Diet, Glycogen Reserves and Resistance to Fatigue in Hatchery Rainbow Trout

1959 ◽  
Vol 16 (3) ◽  
pp. 321-328 ◽  
Author(s):  
R. B. Miller ◽  
A. C. Sinclair ◽  
P. W. Hochachka

In a stream occupied by a resident wild trout population, mortality of introduced hatchery trout is greater than when similar trout are released in a barren stream. From this it has been inferred that in the occupied stream the new-comers cannot find niches and succumb to exhaustion in the open current. A conspicuous rise in blood lactic acid in planted hatchery trout supports this inference.In the present experiment rainbow trout of identical brood stock were raised on two diets; one group received a complete dry pelleted ration, the other, ground liver. After 35 weeks the trout were subjected to varying degrees of exercise, following which blood lactate and liver and muscle glycogen were assayed. It was found that the pellet-fed trout had more glycogen stores before exercise; that during exercise this group maintained its liver glycogen but lost about half the muscle glycogen after 15 minutes of exercise. After 12 hours' rest muscle glycogen had risen to the normal level. In the liver-fed trout liver glycogen was depleted to one-half after 15 minutes' exercise and muscle glycogen fell to one-fifth or lower. Twelve hours rest failed to restore either liver or muscle glycogen. Prolonged exercise in a current of one mile per hour reduced glycogen to about 1/4 in the liver-fed fish; some died during the test, and none returned to normal metabolic states after 24 hours. It is concluded that exhaustion of metabolites such as glycogen plays some part in deaths of planted trout, and that the hatchery diet can materially affect the ability of the fish to survive.

1962 ◽  
Vol 19 (1) ◽  
pp. 127-136 ◽  
Author(s):  
P. W. Hochachka ◽  
A. C. Sinclair

Changes in the glycogen reserves of epaxial and heart muscle of trout were followed after stream planting. Muscle glycogen recovered quickly in large fish; more slowly in smaller ones, and was related to earlier reported changes in liver glycogen and blood lactic acid. Heart glycogen increased initially, but fell again shortly after feeding became stabilized. Muscle glycogen reserves of wild trout were lower in the presence of hatchery fish than in their absence. A depletion of some metabolite, such as glycogen, in conjunction with an increased body demand due to raised basal metabolism was suggested as a factor in delayed mortality.


1961 ◽  
Vol 18 (1) ◽  
pp. 125-135 ◽  
Author(s):  
P. W. Hochachka

Three groups of trout, two introduced populations of Salmo gairdneri and a resident Salmo clarki, were studied in stream sections. Liver glycogen deposits, which were reduced to low levels during transportation to the stream, were restored in 2 to 3 weeks in all groups, with recovery rates being approximately inverse to the population density. Within the hatchery groups, larger fish laid down greater glycogen stores. Wild trout maintained their high glycogen reserves throughout the experiment.


1987 ◽  
Vol 252 (3) ◽  
pp. R587-R593 ◽  
Author(s):  
B. Sonne ◽  
K. J. Mikines ◽  
H. Galbo

In fed rats, hyperglycemia develops during exercise. This contrasts with the view based on studies of fasted human and dog that euglycemia is maintained in exercise and glucose production (Ra) controlled by feedback mechanisms. Forty-eight-hour-fasted rats (F) were compared to fed rats (C) and overnight food-restricted (FR) rats. [3-3H]- and [U-14C] glucose were infused and blood and tissue sampled. During running (21 m/min, 0% grade) Ra increased most in C and least in F and only in F did Ra not significantly exceed glucose disappearance. Plasma glucose increased more in C (3.3 mmol/l) than in FR (1.6 mmol/l) and only modestly (0.6 mmol/l) and transiently in F. Resting liver glycogen and exercise glycogenolysis were highest in C and similar in FR and F. Resting muscle glycogen and exercise glycogenolysis were highest in C and lowest in F. During running, lactate production and gluconeogenesis were higher in FR than in F. At least in rats, responses of production and plasma concentration of glucose to exercise depend on size of liver and muscle glycogen stores; glucose production matches increase in clearance better in fasted than in fed states. Probably glucose production is stimulated by “feedforward” mechanisms and “feedback” mechanisms are added if plasma glucose decreases.


1975 ◽  
Vol 32 (6) ◽  
pp. 753-760 ◽  
Author(s):  
D. J. McLeay ◽  
D. A. Brown

In the static study (no exercise), liver glycogen stores were unchanged during 12-h exposure to 0.8 of the 96-h LC50; longer exposures caused a progressive decrease to levels one fifth those of controls at 72 h. Plasma glucose levels in fish held in 0.8 LC50 effluent for 3–96 h were elevated; at 96 h, glucose had increased threefold. Mean values for plasma lactate were elevated significantly at 3, 6, 24, 72, and 96 h.In the exercise (swimming one body length per second)–rest study, muscle glycogen levels decreased 53–78% during exercise in water or effluent (0.7 LC50) for 4–12 h, and did not recover during 12-h rest in water. Muscle glycogen for fish exercised for 12 h in effluent and then rested for 4 or 12 h in effluent was lower compared to values for fish exercised in effluent and then rested in water. There was no difference in liver glycogen levels offish exercised in effluent or water for 4–12 h. Values of liver glycogen for fish exercised in effluent for 12 h and then rested for 4, 8, or 12 h in effluent decreased 60–70% compared to fish exercised in water for 12 h and then rested in water and by 55–65% from fish exercised in effluent for 12 h and rested in water for 4–12 h. Plasma glucose levels were elevated one- to fourfold during exercise in water or effluent. Fish resting in water for 4, 8, or 12 h following exercise in water had relatively stable glucose levels; whereas for fish exercised and then rested in effluent the glucose levels increased twofold during resting. Plasma lactate levels were elevated five- to sixfold during exercise in water or effluent for 4–12 h, declining to values 1–2 times those of stock fish within 4-h rest. Plasma lactate levels for fish exercised in effluent and then rested in effluent or water were continually higher than those for fish exercised and rested in water.It was concluded that measurement of carbohydrate metabolites, particularly blood sugar levels, in unexercised fish could prove useful as a rapid method for measuring toxicity of pulpmill effluents and other pollutants.


1966 ◽  
Vol 23 (4) ◽  
pp. 471-485 ◽  
Author(s):  
E. Don Stevens ◽  
Edgar C. Black

The effect of intermittent severe exercise of short duration on carbohydrate metabolism was examined using unanesthetized, intact rainbow trout. The levels of muscle glycogen, muscle lactate, blood lactate, and liver glycogen were determined in fish sampled immediately after severe exercise of 3 sec to 5 min, after recovery of 3 min to 60 min, and after re-exercise of 3 sec to 5 min. It appears that rainbow trout are not well adapted to tolerate frequent exercise of short duration.


1994 ◽  
Vol 4 (3) ◽  
pp. 221-236 ◽  
Author(s):  
John A. Hawley ◽  
Steven C. Dennis ◽  
Timothy D. Noakes

Soccer requires field players to exercise repetitively at high intensities for the duration of a game, which can result in marked muscle glycogen depletion and hypoglycemia. A soccer match places heavy demands on endogenous muscle and liver glycogen stores and fluid reserves, which must be rapidly replenished when players complete several matches within a brief period of time. Low concentrations of muscle glycogen have been reported in soccer players before a game, and daily carbohydrate (CHO) intakes are often insufficient to replenish muscle glycogen stores, CHO supplementation during soccer matches has been found to result in muscle glycogen sparing (39%), greater second-half running distances, and more goals being scored with less conceded, when compared to consumption of water. Thus, CHO supplementation has been recommended prior to, during, and after matches. In contrast, there is currently insufficient evidence to recommend without reservation the addition of electrolytes to a beverage for ingestion by players during a game resulting in sweat losses of < 4% of body weight.


1967 ◽  
Vol 24 (8) ◽  
pp. 1701-1715 ◽  
Author(s):  
T. Nakano ◽  
N. Tomlinson

In rainbow trout (Salmo gairdneri) blood plasma concentrations of adrenaline (AD) and noradrenaline (NAD), and liver and heart concentrations of AD increased in response to severe physical disturbance. Skeletal muscle and anterior kidney concentrations of AD and NAD did not change detectably. Maximum plasma concentrations observed during disturbance of the fish were 0.20–0.36 μg AD and 0.05–0.09 μg NAD/ml. These plasma concentrations decreased relatively rapidly during recovery of the fish.Plasma glucose concentrations increased in response to disturbance, the magnitude and duration of the hyperglycemia being greater in those fish with initially high liver glycogen reserves. Liver glycogen concentrations in those fish with initially high (ca. 7%) concentrations apparently decreased in response to disturbance and increased during recovery of the fish, but no change was detected in liver glycogen concentrations in fish in which they were initially low (ca. 2.5%). Heart and skeletal muscle glycogen concentrations decreased in response to disturbance and increased during recovery.In skeletal muscle, the concentration of adenosine 3′,5′-phosphate and the proportion of phosphorylase in the a form increased in response to disturbance of the fish and decreased thereafter.


2014 ◽  
Vol 306 (2) ◽  
pp. R102-R107 ◽  
Author(s):  
Eric A. F. Herbst ◽  
Rebecca E. K. MacPherson ◽  
Paul J. LeBlanc ◽  
Brian D. Roy ◽  
Nam Ho Jeoung ◽  
...  

During recovery from glycogen-depleting exercise, there is a shift from carbohydrate oxidation to glycogen resynthesis. The activity of the pyruvate dehydrogenase (PDH) complex may decrease to reduce oxidation of carbohydrates in favor of increasing gluconeogenic recycling of carbohydrate-derived substrates for this process. The precise mechanism behind this has yet to be elucidated; however, research examining mRNA content has suggested that the less-abundant pyruvate dehydrogenase kinase-4 (PDK4) may reduce PDH activation during exercise recovery. To investigate this, skeletal muscle and liver of wild-type (WT) and PDK4-knockout (PDK4-KO) mice were analyzed at rest (Rest), after exercise to exhaustion (Exh), and after 2 h of recovery with ad libitum feeding (Rec). Although there were no differences in exercise tolerance between genotypes, caloric consumption was doubled by PDK4-KO mice during Rec. Because of this, PDK4-KO mice at Rec supercompensated muscle glycogen to 120% of resting stores. Therefore, an extra group of PDK4-KO mice were pair-fed (PF) with WT mice during Rec for comparison. PF mice fully replenished muscle glycogen but recovered only 50% of liver glycogen stores. Concentrations of muscle lactate and alanine were also lower in PF than in WT mice, indicating that this decrease may lead to a potential reduction of recycled gluconeogenic substrates, due to oxidation of their carbohydrate precursors in skeletal muscle, leading to observed reductions in hepatic glucose and glycogen concentrations. Because of the impairments seen in PF PDK4-KO mice, these results suggest a role for PDK4 in regulating the PDH complex in muscle and promoting gluconeogenic precursor recirculation during recovery from exhaustive exercise.


1962 ◽  
Vol 19 (3) ◽  
pp. 409-436 ◽  
Author(s):  
Edgar C. Black ◽  
Anne Robertson Connor ◽  
Kwok-Cheung Lam ◽  
Wing-Gay Chiu

Experiments upon muscular fatigue in [Formula: see text]-year-old rainbow trout (Salmo gairdneri) were carried out at the trout hatchery at Summerland, British Columbia during the summers of 1958 and 1959. Observations were made on hemoglobin, water content of muscle and whole blood, muscle and liver glycogen, and pyruvate and lactate in muscle, blood and liver. Experimental conditions included 30 min moderate activity, 2–15 min severe exercise, and recovery up to 24 hr following 15 min severe exercise. The results for hemoglobin, muscle and liver glycogen and blood lactate were similar to those reported earlier. Muscle glycogen was depleted 50% or more in the first 2 min of severe activity. Correlated with this rapid depletion of glycogen was a sudden accumulation of muscle pyruvate and lactate. Pyruvate and lactate likewise increased in the blood. While the disappearance of both pyruvate and lactate from muscle began immediately upon cessation of activity, resting levels were not approached until the 8th hr of recovery. During recovery, the levels of pyruvate and lactate in the blood after severe exercise continued to increase for the first hour, remained elevated for at least 8 hr and did not return to the resting level until the 12th–24th hr. Muscle glycogen was not restored above half the resting level at the end of 24 hr. Interpretations of the data in relation to metabolism in rainbow trout are discussed.


1959 ◽  
Vol 196 (6) ◽  
pp. 1253-1257 ◽  
Author(s):  
Joseph E. Sokal ◽  
Edward J. Sarcione

Subcutaneous epinephrine doses of 0.1 mg/kg or more consistently produced declines in muscle glycogen of rats. Transient declines (30%) in liver glycogen, followed by net resynthesis to levels above the control value, were observed after subcutaneous doses 0.2–0.4 mg/kg. Subcutaneous doses of 6.0 mg/kg were required to produce progressive depletion of liver glycogen (82%), over a 3-hour period. However, such depletion was uniformly obtained by intraperitoneal injection of much smaller doses (0.4 mg/kg/hr.). High blood levels of lactate and glucose did not reverse glycogenolysis in liver or in muscle when adequate concentrations of epinephrine were maintained. Although intraperitoneal injection of epinephrine leads to high concentrations at the liver and lower concentrations at skeletal muscle, intraperitoneal doses of 0.1 mg/kg/hr. produced declines in muscle glycogen but not in liver glycogen. It is concluded that the concentration of epinephrine required to produce glycogenolysis in the liver is at least 5–10 times as high as that effective in the muscle. The transient hepatic glycogenolysis observed after relatively small subcutaneous doses of epinephrine may be due to stimulation of endogenous glucagon release.


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