Fanning the coals
Clearing the stem.
18+Reference resource. Nicotine is addictive. Tobacco use harms your health.
Clearing the stem.
A single hookah session measurably raises blood carbon monoxide and lowers oxygen consumption, an effect on exercise tolerance confirmed by instruments. Less is known about endurance with regular smoking: the studies are samples of 10–62 people, mostly men from the Middle East and North Africa, and one key training study has been formally disputed by other researchers.
Hookah smoke is first and foremost CO from smoldering charcoal, not just nicotine. In Theron et al. (S Afr Med J, 2010, N=30: 15 cigarette smokers and 15 hookah smokers), baseline carboxyhemoglobin (COHb) was lower in hookah smokers than in cigarette smokers — 1.0% versus 2.9% — but after a single session it rose by an average of 481.7%, versus 39.9% after a cigarette. In Hawari et al. (Inhal Toxicol, 2013, N=24), after a 45-minute session exhaled CO rose from 3.7 to 24.4 ppm, and resting VO2 fell from 1.86 to 1.70 L/min.
An important detail about the source of CO: in the double-blind placebo-controlled study by Blank et al. (Drug Alcohol Depend, 2011, N=37), COHb rose almost equally from both tobacco and herbal (non-tobacco) mixture — 3.8±0.4% versus 3.9±0.4% — a rise the authors attribute to the burning charcoal, not the tobacco.
For contrast: in clinical CO intoxication after hookah, COHb reached 19–26% in three cases (Verweij et al., 2019), and averaged 26.93%±9.72 on admission in a cohort of 61 such cases (Eichhorn et al., Clin Toxicol, 2018). These are levels requiring medical care, not a typical outcome of an ordinary session, which raises COHb by only a few percent.
No direct measurements of COHb half-life specifically after a hookah session were found. There is data on cigarette smoking and CO in general: in healthy volunteers, daytime COHb half-life is 3.2±0.4 hours in women and 4.5±0.4 hours in men, slower at night — 4.3±1.1 and 8.0±1.6 hours — due to reduced lung ventilation during sleep (Deller et al., 1992). A sheep model shows biphasic CO elimination kinetics on the order of minutes to tens of minutes, but this does not translate to humans — it is given only for order of magnitude (Shimazu et al., J Trauma, 2000). Recommendations like "you can train after so many hours" are not found in the sources — no such study exists.
In 48 regular hookah smokers, a single ad libitum session raised heart rate by +16±1 bpm and mean brachial blood pressure by +6±1 mmHg (p<0.05); carotid-femoral pulse wave velocity rose by +0.66±0.09 m/s, and the augmentation index by +8.76±3.99% (p<0.05), while a control group without smoking (n=14) showed no change. The authors describe the effect on arterial stiffness as comparable in magnitude to cigarettes (Rezk-Hanna et al., Am J Cardiol, 2018) — this does not confirm the claim of hookah as a "safer alternative."
In Chami et al. (Chest, 2023, N=62 versus 34 non-smokers, 22.5±3.0 years), a session raised systolic blood pressure by 4.13 mmHg (95% CI 1.91–6.36), with the augmentation index higher — 9.02% versus 3.06% (p=0.03). In Blank et al. (2011), heart rate rose by 8.6±1.4 bpm from the tobacco mixture versus 1.3±0.9 from placebo with a similar rise in CO — the authors attribute this to nicotine. In Hawari et al. (2013), blood pressure rose from 118.9 to 129.2 mmHg, respiratory rate from 17.7 to 19.7 per minute, and the oxygen pulse during exercise fell from 10.89 to 9.97 mL/beat.
There is a chronic effect too: in regular smokers (N=205, 35+ years) versus 199 non-smokers, blood pressure and the augmentation index were higher — 10.5±3.9 versus 9.4±3.9 mmHg and 28.1±8.4% versus 25.7±8.5% (p=0.01 for both), with a dose-dependent relationship to smoking frequency, years of use and cotinine level; pulse wave velocity did not differ significantly (Chami et al., Blood Press, 2021).
There are few direct "hookah, then a workout" tests, but physical fitness appears to soften the acute vascular response. In Alomari et al. (Atherosclerosis, 2015, N=53), a session produced a small-to-moderate effect on forearm blood flow (d=-0.19), venous outflow (d=0.30) and vascular resistance (d=0.32); the effect was stronger in people with low physical activity — activity level correlated with resting blood flow (r=0.50) and vascular resistance (r=-0.40). This is a correlation in a single sample, not proof that training protects against harm.
A meta-analysis of six studies (Raad et al., Chest, 2011) found significantly lower FEV1 in hookah smokers than non-smokers (SMD=-0.43; 95% CI -0.58…-0.29, ≈-4.04%), with a trend toward lower FVC (≈-1.38%) and FEV1/FVC (≈-3.08%). No significant differences were found between hookah and cigarettes; the authors conclude that hookah "may be just as harmful as cigarettes" — this is their phrasing, not an established fact.
A study of 150 hookah smokers versus 150 non-smoking students (20.6±1.7 years) confirms the direction: FEV1 3.96±0.7 L versus 4.19±0.8 L (p<0.001), FEV1/FVC 85.9±5.7% versus 88.7±4.8% (p<0.001), peak expiratory flow 8.4±1.8 L/s versus 9.2±1.8 L/s (p=0.002); there was no difference in FVC (Nazzal et al., Can Respir J, 2020).
The only study to directly test the effect of training is Koubaa et al. (Libyan J Med, 2015): 10 hookah smokers, 12 cigarette smokers, 11 non-smokers. After 12 weeks of interval training (70% VO2max, 3 times a week), the hookah group's peak expiratory flow rose significantly (+3.4±3.9%, p<0.05), resting heart rate and blood pressure fell (p<0.05 for both), while VO2max itself changed by only +1.5±2.1 mL/min/kg — not statistically significant. The authors themselves note the small sample size as a limitation — and this same paper was formally disputed: the same journal published a separate letter criticizing its methodology (Ben Saad, 2015). Details of the critique were not found in the open access, but the fact of the dispute is confirmed: behind the abstract's conclusion lies an unresolved methodological argument, not a consensus.
Other data also do not favor hookah smokers' endurance. In 360 participants (180 hookah-only smokers with 5+ years of use, 90 non-smokers, 90 cigarette smokers, all 40+ years), 6-minute walk test distance was significantly reduced against non-smokers, with the exact meters not given (Ben Saad et al., Rev Mal Respir, 2010). A review of five studies (only men, four from Tunisia, one from Jordan) summarizes: hookah smokers have lower sub-maximal and maximal aerobic capacity, higher resting heart rate and blood pressure, and a poorer recovery index; the numbers are not given in the abstract (Chaieb, Ben Saad, 2021).
A review on oxidative stress cautiously suggests that training could theoretically partially compensate for it, but presents no human data on endurance recovery — this is a hypothesis (Taati et al., Antioxidants, 2020). The only study with a direct protective effect of training on the heart was done on male Wistar rats (4 groups, 8 weeks): moderate training prevented part of the left-ventricular systolic and diastolic dysfunction caused by hookah smoke (Nakhaee et al., Addict Health, 2019). This is an animal model — its findings do not translate to humans.
No controlled physiological tests on active athletes who smoke hookah were found — all the studies cited above recruited ordinary smokers. There is only prevalence data: among 8,745 students at eight U.S. universities, hookah smoking among varsity athletes and non-athletes occurred at almost the same rate — 27.6% versus 29.5% (p=0.41), while club and intramural athletes had higher rates — 35.1% versus 28.7% and 34.8% versus 27.7% (p<0.001 for both); at the same time, all athletes had lower odds of smoking cigarettes (Primack et al., J Adolesc Health, 2010). Prevalence among athletes is known; the physiological effect specifically on them is not.
Nothing: a targeted search for "hookah and sleep" and "hookah and post-exercise recovery" in PubMed and Europe PMC found no dedicated studies directly measuring sleep or recovery speed in hookah smokers. This is an absence of data, not evidence of no effect.
Does hookah reduce exercise tolerance? Acute effects — a rise in COHb, heart rate, blood pressure and arterial stiffness — have been measured with instruments after a single session. Much less is known about the long-term effect on athletic performance.
How many hours after hookah can you train? No such study exists. There is data on CO clearance from cigarette smoking in general (3.2–8 hours, depending on sex and time of day), but it has never been tested for hookah sessions specifically.
Does training protect against hookah's harm? There is no proof in humans: the rise in VO2max in the one such study was not statistically significant, and the study itself was disputed by other researchers. A protective effect on the heart has only been shown in rats.
Is hookah safer than cigarettes for physical activity? The sources do not support this: the effect on arterial stiffness is called comparable to cigarettes, and no significant difference in lung function was found at all.
Do athletes smoke hookah differently from everyone else? By prevalence — yes, it is more common among club and intramural athletes. There is no data on the physiological effect specifically on athletes.
This topic continues the pieces "How hookah affects health: what science says" and "Top 10 myths about hookah"; on carbon monoxide — "Safety: carbon monoxide, ventilation, how long to smoke"; on reducing risk — "How to minimize the risks of smoking hookah"; on non-smokers nearby — "Secondhand hookah smoke: what non-smokers inhale."