FLW
Tour Tournament Director Bill Taylor said anglers should be conscientious about
which additives they use. Some of them have ingredients not yet approved by the
Federal Drug and Food Administration, he said, and some have warnings on the
package stating that the chemical could be harmful to humans if consumed. Though
all FLW Outdoors tournaments and many others follow the catch-and-release
format, it is entirely possible that any fish released by an angler could
eventually be caught and consumed by another fisherman.
Taylor said he has spoken to many fisheries biologists in different parts of the
country about the use of chemical additives. They recommend not using any
additive that could contaminate a fish and harm either the body of water's fish
population or humans who might catch and eat the fish. Although FLW Outdoors has
seen some success with a few of the additives it has used, Taylor said he is not
convinced that all of them are effective.
“I'm not so sure that any of those additives are of real great benefit,” he
said, adding that a common and safe compound found in most households has
probably been the most effective additive. “With biologists, they say just
regular block salt added into your livewell can be the best additive.”
Non-iodized salt added to a livewell in the right proportion, roughly 1/3 cup
for every five gallons of water, can help reduce fish stress and maintain
electrolyte balances. Some sources suggest that adding salt can also help reduce
the risk of a fish becoming infected.
http://www.flwoutdoors.com/fishing-articles/tech-tackle-reviews/140793/livewells-part-3/
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 in every living
thing is derived from the compound adenosine triphosphate, or 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)
attached to three phosphate groups (triphosphate - TP). When the cell needs
energy the last phosphate bond is broken and chemical energy is released. The
cell converts this chemical energy into the mechanical energy needed to perform
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 recombine
through a series of complicated metabolic pathways to re-form ATP, and the
energy cycle continues. To biochemists, 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 the
energy recycling processes. 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. As long
as oxygen and food (fuel) are readily available, the recycling of energy
continues unimpeded and the energy supply meets demand. Energy metabolism using
oxygen is called "aerobic" metabolism.
Not all energy production relies on oxygen, however. Cells have developed
mechanisms to maintain energy supply 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 for very long. To keep a steady balance between energy utilization
and supply, fish need oxygen.
Fish must rely on constant supplies of energy. And to get the energy they need,
fish also must rely on constant and plentiful supplies of oxygen. Lack of oxygen
will quickly deprive fish of the energy they need to sustain life.
Catching Fish Depletes Energy Reserves
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 use high volumes of oxygen for energy synthesis. As
long as there is a constant supply of oxygen, fish basically never become tired
during this type of exercise.
Sudden bursts of high-intensity swimming are called burst swimming. This type of
swimming normally lasts 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 compounds
are consumed by, or lost from, the fish's tissue. Energy metabolism during burst
swimming is anaerobic, providing only enough energy for a few seconds. If the
exercise continues, tissue energy stores will become completely drained.(1)
Think of this in terms of a sprint-type exercise over a 100-yard dash. When you
sprint your leg muscles totally consume their energy in only seconds. Short rest
between sprints allows the muscle to restore a small amount of energy, but the
next sprint is harder and slower. With continued exercise sprinting becomes
continually difficult until the muscle is totally exhausted and you cannot run
another step. Muscles become weak and spongy, and if you are not used to the
exercise they will be sore for several days. Only the oxygen you breath after
the exercise will allow the energy in your leg muscles to recover, reducing the
soreness and regaining muscle strength. Imagine trying to recover if a plastic
bag was pulled over your head!
Now relate this example to a fish involving its entire body in an all-consuming
sprint-type exercise lasting 30-seconds, two minutes or longer. Energy from the
whole body is recruited and used up. Even in a well-oxygenated environment, like
a trout stream, the fish will need to find a quiet place to rest for several
hours before it regains its energy. Imagine this fish placed in a livewell with
little or no oxygen. Energy cannot recover and the fish will either die, or
become so energy starved it will likely die later. It is not the lack of oxygen
that kills the fish. It is the lack of energy and the inability to recover lost
energy stores.
Factors Affecting Recovery
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, ultimately
reducing the total energy supply of the cell.(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 normal cellular
function, can take anywhere from four to 12 hours. Over this time the fish is
able to restore lost metabolites, but 12-hours still 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 anaerobic energy
metabolism and power requirements of burst exercise in the rainbow trout. In
general, bigger fish require more relative energy to perform burst swimming
exercise. This creates a larger drain on energy reserves, taking longer to
recover.(4)
- Environmental temperature: Clearance rate of lactic acid and
energy-draining metabolites are significantly affected by acclimation to
temperature. Large changes in ambient temperature dramatically effect the fish's
ability to recover.(5) Dramatic heating or cooling of the environment will
reduce recovery rate.
- 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
maintaining salt balance in the fish. Maintaining salt balance is called
osmoregulation and it will be described in more detail later.
- Water pH: Moderate water acidity will help fish recover more quickly.
Higher water pH will slow the recovery process dramatically.(3)
Why are these things important? Stress associated with catch and release can
contribute to catch 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 (ion) balance is fundamental to all life. The
structure and function of cells depend closely on their interactions with water
and things that are dissolved in water, 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 anaerobic energy metabolism is less than 1/10
as efficient as energy metabolism 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 control the movement of salts across the
cell membrane. A disruption ion 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 of highly dilute urine. In fact, they will produce urine
weighing up to 20% of their body weight every day. Imagine a 200-pound man
generating 40-pounds - or about five gallons - of urine every day! While fish
kidneys are highly efficient at removing water from the fish, they are equally
efficient at keeping body salts out of the urine. This mechanism allows the
salts to stay in the body, helping to control salt balance. 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 highly energy dependent and is facilitated by an enzyme called
Na/K-ATPase. This enzyme resides right inside 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
needed to stimulate the heartbeat, and allows all manner of brain and nerve
signals to be transmitted.(9,10)
Imagine yourself to be a Na/K ATPase enzyme in line in a fast food restaurant.
You hand your money to the attendant, pick up your change, and then grab your
number three value meal. The same is true in the fish's cell. A sodium ion is
handed across the cell membrane, a second (different) ion is picked up, and this
ion is brought back into the cell.
Most osmoregulation occurs in the fish's gill. The enzyme Na/K-ATPase is
primarily responsible for maintaining salt balance and it resides in the
membrane of the fish gill cell. There is one pump on the side of the gill cell
next to the blood, and another in the membrane on the side next to the water. In
freshwater fish, the system of osmoregulation works like this…
Ammonia is produced as a waste product of fish metabolism. When fish exercise,
they produce a great deal of ammonia, and that ammonia has to be excreted from
the blood. Unlike higher animals, fish do not excrete ammonia in the urine.
Instead, ammonia (and most all other nitrogen waste) diffuses through the gill
membrane. 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 gill cell. In turn, a sodium ion is passed from the gill cell and into
the blood. The plasma sodium concentration is increased and the sodium
concentration in the gill cell goes down. To replace the sodium ion in the gill
cell and restore its salt balance the cell then passes the ammonia out of the
gill 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.
Bicarbonate is formed when CO2 from cellular respiration combines with water in
the cell. Remember, like us, fish use oxygen in respiration. The byproducts of
respiration are CO2 and water. We get rid of CO2 by simply exhaling, but
obviously fish can't do that. Instead, the CO2 formed in fish respiration
combines with water in the cell to form bicarbonate ion. 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. For a graphic depiction of all this refer to Figure 1.
Figure 1: Diagram of the model of ion transport in the fish gill
(modified after several authors)
These two mechanisms for ion exchange are called absorption and secretion and
occur within two cell types of the fish gill known as 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. Respiratory cells, which are involved in gas exchange,
nitrogenous waste removal and acid-base balance, are more developed in
freshwater fish. They are supplied by arterial flow and are used to exchange
sodium and chloride for ammonia and bicarbonate, respectively.
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 enough energy to drive the ion pumps, these exchanges cannot occur and
water will flood the cells by diffusion, killing the fish. Maintaining control
of salt and water balance is vital and requires considerable metabolic energy to
power it. Energy is the key constituent.
Consequences of Oxygen Starvation on Osmoregulation
After only a few minutes of oxygen starvation the membrane surrounding brain
cells loses it ability to control ion balance causing a release of chemicals
(called neurotransmitters) 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 destruction of DNA, important cellular proteins, and even the cell membrane
itself. Free radicals and nitric oxide are also formed, eating away further at
the cell membrane and attacking intracellular constituents.(12,13) The important
events of this catastrophe are common to most vertebrate brains, including both
fish and humans. Similar events occur in other tissues, like liver(14-16),
muscle(7), blood cells(17) and heart(9). Once calcium has invaded the cells it
takes much more energy to remove it, via the ATP-dependent calcium pumps.
Another consequence of oxygen starvation (or hypoxia) is the release of hormones
from the pituitary gland. Prolactin is the most prevalent of these hormones in
most fish species, both fresh- and saltwater. The release of this hormone
affects the permeability of cell membranes in the gill, skin, kidney, intestine
and urinary bladder and impacts ion transport mechanisms. Prolactin release
helps regulate water-ion balance by decreasing water uptake and promoting
retention of important ions (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 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.
Salt or Oxygen?
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 - like
fighting at the end of a line - energy deprivation is the most vital concern.
Tissues 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 needed to drive the
pathways of energy recovery in the cell. Oxygen deprivation will not allow these
pathways to function efficiently, if at all. And the result is dead fish. They
might not die right away, but they will die. Salt balance, no matter how much
salt there is in the livewell environment, cannot be maintained without large
amounts energy to fuel the process. And while the importance of maintaining ion
balance 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 water 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 - almost certainly leading to delayed fish
mortality.
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! Relying on ice to sufficiently cool a livewell to fully oxygenate the water
is unrealistic.
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.
References:
1. Milligan CL. Metabolic recovery from exhaustive exercise in rainbow trout:
Review. Comp Biochem Physiol, 1996; 113A:51-60.
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.
6. Grau EG. Environmental physiology and comparative endocrinology of estuarine
fish. Available on-line www2.hawaii.edu/zoology/graduate/faculty/grau.htm.
7. Laiz-Carrion R, S Sangiao-Alvarellos, JM Guzman, MP Martin, JM Miguez, JL
Soengas, JM Mancera. Energy metabolism in fish tissues relaed to osmoregulation
and cortisol action: Fish growth and metabolism. Environmental, nutritional and
hormonal regulation. Fish Physiol and Biochem, 2002; 27(3-4):179-188.
8. Morgan JD, GK Iwama. Energy cost of NaCl transport in isolated gills of
cutthroat trout. Am J Physiol, 1999; 277(3 Pt 2):R631-639.
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.
11. Manzon LA. The role of prolactin in fish osmoregulation: a review. Gen
Compar Endocrin, 2002; 125:291-310.
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.
15. Krumschnabel G, C Biasi, W Weiser. Action of adenosine on energetics,
protein synthesis and K(+) homeostasis in teleost hepatocytes. J Exp Biol, 2000;
203(Pt 27):2657-2665.
16. Krumschnabel G, C Manzl, PJ Schwartzbaum. Importance of glycolysis for the
energetics of anoxia-tolerant and anoxia-intolerant teleost hepatocytes. Physiol
Biochem Zool, 2001; 74(3):413-419.
17. Pesquero J, T Roig, J Bermudez, J Sanchez. Energy metabolism by trout red
blood cells: substrate utilization. J Exp Biol, 1994; 193:183-190.
18. Schramm H. Surviving the summer. Guest article, Bassmaster online. Available
at espn.go.com/outdoors/bassmaster/s/bass_biology_surviving_summer.html.
Oxygen systems that deliver pure oxygen must deliver enough pure oxygen continuously to satisfy the cellular oxygen debt and cellular demand for all the bait or fish in the livewell that are in crisis. Any oxygen system that delivers a fixed or limited flow of oxygen may easily deliver less oxygen than a good aerator or water pump which is often deadly every summer. Know and understand the limitations of any pure oxygen system, it's important. Without enough oxygen supplied continuously, all the salt, chemicals, ice and any other life saving efforts will fail.
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