Stresses in Scuba and Breath-Hold Diving

  • Dr. Joe Alcock, MD, MSCr, FAAEM; Dr. Satkirin Khalsa, MD; and Dr. Michael Strauss, MD, FACS, AAoS
  • Volume 06 - Issue 3

This series of Wound Care and Hyperbaric Medicine has focused on the various physiological and psychological stresses that affect divers. This section concerns the travel and surface stresses affecting divers in the predive phase of a dive trip. We will review the behavioral and physiological responses to travel and jet lag, travel-related infections, and sun and heat disorders. We will also discuss the most common cause of death for travelers on dive trips: cardiovascular disease. We suggest ways to mitigate these stresses to improve the health of divers and allow them to get the most out of their dive experience.

Travel Stresses

Divers frequently travel long distances to dive locations. Travel itself can be experienced as pleasurable or stressful or both, although recent studies suggest that air travel in particular is often experienced as a negative and stressful experience.1,2 Features that predict air-travel stress include (a) anxious reactions to air-travel events, (b) negative interactions with other travelers, and (c) a lack of trust in the ability of airlines/airports to provide comfort and safety.1 Travel itself can elicit a physiological stress response involving sympathetic nervous system activation and cortisol production.3

Laboratory simulations of long-haul flights, using crowded conditions and hypobaric or normobaric hypoxia, have been shown to result in increased stress catecholamines, transient immune impairment, sleep disturbance, fatigue, and mood changes.4-6 Although aircraft pressurization and crowding are unlikely to change, careful planning and other coping strategies can mitigate the adverse effects of travel. Successfully resolving these stresses can increase the pleasure from diving and leisure activities, the enjoyment of which has been associated to increased psychological and physical well-being.7

Just as safety concerns can add to air-travel stress, the safety capabilities of dive boats can raise concerns. Most North American dive operators have sophisticated navigation, emergency communication, and safety equipment on board. In developing worlds, where many popular diving destinations are located, a wide degree of variation may be observed for boat maintenance, communication capacity, and safety and emergency medical equipment. Combined with language barriers, these features can vastly influence whether a dive trip is experienced as stressful or pleasurable.

Is Jet Lag an Issue for Divers?

Jet lag is an underappreciated source of stress that can affect a dive trip. Circadian rhythm disruption and jet lag are often unavoidable during long-distance travel over many time zones. The normal pattern of sleep involves an eight-hour sleep cycle with cycles of REM and deeper sleep. The normal timing of sleep is determined by circadian physiology and circadian stimuli known as zeitgebers (“time givers” in German). The most important zeitgeber is light exposure, which sends signals to the suprachiasmatic nucleus (SCN). Output rhythms from the SCN affect physiology and behavior, including the timing of sleep. Changes in light exposure accompanying travel over many time zones causes circadian disruption and sleep loss, as well as daytime sleepiness.8

Sleep restriction causes weight gain and is linked to systemic inflammation. Long-term sleep loss has been associated with a variety of chronic diseases, including hypertension, increased risk of cardiovascular events, and cancer.9 In the shorter term, circadian disruption is associated with mood disturbances, impairment of concentration, and mental fatigue.10 These occur with sleep of shorter duration and increased awakenings, both of which are described in jet lag. Jet lag can induce depressive symptoms that can be treated or prevented with melatonin and melatonin analogs.11 Findings indicate that even a one-hour change in sleep duration can make a big difference.9

The stress of jet lag can be ameliorated by several modalities. Melatonin taken at the sleep time of the destination for several days prior to travel has been shown to make a difference in acclimatization to the new time zone.8 Mainly, recovery from jet lag is accomplished with exposure to daytime light to provide circadian input to the brain and suprachiasmatic nucleus.

Does Stress Predispose Divers to Decompression Illness?
Besides determining whether a trip is pleasurable or not, physical and psychological stresses have hematologic and immune effects that may alter the risk of decompression illness (DCI). Increased DCI from emotional stress has not yet been demonstrated, but evidence suggests a plausible mechanism for such a link.
1. Emotional stress and sleep disturbance are linked with platelet activation, resulting from increased exposure to the catecholamine stress hormones norepinephrine and epinephrine.14
2. Catecholamines, e.g. epinephrine, are well-known stimuli of platelet activation and aggregation when microbubbles are present.15
3. Platelets are critically important in promoting thrombosis from bubbles during decompression illness.15 Bubbles cause platelet aggregation and clotting in animal models of decompression16,17and in humans18 after decompression, platelet adhesiveness increases, free platelet counts decreases, antithrombin III activity decreases, fibrinolysis increases, all markers of a hypercoagulable state16 (Figure 1). In addition to promoting thrombosis, bubbles activate immune pathways that induce inflammation,19 exacerbating tissue damage during DCI.20,21
Because bubbles and catecholamine exposure are potent activators of platelets, travel stresses outlined in this section have the potential to increase harm from activated platelets in DCI. a model showing this hypothesized mechanism is shown in Figure 2. Whether stress hormones worsen DCI has yet to be proven. Either way, it probably makes for a more enjoyable dive when stress and stress hormones are low.


Two other stimuli that have been recognized as important for entraining circadian rhythm are social activity and food. Socializing during the day hours also helps entrain a new circadian rhythm. A nap can reduce jet lag and help adjust the circadian rhythm if daytime sleep is not excessively long. Exercise, especially outdoors, is recommended.12 Yoga and meditation can also help resolve the stress of travel and time change. Finally, an increasing body of work has linked the gut and intestinal microbes to circadian rhythm and the physiological changes seen in jet lag.13 Recovery from jet lag may occur faster by eating at mealtimes appropriate for the new time zone, ensuring adequate dietary fiber, and by avoiding a high-fat diet and excessive alcohol.8

Figure 1. Activation of platelets and clotting by bubbles


Gas bubbles activate immune cells, complement, and platelets, causing a hypercoagulable state.



Figure 2. A model for how exposure to stress hormones interact with bubbles to increase risk for DCI


Nitrogen bubbles interact and stress catecholamines (epinephrine) activates platelets, white blood cells, and endothelial cells, resulting in vasoconstriction, microvascular hemostasis, and tissue hypoxia in DCI.


Figure 3. Yoga for divers


Yoga and breathing exercises (usually performed above water!) are a good way to resolve diving and travel stresses.


Travel Medicine: What’s New in Travel-related Disease?

One important concern for travelers is the potential exposure to travel-related diseases. Because travel medicine risks vary by location, the reader is urged to consult CDC Health Information for International Travel (“The Yellow Book”) before planning a dive trip.22 Because of space constraints, we limit this discussion to travelers’ diarrhea and the mosquito-borne diseases dengue fever and chikungunya. Adequate preparation for these infectious threats can help prevent a trip-ending illness.

Travelers’ Diarrhea

Gastrointestinal upset and diarrhea are common infectious complications that can occur to any traveler in the predive stage or at any other time on the trip. Travelers’ diarrhea (TD) occurs in 30-50% of travelers and may be exacerbated by dietary changes, exposure to infectious disease, as well as physiological stress of travel and jet lag. TD is most often caused by enterotoxigenic E. coli (ETEC). ETEC and other bacteria account for 80-90% of TD. Campylobacter is a common cause of TD in some destinations, including Thailand. Other causes include the protozoan Giardia intestinalis, responsible for a more indolent and persistent diarrheal illness. A notable viral cause of TD is norovirus, which causes epidemic gastroenteritis among travelers, including passengers on cruise ships.

Uncomplicated TD does not involve fever or bloody stool and is generally a self-limited disease. While self- limiting, TD is common, debilitating when present, and can potentially ruin a diving trip. In particular, TD is often associated with dehydration, which puts divers at risk for decompression illness (DCI).

Travelers can prepare for the eventuality of TD by bringing antibiotics, preventative medications, and antidiarrheals (Table 1). Ciprofloxacin reduces the duration of symptoms, although increasing resistance to this medication has been reported. In locations with high ciprofloxacin resistance, the nonabsorbed antibiotic rifaximin is an alternative.26 Travelers should be aware that resistance to rifaximin in E. coli also has been reported recently.27 Azithromycin is safe for treatment of TD in pregnant women and children. Besides these prescription medications, over- the-counter bismuth preparations such as Pepto Bismol® have been shown to help prevent and reduce symptoms of TD.28 Probiotics, such as lactobacilli, also have proven effectiveness and should be considered for prevention of TD.28,29 If symptoms appear, an antimotility agent such as loperamide is reported to be safe for TD and may prove essential when a bathroom is unavailable.30 Loperamide and Lomotil® should not be used if fever accompanies diarrhea. Antimotility agents also are not recommended for children. Oral hydration with solutions such as Pedialyte® is helpful for bacterial TD and is the main treatment for epidemic norovirus gastroenteritis.


TABLE 1. Medications for Travelers' Diarrhea
Trimethoprim/sulfamethoxazole Treatment of TD antibiotic resistance is common. Not recommended for prevention.
Ciprofloxacin Treatment of TD antibiotic resistance is increasing. Not recommended for prevention.
Rifaximin Treatment of and possible prevention of TD antibiotic resistance is emerging. May be used for prevention. Expensive.
Bismuth subsalicylate Treatment and prevention of TD Over the counter. Recommended.
Probiotics Prevention of TD May also be used for treatment
Oral fluid replacement Treatment of TD Pedialyte® of equivalent. Ideal for viral diarrhea.


Dengue Fever and Chikungunya Infection

Mosquito-borne viral diseases are common and increasing in frequency in many popular diving destinations, especially the Caribbean.23 Dengue fever is caused by an arbovirus carried by the mosquito Aedes aegypti, resulting in between 50-100 million cases per year. Sufferers develop a fever and an erythematous macular rash that soon becomes confluent. The common name for dengue disease is “breakbone fever,” which, as the name suggests, involves myalgias and arthralgias as well as headache. This classic presentation is seen mostly in adults; children can have a mild flu-like or asymptomatic presentation. More rarely, dengue infection can progress to dengue hemorrhagic fever, resulting in thrombocytopenia, vasculitis, capillary leak syndrome, and shock.24 Unfortunately, no vaccine or specific treatment is available; fluid therapy and supportive care are mainstays of treatment.

Another increasing problem at many diving destinations is chikungunya virus, carried by the same mosquito that transmits dengue.25 Chikungunya transmission was unknown in the New World until 2013. Since then, chikungunya infections have reached epidemic proportions in most Caribbean islands.23 In the United States, most cases are seen in returned travelers, although sporadic cases of endemic transmission have been reported.


Solar Injury FAQs
1. What is sunburn?
Sunburn erythema is a cutaneous inflammatory response accompanied by DNa damage and cytotoxicity. Microscopy may reveal edema, vasodilation, and endothelial cell swelling. “Sunburn cells” have enlarged nuclei and vacuolated cytoplasm, appearing several hours after exposure.32 Histamine is released, and mast cells degranulate, contributing to the warmth, pain, and discomfort of sunburn.
2. Besides sunscreens, what can mitigate sunburn?
Antioxidants given before, but not after, exposure can decrease erythema, but their effect on DNa damage is unknown. a majority of randomized trials have concluded that topical NSaIDs, antihistamines, and oral steroids are ineffective, shortening the duration of sunburn.33
3. What is the MED?
MED stands for mean erythema dose and is the smallest amount of UVR, generally UVB, that can cause discernable dermal erythema. MED is often measured in time. For example, MED may be 20 minutes of exposure in a fair-skinned person. DNa absorption of UVB correlates with extent of erythema.
4. What is a tan?
Immediate pigment darkening occurs from melanin precursors that are preformed, generally in darker- skinned people. Delayed pigment darkening occurs from UVB and UVa (mostly UVa) when melanocytes proliferate and melanin synthesis occurs.
5. Is the age of solar exposure important developing skin cancer?
yes. australians who arrived from Britain younger than 18 have high rates of basal cell carcinomas.
If they arrived older than 18, immigrants to sunny australia had skin cancer rates similar to their British counterparts.34 Intermittent exposure to sun, fair skin, and red hair are risk factors for skin cancer.
6. Does high cumulative lifetime exposure to uVr cause melanomas?
Increased occupational exposure over a lifetime decreases the risk of melanoma, the most deadly form of skin cancer. Lower latitude and intermittent high doses of UVR, especially at young ages, correlate with melanoma risk. Melanoma is associated with increased number of nevi; nevi numbers increase with childhood UVR. Whether regular sunscreens reduce melanoma and other skin cancers is uncertain and remains controversial. Sunscreens have not conclusively been shown to reduce the risk of melanoma or other cancers.35,36

Originally from Africa, chikungunya is a risk for travelers to that continent, as well as to the Indian Ocean and Western Pacific. In addition to sharing the same vector as dengue, chikungunya causes a similar clinical syndrome to dengue fever. A high fever and myalgias are common. Incapacitating joint pains are often prominent in chikungunya disease. Joint pains may last for weeks or months after the initial infection. Treatment, which involves rest and fluids, is directed at symptoms of the disease. Preventing bites from mosquitoes by using permethrin clothing, DEET-containing repellents, and screened air-conditioned rooms reduces the risk of both dengue and chikungunya.

Solar Injury

Sun exposure causes sunburn, one of the most common conditions experienced by divers. Sunburn is more common in light-skinned individuals, but all divers should take measures to protect their skin and eyes from the sun.

Clearly, solar radiation is not all bad. Some UV exposure is important, because lack of UV inhibits vitamin D production in the skin and can lead to deficiency syndromes such as rickets. Vitamin D and exposure to the sun are linked with a reduced risk of a variety of chronic diseases, including cardiovascular disease, diabetes, and cancer. On the other hand, solar ultraviolet radiation (UVR) causes sunburn and eye injuries that can commonly affect divers and other travelers.

UVR comes in two varieties relevant to human health. UVB measures 290-320nm in wavelength and is responsible for vitamin D production from 7-dehydroxycholesterol via the skin, liver, and kidney. UVB also causes tanning, burning, and some skin cancers. UVA has longer wavelengths (320- 400nm) and contributes to photoaging, tanning, burning, and cancers. UVA is also responsible for the phototoxicity of certain pharmaceuticals.

The amount of UVA and UVB that reaches the skin is affected by time of day, season, and clouds. The majority (65%) of UVR falls between 10 a.m. and 2 p.m., so efforts to protect skin from the sun should focus on those hours. Season is also important. In northern latitudes, June has 100 times more UVR than December. Latitude makes a difference in UVR exposure, with higher intensity in tropical locations.31 As one moves away from the equator, UVR decreases 3% with every degree of latitude. Additionally, surface features such as water and sand reflect UVR. Areas such as the chin, lips, and nose may require protection from reflected light. Albedo is the reflection of solar radiation from white objects, especially snow, reflecting as much as 85% of visible light and UVR. Compared with snow, water reflects less UVR. Clouds attenuate UV radiation by 20-80%, generally 40%, which may not be enough to protect from sunburn.


1. What is the meaning of SPF?

SPF stands for skin protection factor. SPF is calculated by the ratio of MED (mean erythema dose) — measured in time — of skin with sunscreen divided by the MED of unprotected skin.

SPF = MED protected skin

         MED unprotected skin

2. What number SPF should I look for? Is higher better?

SPF 15 blocks 93% of UVB. So, in theory, it should be fine. However, in practice the SPF may be much lower than advertised because of sweating, abrasion, inadequate application, etc. So a higher SPF gives a bigger margin of error. Several real-world and clinical studies suggest that using higher SPF (at least SPF 30) gives increased protection — at least from sunburn.

3. Does the DEET in insect repellant affect my sunscreen?

yes, DEET reduces the efficacy of sunscreen by about 30%. This is another argument for higher SPF sunscreens. In endemic areas, there is a trade-off between mosquito protection (e.g., chikungunya risk) and sunburn protection.

4. How do sunscreens work?

Sunscreens have two mechanisms of action. Physical blockers are generally metals (e.g., zinc or titanium) that reflect and scatter UV radiation away from the skin. These physical agents often appear visible (e.g., white, yellow), but newer micronized formulas are transparent on skin but still reflect/scatter UVR. Physical agents are effective on both UVa and UVB.

The second way that sunscreens work is via chemical agents that absorb solar radiation. These are the most common active ingredients in sunscreens. They are often degraded by the process of absorbing energy and are often used in combination to improve their stability.40

5. Don't some sunscreens cause rashes, even allergies?

One of the first sunscreens developed was PaBa. It is no longer widely used because it sensitizes the skin in about 1 in 20 people. Sensitized people will develop photo eruptions and photo allergy. Despite the discontinuation of PaBa, sunscreens are still the No. 1 cause of photoallergic reactions.41

6. My sunscreen says it is water resistant. What does that mean?

This is an FDa-regulated claim. It means that the sunscreen should retain its SPF rating after 40 minutes of exposure to water or 80 minutes of water exposure as indicated on the label.



Protection from the sun involves protective eyewear and the use of sunscreens (Table 2). However, in warm climates sunscreen effectiveness is compromised by sweating, toweling off, and frequent entry and exit from the water. In those settings, protective clothing and hats are recommended while on land or topside. Sun protection from clothing is variable, depending on the kind of fabric and weave. Synthetics are generally better UV blockers than cotton. On the other hand, denim SPF equivalent is greater than 200, while a T-shirt may be as low as SPF 4. Certain brands (e.g., Solumbra®) make clothing specifically designed to protect from solar UV. These clothes are labeled with UPF, which is similar to SPF; higher UPF indicates better protection from sunburn.

TABLE 2. Sun Protection
Sunscreen physical blockers Titanium or zinc Often opaque, but microsphere preparation does not appear white. Block UVa and UVB. Can harm corals.
Sunscreen chemical filters Oxybenzone benzophenones Block UVa or UVB. Photosensitivity common. Harmful for corals.
Stretch fabric shirt/suit Rash guard, Lycra or spandex Generally, 50+ UPF. Provides sting protections. Safe for corals.
Wetsuit Many brands 50+ UPF. Thermal protection. Provides sting protection. Safe for corals.
Hat Wide-brimmed preferred over baseball cap for UV protection Topside only (although surfing versions exist)
Sunglasses Look for sunglasses that advertise UV protection Protect from UV keratitis. Unknown effectiveness for cataracts and pterygia.


For divers, lycra suits and wetsuits provide thermal protection (from cold) as well as sun protection. Lycra® and wetsuits also offer excellent protection against stings from venomous marine organisms such as jellyfish. Relying on wetsuits/clothing for sun protection has another important benefit relating to marine conservation. Divers should be aware that their activities, including the use of sunscreen, adversely affect coral health.37 Sunscreens have been shown to cause mortality, promote viral infections, and induce bleaching in corals.38 For these reasons, fabrics are preferred to sunscreens in sensitive coral reef areas and where marine stings are anticipated.

For most people, sunglasses are useful for protection against ocular overexposure of UVB. Photokeratitis of the cornea is characterized by corneal edema, corneal surface defects, and blurred vision. Although regular eyeglasses provide some UV protection, most sunglasses block more than 99% of UVR. Sunglasses may provide protection from cataracts and premature aging of the eye, although these benefits remain controversial.39

Figure 4. Clothing sun protection


Lycra® rash guards and wetsuits provide excellent sun protection as well as protection from stinging marine organisms. Unlike sunscreens, fabrics are nontoxic to corals.

Heat Stress

The sun is a source of heat as well as UV radiation. Humans deal with hot environments by shedding heat in four ways: radiation, conduction, convection, and evaporation. Humans rely largely on evaporative cooling with sweating, a strategy that does not work as well in hot and humid environments or when clothing or wetsuits prevent evaporation. Underwater, direct contact with water usually results in heat loss by conduction. Rarely, very warm water causes net heat gain. Heat gain from ambient water is a stress that the human body is poorly equipped to cope with.

Of the two most important heat syndromes, heat exhaustion is serious but less life-threatening than heat stroke. Heat exhaustion is characterized by dehydration induced by sweating and increased demands on the cardiovascular system. Evaporative fluid losses generate a high workload for the heart, especially because cardiac output can increase to 20 liters per minute during acute heat stress. Heat exhaustion is usually reversible by replacing fluid losses and removing the person from the hot environment.

Heatstroke, the most severe form of heat illness, is defined as mental status changes accompanied by a core temperature greater than 40°C. Exertional heat stroke is a shock state caused by thermal injury to critical organs, including the  gut. Cells die because of direct thermal damage, apoptosis, inflammation, and systemic coagulation.42 Thermal injury causes damage to intestinal epithelial cells, reduces tight junction integrity, and allows bacteria to translocate from the bowel into the blood.43 These result in systemic inflammation resulting from endotoxemia, endogenous pyrogens, and elevated levels of the cytokines IL-1 and TNFα. The presence of bacterial products in the blood and elevated pro- inflammatory cytokines in heat stroke highlights its similarity to septic shock, which is a clinical mimic of this condition.

Heatstroke requires emergent treatment including active cooling measures. Ice-water immersion is both fast and effective and is the best immediate method of cooling for heatstroke.44 However, this technique introduces difficulties in monitoring and resuscitating patients. Other treatments include evaporative cooling using cool mist and fans, with the caveat that high ambient humidity limits its effectiveness. Ice packs can be placed on the groin and axillae, and cooled IV saline can be given if available. Antipyretics such as acetaminophen and ibuprofen are not useful in heatstroke.

In addition to cooling the patient, heatstroke victims are uniformly dehydrated and can present in shock. Hypovolemia should be treated aggressively with fluids. Rhabdomyolysis that is a common complication of heat stroke also benefits from volume resuscitation while arranging evacuation to hospital.

Risk to Divers: Heart Disease and Other Drivers

Although this review has focused on common travel risks for divers (jet lag and sunburn) and high-profile travel-related diseases (chikungunya virus), it is worth noting that the most likely causes of mortality for travelers are heart disease and trauma.45 In other words, what can kill you on a dive trip is the same as what can kill you at home. Cardiovascular disease accounted for more than 50% of travel deaths in a large North American sample, whereas travel-related infectious disease caused less than 1%.45 Trauma accounted for 27% of deaths among travelers from the United States and Canada.45,46 By contrast, the risk of DCI was 0.03% per dive in a series of recreational divers reported by Divers Alert Network.47 DCI accounts for a negligible source of travel mortality, mostly from air embolism.47 Many deaths that occur during diving result from drowning, and about 20% of those can be attributed to in-water cardiovascular events.48

The other mortality risk for travelers is trauma. A special kind of trauma occurs when divers collide with boats. Being struck by boat propellers causes devastating injuries and carries a mortality rate of 15-23%.49 Although serious, boat accidents are relatively rare. By contrast, traffic accidents are a major cause of trauma mortality. In the developing world, a recent increase in the number of cars on the road combined with poor road infrastructure has resulted in an epidemic of traffic deaths.50 Compounding this problem, road and automobile safety features are poor, and access to emergency health care is often subpar in developing countries as compared with developed nations.50 These problems make automobile and road trips the most dangerous part of travel to a dive destination in the developing world — certainly a greater risk than DCI. Bottom line: To stay safe on a dive trip, attend to cardiac risk factors, stop smoking, exercise, and wear your set belt!

Ways to Cope with Stress: Physical Fitness, Breathing and Conditioning

Traditionally, exercise during and immediately after diving has been disfavored because of a concern that it increased nitrogen uptake and decompression stress.51 Contradicting this concern, the majority of research during the past 15 years shows a protective effect of regular and acute bouts of exercise for DCI.52-55 In a counterexample, Madden and colleagues showed that vigorous exercise after diving can result in the arterialization of bubbles, resulting in subclinical air embolism, likely through intrapulmonary shunts.56 On balance, the benefits of regular exercise likely outweigh the reported risks. Exercise is recommended for physical fitness and general health and has benefits for mental health and cognitive functioning. Figure 5 summarizes these benefits to divers and travelers.

Figure 5. Benefits of exercise


Exercise has benefits on multiple organ systems, including the immune system, cardiovascular system, muscles, and brain.


The physical and psychological stresses of travel are commonly experienced by divers, particularly during overseas travel. These stresses are an expected and normal response to being in an unfamiliar and unpredictable environment. Divers can prepare by increasing physical fitness through exercise, which has been associated with reduced levels of stress hormones,57 improved sleep,58 enhanced recovery from jet lag,12 and reduced anxiety.59

Exercise and regular physical activity have a variety of benefits for divers. Exercise training is linked with increased vagal tone, improved heart-rate recovery after exercise, and a reduction in cardiovascular events.57 In addition, exercise combined with breath control (e.g., yoga, qigong, and tai chi) have been shown to reduce baseline parameters of stress and reduce anxiety.59 These mind-body practices, involving movements of the upper chest, shoulders, and accessory muscles of breathing, also improve recovery from the stress response.60 Performed regularly, they may have the added benefit of reducing the work of breathing at depth.61

During travel, there are many factors that divers cannot predict or control, but one exception is their own ventilation. Breathing techniques can minimize predive stress and anxiety while also improving ventilatory efficiency. These techniques also augment exercise tolerance and fin-swimming capacity throughout the dive.61-63  Practice with controlled breathing and respiratory muscle training has beneficial neuroendocrine effects. These include activating stretch receptors and vagal activation in the peripheral and central nervous system that inhibit sympathetic nervous activity.64 These practices, as part of a physical exercise program in the months prior to travel and diving, are a useful strategy to improve flexibility and fitness for diving and can help divers get the most out of their dive travel experience.52


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About the Authors


JOE ALCOCK, MD, MS, is an associate professor of emergency medicine at the University of New Mexico Department of Emergency Medicine and is the former chief of the Emergency Medicine Service at the New Mexico VaMC. Dr. Alcock is also an adjunct professor at the UNM Department of Biology, where he teaches a course on evolutionary medicine. In the UNM School of Medicine, Dr. Alcock is the co-director of the UNM Wilderness and Improvisational Medicine program. His current research interest is the effect of sleep and stress on the human gut microbiome.



SATKIRIN K. KHALSA is a graduate of the University of New Mexico School of Medicine. She completed family medicine residency training at the Mayo Clinic in Scottsdale, arizona, in 2007. Dr. Khalsa practices general and integrative medicine in Albuquerque, New Mexico. She has additional training and certifications in yoga, medical acupuncture, plant- based nutrition and Tai Chi: Moving for Better Balance.



Dr. MICHAEL STRAUSS is a clinical professor of Orthopedic Surgery at the University of California Irvine, medical director of the Long Beach Memorial Medical Center Hyperbaric Medicine Program, Long Beach, California, and orthopedic consultant for the PaVE (Preservation-amputation Veterans Everywhere) Clinic at the Veterans affairs Health Care Medical Center, Long Beach, California. His special interests in diving include panic and blackout, disordered decompression, the source of pain in decompression sickness, diving stresses, diving in older age, and mammalian adaptations to diving.


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