Posts Tagged ‘ nitrogen ’

Strategies of Diving Mammals

Introduction

Diving to depth is a typical behaviour observed in many aquatic mammals such as; whales, otters, seals, walrus and many others. Such mammals are well adapted at diving. The Weddell seal for example, is able to dive for periods of 80 minutes and more. Compare this to the average 1-3 minutes in untrained humans and you can see that diving mammals have developed great abilities for diving to depths.

The two major problems associated with diving are; limited oxygen stores (limiting the length of the dive) and hydrostatic pressure (limiting the depth of the dive). Oxygen is an important factor during diving, an absence of oxygen (anoxia) means anaerobic respiration becomes the only source of energy. Anaerobic respiration consists only of glycolysis, which produces around 5% of the energy (ATP) produced during aerobic respiration. Such a great deficit in ATP production can damage brain cells and have fatal consequences. In anaerobic respiration, lactate is produced as a waste product. Normally (in aerobic conditions) the lactate is metabolised by the presence of oxygen, in its absence however, the lactate builds up and dissociates into lactic acid. This causes fatigue, which decreases swimming ability.

The dangers of hydrostatic pressure come include; physical damage as a result of the pressure (barotrauma). Especially gas filled spaces of the body such as the lungs and ears. As well as decompression sickness (referred to as ‘the bends’ in humans), caused by rapid changes in pressure.

Oxygen Stores

The main stores or oxygen in mammals are; the lungs, blood and muscle. Oxygen is also present dissolved in body tissue. In adept diving mammals such as the Weddell seal the primary store of oxygen is the blood (in haemoglobin), followed by the muscle (in myoglobin) and then the lungs. The Weddell seal actually exhales before performing a dive.

Having a large store of oxygen in the lungs causes some problems. A large lung volume can make the dive more energetically costly due to the extra energy spent negating the effect of increased buoyancy. Exhaling pre-dive decreases energy required to dive. Another factor to consider is that, being a gas filled space, the lungs are susceptible to hydrostatic pressure. At large enough depths, the pressure can cause the lungs to collapse. So, a large lung volume is not necessary for accomplished diving mammals and some will exhale before diving to reduce the lung volume further.

The blood has an excellent oxygen carrying capacity, oxygen binds with haemoglobin in the blood and this essentially dissolves the gas, thus reducing the volume and associated problems. Adept divers will have a greater volume of blood (and haemoglobin) and therefore are able to store more oxygen. Humans are typically able to store 15ml of oxygen per Kg of body weight, whereas accomplished divers can store anything between 40-70+ ml Kg-1.

Myoglobin is similar to haemoglobin, it is found in the muscles and transports oxygen, but it has a much higher affinity for oxygen. Large concentrations of myoglobin mean diving mammals are able to dive for much longer, therefore high levels of myoglobin are associated with accomplished divers.

No matter how great the ability to store oxygen, there will always be a time when oxygen stores are exhausted. This is known as the aerobic diving limit. It is the length of time an organism is able to dive and respire aerobically from stored oxygen. Dives longer than the aerobic diving limit are possible, but are often rare even in capable diving mammals. Taking the Weddell seal as an example, 80% of dives occur within the aerobic diving limit (about 18-20 minutes) but some still dive for periods of 80 minutes or more. This shows they have developed systems to help combat the buildup of lactate and the lack of oxygen which occurs during anaerobic dives of 20 minutes or more.

Extending Dives beyond the Aerobic Diving Limit

The body is still able to produce energy (ATP) without oxygen via glycolysis during anaerobic respiration but this is at an effective efficiency of 5%. Therefore glucose and glycogen stores (the body’s fuel) would be depleted at 20x the normal rate if glycolysis increased to match aerobic ATP production. Such an increase is known as the ‘Pasteur Effect’, but if the diving mammal is able to decrease metabolism, this might not be necessary.

Diving mammals are able to undergo metabolic depression, which reduces the energy demand of certain body systems by reducing their output. The only problem is that the mammalian brain is very energy hungry and requires a lot of ATP to remain functional.

The ‘Diving Reflex’ is observed when diving past the aerobic diving limit. This reflex includes the slowing of the heart rate (bradycardia) and regional vasoconstriction to produce metabolic depression.

The Diving Reflex

The bradycardia seen in the diving reflex, reduces the heart rate from around 60-70 to 5-10 beats per minute. This is combined with regional vasoconstriction to increase the length of dives. The regional vasoconstriction is seen across the body except the brain as it would be unable to survive any reduction in blood flow. The amount by which blood flow is reduced across the rest of the body varies from 80-95%. This essential sets up a near closed blood flow from the lungs, to the heart, to the brain. Blood flow from the heart to the rest of the body is minimal.

Bradycardia prevents a change in stroke volume, blood pressure and blood flow, which if altered may damage the body. So even though the dimensions of the cardiovascular system have been reduced, the blood flows around the ‘closed circuit’ of the heart, lungs and brain as it would flow round the complete cardiovascular system under aerobic conditions.

The ‘closed circuit’ is able to remain aerobic from oxygen stores in the blood, muscles and lungs. The rest of the body remains aerobic only for as long as the oxygen bound to the myoglobin of the muscles lasts, barely any oxygen is received from the blood or lungs due to the extreme vasoconstriction. This means the rest of the body becomes anaerobic much faster than the ‘closed circuit’, the anaerobic respiration results in production of lactate.

Because of this, high levels of lactate are observed in the muscles, whereas levels are low in heart, lung and brain. Lactate produced by anaerobic respiration of the rest of the body is stored in the muscles until resurfacing. Lactate remains in the muscles due to the regional vasoconstriction, which essentially has disconnected them from the blood flow.

Upon resurfacing, regional vasoconstriction and bradycardia cease. This results in a ‘Wash out’ of lactate. All the lactate stored in the muscles during the dive is released into the bloodstream, thus increasing blood lactate levels. The lactate is metabolised however, in the presence of oxygen. The lactate produced during the dive must be metabolised before another anaerobic dive may occur. Therefore the longer the dive, the longer it takes before another dive may occur. The period of time between dives spent metabolising lactate, is known as the recovery period. Because of this, long dives are not desirable (unless necessary, such as escaping a predator) as it means less time can be spent beneath the water.

Energy Saving Behaviour

To further preserve energy, diving mammals will perform diving locomotion which reduces muscle energy requirements as much as possible. Diving mammals will use a combination of actively stroking for propulsion and gliding to preserve energy. Typically the descent of a dive requires stroking (combined with brief glides) to reach large depths due to buoyancy of the animal. The ascent however consists almost completely of long gliding behaviour in an attempt to expend as little energy as possible. Stroking it is not needed due to buoyancy, which causes the animal to rise to the surface.

Another energy saving behaviour is the induction of voluntary hypothermia. Whilst diving, mammals actively seek cooler waters, as a decrease in temperature causes a decrease in metabolic rate. If the animal is able to decrease their metabolic rate, the length of the dive can be extended.

Hydrostatic Pressure

Pressure can be measured in terms of atmospheres. At sea level (0m), pressure is the equivalent of 1 atmosphere or 1atm.Underwater, the pressure increases by 1atm per 10 meters, therefore at 10 meters below sea level, the pressure is 2atms. At 100 meters below sea level, the pressure rises to 11atms.

Boyle’s law states that pressure multiplied by volume equals a constant value (at a constant temperature) or PV= Constant. This means, if pressure increases, volume decreases (and vice versa). This is important because the body contains many gas filled spaces such as the lungs. Gas is easy to compress, and so as pressure increases (i.e. As we travel deeper into the ocean) the volume of these gas filled spaces within the body decrease in volume.

In order to understand the changes of the body with pressure, there are two other important pressure laws, these are:

Dalton’s Law – The total pressure of a gas constitutes all of the partial pressures within the gas. For example, the total pressure of air at sea level (or Ptot) = 1atm. This means all partial pressures of gases within air must total to 1atm. PN2 (or the partial pressure of nitrogen) = 0.78atm and PO2 = 0.21atm therefore the partial pressures of all the other gases in air must equal 0.01atm.

Henry’s Law – The solubility of a gas in a liquid is proportional to the partial pressure of the gas (above the liquid). This means that if the PN2 in the lungs increases, the amount of nitrogen which dissolves into the blood also increases.

Problems Associated with Hydrostatic Pressure

The main concerns of hydrostatic pressure are; the toxicity of the gases, decompression sickness and barotrauma. The potential of damage being caused by these factors increases as hydrostatic pressure increases.

At certain depths, nitrogen and oxygen can become toxic. At around 20m depth nitrogen can begin to have affect consciousness – altering perception. At around 50m oxygen can cause damage to the central nervous system, lungs and eyes.

Barotrauma is physical damage as a result of pressure. Gas filled spaces are prone to such damage. Major targets of barotrauma are the thorax and the trachea, if the trachea is not strengthened at great depths, the high pressure can cause the trachea to collapse. This is similar with the thorax, as pressure increases, the size of the lungs decreases. At a depth of 40m the lungs are 1/5 of their size at sea level. Such a large decrease in size could cause damage to thoracic muscles. By having a strengthened trachea, elastic diaphragm and strong sternum, it is possible to prevent such damage.

Decompression Sickness

Decompression sickness occurs due to resurfacing too quickly, this is a result of how pressure of nitrogen changes within the body at depth:

Pre-dive

PN2 (0.8atm) is equilibrated between the lungs blood and tissues.

Dive to 30 meters (Compression)

Ptot has increased to 4atms. Due to Dalton’s law, PN2=3.2atms. Due to Boyle’s law, the volume of the lungs has decreased.

PN2 in the lungs quickly reaches 3.2atms, due to their compression. PN2 in the blood slowly equilibrates followed by the tissues. Eventually lungs, blood and tissues have all equilibrated to PN2=3.2atms.

Resurfacing (Decompression)

Resurfacing too quickly means PN2 in the blood and tissues remains at a value near 3.2atms as there was not a chance to equilibrate with the lungs. At the surface, PN2=0.8atms in the lungs, whilst blood and tissues PN2 still equals 3.2atms. This results in a rapid release in pressure resulting in the formation of bubbles in the blood. The bubbles consist of nitrogen at a partial pressure of 0.8atms and so it is energetically favourable for any remaining dissolved nitrogen to diffuse into these bubbles. Because of this, the bubbles can quickly grow in size.

Decompression sickness arises due to any rapid change in pressure (not just changes in pressure when diving). It is also known as either ‘Caisson’s Disease’ or the ‘Bends’. The only treatment available is to contain the sufferer in a hyperbaric chamber – a chamber where pressure can be controlled and allowed to rise steadily, preventing further formation of nitrogenous bubbles in the blood.

Decompression sickness can arise due to the rapid resurfacing from large depths underwater, this results in a large gradient of partial pressures between the blood, lungs and tissues. The offloading of nitrogen from the blood into the lungs is a relatively slow process and therefore takes time. By resurfacing too fast, the pressure is quickly released causing gases (nitrogen) to go out of solution. This results in the formation of nitrogen bubbles in the blood. The bubbles can join together to become larger and more dangerous, whilst nitrogen is able to diffuse in, further increasing the size. It is energetically favourable for nitrogen to diffuse into the bubbles as they are at normal atmospheric pressure. If decompression sickness reaches the spinal cord, it can result in paralysis.

Avoiding Decompression Sickness

There are basically two ways to combat decompression sickness; limit the load of nitrogen into the body and prevent its distribution. To limit the load of nitrogen, diving mammals have evolved specialised alveoli.

An alveolus consists of a sac-like, bulbous area (where gas exchange takes place) and a terminal bronchiole (a tube connecting to the alveolus where no gas exchange takes place). In terrestrial mammals, pressure (such as that experienced whilst diving) causes the bronchiole to collapse, trapping nitrogen within the bulbous end of the alveoli. With nowhere to go, the nitrogen moves out into the tissues and blood (increasing nitrogen load and the possibility of decompression sickness).

The bronchioles of diving mammals on the other hand consist of strengthened cartilage, preventing them from collapse. Under pressure it is the alveoli which compresses first. Nitrogen in the alveolus moves out into the bronchiole. As no gas exchange occurs in the bronchiole, nitrogen is not able to move into the surrounding blood and tissues. Nitrogen load is therefore decreased as is the possibility of suffering from decompression sickness upon resurfacing. Such alveolar collapse occurs at a depth of 30m in Weddell seals, meaning the partial pressure of nitrogen in the tissues does not increase further than 3.2atms.

The other method of avoiding decompression sickness is to limit the distribution of nitrogen. This is done by peripheral vasoconstriction. As with oxygen limited dives that extend past the aerobic diving limit, regional or peripheral vasoconstriction result in decreased blood flow to the body. Blood flow is only preserved to the lungs, heart and brain. The benefit of this is that fatty tissue (i.e. the areas to where blood flow is restricted) has high nitrogen solubility, so reducing the blood flow to these areas also reduces the amount of nitrogen able to dissolve into the tissue. The brain on the other hand consists mainly of watery tissue which has much lower nitrogen solubility; it also offloads nitrogen much faster and therefore has a reduced risk of bubble growth.

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Comparative Nitrogen Excretion

Introduction

In animals all waste products must be excreted from the body in some manner. The urinary system is involved in the excretion of nitrogenous waste products such as urea, uric acid or ammonia. The excretion of nitrogenous waste from animals is important because if it is allowed to build up, it can prove toxic. We obtain nitrogen from protein in the diet, when protein is metabolised it produces amino groups which are able to form the highly toxic ammonia. Different classes and species of animals deal with toxic ammonia in different ways. A summary:

Compound Chemical Formula Toxicity Water Solubility Animals
Ammonia NH3 High High Aquatic Animals
Urea (NH2)2CO Moderate Moderate Terrestrial Animals
Uric Acid C5H4N4O3 Low Low Reptiles and Birds

Method of Excretion by Species:

Fish

Fish excrete nitrogenous waste as ammonia; this is unusual because ammonia is highly toxic therefore storage in the body can pose a risk. However, fish are able to cope due to their environment – the large volumes of water they reside in allow them to continuously excrete ammonia (without the need for storage) directly into the water, diluting the ammonia to non-toxic levels.

Fish deaminate (remove the amine group) amino acids (obtained in the diet by protein consumption) in the gills. The pure ammonia diffuses into the respiratory water which is leaving via the gills; it is therefore excreted at the site of production with minimal time in the body to reduce toxicity.

There are two extremes of environment which fish have to adapt to however – marine and freshwater. The difference in concentration of salt between these two environments has led to slightly different methods of dealing with nitrogenous waste. Osmoregulation of fish living in fresh water requires them to excrete large volumes of dilute urine. This is due to osmosis, which allows large volume of water to enter body fluid from the surrounding hypotonic freshwater.

The converse is true for marine fish, the hypertonic water means water leaves bodily fluid by passive osmosis, in an attempt to conserve water small amounts of concentrated urine are released.

Elasmobranches, such as sharks, primarily live in seawater and are able to produce urea as well as ammonia. This is important for osmoregulation, as said earlier the hypertonic seawater means water is able to leave bodily fluids by osmosis. By producing urea (which is less toxic than ammonia and therefore storable), elasmobranches are able to increase their osmolarity higher than the seawater and therefore take up water from the sea like freshwater species. This is due to the urea being retained in the blood and therefore increasing the osmolarity of the blood.

Fish still have kidneys however, despite nitrogen excretion being handled by the gills. Instead the kidneys are involved in the excretion of excess water and divalent ions, e.g. Mg2+ and SO42-.

Lungfish, which are able to live out of water, have another adaption. They excrete ammonia in the usual way when in the water, but during times of drought when the lungfish buries itself in the mud the production of toxic ammonia could prove fatal. So instead, when buried in the mud, the lungfish produces urea which can be accumulated and excreted into the environment at less toxic levels.

Amphibians

As with fish the type of nitrogenous excretion depends entirely on environment. Typically tadpoles use the same method as fish – ammonia excretion via the gills. However adult amphibians produce urea as they do not remain constantly in the water. The urea is stored, diluted in the bladder, but as amphibians may be prone to desiccation they have adapted the ability to reabsorb water from the urine when needed. This requires them to have relatively large bladders for storage.

Amphibians do not drink to obtain water; instead they are able to absorb water through a region of the skin called the ventral pelvic area.

Birds

All birds excrete a paste like substance called uric acid (which contains the waste nitrogen) independent of habitat. It initially begins as watery urine which travels down the ureters, from the kidney to the cloaca. The cloaca is a unified exit for the gastrointestinal, urinary and reproductive systems.

In the cloaca, the urine mixes with faecal matter from the digestive tract and as much water is removed as possible to produce a dry, crystalline paste containing uric acid. A small amount of watery urine may be excreted as well.

Reptiles

The method of nitrogen excretion depends on the habitat; aquatic reptiles (e.g. turtles) will mainly excrete ammonia (possibly urea) as with fish. Whilst reptiles living in drier conditions (e.g. lizards, snakes & tortoises) excrete uric acid – the low toxicity, crystalline paste. This helps to conserve water and during development in the egg, a build-up is not fatal. Uric acid, as with birds, is excreted from the cloaca.

The kidneys of reptiles do not have loops of Henle and so they are unable to produce concentrated urine also, whilst a large bladder is present in chelonians (turtles) snakes and some lizards do not have a bladder at all.

Mammals

All mammals produce primarily urea (sometime ammonia) which is excreted in urine. Mammals are able to osmoregulate and maximise water conservation by varying the concentration of urine depending on the hydration of the body. Mammals living in environments with plentiful access to fresh water will excrete large amounts of dilute urine. Mammals living in dry or marine environments will excrete small amounts of concentrated urine.

Osmoregulation in mammals is mainly controlled by the hormone ADH, its release (when a mammal is dehydrated) will result in the reduction of water loss and increased reabsorption of water in the kidneys by the loop of Henle.

Osmoregulation

Osmoregulation has been mentioned above in some cases, it can be associated with the excretion of nitrogenous waste because without correct osmoregulation, levels of ammonia can build within the body. A well osmoregulated animal will be taking on water and balancing ions well enough to ensure that nitrogen can be excreted and not build up.

The primary problem facing osmoregulation is the build-up of salt ions, this can occur with animals living in marine habitats.

  • Fish can actively excrete NaCl via gills
  • Some cartilaginous fish such as sharks have specialised salt-excreting glands in their rectum
  • Birds and reptiles have specialised salt-excreting glands on their heads
  • Marine mammals are able to excrete salt in urine efficiently