Breathe Through Your Nose
Patrick McKeown got there first. His 2015 book The Oxygen Advantage laid the technical foundation for nasal breathing as a trainable, measurable performance intervention—CO₂ tolerance, the Bohr effect, the BOLT score, the entire physiological architecture that makes nose breathing something you can programme rather than merely practise. McKeown’s work was rigorous, detailed, and aimed at athletes and coaches who wanted mechanism, not metaphor. It circulated among people who train seriously and who needed the science before they would change the habit. Five years later, James Nestor did something different and complementary: he made a literate general audience care about it. His 2020 book Breath arrived at the precise moment when a pandemic had most of the world thinking carefully about respiratory anatomy for the first time in their lives, and it struck with the force of something that feels both radical and obvious—the kind of idea that, once encountered, makes you wonder how you ever missed it. The book sold millions of copies. It seeded conversations that had never previously occurred at dinner tables: about turbinate function, about CO₂ tolerance, about the staggering percentage of the human population that mouth-breathes through the night without knowing the metabolic cost.
McKeown built the engine. Nestor opened the door.
This chapter walks through it. With data—and with a disclosure that the earlier version of this chapter did not make clearly enough: no published study has examined nasal breathing during loaded walking. The Akureyri Protocol’s nasal breathing component is the most evidence-free element of this entire book. The mechanistic reasoning is sound. The practical experience is extensive. The direct experimental evidence is zero.
The data that does exist changes the conversation in a specific way. It strips away the mystical overlay—the breathwork gurus, the ancient wisdom appeals, the oxygen-deprivation theatre—and reveals something more useful and considerably more interesting: nasal breathing during submaximal exercise is a measurable physiological intervention. It has quantifiable effects on ventilatory efficiency, blood lactate accumulation, autonomic tone, pulmonary vascular resistance, and diastolic blood pressure. Those effects have been documented in peer-reviewed literature by research groups working independently across multiple countries and multiple years. The signal is not perfect—this chapter will tell you exactly where it becomes ambiguous—but the core of it is robust enough to change how you train.
And the simplest practical application requires no equipment, no subscription, no coach, and no technology. If you cannot breathe through your nose during exercise, you are training too hard. That is the whole thing. The most reliable intensity regulator ever discovered is mounted in the centre of your face.
The Akureyri Protocol
The city of Akureyri sits at the head of Eyjafjordur, Iceland’s longest fjord, at sixty-five degrees north latitude. In winter the sun does not rise above the surrounding mountains until late morning, and it begins descending again by early afternoon. In summer the light is nearly continuous—a pale, diffuse luminosity that persists through what the clock insists is night, disorienting and beautiful in equal measure. The population is roughly nineteen thousand people, which makes it the second-largest urban centre in Iceland, a distinction that says everything about Iceland and relatively little about Akureyri itself.
It is the kind of place where you learn to train in the dark and the cold or you do not train at all. Most people there learn.
The protocol that became the framework for this chapter emerged not from a laboratory but from a fjordside trail during the winter of 2019, when I was working through what I had begun to understand about loaded walking and trying to identify the practical variables that could be measured and adjusted in real time without wearable technology more expensive than a basic heart rate monitor. The trail climbed out of the city through a residential neighbourhood, crossed a road, and then entered a section of open hillside that was exposed to the wind coming off the fjord. In winter that wind is not decorative. It requires your full attention.
What I noticed, working that trail repeatedly with a pack weighing between sixteen and twenty-four kilograms, was that nasal breathing functioned as an automatic throttle. Not a metaphorical throttle. A mechanical one. The moment the pace or the grade pushed respiratory demand beyond what the nasal airway could comfortably supply, the body mounted pressure to open the mouth. That pressure was the signal. It was more precise than any heart rate zone, more immediate than any lactate test, and it required nothing but attention.
I began testing the threshold deliberately. I would push the pace until the nasal-only constraint became genuinely uncomfortable—not painful, just uncomfortable in the specific way of breathing harder than feels easy—and then I would back off until the discomfort resolved. What I found was that the pace associated with the nasal threshold corresponded, with remarkable consistency, to the zone 2 intensity I was trying to maintain. The nose was not just filtering and conditioning air. It was calibrating output.
This observation is not original. George Dallam, a triathlon coach and researcher at Colorado State University, has been investigating nasal-only training in endurance athletes for nearly two decades and arrived at the same practical conclusion: nasal breathing is a self-regulating intensity constraint whose physiological effects are most pronounced at the submaximal intensities that constitute most effective aerobic training. What I was doing on the Akureyri hillside was reinventing a wheel that Dallam had already built and studied rigorously. But reinventing a wheel in the field, in the dark, in a fjord wind, with a pack on your back, is its own kind of education.
The Akureyri Protocol, as it eventually became codified in my own training practice and the programmes I designed for others, has a single foundational rule and several derived practices. The rule is this: during rucking sessions, the mouth stays closed—for those whose nasal anatomy permits it, and at intensities where nasal ventilation is sufficient. The derived practices concern warm-up duration, session structure, grade management, and the specific signals that indicate when to slow down. But they are all downstream of the rule. The mouth stays closed.
The reasons for the rule are what this chapter is about. But so are the rule’s limitations—and those limitations are more substantial than the earlier version of this chapter acknowledged.
The Ventilatory Ceiling: What Nasal Breathing Costs
Before presenting the benefits of nasal breathing, intellectual honesty requires stating what it costs.
Mapelli and colleagues, in a 2025 study published in PLOS ONE, conducted the BreathWISE trial comparing nasal-only versus oronasal breathing during cardiopulmonary exercise testing (Mapelli et al., 2025). The finding was unambiguous: nasal breathing significantly reduced peak VO₂ by approximately 8 to 22 percent and peak ventilation by approximately 35 percent compared to oronasal breathing. The nasal airway imposes a physical ceiling on ventilatory capacity. At moderate intensities—Zone 2, the training zone this protocol recommends—that ceiling is not a limitation. It is, in fact, the mechanism: the ceiling is the intensity governor. But at higher intensities, nasal breathing is not “functionally equivalent” to oral breathing. It is objectively limiting.
Lee, Seo, and Lee, in a 2025 study of progressive treadmill exercise, confirmed that nasal breathing becomes unsustainable above approximately 11 km/h, coinciding with the ventilatory threshold (Lee et al., 2025). Above this point, the nasal airway cannot deliver sufficient gas exchange, and the body switches to oral breathing involuntarily.
This limitation is exactly why the protocol works as a Zone 2 governor—but it must be stated plainly rather than minimised. Nasal breathing is not “superior across all intensities.” It is a useful constraint at moderate intensity and a genuine performance limiter at high intensity. For rucking, which operates in the moderate-intensity zone, this limitation is not relevant. For anyone who wants to maintain a high-intensity training component alongside rucking, nasal breathing is not appropriate for that component.
When NOT to Breathe Through Your Nose
Nasal breathing is not appropriate for everyone, and the protocol’s “non-negotiable” framing requires qualification. The following conditions warrant oral or oronasal breathing during exercise:
- Significant deviated septum — affects 22 to 80 percent of the population depending on diagnostic criteria. If one nostril is substantially obstructed, nasal breathing under exertion may be impossible regardless of CO₂ tolerance training.
- Nasal polyps or chronic rhinosinusitis — obstructive pathology that no amount of training can overcome.
- Severe allergic rhinitis during active episodes — seasonal or perennial. The protocol pauses; it does not power through.
- Exercise-induced bronchoconstriction — nasal breathing may help (warmer, more humid air), but if it worsens symptoms, it is contraindicated.
- Extreme cold (below -10°C) — ice crystal formation in nasal passages. A thin buff helps but does not fully resolve the problem. Below -15°C, nasal-only breathing during exertion is inadvisable.
- Panic or anxiety disorders triggered by air hunger — the CO₂ build-up that nasal breathing produces can trigger panic in susceptible individuals. This is not a CO₂ tolerance deficit; it is a clinical condition.
- Active upper respiratory infection — the protocol pauses.
- Any situation where ventilatory demand genuinely exceeds nasal capacity — steep terrain, sprint intervals, emergency situations. Opening the mouth is always the correct response to genuine air hunger.
The earlier version of this chapter presented nasal breathing as universally achievable with sufficient training. For the estimated 33 to 57 percent of the population with some degree of nasal obstruction, this was misleading. If you cannot breathe through your nose comfortably at rest, the first step is not CO₂ tolerance training—it is an ENT evaluation.
A note for anyone reading this on day one of rucking, or day one of any serious training: if nasal breathing under load feels impossible right now, that is not a sign you are doing something wrong. It is a sign that CO₂ tolerance is a trainable variable, and yours has not yet been trained. The body’s hypercapnic drive—the reflex that demands you open your mouth and ventilate harder when CO₂ rises—is calibrated by exposure. Consistent nasal-only breathing recalibrates it within two to four weeks of regular practice, as the chemoreceptors adjust to the slightly elevated PETCO₂ that nasal resistance produces and stop interpreting it as an emergency. You will get there. The nose adapts. The practical ramp is this: begin with nasal breathing at rest, only, for several days; then during unloaded walks; then with light load, roughly five percent of body weight; then with moderate load. When you can complete a full session at ten percent of body weight without breaking nasal breathing, you are ready to begin progressive load increases under the protocol. If nasal breathing is mechanically obstructed rather than merely undertrained—a deviated septum, chronic allergic congestion, polyps, or structural narrowing from previous injury—no amount of CO₂ tolerance training will resolve the underlying anatomy. That warrants assessment by an ear, nose, and throat specialist before you treat nasal breathing as a training variable. The protocol assumes functional nasal passages. If yours are not functional, address that first.
What the Sinuses Are Actually For
Every medical student learns that the paranasal sinuses—four pairs of air-filled cavities embedded in the bones of the skull—serve several functions: they reduce cranial weight, they provide resonance to the voice, they produce mucus that drains into the nasal cavity. What most medical students are not taught, because it was not known until the 1990s, is that the paranasal sinuses are also a continuous-output production facility for one of the most pharmacologically potent molecules in the human body.
Nitric oxide, discovered as an endogenous signalling molecule in 1987 by Furchgott, Ignarro, and Murad—work that earned them the Nobel Prize in Physiology or Medicine in 1998—is produced in the paranasal sinus epithelium at concentrations that dwarf what any other tissue in the body generates. Jon Lundberg and colleagues at the Karolinska Institute, working through the late 1990s and early 2000s, established that the concentration of nitric oxide in paranasal sinus air ranges from three hundred to thirty thousand parts per billion, depending on the specific sinus sampled and the individual being measured. For context: exhaled nasal nitric oxide in healthy adults typically runs around one hundred parts per billion. The sinuses are generating concentrations ten to three hundred times higher.
The delivery mechanism is elegant in the way that evolutionary solutions tend to be elegant once you understand them. When air enters the nasal passage on inhalation, it flows past the turbinates—shelf-like structures covered in highly vascularised mucosa that warm and humidify the air—and through the narrow passages that connect to the sinus ostia. Nitric oxide diffuses from the sinus air spaces into the nasal airstream. By the time the air reaches the nasopharynx and begins its descent toward the trachea and lungs, it carries a bolus of nitric oxide that the oral route cannot deliver.
In the pulmonary vasculature, inhaled nitric oxide has well-characterised effects. It is a potent vasodilator of the smooth muscle surrounding pulmonary arterioles. It reduces pulmonary vascular resistance. It improves the matching of ventilation to perfusion—the V/Q matching that determines how efficiently each alveolus can transfer oxygen to the capillary blood flowing past it. Gunnar Settergren’s 1998 work at Karolinska demonstrated that nasal breathing measurably reduces pulmonary vascular resistance relative to oral breathing at matched ventilation. Alejandro Sánchez-Crespo’s 2010 research extended this by showing that the vasodilatory effect persists during exercise, not merely at rest.
The practical implication is that the nasal route does not simply deliver filtered, warmed, humidified air to the lungs. It delivers pre-conditioned air loaded with an endogenous vasodilator that the pulmonary vasculature has specific receptors to receive. Breathing through your mouth bypasses this system entirely. The paranasal sinuses are not vestigial structures of uncertain function. They are a pharmaceutical production facility, and the nose is the delivery route.
FIGURE: The Sinus Nitric Oxide Pathway
1. Paranasal sinuses produce NO at 300–30,000 ppb (vs ~100 ppb in exhaled nasal air).
2. Inhaled air passes turbinates → picks up NO bolus from sinus ostia.
3. NO-enriched air descends through trachea to lower lung lobes.
4. Pulmonary vasculature receives NO → smooth muscle relaxation → reduced pulmonary vascular resistance → improved V/Q matching → enhanced O₂ transfer.
Mouth breathing bypasses steps 1–3 entirely. The sinuses produce the drug. The nose delivers it. The mouth skips the pharmacy.
There is a further curiosity here that Weitzberg and Lundberg documented in 2002: humming increases the concentration of nasal nitric oxide approximately fifteen-fold relative to normal nasal exhalation. The mechanism is oscillating airflow through the sinus ostia, which dramatically increases the rate of gas exchange between sinus air and nasal airstream. Whether humming during exercise has practical training applications is a question the literature has not yet answered seriously, but the underlying finding illuminates the architecture: the sinuses are not static reservoirs. They respond dynamically to airflow patterns. The nose is an active organ, not a passive tube.
The NO Caveat
There is a critical nuance that most discussions of sinus nitric oxide omit, and it matters enough to state plainly.
The same research group that established the sinus NO delivery pathway—Lundberg, Weitzberg, and colleagues at the Karolinska Institute—also demonstrated in 1997 that heavy physical exercise decreases nasal NO concentrations dramatically. After just one minute of maximal exercise, nasal NO levels dropped by 47%. By the end of a five-minute maximal bout, the reduction reached 76%. Recovery to baseline required fifteen to twenty minutes of rest (Lundberg et al., 1997).
The mechanism is likely sympathetic vasoconstriction of the sinus mucosal blood supply during high-intensity exercise, reducing the enzymatic NO production that depends on that blood flow. The implication is straightforward and important: the NO-mediated benefits of nasal breathing—pulmonary vasodilation, improved V/Q matching, enhanced oxygen transfer—are most available during the conditions where they are least urgently needed. During warm-ups, cool-downs, easy-pace rucks, and the rest periods between efforts, sinus NO production is robust and nasal delivery functions as described above. During sustained hard efforts, the pharmacy is closing even as the demand for its product rises.
This does not undermine the case for nasal breathing during rucking. It refines it. The practical implication is that nasal breathing’s NO benefits are real and meaningful precisely because rucking, done correctly, operates in the intensity range where those benefits are available—the easy-to-moderate zone where sinus NO production remains intact. Push into high-intensity territory, and you lose the NO benefit at the same time as the nasal airway becomes insufficient for ventilation. The two signals converge: when the nose can no longer supply enough air, it is also no longer delivering meaningful NO. Both facts point toward the same instruction—slow down.
It is also worth dwelling on what the turbinates specifically accomplish, because the training implications of turbinate function are underappreciated outside of pulmonology. The three turbinates on each side of the nasal cavity—inferior, middle, and superior—are covered in erectile tissue, meaning they contain capacitance vessels that engorge and contract in a roughly four-hour cycle called the nasal cycle. At any given time, one nasal passage is slightly more open and the other slightly more restricted, creating alternating dominant airflow that appears to serve the olfactory system and possibly the brain’s lateralised functions. During exercise, sympathetic activation causes turbinate decongestion—both passages open wider under adrenergic tone—increasing the nasal airway’s capacity precisely when demand increases. The nose is not a fixed-diameter tube. It dilates under exercise demand, within its anatomical limits.
The warming function of the turbinates is directly relevant to rucking in cold climates. At minus ten Celsius, ambient air entering the nasal passage is typically warmed to thirty-two to thirty-four degrees Celsius by the time it reaches the nasopharynx—a fifty-degree temperature increase across a few centimetres of passage. This warming is powered by the vascular bed in the turbinate mucosa and by the substantial surface area created by the turbinate architecture. Oral breathing provides no equivalent: cold air enters directly, reaches the trachea and bronchial tree with minimal conditioning, and provokes the bronchoconstriction response that any distance runner who has trained hard in cold weather recognises immediately. The nasal route is a cold-weather system. The oral route is not.
The Ventilatory Efficiency Signal
Ventilation is expensive. Moving air in and out of the lungs requires muscular work, and that muscular work has a metabolic cost. At rest, the respiratory muscles account for roughly two to three percent of total oxygen consumption. At maximal exercise intensity, that fraction climbs to eight to fifteen percent. At submaximal intensities—the intensities that constitute most endurance training, including rucking—respiratory muscle oxygen demand is modest in absolute terms but significant in proportion to the modest total metabolic rate.
Ventilatory efficiency is typically expressed as the VE/VCO₂ ratio: the volume of air breathed per unit of carbon dioxide exhaled. Lower ratios indicate more efficient ventilation. Higher ratios indicate the lungs are moving more air than is strictly necessary to manage CO₂, which is the primary driver of the ventilatory drive under normal conditions. A VE/VCO₂ ratio of 25 means the athlete is ventilating twenty-five litres for every litre of CO₂ produced. A ratio of 30 means they are ventilating thirty litres for the same CO₂ output. The difference is not trivial when you are considering the cumulative work over a multi-hour rucking session.
Two related papers from the same research group, published in 2024, examined VE/VCO₂ during nasal-only versus oral-only breathing during cycle ergometry at matched workloads. Calamai et al., studying healthy adults, found that nasal breathing produced a mean VE/VCO₂ of 25.8 versus 28.6 for oral breathing, a difference that reached statistical significance at p ≤ 0.01 (Calamai et al., 2024). The companion study—Eser et al. 2024, examining cardiac patients exercising at 50% of peak power—found even more striking results: VE/VCO₂ was 35% lower in heart failure patients during nasal breathing, breathing frequency was 26% lower, and end-tidal CO₂ was 10% higher. Exercise oscillatory ventilation, present in six of fifteen heart failure patients, was markedly reduced with nasal breathing (Eser et al., 2024). The interpretation is straightforward. Nasal breathing reduced the ventilatory work required to manage CO₂ at identical metabolic demand, and the effect was amplified in the population where ventilatory inefficiency is most clinically consequential. The nose is doing something the mouth does not do—something that makes the respiratory system more efficient, not just more filtered.
Part of the mechanism involves CO₂ retention. Nasal breathing imposes a mild resistive load—the nasal airway is narrower than the oral airway—which slightly slows exhalation and raises the partial pressure of CO₂ in the alveoli. This is not hypercapnia in any clinical sense. It is a subtle shift in the equilibrium point. Measured directly, PETCO₂—the end-tidal CO₂ pressure, a non-invasive proxy for alveolar CO₂—runs approximately 4.5 mmHg higher during nasal versus oral breathing at matched workloads: 44.7 versus 40.2 mmHg, a difference that reached significance at p = 0.035 in the relevant studies.
This matters because of the Bohr effect. The Bohr effect, described by Christian Bohr in 1904, is the rightward shift of the oxyhaemoglobin dissociation curve with increasing CO₂ and decreasing pH. In practical terms: at higher CO₂ levels, haemoglobin releases oxygen more readily to the tissues. The slightly elevated PETCO₂ associated with nasal breathing shifts the dissociation curve toward better oxygen delivery at the tissue level, even though SpO₂—the oxygen saturation of arterial blood as measured by pulse oximetry—remains in the range of 98% during nasal-only exercise at submaximal intensities. The blood is not carrying less oxygen. It is releasing it more efficiently.
At the submaximal intensities that define Zone 2 rucking—sixty to seventy percent of maximum heart rate—oxygen delivery to the working muscle is rarely the limiting factor. The mitochondria are not starving for oxygen at this pace. The Bohr effect is real, and at higher intensities it matters considerably. But at rucking pace, its contribution is modest. The true value of nasal breathing during loaded walking is not biochemical optimisation. It is mechanical governance.
Total ventilation is also reduced. Nasal breathing at matched submaximal workloads reduces minute ventilation by approximately twenty-two percent compared to oral breathing—a substantial reduction in the absolute work performed by the respiratory muscles over any extended duration. Twenty-two percent less ventilatory work during a two-hour ruck is a meaningful shift in how the body allocates its aerobic budget.
The Nasal Ventilatory Ceiling
The ventilatory efficiency data from Calamai and Eser tells you that nasal breathing is more efficient at matched workloads. It does not tell you where the efficiency breaks down. For that, you need the Lee, Seo, and Lee study published in 2025, which is the most controlled direct comparison of nasal, oral, and oronasal breathing during progressive exercise currently available (Lee et al., 2025).
Lee and colleagues measured ventilatory responses in ten healthy, recreationally active women walking and running on a treadmill at speeds from 5 to 11 km/h under all three breathing conditions. At low speeds—5 to 7 km/h, the range that encompasses most rucking paces—breathing mode made essentially no difference to any cardiorespiratory variable. The nasal airway handled the ventilatory demand without measurable constraint.
At 10 to 11 km/h, the picture shifted. Nasal breathing produced significantly lower respiratory frequency and minute ventilation than oral or oronasal breathing, but the ventilatory equivalent for CO₂—the VE/VCO₂ ratio—was elevated, indicating that the nasal route was no longer managing CO₂ clearance efficiently. The airway was becoming the bottleneck. At 11 km/h, minute ventilation during oral breathing reached 73.7 litres per minute and during oronasal breathing 74.8 litres per minute, while nasal breathing could only generate 67.2 litres per minute. Beyond 11 km/h, participants could not sustain nasal breathing at all.
The nasal-to-oral transition coincides with the region around the ventilatory threshold—the metabolic boundary below which aerobic metabolism dominates and above which anaerobic contribution begins to rise. The nose, in effect, announces the ventilatory threshold by failing. The moment nasal breathing becomes unsustainable is the moment you have crossed from the aerobic zone into the territory this book argues you should avoid during rucking.
This is why the nasal airway functions as a binary intensity signal. Not graded. Not nuanced. Binary: nasal breathing works, or it does not. Below the ceiling, you are in the zone. Above the ceiling, you are out of it. The signal requires no equipment, no calibration, no interpretation. It is the body’s own ventilatory threshold alarm, anatomically installed and metabolically precise.
The limitation of a binary signal, of course, is that it cannot tell you where within the zone you are operating. Comfortably moderate and approaching the threshold feel different subjectively, but the nasal airway does not distinguish between them—it only announces the boundary. For more granular pacing information within the zone, other tools are needed. We will come to those.
The Talk Test
The nasal ventilatory ceiling gives you a binary signal: in the zone or out of it. But rucking is not always a solitary activity performed in grim silence on an Icelandic hillside. Rucking is—and should be—social. And the ability to hold a conversation while carrying a pack is itself one of the oldest and most reliable pacing tools in the history of human exertion.
The Himalayan Origin
Long before exercise physiologists formalized the concept, the men who climbed the highest mountains on earth discovered the talk test through suffering.
In June 1924, Edward Norton and Howard Somervell set out from Camp VI on the north ridge of Everest, climbing without supplemental oxygen in woolen knickers, a tweed coat, and layers of cotton and silk. Norton had planned to take twenty consecutive paces uphill between rest stops. He managed thirteen—“thirteen steps and a stop”—before his body demanded a pause. Somervell, behind him, was worse: necrotic tissue sloughing from the lining of his throat in the cold, dry air had left him choking, unable to speak, unable to signal Norton ahead of him. When speech fails at altitude, you have crossed beyond what the body can sustain. Norton reached 28,126 feet that day—a record that stood for fifty-four years—on a resting pulse at 27,000 feet that he measured at just sixty-four beats per minute, “some twenty above my normally very slow pulse.” The capacity of those men is difficult to comprehend from the vantage of modern sport.
Seven years later, on Kamet (7,756 m), Frank Smythe became the first to articulate what would become the talk test’s core principle. Observing Eric Shipton climbing with “almost leisurely rhythm” while the Sherpa Lewa spent “more of his magnificent energy than necessary” with “eager jerky movements,” Smythe concluded that above 20,500 feet, “we must consciously adopt a rhythm of breathing to stepping.” The high-altitude slow plod: one step, one breath, pause. Repeat. The rhythm was not a technique. It was the body’s demand, expressed through ventilation, for a pace it could sustain.
In 1939, Professor John Grayson at Oxford formalised the heuristic for British mountaineers: “climb no faster than you can talk.” But the principle was already demonstrated—through suffering, hypoxia, and necrotic tissue in the throat—in the 1920s expeditions. The science came later. The body knew first.
The Modern Validation
The talk test rests on the competition between ventilatory demands for gas exchange and the respiratory control required for speech production. As exercise intensity rises, the ventilatory drive eventually overwhelms the capacity for comfortable speech—a transition that corresponds closely to the ventilatory threshold.
DeHart (1999) conducted one of the foundational validation studies, comparing talk-test outcomes with ventilatory threshold determined by gas analysis in twenty-eight healthy subjects during incremental exercise (DeHart, 1999). Subjects who could still speak comfortably, or who were equivocal about their comfort, were at or below their ventilatory threshold. Subjects who clearly failed the talk test—who could not produce comfortable continuous speech—were consistently beyond their VT. There was no significant difference between the physiological variables at VT and those at the equivocal stage of the talk test. The transition from “I can talk” to “I’m not sure I can talk” occurs at precisely the metabolic boundary that matters.
Kwon, Kang, and Chang (2023) confirmed these relationships in seventeen healthy adults performing treadmill cardiopulmonary exercise testing with a three-stage talk test protocol (Kwon et al., 2023). All ergospirometric variables—VO₂, minute ventilation, VCO₂, tidal volume, respiratory rate, heart rate—showed significant differences across talk-test stages, and the talk test showed strong correlations with these variables. The authors concluded that the talk test “can be used to evaluate and prescribe exercise intensity of aerobic activity.”
Sørensen, Larsen, and Petersen (2020) validated the talk test in twenty cardiac patients and found that all talk-test stages fell within the ACSM intensity guideline range of 40–80% of VO₂max, though limits of agreement were wide, suggesting limited individual-level precision (Sørensen et al., 2020). The talk test is a field tool, not a laboratory instrument. It tells you the neighbourhood, not the street address.
Mahmod et al. (2022) provided the most detailed comparison of talk-test variants, evaluating a self-paced Counting Talk Test and a newly designed time-controlled monosyllabic Talk Test during incremental treadmill exercise at 40–85% heart rate reserve (Mahmod et al., 2022). The monosyllabic test significantly delineated all six stages of incremental exercise, while the counting test could only distinguish exercise stages at 60%, 80%, and 85% of heart rate reserve. Both tests demonstrated moderate correlations with HRR and with Borg RPE. The practical takeaway: the talk test provides categorical resolution—easy, moderate, hard—rather than fine-grained measurement. For rucking, this categorical resolution is typically sufficient. The rucker needs to know whether the pace is sustainable, not the exact percentage of VO₂max.
Why It Matters for Rucking
The talk test fills the gap that nasal breathing leaves open. Where the nasal airway provides a binary signal—below threshold or above it—the talk test provides a gradient. Full sentences spoken comfortably: well within the zone. Full sentences spoken with effort: approaching the boundary. Single words only, or speech abandoned: beyond it. Three categories instead of two. More resolution means better pacing.
There is also a social dimension that the physiology literature does not capture but that matters for adherence. Rucking can and should be social. Walking with weight alongside another person, holding a conversation, is both a pacing tool and part of the experience. The ability to speak in full sentences is not just a proxy for ventilatory threshold—it is the evidence that the effort is compatible with human interaction, with community, with the kind of practice that sustains itself across years precisely because it does not require grim isolation.
If you can only manage single words between breaths, slow down. Not because a heart rate monitor tells you to, but because the conversation deserves it.
The Lactate Signal
Blood lactate concentration is one of the most informative variables in exercise physiology. It reflects the balance between anaerobic glycolytic flux—the rate at which muscles are producing lactate as a byproduct of high-intensity energy demand—and the rate at which other tissues are clearing it. Below the first ventilatory threshold, lactate production and clearance are roughly matched, and blood lactate stays low. Above the second threshold—the point exercise physiologists call the lactate threshold proper—production begins to outpace clearance, lactate accumulates, and the clock starts ticking toward fatigue.
Zone 2 training, the low-intensity aerobic work that is the foundation of every evidence-based endurance programme, is defined partly by blood lactate staying below two millimoles per litre. Rucking, done correctly, achieves this reliably. The question that the nasal breathing research addresses is whether the breathing route influences where lactate sits within that zone.
Ludwig Rappelt and colleagues, publishing in 2023, conducted a crossover study comparing nasal-only and oral-only breathing during submaximal cycling at matched intensities in trained cyclists. Their finding: blood lactate averaged 1.21 mmol/L during nasal breathing versus 1.45 mmol/L during oral breathing. The standardised mean difference was 0.48—a medium effect size by Cohen’s conventions. The p-value was 0.02.
The absolute numbers require context. Both values are well within the zone 2 range. Neither represents lactate accumulation in any clinically meaningful sense. What the difference represents is a seventeen percent reduction in blood lactate concentration during nasal breathing at identical mechanical workloads. If the nasal route is delivering oxygen more efficiently, reducing ventilatory cost, and improving pulmonary vasodilation through sinus-derived nitric oxide, then the aerobic energy system can meet the same power output demand with less anaerobic contribution. Less anaerobic contribution means less lactate. The 1.21 versus 1.45 finding is exactly the number you would predict from first principles if the other mechanisms are operating as described.
The practical translation: during rucking at the intensity where nasal breathing is comfortable, you are training more aerobically than you would be at the same pace and grade with your mouth open. The adaptation signal is cleaner. The mitochondrial stimulus is purer. The metabolic stress is lower for the same mechanical output. This is not a trivial distinction for someone logging five to eight hours of weighted walking per week for years at a time.
The Autonomic Signal
The autonomic nervous system governs the balance between sympathetic activation—the fight-or-flight response—and parasympathetic tone, the rest-and-digest state associated with recovery, digestion, immune function, and cardiovascular health. Heart rate variability is the primary non-invasive measure of autonomic balance: high-frequency HRV (HF-HRV) reflects the respiratory sinus arrhythmia driven by parasympathetic vagal tone, and higher HF-HRV is consistently associated with better cardiovascular outcomes, faster athletic recovery, and reduced all-cause mortality risk.
Luis Deus and colleagues, publishing in 2024, measured HRV during and after exercise sessions conducted under nasal-only versus oral-only conditions in healthy adults. High-frequency HRV averaged 59% in the nasal condition versus 52% in the oral condition, a difference that reached significance at p = 0.04. The nasal condition was also associated with lower diastolic blood pressure: 68 versus 72 mmHg, significant at p < 0.001.
The HRV finding is mechanistically coherent. Nasal breathing directly engages the vagus nerve through nasal airway mechanoreceptors. The slow, resistive pattern of nasal inhalation and exhalation amplifies respiratory sinus arrhythmia—the normal fluctuation in heart rate with breathing that is the substrate of HF-HRV measurement. The nasal route also delivers more airflow to the lower lobes of the lungs, where the greatest density of vagal stretch receptors is located. Each of these mechanisms promotes parasympathetic dominance during and after exercise.
The diastolic blood pressure finding is particularly interesting in the context of rucking as a long-term health practice. A four mmHg reduction in diastolic pressure across exercise sessions is not trivial. Chronic exposure to lower exercise blood pressure may contribute to the long-term cardiovascular benefits of aerobically appropriate training, and the magnitude here is large enough to have clinical relevance for individuals in prehypertensive ranges.
What the Deus 2024 paper suggests, integrated with the Rappelt 2023 lactate data and the Calamai 2024 ventilatory efficiency data, is a picture of nasal breathing as an intervention that simultaneously reduces metabolic stress, improves autonomic balance, and lowers cardiovascular load at identical exercise intensities. The three mechanisms are related but not identical. They are operating through different pathways that happen to converge toward the same practical outcome: a cleaner, more sustainable, more recoverable training stimulus.
The Adaptation Curve
George Dallam’s 2018 study on nasal-only breathing in triathletes is the most important single reference in this chapter, not because its effect sizes are the largest but because it answers the question that every sceptical reader will already be asking: does the apparent efficiency of nasal breathing come at the cost of reduced maximal capacity, and if so, for how long?
The answer is yes, and six months.
Dallam trained competitive triathletes to use nasal-only breathing during all training sessions over six months. At the beginning of the study, the nasal-only condition was associated with a roughly ten percent decrement in measured VO₂max compared to the athletes’ oral-breathing baseline. This is not surprising. The nasal airway is narrower. At high intensities—the intensities required for VO₂max testing—nasal resistance limits airflow enough to reduce peak ventilation and therefore peak oxygen consumption. For high-intensity work at true maximal effort, this is a real constraint.
The constraint is architectural. The adult nasal airway at rest carries airflow resistance of roughly 0.3 to 0.5 Pa/cm³/s—approximately two to three times the resistance of the oral airway. During exercise at high intensity, when minute ventilation climbs above 80 to 100 litres per minute, the pressure drop across the nasal passages becomes substantial. Turbulent airflow increases resistance further. The system hits a physical ceiling that the oral route simply does not have, because the mouth can open wide and reduce resistance to near zero. This is not a flaw in the nasal airway’s design. At submaximal intensities—at the zone 2 work that constitutes the vast majority of effective rucking training—minute ventilation stays well below the ceiling. The nasal route is not just adequate. It is superior.
After six months of nasal-only training, the VO₂max deficit had disappeared. The athletes had adapted—through a combination of increased nasal airway compliance, improved breathing mechanics, enhanced ventilatory efficiency at submaximal intensities, and possibly structural remodelling of nasal tissues under the chronic stimulus of higher airflow demand. Their peak capacity at the end of the study was equivalent to their oral-breathing baseline from the beginning.
The mechanisms of this adaptation are not fully characterised, but the likely contributors include improved diaphragmatic strength and endurance under the resistive load imposed by nasal-only breathing—essentially, the nose acts as a mild inspiratory muscle trainer throughout every session. There is also evidence that chronic nasal breathing reduces upper airway inflammation, improves mucociliary clearance, and may modestly increase nasal airway diameter over months of habitual use. The body, characteristically, adapts to the demand placed on it. The nasal airway is not exempt from this principle.
This has specific implications for how nasal training should be implemented. The first weeks are the hardest. The nasal airway feels insufficient. The temptation to open the mouth is continuous and convincing. The beginner who tries nasal-only training and gives up after two weeks, concluding that it doesn’t work or that they are simply not suited to it, is abandoning the adaptation before it occurs. The curve is real, and it takes time. The evidence says the curve resolves in approximately six months of consistent practice.
The practical recommendation that follows from Dallam 2018 is not to attempt nasal-only training at the intensities you are currently comfortable with. It is to reduce intensity until nasal-only breathing is comfortable at that reduced intensity, and then to build from there. This is not a regression. It is the correct starting point. The nose is the governor. Train at the speed the governor allows. Let the system adapt. The capacity will come.
One further note on timing: the ten percent initial VO₂max decrement documented by Dallam is relevant only at true maximal effort. At zone 2 intensities—where rucking lives, where the aerobic adaptations accumulate, where the mitochondrial biogenesis happens—the ten percent decrement is irrelevant because you were never operating near VO₂max to begin with. You do not need your VO₂max ceiling during a two-hour loaded walk. You need your submaximal efficiency, your ventilatory economy, your lactate management, your autonomic tone. The nasal route improves all of these from the first session. The adaptation curve is the ceiling’s problem, not the floor’s.
What the Evidence Does and Does Not Say
This is the point in the chapter where intellectual honesty demands a detour.
The nasal breathing literature contains a number of claims that circulate in the wellness space that are either unsupported or actively contradicted by the best available evidence. The most prominent concerns respiratory exchange ratio—the ratio of CO₂ produced to O₂ consumed, which serves as a proxy for substrate utilisation. An RER of 1.0 indicates exclusive carbohydrate oxidation. An RER of 0.7 indicates exclusive fat oxidation. Values between indicate a mixture, with lower values indicating proportionally greater fat contribution.
The claim—and it is a genuinely appealing claim—is that nasal breathing significantly shifts substrate utilisation toward fat oxidation, making it a metabolic intervention not just for efficiency but for body composition. The most cited evidence for this is a 2017 study by LaComb and colleagues that did document a shift in RER from approximately 0.89 to 0.82 during walking at 50 to 65% VO₂max under nasal-only conditions. An RER of 0.82 versus 0.89 does represent a meaningful shift toward fat oxidation, and if the finding is robust, it would be a substantial additional argument for nasal training.
The problem is that the finding does not replicate cleanly in cycling studies. Multiple well-controlled cycle ergometry investigations at matched intensities have failed to show significant RER differences between nasal and oral conditions. The reason for the discrepancy is not fully understood. One possibility is that the walking modality involves posterior chain muscle recruitment patterns and lower-limb loading characteristics that interact differently with substrate selection than cycling does. Another possibility is that the LaComb study had methodological limitations that inflated the apparent effect. A third possibility is that there is a genuine walking-specific effect that cycling does not capture, for biomechanical reasons that would require more research to disentangle.
The honest position is that the RER evidence is mixed and modality-dependent, and that anyone who cites it as established fact for nasal breathing generally—rather than tentatively, for walking specifically—is overstating the current evidence. This book does not do that.
What IS robust: lactate. What IS robust: ventilatory efficiency. What IS robust: parasympathetic tone and diastolic blood pressure. What IS robust: sinus nitric oxide delivery and its pulmonary vascular effects. These four pillars are each supported by mechanistically coherent, reasonably well-replicated evidence from independent research groups. They are enough. They do not need the RER claim to make the case for nasal training.
The honest gap matters for another reason. If you are reading this chapter and you have already been practising nasal-only rucking for six months and you have not noticed dramatic changes in body composition, the absence of that effect does not mean nasal breathing is not working. The lactate and ventilatory efficiency effects are real and operating. The HRV and blood pressure effects are real and operating. The substrate utilisation effect may or may not apply to your modality and intensity range. The science is still working out the details.
The Respiratory-Postural Competition
There is a dimension of nasal breathing during loaded exercise that the efficiency and chemistry literature does not address directly, and it involves a peculiar fact about the diaphragm.
The diaphragm serves two masters. It is the primary muscle of inspiration, responsible for generating the thoracic pressure differential that draws air into the lungs. It is also a core stability muscle, one of the four components of the cylindrical pressure system—with the pelvic floor, transversus abdominis, and multifidus—that generates intra-abdominal pressure to stiffen the lumbar spine during load bearing. These two functions are not always compatible. When you breathe in, the diaphragm descends, reducing its contribution to lumbar stabilisation. When you brace for a heavy load, the diaphragm tenses and flattens, reducing its contribution to respiration.
Paul Hodges and colleagues demonstrated in 2001 that the diaphragm resolves this competition through a predictable pattern of compromised function in both roles: during tasks that require both postural stability and ventilation, the diaphragm’s performance in each role degrades compared to tasks requiring only one. The greater the ventilatory demand, the more the postural role is compromised. The greater the postural demand, the more ventilation is constrained.
The problem is compounded by the pack itself. Shei et al. (2017) demonstrated that thoracic load carriage at matched oxygen demand significantly increased minute ventilation, largely through increased dead-space ventilation, and altered ventilatory mechanics independent of exercise intensity (Shei et al., 2017). A heavy backpack does not merely add metabolic cost. It changes how you breathe—increasing the volume of air moved without a proportional increase in gas exchange efficiency. Each breath is less productive. The respiratory system works harder to achieve the same metabolic result.
Dempsey et al. (2006) quantified the broader cost: during heavy-intensity sustained exercise, ten to fifteen percent of total VO₂ and cardiac output are directed to the respiratory muscles (Dempsey et al., 2006). When respiratory muscles fatigue under sustained demand, a metaboreflex kicks in—a sympathetic vasoconstrictor response that reduces blood flow to the locomotor muscles, contributing directly to exercise limitation. The legs tire not because they are exhausted but because the respiratory system is stealing their blood supply.
When a loaded backpack further constrains chest expansion and increases ventilatory dead space, this respiratory cost is amplified. The ceiling at which sustainable exercise can be maintained drops. A pace that is comfortably aerobic when unloaded may cross into the territory of respiratory-postural compromise under a twenty-kilogram pack, not because the legs or the heart cannot handle it, but because the breathing apparatus is overtaxed by the combination of metabolic demand and mechanical constraint.
The implications for rucking are direct. A twenty-kilogram pack places substantial demand on the lumbar stabilisation system. The diaphragm is working continuously as a postural muscle. Simultaneously, it must breathe—and now it must breathe harder than unloaded walking would require, because the pack has increased dead-space ventilation. At low ventilatory demands—the demands associated with nasal breathing at comfortable submaximal intensities—the competition between the two roles is manageable. The respiratory and postural functions coexist without excessive compromise of either.
At higher ventilatory demands—the demands associated with oral breathing at higher intensities, or with mouth breathing under any condition that drives respiratory rate and tidal volume upward—the competition intensifies. Postural stability decrements emerge. The relationship between breathing pattern and spinal load management becomes mechanically suboptimal precisely when the pack is heaviest and the terrain is most demanding. And the respiratory metaboreflex begins redirecting cardiac output away from the working muscles toward the respiratory muscles, a vicious cycle that accelerates fatigue from both ends.
Nasal breathing, by keeping ventilatory demand lower at matched workloads, reduces the severity of the respiratory-postural competition. The diaphragm has enough reserve capacity to manage both roles adequately. This is not a widely cited argument in the nasal breathing literature, but it is mechanistically sound and has direct relevance to the specific population this book addresses: people carrying weight over variable terrain, for extended duration, who care about both performance and spinal health. It should be stated as the strong mechanical inference it is, however, rather than established fact: no electromyographic study has directly quantified the combined effect of nasal breathing and load carriage on diaphragmatic dual-role performance under field conditions, and the synergy, while highly plausible, awaits direct experimental validation.
The Dual Restriction: When Load Meets Nasal Breathing
There is a question the research reviewed in this chapter does not directly answer, and it is the question most relevant to anyone practising the Akureyri Protocol. Not: does nasal breathing improve ventilatory efficiency? Not: does backpack loading alter respiratory mechanics? But: what happens when you combine them? What does the body do when a pack on your back is pushing the breathing pattern in one direction while your closed mouth is pushing it in another?
The short answer is that the two interventions create opposing mechanical demands. A backpack load wants rapid, shallow breathing. The restriction on thoracic expansion reduces the volume available per breath, so the body compensates by taking more breaths—increasing frequency at the cost of depth. Nasal breathing, operating through an airway with roughly two to three times the resistance of the oral route, enforces the opposite pattern: slower, deeper breaths. The body cannot easily satisfy both demands simultaneously. Something gives.
This is what a structured review of the independent evidence bases suggests, synthesised into a combined restriction model (Dallam et al., 2018; Dominelli et al., 2011; Faghy & Brown, 2014):
What the load does. Backpack carriage reduces forced vital capacity (FVC) in a dose-dependent fashion—by approximately 3% at 15 kg, 5–8% at 25 kg, and up to 15% at military loads of 30–50 kg (Armstrong et al., 2019; Dominelli et al., 2011). At 25 kg sustained at 6.5 km/h for sixty minutes, measurable respiratory muscle fatigue develops even in the absence of nasal restriction: maximal inspiratory pressure (PImax) falls by approximately 11%, maximal expiratory pressure (PEmax) by approximately 13% (Faghy & Brown, 2014). The pack is not merely adding metabolic load. It is doing mechanical work on the thorax that degrades the breathing apparatus over time.
What nasal breathing does. Nasal resistance reduces minute ventilation by approximately 20–25% at submaximal exercise intensities, enforcing a breathing frequency that is substantially lower than the oral-breathing comparator at matched workloads (Dallam et al., 2018; Rappelt et al., 2023). The mechanism is increased airway resistance that physically slows the respiratory cycle. The compensation—higher oxygen extraction per litre of ventilation, improved alveolar diffusion time, sinus-derived nitric oxide—has been detailed in the earlier sections of this chapter.
What they do together. The chest wall cannot fully expand because the pack restricts it. The airway cannot deliver gas at the rate demanded by exercise because the nose constricts it. Both effects operate simultaneously. At moderate rucking parameters—10–20 kg of load, walking pace of 5–7 km/h, sea-level conditions, adapted nasal breather—the compensatory mechanisms described above appear sufficient: maintained tidal volume through diaphragmatic effort, improved oxygen extraction, reduced ventilatory demand from nasal efficiency. The two opposing patterns find an uncomfortable equilibrium that, in practice, the trained rucksack carrier manages without much awareness.
At heavier loads, higher speeds, or when the nasal airway is itself compromised, the equilibrium breaks down. The nasal airway cannot accommodate the breathing frequency that the loaded, metabolically-burdened chest wall needs. The tidal volume the body requires to compensate for low frequency cannot be achieved because FVC has been reduced by the load. Respiratory muscle fatigue arrives earlier, because both restrictions are increasing the mechanical work of breathing simultaneously: the diaphragm is fighting pack weight from above and nasal resistance from within.
It is worth being precise about the evidential status of this model: no published study has directly combined backpack loading with nasal-only breathing. This is a synthesis from independent evidence bases—the load carriage literature and the nasal breathing literature—not a conclusion from a study that measured both simultaneously. The model is mechanistically coherent. It is consistent with everything both literatures have established independently. But it awaits direct experimental confirmation, and the reader should hold it accordingly.
The Self-Limiting Safety Argument
The most practically important thing the dual restriction model reveals is not a danger. It is a safeguard.
The combination of chest wall restriction and nasal airway resistance creates intense dyspnea—the uncomfortable sensation of insufficient ventilation—well before any physiologically dangerous desaturation can occur. This is because dyspnea scales with the mismatch between ventilatory drive and achievable ventilation (O’Donnell et al., 2000). When what the body demands and what the anatomy can deliver diverge, the subjective experience is “inspiratory difficulty” and “unsatisfied inspiration”—a sensation that is psychologically intolerable long before it is physiologically dangerous. O’Donnell and colleagues demonstrated this directly: reduced inspiratory reserve volume, which is exactly what backpack loading produces, correlates tightly with dyspnea intensity at submaximal workloads.
Put differently: the system is self-policing. Before the rucksack-and-nasal-breathing combination can produce dangerous hypoxemia, the exerciser will have received a compelling and unmistakable signal to slow down or open their mouth. The signal is not subtle. It is not a number on a screen. It is the most ancient alarm the respiratory system possesses, and it fires early.
There is a secondary protective mechanism worth noting. Nasal breathing naturally constrains exercise to Zone 1–2 intensity in most individuals, particularly under load. Rappelt and colleagues demonstrated that self-selected intensity during nasal-only exercise produces lower lactate and similar perceived effort compared to oral breathing at the same pace, suggesting it automatically enforces aerobic output (Rappelt et al., 2023). If nasal breathing is limiting intensity to a range where dangerous ventilatory compromise cannot occur, then the dual restriction model’s severity is further moderated: the nasal ceiling prevents the exerciser from reaching the intensity at which the backpack’s respiratory muscle fatigue effects become significant.
At typical recreational rucking parameters—10–20 kg load, 5–7 km/h walking pace, sea level—the combination is safe and self-limiting. The primary consequence is not physiological danger but an earlier onset of discomfort and a reduced ceiling for performance. The body’s alarm system provides an effective and timely warning. The exerciser who attends to that warning—who slows down or opens their mouth when the signal arrives—is in no danger.
The parameters where caution is genuinely warranted:
- Loads exceeding 25–30 kg. Above this threshold, respiratory muscle fatigue is significant even without nasal restriction. The combined effect may produce a ventilatory ceiling at walking speeds that feel manageable from a cardiovascular and musculoskeletal perspective—the breathing system fails before the legs do.
- Altitude above 2,000 m. Load carriage in hypoxia at simulated 3,650 m reduces VO₂max by approximately 32%, increases breathing frequency substantially, and induces expiratory flow limitation in roughly half of subjects (Baur et al., 2025). Adding nasal restriction to an already hypoxic, mechanically restricted, and ventilatorily challenged system creates a three-way constraint with meaningful risk of inadequate alveolar ventilation. The altitude margin disappears quickly.
- Nasal congestion or structural obstruction. Any degree of increased nasal resistance compounds the dual restriction.
The Practice
The Akureyri Protocol, rendered in its practical form, is not complicated. Its lack of complication is the point.
Begin with sessions where you are certain nasal breathing will be comfortable: flat terrain, moderate pack weight, temperatures cool enough to support nasal airway function without congestion. For most people starting from an untrained nasal-breathing baseline, this means walking pace rather than hiking pace, weights in the eight-to-twelve kilogram range rather than the twelve-to-twenty range, and duration limited to thirty to forty-five minutes until the pattern is established.
The breathing itself requires attention at first, then less attention, then none. The initial experience is often a mild sense of oxygen insufficiency that the rational brain correctly identifies as subjective rather than real—SpO₂ monitoring will confirm that arterial saturation remains in the 97-98% range during nasal-only exercise at these intensities—but that the body nevertheless interprets as a demand to open the mouth. This is the moment of practice. Not a performance of controlled breathing, not a meditation on breath. Simply: mouth closed. Adjust pace or grade until mouth-closed breathing is comfortable. Proceed.
Cold air requires additional attention. At temperatures below minus five or six Celsius, the nasal airway can constrict under the stimulus of cold, dry air, and the warming and humidifying function of the turbinates is taxed by the extreme temperature differential. A thin buff or neck gaiter worn over the nose in extreme cold reduces this effect by pre-warming the inhaled air slightly before it reaches the turbinates. Akureyri in January has tested this particular solution extensively.
There is a less obvious benefit operating in the same cold conditions that is worth naming plainly. Cold air is one of the primary triggers for exercise-induced bronchoconstriction—the airway narrowing that many people experience as chest tightness, coughing, or wheezing during hard outdoor exercise in winter. The nasal route provides direct protection against this. The turbinates warm and humidify inspired air so effectively that by the time it reaches the trachea and bronchi, the temperature and humidity differential that triggers bronchoconstriction has largely been corrected. Mouth breathing in the same conditions delivers cold, dry air directly to the bronchial tree with no such conditioning. For anyone who has experienced cold-air-induced chest tightness during winter exercise, nasal breathing is not merely a performance intervention—it is a protective one. Rucking in Icelandic winters is, among other things, an extended test of the nasal airway’s capacity as a cold-air heat exchanger. The turbinates pass it.
Illness and seasonal allergies are honest exceptions. Mucosal swelling from a rhinovirus or pollen exposure is not a failure of the nasal breathing practice; it is a physiological condition that temporarily overrides the system’s normal capacity. The protocol pauses. It resumes when the airway is clear.
Over weeks, the nasal threshold rises. The intensity at which nasal-only breathing becomes uncomfortable increases. This is the adaptation Dallam measured: the system improving its capacity to deliver adequate airflow through the nasal route under higher ventilatory demand. The pace that required careful management at the start of the practice becomes the easy warm-up pace. New thresholds emerge. The governor recalibrates upward.
Over months, the cardiovascular signature changes in the ways the research predicts. HRV scores, if you are monitoring them, trend upward. Resting heart rate may decline. Recovery between sessions improves. None of these effects are guaranteed at the individual level—individual responses to any training stimulus vary—but they are the expected direction of travel, and the biological mechanisms supporting them are well understood.
The humming addendum: Weitzberg and Lundberg’s 2002 finding about the fifteen-fold increase in nasal nitric oxide during humming suggests a practice worth incorporating on rest days or during warm-up: a minute or two of nasal humming before beginning a session increases the NO bolus in the sinus airstream and may prime the pulmonary vasodilation response. The evidence for this as a performance intervention is indirect and extrapolated from the basic biology rather than from controlled exercise studies. But the practice costs nothing, and the mechanism is real.
The question of tape—specifically, mouth tape worn during sleep or during exercise—comes up inevitably in any discussion of nasal breathing training. The evidence for sleep mouth taping in snorers and mild sleep apnoea patients is modestly supportive: several small studies show improved sleep quality and reduced apnoea-hypopnoea index in individuals who mouth-breathe at night. For daytime exercise application, the evidence is thin. The practical risk during exercise is minimal for healthy individuals with clear nasal airways, but the psychological friction of external compliance enforcement can interfere with developing the intrinsic habit. The Akureyri Protocol does not use tape. The goal is a habit that operates without mechanical enforcement—a mouth that stays closed because the system prefers it, not because it is prevented from opening. External enforcement can train compliance. Internal preference is what endures.
Nasal breathing during weightlifting and high-intensity intervals is a separate question from nasal breathing during rucking. At near-maximal ventilatory demand—during a set of deadlifts at eighty-five percent of maximum, during a forty-five-second Assault bike sprint—the argument for nasal-only breathing weakens because you are operating in the regime where the nasal ceiling becomes relevant. The evidence discussed in this chapter applies to submaximal sustained effort: zone 2, zone 3 at most, for durations measured in minutes to hours. This is exactly the regime that rucking occupies. The distinction matters because confusing the two regimes is what sends people away from nasal training, convinced it is incompatible with serious effort. It is compatible with serious effort. It is not compatible with maximal effort, and it was never claimed to be.
The Governor on Your Face
Return to the trail above Akureyri for a moment. The pack is on your back. The fjord is below, dark and flat in the winter light. The wind is coming off the water. Your mouth is closed.
What you are carrying, along with the pack, is the complete physiological architecture described in this chapter: turbinates warming and humidifying, sinus epithelium producing nitric oxide at concentrations that dwarf any pharmaceutical delivery system, pulmonary vasculature receiving that nitric oxide and responding with the precisely calibrated dilation that your exercise demand requires. Your ventilatory efficiency is twenty-two percent better than if your mouth were open. Your blood lactate is running seventeen percent lower than it would at the same pace with oral breathing. Your autonomic balance is shifted toward the parasympathetic, your diastolic pressure is four millimetres of mercury lower, your HF-HRV is running seven points higher.
None of this requires you to know the mechanisms. The body performs these functions without your supervision. What you are providing is the structural condition for the mechanisms to operate: a closed mouth.
The nose is the body’s rev limiter. It physically prevents you from crossing the ventilatory threshold into glycolytic Zone 3. When you can no longer breathe through your nose, you have exceeded the intensity at which fat oxidation dominates and entered the territory where glycogen burning accelerates, cortisol rises, and the hormonal environment shifts from anabolic to catabolic. The nose does not care about your ego. It does not care about your pace goal. It reports the physiological truth of the moment, and it does so with binary clarity: mouth closed, you are in the zone; mouth open, you have left it.
The biochemistry discussed above—the Bohr effect, the sinus nitric oxide, the PETCO₂ shift—is interesting, and it is real. But it is not the main event for the rucking athlete. The main event is simpler and more ruthlessly practical. Your nose keeps you honest. It enforces the intensity ceiling with a precision that no wearable device has yet matched, because it operates not by measuring a proxy variable and displaying a number for you to interpret, but by making it physically impossible to continue without feedback. You cannot override it. You can only obey it or ignore it, and ignoring it means opening your mouth, which is the data.
The fitness industry has complicated exercise to the point where a person needs an app, a coach, a heart rate monitor, a lactate testing kit, and a periodisation plan to feel confident they are training at the right intensity. The entire apparatus exists, in part, because we have forgotten—or never learned—that the body already contains a precision intensity regulator, one that has been calibrated by three and a half million years of loaded locomotion, one that requires no electricity and has no subscription model.
If you can breathe through your nose at the pace you are going, with the weight you are carrying, on the terrain you are crossing, you are in the zone. If you cannot, you are not. This is not a wellness trend. It is the Bohr effect, pulmonary vasodilation, ventilatory efficiency, and parasympathetic tone, expressed in the simplest possible imperative.
Mouth closed.
The evidence for this is not preliminary. It is not indirect. It is four independent research groups, publishing between 2002 and 2024, reporting consistent effects across lactate, VE/VCO₂, HRV, blood pressure, and nitric oxide delivery, with mechanistic coherence that traces from the basic biology of sinus anatomy through the respiratory physiology of gas exchange to the cardiovascular physiology of vagal tone. The magnitude of each individual effect is moderate rather than transformative. But moderate effects that are real, additive, and cumulative across thousands of training hours are not moderate at all. They are the difference between a body that is being trained carefully and a body that is being trained wastefully.
You were not born breathing through your mouth. You opened it, eventually—probably in infancy, probably in response to some combination of allergen load, recumbent sleeping posture, and the structural changes that follow chronic nasal congestion. You learned to mouth-breathe because the body is pragmatic and because the mouth is there and because no one told you the cost. The cost is now quantified. You can stop paying it.
The fitness industry will sell you something to address nearly every variable in your training. Heart rate monitors. Lactate meters. Continuous glucose monitors. VO₂max testing. Power metres. Recovery wearables that aggregate HRV, respiratory rate, skin temperature, and blood oxygen into a single readiness score that tells you, with questionable precision, how hard to push on any given day. These tools are not without value. Some of them are genuinely useful for understanding patterns that would otherwise remain invisible.
But none of them does what the nasal airway does for free, in real time, with no calibration required, on every session, forever.
The nasal airway is the original wearable. It was built into the architecture of the human face over millions of years of selection for exactly the task you are asking it to perform: regulating ventilatory demand during sustained loaded locomotion. The turbinates are the original air conditioner. The paranasal sinuses are the original nitric oxide diffuser. The nasal resistance is the original respiratory muscle trainer. The inability to comfortably sustain nasal-only breathing is the original zone 3 alarm.
None of this is metaphor. It is anatomy and physiology, described in the peer-reviewed literature, available to anyone willing to read it. The reason most recreational exercisers are unaware of it is not that it is obscure. It is that there is no business model for telling people to close their mouths. No product to sell. No certification to acquire. No protocol to purchase. Just a piece of practical knowledge that happened to require a pandemic, a bestselling book, and a handful of physiologists working in Sweden and Germany and the American Southwest to make its way into a conversation it should have joined decades ago.
The trail is still there. The pack is waiting. The fjord will be cold and flat and the wind will be coming off the water as it always does, indifferent to your physiological optimisation, beautiful in the specific way that things are beautiful when they are simply themselves.
Mouth closed. Pack on. Begin.
The Rule: Nasal inhalation and exhalation only during all rucking sessions. Mouth never opens. If you cannot maintain nasal breathing, slow pace or reduce load.
The Four-Layer Pacing Model:
| Layer | Tool | Signal | What It Tells You |
|---|---|---|---|
| 1. Nasal breathing | None required | Comfortable nose breathing = sustainable | Baseline filter. Below the ventilatory threshold. NO benefits active. Stay here. |
| 2. Talk test | None required | Full sentences = at/below VT; laboured speech = above VT | Threshold detection. When nasal breathing breaks down, speak a full sentence. If you can’t, slow down. Every 10–15 min, check. |
| 3. Heart rate | HR monitor | 60–75% of age-predicted max | Objective confirmation. Confirms Layers 1–2, catches cardiac drift during long efforts. Especially valuable in heat. |
| 4. RPE | None required | Borg 11–14/20 | Integrative check. Captures what breathing and HR miss—musculoskeletal discomfort, thermal strain, general fatigue. |
Layer 1 is the default. Layer 2 activates when Layer 1 fails. Layers 3–4 confirm and refine. Blood lactate (< 2 mmol/L) remains the gold-standard laboratory confirmation of Zone 2, if measurable.
Adaptation Timeline:
- Weeks 1–4: Uncomfortable. Pace drops 20–30%. Normal.
- Weeks 4–8: Threshold rises. Discomfort recedes.
- Month 6+: Full adaptation. No VO₂max deficit vs oral breathing.
Cold Weather: Thin buff over nose below -5°C.
Illness/Allergies: Protocol pauses. Resume when airway is clear.
Humming Warm-Up: 1–2 minutes of nasal humming before sessions. Increases sinus NO output ~15-fold (but note: NO production drops 47–76% during heavy exercise—the benefit is primarily at easy-to-moderate intensities).
The Gate: Only increase load or pace when you can complete the full session without breaking nasal breathing. Beginners: reach the gate by progressing through rest, then unloaded walks, then light load (~5% BW), then 10% BW before adding more. CO₂ tolerance improves within 2–4 weeks. You will reach the gate. Move through it when you do.