Sliding filament theory
In 1954, two researchers, Jean Hanson and Hugh Huxley from the Massachusetts Institute of Technology, made a model for muscle tissue contraction which is known as the sliding filament theory. This theory describes the way a muscle cell contracts or shortens as a whole by the sliding of thin filaments over thick filaments and pulling the Z discs behind them closer.
Six different proteins and molecules participate in the contraction of a sarcomere, namely:
Some of these combine together to form thick and thin filaments.
Myosin molecules are bundled together to form thick filaments in skeletal muscles. A myosin molecule has two heads which can move forward and backward and binds to ATP molecule and an actin binding site. This flexible movement of head provides power stroke for muscle contraction.
The thin filaments are composed of three molecules - actin, tropomyosin and troponin. Actin is composed of actin subunits, joined together and twisted in a double helical chain. Each actin subunit has a specific binding site to which myosin head binds. Tropomyosin entwines around the actin. This cover the binding sites of actin subunits, preventing myosin heads from binding to them in an unstimulated muscle. Troponin molecules are attached to tropomyosin strands and facilitate tropomyosin movement so that myosin heads can bind to the exposed actin binding sites. The sarcomeres can hence shorten. This hoever can only occur with the binding of Ca2+ ions to troponins first.
Mechanism of contraction of the sliding filament
Once an action potential arrives at the axon terminal, acetylcholine is released, resulting in the depolarization of motor end plate as shown in Figure 1. This action potential propagates along the sarcolemma and down the T-tubules causing release of Ca2+ ions from the terminal cisternae into the cytosol. Ca2+ ions then bind to troponin causing a conformational change in the troponin-tropomyosin complex, which exposes the binding sites on actin. As illustrated in Figure 3, the myosin head is already energised, as an ATP molecule binds to a myosin head where an enzyme called myosin ATPase hydrolyses the ATP. This releases the energy resulting in an extension of myosin head, carrying high energy, while holding ADP and a phosphate group temporarily.
This energised and cocked myosin head binds to an active site on the exposed actin binding site as shown in Figure 3. With a power stroke, the thin actin filaments slides along the myosin. The myosin hear changes from a high energy extended position to a low energy flexed position. ADP and a phosphate group are released. The myosin head still remains bound to actin filament until it binds to a new ATP molecule. Once a new ATP binds to myosin head, it releases actin and changes back to a high energy extended position, ready for a next cycle of causing power stroke. Such alternative power stroke occurs concurrently in thousands of myosin heads with actin filaments, resulting in an overall contraction of a muscle fibre. These contractions occuring in millions of muscle fibres in turn cause an entire skeletal muscle to contract.
After a brief time, the acetylcholine diffuses away from their receptor sites causing the acetylcholine receptors to close back as shown in Figure 4. The acetylcholine is then broken down by an enzyme acetylcholinesterase present at the synaptic cleft. Soon after contraction, Ca2+ ions is actively transported from cytosol back to sarcoplasmic reticulum via specialised Ca2+ pumps. ATP is expended in this process of active transport. After the Ca2+ ions are removed from cytosol, the troponin-tropomyosin complex covers the active binding sites of actin subunits once again, so that myosin heads cannot bind to actin. This results in the relaxation of a muscle cell.
Muscle Fibre Types
Within skeletal muscle there are three types of fiber. Type one (I), type two A (IIa) and type two B (IIb). Each fiber types has different qualities in the way they perform and how quickly they fatigue.
Type I fibers are also known as slow twitch fibers. They are red in colour due to the presence of large volumes of myoglobin and so oxygen and high numbers of Mitochondria. Due to this fact they are very resistant to fatigue and are capable of producing repeated low-level contractions by producing large amounts of ATP through an aerobic metabolic cycle.
For this reason the muscles containing mainly type I fibers are often postural muscles such as those in the neck and spine due to their endurance capabilities Also, athletes such as marathon runners have a high number of this type of fiber, partly through genetics, partly through training.
Type IIa fibers are also sometimes known as fast oxidative fibres and are a hybrid of type I and II fibers. These fibers contain a large number of mitochondria and Myoglobin, hence their red colour. They manufacture and split ATP at a fast rate by utilising both aerobic and anaerobic metabolism and so produce fast, strong muscle contractions, although they are more prone to fatigue than type I fibers. Resistance training can turn type IIb fibers into type IIa due to an increase in the ability to utilise the oxidative cycle.
Often known as fast glycolytic fibers they are white in colour due to a low level of myoglobin and also contain few mitochondria. They produce ATP at a slow rate by anaerobic metabolism and break it down very quicky. This results in short, fast bursts of power and rapid fatigue. As mentioned above, this type of fiber can be turned into type IIa fibers by resistance training. This is a positive change due to the increased fatigue resistance of type IIa fibers. These fibers are found in large quantities in the muscles of the arms.
There Are Three Primary Muscle Fiber Types In Humans:
Type I are referred to as "slow twitch oxidative", Type IIA are "fast twitch oxidative" and Type IIB are "fast twitch glycolytic" As their names suggest, each type has very different functional characteristics. Type one fibers are characterized by low force/power/speed production and high endurance, Type IIB by high force/power/speed production and low endurance, while Type IIA fall in between.
These characteristics are a result, primarily, of the fiber's Myosin Heavy Chain (MHC) composition, with Mysosin heavy chain isoforms I, IIa and IIx corresponding with muscle fiber types I, IIA, and IIB.
Individual muscles are made up of individual muscle fibers and these fibers are further organized into motor units grouped within each muscle. A motor unit is simply a bundle or grouping of muscle fibers. When you want to move the brain nearly instantaneously sends a signal or impulse through the spinal cord that reaches the motor unit.
The impulse then tells that particular motor unit to contract it's fibers. When a motor unit fires all the muscle cells in that particular motor unit then contract with 100% intensity. So, a muscle cell either contracts 100% or not at all. A motor unit is either recruited 100% or not at all. Therefore, there is no such thing as a partially firing motor unit or a partially contracted muscle fiber.
When you engage in very low intensity activities like lifting a spoon to your mouth, your brain recruits motor units that have a smaller number of muscle fibers and the fibers that make up these smaller motor units are slow twitch, meaning they don't contract as fast or contract with the same level of force as type II fast twitch motor units and fibers. If they did you'd be knocking yourself in the head with a spoon everytime you sat down to eat!!
These smaller motor units are termed low threshold motor units. As the intensity needed to apply force increases, so does the number of motor units involved in the task, particularly the number of fast twitch or high threshold motor units. The main difference between a slow twitch motor unit and a fast twitch motor unit is the fast twitch motor unit controls more muscle fibers or cells and these cells are bigger.
In much the same way, the main difference between a slow twitch muscle fiber and a fast twitch muscle fiber is the fast twitch fiber is larger and can thus produce more force. During an activity such as curling a dumbbell, not only does your body recruit the same motor units as it does when you lift a spoon, but, since curling a dumbbell requires more force, it recruits enough additional fast twitch motor units until enough have been recruited to do the job.
The body recruits the lower threshold motor units first (slow-twitch), followed by the higher threshold motor units (fast-twitch) and continues to recruit and fire motor units until you've applied enough force to do whatever it is you're trying to do regarding movement. When you are lifting something extremely heavy or applying a lot of force your body will contract practically all the available motor units for that particular muscle.
When engaging in high intensity or high force activities you get lots of motor unit activation and thus a lot of force. So how does this relate to the fiber in the available motor units? Well type I muscle motor units contract less forcefully and a little slower then type II fast twitch motor units and they reach peak power slower. They are also highly resistant to fatigue so they have good endurance. This is why you can sit and eat all day or play Playstation all day and never get tired!
The type II motor units are divided into type IIA and type IIB. Both of these sub-groups are capable of greater levels of absolute force than type I and also fatigue a lot quicker. Type IIA and IIB are capable of roughly the same amount of peak force, but the IIA fibers take longer to reach their peak power in comparison to type IIB.
Type IIA fibers reach peak power in about 50 milliseconds whereas type IIB reaches peak power in about 25 milliseconds. Because of their greater contraction speeds, the total peak power by IIB can be up to 5 times higher then the IIA's.
Fiber Type Contraction Speed Time To Peak Power Fatigue
I (slow twitch) Slow 100 milliseconds Slowly
IIA (fast twitch) Fast 50 milliseconds Fast
IIB (fast twitch) Very Fast 25 milliseconds Fast
Muscle Fibers & Nerves
You see, the type of fiber expressed as far as type I vs Type II is controlled by the nervous system. Nerves that control and connect to a group of motor units run from the brain to the motor unit and are hardwired in the brain. Fast twitch motor units are controlled by fast twitch nerves. Slow twitch motor units are controlled by slow twitch nerves.
In the laboratory you can take a nerve from a motor unit that supplies a slow twitch muscle fiber and replace it with one that supplies a fast twitch fiber and the slow twitch fiber will behave just like a fast twitch fiber! The reverse is also true.
You can take a slow twitch nerve and connect it to a fast twitch motor unit and the fast twitch will behave like slow twitch. Unforunately, it's impossible to change a slow twitch nerve into a fast twitch nerve and vice versa. However, you can make the Myosin Heavy chain expressed in a fast twitch fiber either more or less fast twitch or a slow twitch fiber more or less slow twitch but more on that later.
At higher altitudes, the pressure of the air around you (barometric pressure) decreases so there is less oxygen in surrounding air. People can live comfortably at moderately high altitudes, but the body must make some adjustments, and this takes time. If you ascend to altitudes above 8,000 feet, you will be in danger of developing uncomfortable or dangerous symptoms from the change in altitude.
Symptoms of altitude sickness that are not life threatening are called acute mountain sickness. Mountain climbers on any high mountain and skiers in high-altitude locations such as Colorado are at risk of developing acute mountain sickness. Symptoms from acute mountain sickness improve if you descend to lower altitude quickly. For very mild symptoms, a delay before further climbing may be enough to allow symptoms to go away.
Acute mountain sickness is the least dangerous of several kinds of altitude illnesses that can occur. This sickness affects close to half of all people who begin near to sea level and climb to 14,000 feet of elevation without scheduling enough rest time.
Symptoms that develop at high altitude should be taken very seriously, since some altitude problems can develop into fatal illnesses. One dangerous reaction to high altitude is a condition called high-altitude cerebral edema (HACE), in which the brain accumulates extra fluid, swells and stops working properly. A related illness, high-altitude pulmonary edema (HAPE), can occur with or without warning symptoms that signal altitude sickness. HAPE causes fluid to enter the lungs. A type of altitude sickness called high-altitude retinal hemorrhage (HARH) can cause eye damage. Coma and death are the most serious consequences of altitude sickness.
Altitude sickness is more likely to occur in people who have a previous history of altitude sickness. It is more likely if you climb quickly, if you exercise vigorously during your first few days of altitude exposure, and if you have been living at low elevation prior to your climb. Obesity appears to increase the risk for altitude sickness. Genetics may also put some people at increased risk, particularly for high altitude pulmonary edema (HAPE).
As your body makes normal adjustments to adapt to a high altitude, you may experience a few symptoms that are bothersome but are not cause for concern. They include rapid (but still comfortable) breathing, shortness of breath with strenuous exercise, occasional short pauses in breathing while you sleep, and frequent urination. The last two symptoms are caused by a low carbon dioxide level, which triggers adjustments in the brain and kidney.
More serious symptoms are caused by low levels of oxygen in the blood and adjustments that are made by your circulation system.
Acute mountain sickness usuallycauses symptoms at least 8 to 36 hours after ascent.
Symptoms of acute mountain sickness can include:
Headache that is not relieved by over-the-counter pain medicine
Nausea or vomiting
Dizziness or lightheadedness
Weakness or fatigue
Loss of appetite
High-altitude cerebral edema is considered by many experts to be an extreme form of acute mountain sickness. It usually develops after symptoms of acute mountain sickness. Symptoms of this more severe altitude disease may not be noticed immediately because the illness can begin during the night. Because this low-oxygen injury affects the brain and thought process, a person with high-altitude cerebral edema may not understand that symptoms have become more severe until a traveling companion notices unusual behavior.
Symptoms may include:
Worsening headache and vomiting
Walking with a staggering gait
Visual hallucinations (seeing things that are not real)
Changes in the ability to think
Changes in normal behavior
Coma (in advanced cases)
High-altitude pulmonary edema, which is the lungs' response to an increase in altitude, may occur with or without other symptoms of altitude illness. A low oxygen concentration can trigger blood vessels in the lungs to constrict (tighten), causing a higher pressure in the lung arteries. This causes fluid to leak from the blood vessels into the lungs. Symptoms of high-altitude pulmonary edema commonly appear at night and can worsen during exertion.
Symptoms of high-altitude pulmonary edema include:
Chest tightness or fullness
Inability to catch your breath, even when resting
Blue or gray lips and fingernails
Coughing, which may produce pink frothy fluid
Fever (temperature is above normal but is less than 101° Fahrenheit)
Noises when breathing, such as rattling or gurgling sounds
High-altitude retinal hemorrhage can occur with or without symptoms. It usually is not noticeable unless the area of the eye that provides the most detailed vision (the macula) is involved.
Blurred vision is the main symptom of high-altitude retinal hemorrhage.
You must be able to recognize the early symptoms of altitude sickness, and you should watch carefully for symptoms when you are at risk because altitude illnesses can be life threatening.
If headache is your only symptom, you should stop climbing and take a mild pain reliever. If you have a headache that does not go away or if you have other symptoms that suggest acute mountain sickness, this illness can be diagnosed without tests.
High-altitude cerebral edema can make it difficult to walk a straight line, and can lead to changes in thinking, hallucinations or an unexplained change in personality. If a person has these symptoms at high altitude, you should assume that the person has high-altitude cerebral edema. A person with these symptoms should descend immediately and seek medical care. Once a person with high-altitude cerebral edema has been transported to a medical center, a magnetic resonance imaging (MRI) scan may be done to confirm the cause of the symptoms. An MRI can show brain swelling.
Recognizing high-altitude pulmonary edema can be difficult in its early stages because fatigue may be the only sign. Symptoms that should be of concern include difficulty exercising, dry cough, rapid heart rate (more than 100 beats per minute), and shortness of breath while resting. Listening to the lungs with a stethoscope may reveal a crackling noise with each breath. If blood oxygen levels were measured, they would be lower than expected for your altitude. X-rays may show signs of fluid filling one or more areas within the lungs, giving an appearance that is similar to pneumonia.
High-altitude retinal hemorrhage can be diagnosed by a doctor who examines the eye with a hand-held instrument called an ophthalmoscope.
If you are climbing and do not move back down to an elevation where you last felt well, your symptoms can worsen and can be deadly. Symptoms from acute mountain sickness will go away after two or three days of rest at a lower altitude. Severe syndromes such as HAPE can take weeks to disappear, and will require medical attention and possible hospitalization.
Gradual changes in altitude will help your body adapt to the low-oxygen environment and can reduce your chances of developing all forms of altitude sickness. People adapt at different rates, but there are four general guidelines for climbing above 10,000 feet that are practical for climbers to follow:
Do not increase your altitude by more than 1,000 feet per night.
Each time you increase your altitude by 3,000 feet, spend a second night at this elevation before going farther.
Limit your physical exertion to reasonable levels during your first few days of ascent to altitude.
Drink plenty of fluid during your altitude exposure.
If you develop early signs of altitude sickness, you can keep from getting worse if you immediately stop ascending or if you descend.
Mild symptoms of altitude adjustment, such as headache, can be prevented or at least limited by taking ibuprofen.
If you have experienced high-altitude illness in the past and are planning to again go to high altitude, you may want to discuss with your doctor the option of taking a prescription drug. The ones used are acetazolamide (Diamox, generic versions) and the corticosteroid medicine dexamethasone (Decadron, generic versions). Acetazolamide can cause frequent urination and a metallic taste in the mouth. These drugs do not prevent serious forms of altitude sickness.
If you previously have developed HAPE, you may receive the oral drug nifedipine (Procardia), the inhaled drug salmeterol (Serevent), or both medicines for a future rise to altitude. These medications may stabilize the blood-flow pattern in your lungs.
The first rule of treatment for mild symptoms of acute mountain sickness is to stop ascending until your symptoms are completely gone. If you have more severe symptoms or any symptoms of high-altitude cerebral edema, high-altitude pulmonary edema, or blurred vision, you need to move to a lower altitude as soon as possible, even if it's the middle of the night. If you remain at your current altitude or continue going higher, the symptoms will get worse and the sickness can be fatal.
Besides moving to a lower altitude, you can treat mild altitude sickness with rest and pain relievers. The drug acetazolamide can speed recovery. This drug balances your body chemistry and stimulates breathing.
If you have symptoms of altitude sickness, avoid alcohol, sleeping pills and narcotic pain medications. All of these can slow your breathing, which is extremely dangerous in low-oxygen conditions.
Besides moving to a lower altitude — or if a descent must be delayed — you can treat high-altitude cerebral edema with supplemental oxygen and the drug dexamethasone, which decreases brain swelling. If one is available, this condition is also helped by time spent in a portable hyperbaric (pressure) chamber, which simulates descent to a lower altitude, during the time that supervision and transportation arrangements are being made for descent to lower altitude. Additional treatment for high-altitude pulmonary edema includes oxygen and nifedipine, as well as the use of a standard hyperbaric chamber.
Altitude sickness, also known as acute mountain sickness (AMS), is negative health effect of high altitude, caused by acute exposure to low amounts of oxygen at high altitude.
Although minor symptoms such as breathlessness may occur at altitudes of 1,500 metres (5,000 ft), AMS commonly occurs above 2,400 metres (8,000 ft). It presents as a collection of nonspecific symptoms, acquired at high altitude or in low air pressure, resembling a case of "flu, carbon monoxide poisoning, or a hangover". It is hard to determine who will be affected by altitude sickness, as there are no specific factors that correlate with a susceptibility to altitude sickness. However, most people can ascend to 2,400 metres (8,000 ft) without difficulty.
Acute mountain sickness can progress to high altitude pulmonary edema (HAPE) or high altitude cerebral edema (HACE), both of which are potentially fatal, and can only be cured by immediate descent to lower altitude or oxygen administration.
Chronic mountain sickness is a different condition that only occurs after long term exposure to high altitude.
Signs and symptoms
People have different susceptibilities to altitude sickness; for some otherwise healthy people, acute altitude sickness can begin to appear at around 2,000 metres (6,600 ft) above sea level, such as at many mountain ski resorts, equivalent to a pressure of 80 kilopascals (0.79 atm). This is the most frequent type of altitude sickness encountered. Symptoms often manifest themselves six to ten hours after ascent and generally subside in one to two days, but they occasionally develop into the more serious conditions. Symptoms include headache, fatigue, stomach illness, dizziness, and sleep disturbance. Exertion aggravates the symptoms.
Those individuals with the lowest initial partial pressure of end-tidal pCO2 (the lowest concentration of carbon dioxide at the end of the respiratory cycle, a measure of a higher alveolar ventilation) and corresponding high oxygen saturation levels tend to have a lower incidence of acute mountain sickness than those with high end-tidal pCO2 and low oxygen saturation levels.
Headaches are the primary symptom used to diagnose altitude sickness, although a headache is also a symptom of dehydration. A headache occurring at an altitude above 2,400 metres (7,900 ft) – a pressure of 76 kilopascals (0.75 atm) – combined with any one or more of the following symptoms, may indicate altitude sickness:
Gastrointestinal disorder: Loss of appetite, nausea, or vomiting, excessive flatulation
Nervous system disorder: Fatigue or weakness, headache with or without dizziness or lightheadedness, insomnia
Locomotory system disorder: Peripheral edema (swelling of hands, feet, and face)
Respiratory system disorder: Nose bleeding, shortness of breath upon exertion
Cardiovascular system disorder: Persistent rapid pulse
Others: Pins and needles, general malaise
Symptoms that may indicate life-threatening altitude sickness include:
Pulmonary edema (fluid in the lungs)
Symptoms similar to bronchitis
Persistent dry cough
Shortness of breath even when resting
Cerebral edema (swelling of the brain)
Headache that does not respond to analgesics
Gradual loss of consciousness
Increased nausea and vomiting
The most serious symptoms of altitude sickness arise from edema (fluid accumulation in the tissues of the body). At very high altitude, humans can get either high altitude pulmonary edema (HAPE), or high altitude cerebral edema (HACE). The physiological cause of altitude-induced edema is not conclusively established. It is currently believed, however, that HACE is caused by local vasodilation of cerebral blood vessels in response to hypoxia, resulting in greater blood flow and, consequently, greater capillary pressures. On the other hand, HAPE may be due to general vasoconstriction in the pulmonary circulation (normally a response to regional ventilation-perfusion mismatches) which, with constant or increased cardiac output, also leads to increases in capillary pressures. For those suffering HACE, dexamethasone may provide temporary relief from symptoms in order to keep descending under their own power.
HAPE can progress rapidly and is often fatal. Symptoms include fatigue, severe dyspnea at rest, and cough that is initially dry but may progress to produce pink, frothy sputum. Descent to lower altitudes alleviates the symptoms of HAPE.
HACE is a life-threatening condition that can lead to coma or death. Symptoms include headache, fatigue, visual impairment, bladder dysfunction, bowel dysfunction, loss of coordination, paralysis on one side of the body, and confusion. Descent to lower altitudes may save those afflicted with HACE.
Altitude sickness can first occur at 1,500 metres, with the effects becoming severe at extreme altitudes (greater than 5,500 metres). Only brief trips above 6,000 metres are possible and supplemental oxygen is needed to avert sickness.
As altitude increases, the available amount of oxygen to sustain mental and physical alertness decreases with the overall air pressure, though the relative percentage of oxygen in air, at about 21%, remains practically unchanged up to 21,000 metres (70,000 ft). The RMS velocities of diatomic nitrogen and oxygen are very similar and thus no change occurs in the ratio of oxygen to nitrogen until stratospheric heights.
Dehydration due to the higher rate of water vapor lost from the lungs at higher altitudes may contribute to the symptoms of altitude sickness.
The rate of ascent, altitude attained, amount of physical activity at high altitude, as well as individual susceptibility, are contributing factors to the onset and severity of high-altitude illness.
Altitude sickness usually occurs following a rapid ascent and can usually be prevented by ascending slowly.In most of these cases, the symptoms are temporary and usually abate as altitude acclimatization occurs. However, in extreme cases, altitude sickness can be fatal.
At high altitude, 1,500 to 3,500 metres (4,900 to 11,500 ft), the onset of physiological effects of diminished inspiratory oxygen pressure (PiO2) includes decreased exercise performance and increased ventilation (lower arterial partial pressure of carbon dioxide- PCO2). While arterial oxygen transport may be only slightly impaired the arterial oxygen saturation, SaO2, generally stays above 90%. Altitude sickness is common between 2,400 and 4,000m because of the large number of people who ascend rapidly to these altitudes.
Very high altitude
At very high altitude, 3,500 to 5,500 metres (11,500 to 18,000 ft), maximum SaO2 falls below 90% as the arterial PO2 falls below 60mmHg. Extreme hypoxemia may occur during exercise, during sleep, and in the presence of high altitude pulmonary edema or other acute lung conditions. Severe altitude illness occurs most commonly in this range.
Above 5,500 metres (18,000 ft), marked hypoxemia, hypocapnia, and alkalosis are characteristic of extreme altitudes. Progressive deterioration of physiologic function eventually outstrips acclimatization. As a result, no permanent human habitation occurs above 6,000 metres (20,000 ft). A period of acclimatization is necessary when ascending to extreme altitude; abrupt ascent without supplemental oxygen for other than brief exposures invites severe altitude sickness.
The physiology of altitude sickness centres around the alveolar gas equation; the atmospheric pressure is low, but there is still 20.9% Oxygen, water vapour still occupies the same pressure too, this means that there is less oxygen pressure available in the lungs and blood. Compare these two equations comparing the amount of oxygen in blood at altitude:
The hypoxia leads to an increase in minute ventilation (hence both low CO2, and subsequently bicarbonate), Hb increases through haemoconcentration and erythrogenesis. Alkylosis shifts the haemaglobin dissociation constant to the left, 2,3-DPG increases to counter this. Cardiac output increases through an increase in heart rate.
The body's response to high altitude includes the following:
↑ Erythropoietin → ↑ hematocrit and hemoglobin
↑ 2,3-BPG (allows ↑ release of O2 and a right shift on the Hb-O2 disassociation curve)
↑ kidney excretion of bicarbonate (use of acetazolamide can augment for treatment)
Chronic hypoxic pulmonary vasoconstriction (can cause right ventricular hypertrophy)
People with high-altitude sickness generally have reduced hyperventilator response, impaired gas exchange, fluid retention or increased sympathetic drive. There is thought to be an increase in cerebral venous volume due to increase in cerebral blood flow and hypocapnic cerebral vasoconstriction causing oedema.
Ascending slowly is the best way to avoid altitude sickness. Avoiding strenuous activity such as skiing, hiking, etc. in the first 24 hours at high altitude reduces the symptoms of AMS. Alcohol and sleeping pills are respiratory depressants, and thus slow down the acclimatization process and should be avoided. Alcohol also tends to cause dehydration and exacerbates AMS. Thus, avoiding alcohol consumption in the first 24–48 hours at a higher altitude is optimal.
Pre-acclimatization is when the body develops tolerance to low oxygen concentrations before ascending to an altitude. It significantly reduces risk because less time has to be spent at altitude to acclimatize in the traditional way. Additionally, because less time has to be spent on the mountain, less food and supplies have to be taken up. Several commercial systems exist that use altitude tents, so called because they mimic altitude by reducing the percentage of oxygen in the air while keeping air pressure constant to the surroundings.
Altitude acclimatization is the process of adjusting to decreasing oxygen levels at higher elevations, in order to avoid altitude sickness. Once above approximately 3,000 metres (10,000 ft) – a pressure of 70 kilopascals (0.69 atm) – most climbers and high-altitude trekkers take the "climb-high, sleep-low" approach. For high-altitude climbers, a typical acclimatization regimen might be to stay a few days at a base camp, climb up to a higher camp (slowly), and then return to base camp. A subsequent climb to the higher camp then includes an overnight stay. This process is then repeated a few times, each time extending the time spent at higher altitudes to let the body adjust to the oxygen level there, a process that involves the production of additional red blood cells. Once the climber has acclimatized to a given altitude, the process is repeated with camps placed at progressively higher elevations. The rule of thumb is to ascend no more than 300 m (1,000 ft) per day to sleep. That is, one can climb from 3,000 m (9,800 ft) (70 kPa or 0.69 atm) to 4,500 m (15,000 ft) (58 kPa or 0.57 atm) in one day, but one should then descend back to 3,300 m (10,800 ft) (67.5 kPa or 0.666 atm) to sleep. This process cannot safely be rushed, and this is why climbers need to spend days (or even weeks at times) acclimatizing before attempting to climb a high peak. Simulated altitude equipment such as altitude tents provide hypoxic (reduced oxygen) air, and are designed to allow partial pre-acclimation to high altitude, reducing the total time required on the mountain itself.
Altitude acclimatization is necessary for some people who move rapidly from lower altitudes to intermediate altitudes (e.g., by aircraft and ground transportation over a few hours), such as from sea level to 8,000 feet (2,400 m) as in many Colorado, USA mountain resorts. Stopping at an intermediate altitude overnight (for example, staying overnight when arriving through Denver, at 5,500 feet (1,700 m), when traveling to the aforementioned Colorado resorts) can alleviate or eliminate occurrences of AMS.
The only reliable treatment, and in many cases the only option available, is to descend. Attempts to treat or stabilize the patient in situ (at altitude) are dangerous unless highly controlled and with good medical facilities. However, the following treatments have been used when the patient's location and circumstances permit:
Oxygen may be used for mild to moderate AMS below 3,700 metres (12,000 ft) and is commonly provided by physicians at mountain resorts. Symptoms abate in 12 to 36 hours without the need to descend.
For more serious cases of AMS, or where rapid descent is impractical, a Gamow bag, a portable plastic hyperbaric chamber inflated with a foot pump, can be used to reduce the effective altitude by as much as 1,500 m (5,000 ft). A Gamow bag is generally used only as an aid to evacuate severe AMS patients, not to treat them at altitude.
The folk remedy for altitude sickness in Ecuador, Peru and Bolivia is a tea made from the coca plant. See mate de coca.
Steroids can be used to treat the symptoms of pulmonary or cerebral edema, but do not treat the underlying AMS.
Heat illness or heat-related illness is a spectrum of disorders due to environmental exposure to heat. It includes minor conditions such as heat cramps, heat syncope, and heat exhaustion as well as the more severe condition known as heat stroke.
A number of heat illnesses exist including:
Heat stroke - Defined by a body temperature of greater than 40 °C (104 °F) due to environmental heat exposure with lack of thermoregulation. Symptoms include dry skin, rapid, strong pulse and dizziness.
Heat exhaustion - Can be a precursor of heatstroke; the symptoms include heavy sweating, rapid breathing and a fast, weak pulse.
Heat syncope - Fainting or dizziness as a result of overheating.
Heat cramps - Muscle pains that happen during heavy exercise in hot weather.
Heat rash - Skin irritation from excessive sweating.
Heat tetany - Usually results from short periods of stress in intense heat. Symptoms may include hyperventilation, respiratory problems, numbness or tingling, or muscle spasms.
Prevention includes avoiding medications that can increase the risk of heat illness (e.g. antihypertensives, diuretics, and anticholinergics), gradual adjustment to heat, and sufficient fluids and electrolytes.
Mild disease can be treated with fluids by mouth. In more significant disease spraying with mist and using a fan is useful. For those with severe disease putting them in lukewarm water is recommended if possible with transport to a hospital.
Heat stroke is relatively common in sports and is the cause of about 2 percent of deaths. Football in the United States has the highest rates.
Between 1999 and 2003, the US had a total of 3442 deaths from heat illness. Those who work outdoors are at particular risk for heat illness, though those who work in poorly-cooled spaces indoors are also at risk. Between 1992 and 2006, 423 workers died from heat illness in the US.