The Soberg Principle: Why Ending on Cold Matters

The Søberg Principle is a practical guideline for contrast therapy stating that you should end your session on cold rather than warm. Named after Danish researcher Susanna Søberg, the idea is straightforward: when you alternate between heat (like a sauna) and cold (like a cold plunge), finishing with cold forces your body to burn energy reheating itself without external help. That metabolic work, driven largely by brown adipose tissue, is where much of the claimed benefit lives. The principle has gained wide popularity in wellness and biohacking circles, but the underlying physiology is more layered than a single rule suggests.

Why Ending on Cold Matters

The core logic of the Søberg Principle rests on what happens after you get out of cold water. Your body does not passively drift back to its normal temperature. Rewarming is an active, energy-hungry process. Research on post-cold-water-immersion recovery shows that the rewarming period is non-linear and metabolically costly, with oxygen consumption in body regions that were not even submerged rising significantly above baseline due to thermogenesis.¹ In other words, your body does not just warm up from the outside in. It actively generates heat internally, and that costs calories.

If you end on warm instead, say by stepping into a hot shower or sauna after your cold dip, you hand that rewarming job to the external heat source. Your body no longer has to do the metabolic work. The Søberg Principle argues that you are leaving benefits on the table by doing this. The metabolic rate during global rewarming after cold exposure has been measured at roughly double the resting metabolic rate, and that elevation persists until tissue temperatures recover.² While that particular measurement comes from king penguins (which are built for extreme cold tolerance), the directional finding aligns with what human studies show about the energetic demands of rewarming.

So the principle is less about cold exposure itself and more about what your body does afterward. The cold is the stimulus; the rewarming is where the metabolic payoff occurs. Jumping into a warm environment right after cold exposure short-circuits that process.

Brown Fat and the Heating Engine

The tissue most responsible for the rewarming effect is brown adipose tissue, commonly called brown fat. Unlike regular white fat, which stores energy, brown fat burns it to produce heat. It does this through a protein called UCP1, which essentially uncouples the normal energy-production process in mitochondria so that chemical energy is released as warmth instead of being stored. In mice, UCP1 has been shown to be the only protein capable of mediating the adaptive non-shivering thermogenesis that improves with cold acclimation. No alternative pathway can take over when UCP1 is absent.³

Cold exposure ramps up metabolic activity in brown fat dramatically. The glycolysis pathway, which breaks down glucose for energy, is enhanced as a direct consequence of UCP1-mediated thermogenesis, as demonstrated in mouse studies comparing normal and UCP1-deficient animals.⁴ In humans, brown fat is found mainly around the neck, collarbones, and along the spine, and its activity varies significantly between individuals. Proponents of the Søberg Principle argue that by ending on cold, you are essentially training this tissue to activate more robustly and frequently.

Cold also triggers changes at a deeper cellular level. In skeletal muscle and white fat, exposure to cold increases expression of PGC-1α, a key regulator of mitochondrial biogenesis, meaning the body creates more mitochondria in response.⁵ When exercise and cold exposure are combined, the PGC-1α response can actually be amplified beyond what either stimulus produces alone.⁶ This has led some researchers to suggest that strategic cold exposure may enhance certain metabolic adaptations to exercise, though the timing matters considerably, as we will see.

Where Heat Fits Into the Protocol

The Søberg Principle is not exclusively about cold. It typically involves alternating between sauna or hot bath sessions and cold immersion. The heat component carries its own set of physiological effects. Chronic, repeated use of hot baths or saunas has been linked to improvements in cardiovascular health through a growing body of research.⁷ These benefits include improvements in blood vessel function, reductions in blood pressure, and favorable shifts in blood lipid profiles.

On the lipid front, a study of physically active young men found that a three-week sauna program significantly decreased total cholesterol and LDL cholesterol, with the improvements persisting into the week following the last session.⁸ Triglycerides also dropped measurably after individual sessions. Heat therapy has also been proposed to improve insulin sensitivity through mechanisms that overlap with those of aerobic exercise, including boosting nitric oxide production in blood vessels.⁹ In diabetic patients specifically, sauna use has been shown to accelerate insulin absorption from injection sites and lower blood glucose concentrations by a meaningful margin.¹⁰

The contrast between heat and cold is thought to amplify the cardiovascular challenge. Alternating sessions cause blood vessels to dilate then constrict, heart rate to rise then fall, and blood pressure to shift in both directions. In a study of normotensive women cycling through Finnish sauna heating and cold water immersion, systolic blood pressure rose during the first heating session and fell progressively across subsequent heat exposures, while heart rate was significantly elevated during all heating sessions.¹¹ The cardiovascular system essentially gets a workout from the thermal stress alone.

Cold and Your Nervous System

Beyond metabolism, cold exposure produces measurable changes in the autonomic nervous system, specifically by activating the parasympathetic branch, sometimes called the “rest and digest” system. Cold applied to the skin triggers what researchers call cardiac-vagal activation: a slowing of heart rate and an increase in heart rate variability, both of which are markers of a healthy, resilient nervous system. Cold stimulation on the lateral neck in particular produced significantly higher heart rate variability and lower heart rate compared to a control condition in a randomized trial.¹²

This parasympathetic response is part of what makes cold exposure feel calming after the initial shock. Facial cooling in particular activates the dive reflex, a set of involuntary responses that include substantial heart rate drops. Research using a facial cooling mask during psychosocial stress testing found peak heart rate reductions of roughly 20 to 27 percent during cold application, with accompanying increases in parasympathetic markers.¹³ The effect lessened somewhat with repeated stress cycles, but remained present throughout.

Even cold water ingestion, not just immersion, triggers autonomic shifts. Drinking cold water decreased heart rate by about 9 percent and increased a key heart rate variability measure by more than 40 percent, with responses peaking within 17 to 30 minutes. A second cold drink produced additional but attenuated responses, with shorter recovery times, suggesting the body begins adapting even within a single session.¹⁴

This nervous system activation is one reason some advocates of the Søberg Principle frame ending on cold as a resilience practice, not just a metabolic one. Brief, controlled cold stress appears to promote adaptive tuning of the brain’s arousal systems, potentially blunting hyperreactivity over time and offering benefits for mood and anxiety regulation.¹⁵

The Timing Problem With Exercise

If you train with weights and want to build muscle, the Søberg Principle creates a genuine tension. Cold water immersion after resistance training blunts some of the molecular signals that drive muscle growth. Research has shown that key muscle-building signaling molecules are significantly less activated after cold immersion compared to active recovery. One study found that a critical anabolic signaling marker was 90 percent higher after active recovery compared to cold water immersion at two hours post-exercise, and 60 percent higher at 24 hours.¹⁶

A separate study confirmed these findings over a longer training period, showing that cold water immersion blunted both anabolic signaling and actual muscle fiber hypertrophy, though interestingly, maximal strength gains were not significantly impaired.¹⁷ The mechanism appears to involve both reduced protein building and increased protein breakdown in cold-exposed muscle. So if your primary goal is gaining muscle size, cold immersion right after lifting works against you. Strength gains seem more resilient to the interference, but hypertrophy clearly takes a hit.

Most practitioners who follow the Søberg Principle and also lift weights try to separate their cold exposure from their training by at least several hours. The principle itself does not require immediate post-workout cold; it only requires that your contrast session ends cold rather than warm. Doing your sauna-cold cycle in the morning and lifting in the evening, or on separate days entirely, sidesteps the conflict.

Sex Differences in Cold-Induced Thermogenesis

How much metabolic benefit you get from ending on cold is not uniform across people, and sex is one of the major variables. Women, particularly pre-menopausal women, tend to have a stronger cold-induced thermogenic response than men. One study found that cold-induced thermogenesis was significantly higher in women, and that estradiol levels were positively associated with this response regardless of age, sex, or body fat percentage.¹⁸ Intriguingly, this advantage was not static across the menstrual cycle. During the luteal phase, women’s cold-induced thermogenesis dropped to levels similar to men’s.

Brown fat temperature responses tell a complementary story. Women showed greater adaptive brown fat temperature responses to cold than men overall, but during the follicular phase, the increase in brown fat temperature during cold exposure was diminished compared to both men and women in the luteal phase.¹⁹ The relationship between sex hormones and brown fat activity is clearly complex, and it means that the metabolic return on cold exposure fluctuates for women in ways that it does not for men.

Your Brown Fat Changes With the Seasons

Brown adipose tissue does not operate at the same level year-round. People who had serial imaging scans showed dramatic seasonal swings in brown fat activity, with average activity roughly six times higher in January than in July. Surprisingly, this variation tracked more closely with day length than with outdoor temperature, suggesting that seasonal light exposure plays a role in regulating brown fat beyond just ambient cold.²⁰

Cold-induced thermogenesis itself follows a seasonal pattern. In people with metabolically active brown fat, the extra calories burned during cold exposure increased substantially from summer to winter, averaging about 186 extra kilocalories per day in winter versus about 18 in summer. People with low brown fat activity saw a much smaller seasonal shift.²¹ Winter also appears to make brown fat more efficient at its job, with greater heat output from the supraclavicular region (where brown fat concentrates) during mild cold in winter compared to summer, even without an increase in overall metabolic rate.²²

For anyone following the Søberg Principle, the practical implication is that the metabolic payoff of ending on cold is likely greater in winter than in summer. Your brown fat is already primed by shorter days and cooler ambient temperatures. In summer, you may still get autonomic and psychological benefits from cold exposure, but the raw calorie-burning effect is muted.

Does the Body Stop Responding Over Time

One concern with any deliberate cold practice is habituation. If your body adapts to the cold, does it stop generating as much heat, effectively erasing the metabolic benefit the Søberg Principle depends on? The answer is nuanced. Cold habituation does occur with repeated short, mild exposures, and it manifests as reduced shivering, higher skin temperatures during cold, and diminished perception of cold.²³ These changes actually serve a useful purpose: they help protect peripheral tissues and conserve energy during non-threatening cold stress.

But habituation and metabolic adaptation are not the same thing. The reduction in shivering that comes with habituation is partly offset by increased non-shivering thermogenesis from brown fat, which actually becomes more active with repeated cold acclimation. This is the adaptation the Søberg Principle is trying to cultivate. You shiver less, but your brown fat works harder. The cold feels less miserable while the internal furnace burns hotter. Whether this net effect remains stable over months or years of practice is harder to say with certainty, as most cold acclimation studies run for weeks, not years. But the seasonal data showing persistent brown fat activity in winter across repeated years of scanning suggests the system does not simply shut off from overexposure.

Sleep After Cold Immersion

An effect that gets less attention in discussions of the Søberg Principle is what cold exposure does to sleep. In well-trained male endurance runners, whole-body cold water immersion increased the proportion of slow-wave sleep (the deepest, most restorative stage) during the first three hours of the night compared to partial immersion. Both whole and partial immersion reduced arousals throughout the night, and whole-body immersion additionally decreased limb movements during sleep.²⁴ Deeper cold exposure appeared to produce a more pronounced improvement in sleep architecture.

This makes intuitive sense in the context of thermoregulation. Your core body temperature naturally drops as you fall asleep, and cold exposure in the hours before bed accelerates that decline. For people who practice the Søberg Principle in the evening, ending on cold could enhance this natural temperature dip and facilitate faster, deeper sleep onset. Whether this holds true for people who are not elite athletes is uncertain, as the study population was quite specific, but the direction of the finding aligns with broader thermoregulation research on sleep.

What the Principle Does Not Address

The Søberg Principle is a useful heuristic, but it leaves several things unspecified. It does not prescribe water temperature, immersion duration, number of contrast cycles, or the ratio of hot to cold. These variables all matter. A 30-second splash under cool water is not physiologically equivalent to three minutes in water near freezing. The principle also does not account for individual variation in brown fat quantity, body composition, cold tolerance, or cardiovascular health. People with very little brown fat, older adults, or those with uncontrolled hypertension face different risk-benefit calculations than a healthy 30-year-old with abundant brown fat.

The cardiovascular demands of contrast therapy are real. Rapidly alternating between vasodilation in the sauna and vasoconstriction in cold water stresses the heart and blood vessels. While this appears to be beneficial for healthy people, the acute blood pressure swings documented during sauna-cold cycling are not trivial.²⁵ Anyone with a heart condition, uncontrolled blood pressure, or a history of fainting episodes should consult a physician before adopting this practice. The principle’s viral popularity sometimes obscures the fact that what it describes is a significant physiological stressor, and stressors require a body capable of handling them.