nitric oxide (NO). NO is widely leveraged in cardiopulmonary care and sports-nutrition pathways via dietary nitrate → nitrite → NO, e.g., beetroot. If you’re pursuing legal, safer performance support for blood flow and oxygen delivery, focus on nitrate-rich whole-food strategies; see PURECLEAN BEET JUICE for a practical route within that paradigm.
Re-organized source excerpts (kept for readers who want depth)
Article #1: Carbon monoxide is a killer—yet a signaling molecule
Background and toxicity statistics with mechanistic notes and cytoprotective research links appear above. Original references preserved: CDC, Mayo Clinic, Nature Med, Immunity, J Exp Med, and disease-model links above. Original feature: C&EN.
Article #2: CO and endurance adaptations
Summary of the Bayreuth group’s work on chronic, low-dose CO exposure—hematological and VO₂max changes—plus collaboration notes and citation: MSSE 2020. Media summary preserved: innovations-report.
Article #3: CO—bad and good sides: neuronal injury vs. anti-inflammatory actions
Review on CO’s dual roles, delayed neuropathology after poisoning, debates on hyperbaric oxygen in CO poisoning, and CO-releasing molecules in inflammation models. PubMed record preserved: PMID: 16955388.
Bottom line
CO is unequivocally dangerous at high levels. At strictly controlled, low exposures in clinical settings, it shows signaling effects with potential therapeutic uses. That is a research and regulatory domain—not a DIY performance strategy. For legal, practical oxygen-delivery support, prioritize nitric-oxide dietary pathways and respiratory training approaches, not CO exposure.
Further reading: Nobel Prize perspective on NO signaling (link), hydrogen sulfide research (overview), EPOC primer (ACE), RBC production context (overview), nicotine note (PubMed), and historical anecdotes (We Love Cycling).