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Salt or Oxygen?
Given this choice, what’s best for taking stress out of fish?

 By Adam Johnson

 

Fighting, handling and holding fish in captivity place severe metabolic demands on brain, muscle, heart, gill and other organ tissues putting them at considerable physiological risk.  In general terms we call this stress, but the physiological situation is highly complicated.  The degree of stress fish realize, and the potential for subsequent recovery, depends on the type and duration of the physiological stress we place them in and the environment in which they are allowed to recover.  To gain a better understanding of fishing-related stress, we must first gain a basic understanding of some of the physiological mechanisms involved. 

Energy Metabolism – A Continued Need for Oxygen 

The energy used to fuel virtually all cellular functions is derived from the compound adenosine triphosphate (ATP).  ATP is needed to make muscles contract, drive brain impulses, allow the heart to beat, provide oxygen uptake by the gills and on an on.  ATP is made up of adenosine (a compound formed from adenine and ribose, a carbohydrate) attached to three phosphate groups.  As the last phosphate bond is broken (actually called a phosphoryl bond by biochemists), chemical energy is released.  The cell converts this chemical energy into mechanical energy to do the work of the cell.  The by-products remaining after this reaction are adenosine diphosphate (ADP) and inorganic phosphate (Pi).  In the cell, ADP and Pi can again combine through the work of complicated metabolic pathways to form ATP, and the energy cycle continues.  The metabolic reaction looks like this: 

ATP « ADP + Pi 

Most freshwater fish rely heavily on oxygen in their environment.  This oxygen is used, primarily, to help fuel the biochemical mechanisms associated with energy production.  Oxygen-associated energy metabolism is highly efficient, and produces the constant supply of energy that fish (or people, for that matter) rely upon to support basically all physiological functions.  Aerobic energy metabolism takes place in a cellular organelle called the mitochondria using a metabolic process known as oxidative phosphorylation.  Cellular energy synthesis is the sole job of the mitochondria and cells can hold literally thousands of these tiny power plants.  All types of foods (fuels) are metabolized for aerobic energy production, including fats, carbohydrates and proteins. 

However, not all energy production relies on oxygen.  Cells have developed mechanisms to keep energy supplied to tissue high during short bursts of sudden, high-intensity exercise, or for short periods when oxygen levels are inadequate (a situation known as hypoxia, or lack of oxygen).  Anaerobic or hypoxic energy metabolism is inefficient and cannot be relied on to produce enough energy to keep tissues functioning in the long term.  Glucose (a six-carbon sugar) is the primary energy substrate for anaerobic energy production.  Glucose is converted to energy down a non-oxidative metabolic pathway called glycolysis.  

Fish must rely on constant supplies of energy.  This energy is most often provided by the oxygen utilization metabolic pathways of oxidative phosphorylation in the mitochondria. 

Fish can swim continuously for long distances without tiring at a broad range of speeds.  This type of swimming, called steady state swimming, is used by fish during normal cruising, or for long distance travel.  Muscles that are used in this type of exercise have a large number of mitochondria and use oxygen for energy synthesis.  As long as there are constant supplies of oxygen, fish basically never become tired during this type of exercise.1  

Sudden bursts of high-intensity swimming are called burst swimming.  This type of swimming normally last for only seconds (possibly minutes) and ends in a physical state of exhaustion.1,2  Burst swimming is critical when fish attack prey, when they migrate against strong currents or up waterfalls, or when they are fighting after being hooked.  This high-intensity exercise totally drains fish of energy reserves.  Recovery from such exhaustive exercise may take hours, or sometimes days, depending on the availability of oxygen following the exercise, the duration of the exercise and the degree to which energy substrates are consumed by (or lost from) the tissue.  Energy metabolism during burst swimming is anaerobic. 

Associated with the depletion of energy reserves during burst swimming is an increase in tissue (including blood) lactic acid (or lactate).  As an acid, lactate produces hydrogen ions that lower the pH of the tissue and reduce the total energy supply of the cell (called its energy charge).1,3  It also drains the cell of important metabolites it needs to recover.  Once these metabolites are exhausted, the fish will not be able to perform another burst of exercise until they are replenished.  Clearance of lactic acid, and restoration of cellular stasis, can take anywhere from four to 12 hours.  This allows the fish sufficient time to restore lost metabolites, but may not be sufficiently long to allow cellular energy levels to rebound.  Factors such as body size, water temperature, water hardness, water pH and oxygen availability all play a part in time to recovery. 

The following is a list summarizing the effects of certain factors on the physiology and recovery from exhaustive exercise in fish: 

  • Body size:  There is a positive correlation between the activity of enzymes associated with anaerobic energy metabolism and/or power requirements of burst exercise in the rainbow trout.  The bigger the fish, the more relative energy is required, the larger the drain on energy reserves and the longer it takes to recover.4 

  • Environmental temperature:  Clearance rate of lactic acid and other metabolic protons (hydrogen ions) are significantly affected by acclimation to temperature.  Large changes in ambient temperature dramatically effect the fish’s ability to recovery.5 

  • Water hardness:  A reduction in the hardness of environmental water has a minimal, but important, effect on the metabolic and acid-base status of the blood.3  Much of the work describing this effect has been conducted in saltwater species, so it is not fully known if the results are directly transferable to freshwater fish.  What is known, however, is that when freshwater fish are stressed, water flows across cell membranes (particularly those of the gills) and the blood becomes diluted.  This dilution puts additional pressure on maintenance of ion balance in the fish (osmoregulation), as will be described below.

  • Water pH:  Moderate acidity has the result of faster recovery of muscle energy.  Higher water pH will slow the recovery process dramatically.3

Why is this important?  Stress associated with catch and release can contribute to stress related mortality.  The lessons learned from studies investigating the affects of, and recovery from, exhaustive exercise have the potential to decrease the number of stress-related deaths and increase fish productivity.  Understanding the energy metabolism of fish, and the factors that affect energy metabolism, are critical to understanding how fish must be handled and treated when caught.  

Osmoregulation – Maintaining Salt Balance in Stressed Fish 

The regulation of salt balance is fundamental to life.  The structure and function of cells depend closely on their interactions with water and its solutes, and few factors affect the viability of an organism as extensively as osmoregulation.  Thus, fish invest considerable energy in controlling the composition of intracellular and extracellular fluids.  In fish, osmoregulation typically consumes 25% - 50% of the total metabolic energy output, possibly the largest energy consumer in the animal.6,7,8  

The mechanisms used by fish to maintain salt balance are highly complicated and extremely energy dependent.  Since every molecule of glucose that is used to generate energy in a hypoxic environment is less than 1/10 as efficient as it is in an oxygen rich environment, the energy demand of tissue osmoregulation cannot be met by anaerobic energy metabolism alone.  A rapid fall in cellular ATP levels causes a slow-down, and eventual stop, in the cellular pumps used to move sodium, potassium and other ions across the cell membrane (called Na/K pumps).  A disruption in Na/K pump activity causes the cell to lose ion homeostasis, and ions are then free to run down their concentration gradients putting the survival of the cell – and the fish – at risk. 

Both fresh- and saltwater fish are constantly faced with the challenge of ionic and osmotic regulation.  Freshwater fish, in which tissue ion concentrations are much greater than the water in their surrounding environment, must deal with osmotic water uptake and loss of ions through permeable epithelial tissues and via the urine.  The opposite is obviously true in saltwater fish.  Freshwater fish produce copious amounts (up to 20% of the body weight per day) of highly dilute urine.  Fish kidneys are highly efficient at keeping body salts (ions) out of the urine, allowing them to stay in the body.  While very small amounts of salt are passed in the urine, most osmoregulation is managed by cells in the fish’s gills. 

Sodium is the primary ion found in tissue.  Transport of sodium across cell membranes is energy dependent and is facilitated by an enzyme called Na/K-ATPase.  This enzyme is integral to the cell membrane and uses the energy supplied by ATP to move sodium in one direction across the cell membrane, while its counter-ion (potassium or whatever) moves in the other direction.  This process allows muscles to contract, it provides the electrochemical gradient to stimulate the heartbeat and allows all manner of neuronal signals to be transmitted.9,10 

Osmoregulation occurs in the fish gill.  The enzyme Na/K-ATPase is found in the basolateral membrane of the gill lamellae.  In freshwater fish, the system works like this: 

Ammonia is produced as a waste product of fish metabolism.  Unlike higher animals, fish do not excrete ammonia in the urine, although some urea, another nitrogenous waste, is excreted that way.  Instead, ammonia (and most of the urea) diffuses through the gill epithelium.  About 80% - 90% of the nitrogenous waste of fish metabolism are excreted via the gills. 

Ammonia from the blood is exchanged across the gill cell membrane for sodium.  This removes the ammonia from the blood and increases the ammonia concentration in the epithelial cell.  In turn, the plasma sodium concentration is increased and the sodium concentration in the gill cell goes down.  To restore osmotic balance in the gill cell, the cell then passes the ammonia out of the cell into the environment and exchanges it for another sodium ion from the water.  In like fashion, chloride ions from the water are exchanged for bicarbonate (formed as CO2 from cellular respiration combines with water in the cell).  Chloride ions move into the cell and bicarbonate moves out of the cell and into the environment.11  Hydrogen ions can also be exchanged for sodium in this manner, helping to control blood pH (Figure 1). 

These two mechanisms for ion exchange, absorption and secretion, occur within two cell types of the fish gill, respiratory cells and chloride cells.  Given that chloride cells are used to eliminate salts, they are larger and more highly developed in saltwater species and not well established in freshwater species.  These two cell types are found in two anatomically distinct locations within the gill with very different exposures to blood flow.  Respiratory cells are supplied by arterial flow, while chloride cells are found in portions of the gill supplied with venous blood.  These positional differences support the ion exchange mechanisms described here.  Respiratory cells, which are involved in gas exchange, nitrogenous waste removal and acid-base balance, are supplied by arterial flow and they exchange sodium and chloride for ammonia and bicarbonate, respectively.  Chloride cells, which deal strictly with salt excretion, are located away from the respiratory cells. 

Again, the most important point to remember is that the exchange of ions that takes place in these cells is highly dependent on energy availability.  If there is not sufficient energy to drive the Na/K pumps, these exchanges cannot occur and water will flood the cells by diffusion.  Maintaining control of salt and water balance is vital and requires considerable metabolic energy to power it.  Energy is the key constituent. 

Figure 1:  Diagram of the model of ion transport in the teleost gill
(modified after several authors)

Consequences of Oxygen Starvation on Osmoregulation 

After only a few minutes of hypoxia there is a general depolarization of the membrane surrounding brain cells causing a release of neurotransmitters (particularly amino acids and most importantly glutamic acid) that speed up calcium influx into the cell.  The increased level of calcium in the cells triggers a number of degenerative processes that can lead to neurological damage or death.  These processes involve the degradation of DNA, proteins and the cell membrane itself, and besides calcium and glutamate involve enzymes that eat away at cell membrane constituents (called lytic enzymes), free radicals and nitric oxide.12,13  The important events of this anoxic catastrophe are common to most vertebrate brains.  Similar events occur in other tissues, like liver14-16, muscle7, blood cells17 and heart9.  Once calcium has invaded the cells it takes much more energy to remove it, via the ATP-dependent calcium pumps. 

Another consequence of anoxia is the release of pituitary hormones, notably prolactin, in most fish species, fresh- and saltwater.  The release of this hormone affects the permeability of osmoregulatory surfaces (gill, skin, kidney, intestine and urinary bladder) and ion transport mechanisms.  Prolactin release regulates water-ion balance by decreasing water uptake and promoting ion retention (especially Na+ and Cl-).  In doing so, prolactin helps to maintain the salt balance of the blood and tissues and keeps the fish from swelling with water.11 

The main threat to freshwater fish is the loss of ions by diffusion into the external hypoosmotic environment, rather than the elimination of excess water.  Even though the regulation of water balance may be important, it is secondary to the importance of ion retention.  However, the effect of prolactin on water permeability should not be dismissed as inconsequential.  Prolactin decreases the osmotic permeability of the gills, retaining ions and excluding water.  It also increases gill mucous secretion, contributing to ion-water balance by impeding the passage of molecules across the membrane. 

So, which is more important, salt or oxygen?  The answer is clear.  In fish that have been stressed by sudden bursts of high-intensity exercise, energy deprivation is a vital concern.  Tissues use up and become almost totally depleted of energy, and it takes several hours (or perhaps days) for them to recover.  Anaerobic energy metabolism cannot keep pace with cellular demand and large amounts of oxygen are required to drive the oxidative pathways of energy metabolism in cellular mitochondria.  Oxygen deprivation will not allow these pathways to function efficiently, if at all. 

Salt balance, no matter the osmolarity of the livewell environment, cannot be maintained without large amounts energy to fuel the process.  And, while the importance of maintaining ion homeostasis cannot be over emphasized, the first consideration must be providing stressed fish the energy they need to turn on the osmoregulatory processes.  

How Much Oxygen is Enough?

 Oxygen, not temperature or salt level, is the main culprit in fish death in the livewell or in catch-related stress.  However, livewell water temperature is a main determinant of how much oxygen can be made available to fish and how quickly they will utilize what’s available. 

The maximum amount of dissolved oxygen in water is called its saturation level.  Saturation level decrease as the temperature of the water increases.  For example, at 70 degrees, water saturates at 8.9 parts per million (ppm).  At 80 degrees, saturation is achieved at 8.0 ppm, and at 90 degrees only 7.3 ppm.  At higher temperatures, fish metabolism also increases and they use oxygen faster.  Therefore, at 80 degrees, oxygen concentrations below 5.0 ppm may prove quickly fatal.  

Here is an example used by Hal Schramm, noted fisheries biologist, that will put this temperature/metabolism/oxygen relationship into perspective.  Ten pounds of bass in a 15-gallon livewell will reduce the oxygen concentration from 75% saturation to stress levels in about eight minutes at 60 degrees; in seven minutes at 70 degrees; and in only 2.5 minutes at 85 degrees.18  

Standard livewell aeration systems simply cannot keep up with this oxygen demand.  A recirculating aeration system will raise the oxygen level in a 15-gallon livewell from 3 ppm to 7 ppm in about eight minutes when the water is 60 degrees.  It will take about 14 minutes at 70 degrees.  At 85 degrees, a standard livewell system simply cannot get to 7 ppm.  With several fish in the livewell, a standard livewell system is not able to keep the oxygen level above stressful limits that may prove fatal, or will certainly create stress on the fish that may not be recoverable.  

Decreasing the water temperature with ice is one solution, but remember that too great a change in water temperature adds its own element of stress.  Large changes in water temperature affect lactic acid clearance and slow metabolic recovery.  In addition, to lower the water temperature by five degrees for a full tournament day in temperatures above 85 degrees could require up to 50-pounds of ice.  

Supplemental oxygen is required, along with temperature control of the livewell, to supply fish the oxygen they need to recover from metabolic stress and promote osmoregulation.  There are no two ways about it; oxygen delivery is the key to helping fish overcome the stress that comes with angling and survival in the livewell.

For More Information Contact:
Adam Johnson
Adam Johnson Outdoors

218.825.0096 (Home/Office)

763.350.5326 (Mobile)
www.adamjohnsonoutdoors.com

References:

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  2. Moyes CD, TG West.  Exercise metabolism in fish.  In:  Biochemistry and Molecular Biology of Fishes, Volume 4 (Eds. Hochachka and Mommsen).  Elsevier Science, 1995, Boston. 
  3. Rossiter AM.  Physiology and survival of Atlantic salmon following exhaustive exercise in soft and acidic water:  implications for the catch and release fishery.  M.Sc. Thesis.  1996.  Queen’s University, Kingston, Canada.  86pp.
  4. Ferguson RA, JD Kieffer, BL Tufts.  The effects of body size on the acid-base and metabolic status in the white muscle of rainbow trout before and after exhaustive exercise.  J Exp Biol, 1993; 180:195-207.
  5. Kiefer JD, S Currie, BL Tufts.  Effects of environmental temperature on the metabolic and acid-base responses on rainbow trout to exhaustive exercise.  J Exp Biol, 1994; 194:299-317.
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  9. MacCormack TJ, WR Driedzic.  Mitochondrial ATP-sensitive K+ channels influence force development and anoxic contractility in a flatfish, yellowtail flounder Limanda ferruginea, but not Atlantic cod Gadus morhua heart.  J Exp Biol, 2002; 205:1411-1418.
  10. Slagle R.  Gill Na,K-ATPase and osmoregulation in the sailfin molly, Poecilia latipinna.  Honor’s Thesis, 1986.  Lafayette College, Easton, Pa.
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  12. Nilsson GE, M Perez-Pinzon, K Dimberg, S Winberg.  Brain sensitivity to anoxia in fish as reflected by changes in extracellular potassium-ion activity.  Am J Physiol, 1993; 264:R250-R253.
  13. Hylland P, GE Nilsson, D Johansson.  Anoxic brain failure in an ectothermic vertebrate: release of amino acids and K+ in rainbow trout thalamus.  Am J Physiol, 1995; 269:R1077-R1084.
  14. Krumschnabel G, PJ Schwarzbaum, J Lisch, C Biasi, W Weiser.  Oxygen-dependent energetics of anoxia-intolerant hepatocytes.  J Mol Biol, 2000; 203(Pt 5):951-959.
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