Caffeine can potentially enhance the dopamine-mediated effects of cold exposure, which works at least in part by increasing the amount of dopamine-receptor availability in the brain. In a 2015 trial that investigated caffeine's effect on dopamine receptors, increased dopamine receptor availability was observed 60 to 120 minutes after the participants took a single 300-milligram dose of caffeine.^[28] Because cold exposure actually increases dopamine levels,^[3] the results of the 2015 trial suggest that taking a similar dose of caffeine 60 minutes before cold exposure could enhance some of its dopamine-related benefits.

Capsinoids such as capsaicin — the component of chili peppers that makes them hot — can both mimic and enhance cold-exposure-induced thermogenesis.^[29][30] Capsaicin mimics the effects of cold exposure on thermogenesis in brown adipose tissue (BAT; a type of body fat) by activating the transient receptor potential (TRP) channels, a specialized group of ion channels that span the cell membranes and transmit information about environmental changes such as touch, temperature, and pain to the brain.^[31] Capsaicin activates TRPV1, one of the TRP receptors that senses cold, which causes the brain to increase BAT activation through the sympathetic nerves connected to BAT and triggers thermogenesis in this tissue.^[29][32]

The efficacy of capsaicin in increasing energy expenditure through BAT activation may depend on the presence of active BAT because participants without active BAT in one trial did not have significantly increased energy expenditures after a single dose of capsaicin.^[33] However, another trial found that taking a single 9-milligram dose of a capsinoid extract for 6 weeks increased cold-induced thermogenesis in participants with low BAT activity.^[34] Additionally, a study in rodents found that daily capsinoid ingestion in combination with mild cold exposure at 17°C (63°F) enhanced the beiging of white adipose tissue (WAT; another type of body fat), which prevented obesity in animals that were fed an experimental high-fat diet.^[35] Although the ability of capsaicin to enhance WAT beiging in humans is uncertain, an cell-culture study published in 2022 confirmed that capsaicin induces the beiging of human white adipocytes that were derived from dermal fibroblasts (a type of skin cell) and were growing in culture.^[26] Given the ability of capsaicin to induce beiging in human fat cells growing in culture, capsaicin may have the potential to enhance WAT beiging in the human body. However, randomized controlled trials specifically designed to test for this in humans are needed.

Because norepinephrine levels play a significant role in depression,^[36] cold exposure has been investigated for some time as an additional treatment alongside standard therapies.^[37] The results to date have been encouraging. After adults diagnosed with depression were exposed to 10 cryotherapy sessions in a randomized controlled trial, significant improvements were noted in depression symptoms, disease acceptance, quality of life, and self-assessed mood.^[38] These results are consistent with reports of similar results from additional trials.^[39][37][40] Although promising, the studies on cold exposure and depression to date have been less rigorous and tend to involve small numbers of participants and short follow-up periods. More research is needed to determine the long-term efficacy and optimal cold exposure protocols for different populations.^[40]

Some small trials on cold water immersion found that cold exposure can increase insulin sensitivity^[41] and reduce fasting insulin levels.^[42][43] However, these studies all involved small numbers of participants and either were observational in design^[42][43] or lacked blinding and randomization.^[41] Although the research is potentially promising, more rigorous studies are needed to validate these results and to determine whether the effects are clinically relevant. If future studies on cold exposure do end up confirming a significant effect on glucose metabolism, its effect on glucose homeostasis may occur through the increased production of adiponectin, an agent with insulin-sensitivity-enhancing effects.^[44]

Trials that tested the effects of cold exposure on body weight and fat loss have reported inconsistent results,^[45] and the long-term efficacy of cold exposure interventions on obesity has yet to be established.^[46]

Although research to date points toward a lack of efficacy for cold exposure as a stand-alone long-term weight loss intervention, there have been promising results over smaller timescales. In a randomized controlled trial with 51 participants, 2 hours of daily cold exposure at 17°C (63°F) for 6 weeks resulted in increases in energy expenditure, thermogenesis, and brown adipose tissue (BAT) activation that resulted in a significant amount of fat loss compared to the control participants who were not exposed to the cold.^[34] Because people with overweight or obesity tend to have lower amounts of BAT^{[47][48][49][50][51][52]} and cold exposure interventions may improve metabolic health through the expansion of BAT stores and increased nonshivering thermogenesis,^[45] more research is warranted to determine whether cold exposure could be helpful alongside other interventions that target obesity.

It’s important to make the distinction between recovery and adaptation when considering the effects of cold water immersion postexercise. Part of the stimulus for muscle adaptation to any type of exercise involves damage to the local tissues, to a certain degree, which triggers an inflammatory response and frequently delayed-onset muscle soreness, which results in a temporary reduction in strength and range of motion.^[53][54] Recovery is the process of restoring normal function after the training stimulus, such as repairing tissue damage and replenishment of fuel stores. In contrast, exercise adaptation is a longer-developing process that involves physiological changes that better equip the body to handle similar types of training stress in the future. Examples of exercise adaptation include the development of larger, stronger muscles from weight training or the development of increased endurance from endurance training such as running, cycling, or swimming.^[55]

We consider the effects of postexercise cold water immersion on adaptation from weight training and endurance exercise separately below.

Weight training: Postexercise cold water immersion has a suppressive effect on gains in strength and muscle mass from weight training,^{[56][57][58][59]} so it should be avoided for at least several hours after weight training. Although research to better understand the mechanisms involved is still ongoing, cold water immersion seems to have a suppressive effect on the short-term anabolic (muscle-building) signaling processes that are important for triggering longer-term muscle adaptations.^[56]

Endurance exercise: In contrast to the clear suppressive effect on muscle adaptations after weight training, most studies have found that cold water immersion has negligible effects on adaptation from endurance exercise.^{[59][60][61][62]}

Cold exposure can potentially cause heart attacks in certain individuals. The cold-shock response activates the sympathetic (“fight or flight”) nervous system, which increases the heart rate and blood pressure. Although this response is important for preserving core body temperature in the cold and is well tolerated by individuals without apparent health conditions, the sudden increase in stress on the heart could potentially cause a heart attack in people who may be vulnerable.^[67][27]

Vulnerable individuals also may be at an increased risk for sudden cardiac death when the face is submerged during cold water immersion. Although cold water immersion typically involves immersion up to the chest or neck, which triggers the cold shock response and activates the sympathetic nervous system, full-body submersion, in which the face is under water, also triggers the “diving response,” which slows heart rate through a parasympathetic (“rest and digest”) nervous system response. The conflicting signals coming from the two limbs of the autonomic nervous system to the heart have been proposed to cause an “autonomic conflict”, which could potentially cause sudden cardiac death in vulnerable individuals.^[24] Although this has yet to be proven, cold water submersion is known to increase the incidence of cardiac arrhythmias in individuals without known health conditions,^[68][69][70] and it has been proposed that sudden cardiac death may at times be the actual cause of deaths from cold water submersion that were previously attributed to drowning or hypothermia.^[24]

Because the types of fat cells (adipocytes) that make up white adipose tissue (WAT) come from a different developmental lineage than the brown adipocytes in brown adipose tissue (BAT), the cells in WAT can’t transform into brown adipocytes.^[63] However, in response to regular cold exposure, the adipocytes in WAT undergo a transition to a thermogenesis-capable state by expressing some of the same proteins that facilitate heat production in BAT, such as uncoupling protein 1 (UCP1, also known as thermogenin).^[64] The cold-adapted white cells appear light brown in comparison to their non-cold-adapted counterparts and are often referred to as “beige” adipocytes due to their darker color. Papers in the research literature commonly refer to the cold adaptation process in WAT as “beiging” or “browning”.^[65]

Although the intense shivering that is induced by unaccustomed cold exposure can cause significant increases in the metabolic rate, shivering isn’t necessary to get a metabolic boost from cold exposure. In one study, participants who were exposed to mild cold (66°F/19°C) for 10 hours every night for a month had a 42% increase in brown fat volume and a 10% increase in fat metabolic activity.^[6] Although the participants in that particular study resided in a clinical research unit for the duration of the study, which allowed the researchers to test a specific set of conditions that may not reflect those of free-living humans, it is clear that humans acclimate to cold temperatures in part through increased brown adipose tissue activity and nonshivering thermogenesis.

Additionally, with regular cold exposure, shivering thermogenesis (ST) attenuates (decreases over time with exposure) and nonshivering thermogenesis (NST) increases.^[66] The transition from ST to NST can occur relatively fast, as noted in the above study, in which daily cold water immersion for 1 hour in 14°C (57°F) water reduced shivering thermogenesis by 20% without a change in total heat production.^[66]