Glycogen Stores in Trout Tissues Before and After Stream Planting

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.

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.


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.


1992 ◽  
Vol 263 (5) ◽  
pp. H1499-H1505 ◽  
Author(s):  
L. I. Sinoway ◽  
K. J. Wroblewski ◽  
S. A. Prophet ◽  
S. M. Ettinger ◽  
K. S. Gray ◽  
...  

Post leg exercise circulatory arrest (PLE-CA) raises blood pressure (BP) and reduces peak forearm vascular conductance (C). This reflex is evoked by activation of muscle afferents that are often sensitive to lactic acid. We tested the hypothesis that lactic acid reductions induced by muscle glycogen depletion would attenuate the lower-limb metaboreceptor-mediated pressor and forearm vasoconstrictor responses. Eleven subjects had C measured (plethysmography) during post leg exercise circulatory arrest (PLE-CA) (supine bicycle exercise for 9 min, 10 s at 75% VO2max before and after undergoing a glycogen-depletion paradigm (24-h fast followed by 10 min of supine leg exercise at 75% VO2max). In six subjects with lower lactate values, C during PLE-CA was higher after glycogen depletion (0.39 +/- 0.05 vs. 0.21 +/- 0.01 ml.min-1.100 ml-1 x mmHg-1; P < 0.01) and BP was lower (113 +/- 6 vs. 128 +/- 6 mmHg, P < 0.01). In five subjects without attenuated lactate responses, C and BP during PLE-CA were not different. Muscle biopsies (n = 5) demonstrated that the paradigm lowered muscle glycogen concentrations. Thus glycogen depletion-induced reductions in muscle lactate are associated with reduced muscle metaboreceptor-mediated responses.


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.


1968 ◽  
Vol 25 (5) ◽  
pp. 837-851 ◽  
Author(s):  
F. W. H. Beamish

In Atlantic cod, muscle glycogen was reduced by about 50% at moderate swimming speeds and over 80% at higher speeds. Muscle glycogen for a given swimming speed was generally lower after 30 min exercise than after 15 min exercise. During the 8-hr period after strenuous exercise, muscle glycogen increased but remained well below the level for unexercised fish.At moderate swimming speeds, fish exhibited comparatively small amounts of muscle and blood lactic acid. At higher swimming speeds, fish accumulated significantly larger quantities of lactic acid in the muscle and blood. During the recovery period after strenuous exercise, muscle and blood lactic acid increased precipitously. Muscle lactic acid remained high for 1 hr after exercise and then decreased in 8 hr to levels similar to those of unexercised cod. Blood lactic acid followed a similar pattern except that it continued to increase for 1.5 hr after exercise.Serial samples of blood taken before and after 30 min strenuous exercise showed marked differences in lactic acid among individuals. Blood lactic acid usually continued to increase for 30–60 min after exercise, and decreased to the level for unexercised fish about 24 hr after exercise.No mortalities attributable to muscular fatigue occurred among cod.


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.


2015 ◽  
Vol 309 (12) ◽  
pp. E1032-E1039 ◽  
Author(s):  
Javier T. Gonzalez ◽  
Cas J. Fuchs ◽  
Fiona E. Smith ◽  
Pete E. Thelwall ◽  
Roy Taylor ◽  
...  

The purpose of this study was to define the effect of glucose ingestion compared with sucrose ingestion on liver and muscle glycogen depletion during prolonged endurance-type exercise. Fourteen cyclists completed two 3-h bouts of cycling at 50% of peak power output while ingesting either glucose or sucrose at a rate of 1.7 g/min (102 g/h). Four cyclists performed an additional third test for reference in which only water was consumed. We employed 13C magnetic resonance spectroscopy to determine liver and muscle glycogen concentrations before and after exercise. Expired breath was sampled during exercise to estimate whole body substrate use. After glucose and sucrose ingestion, liver glycogen levels did not show a significant decline after exercise (from 325 ± 168 to 345 ± 205 and 321 ± 177 to 348 ± 170 mmol/l, respectively; P > 0.05), with no differences between treatments. Muscle glycogen concentrations declined (from 101 ± 49 to 60 ± 34 and 114 ± 48 to 67 ± 34 mmol/l, respectively; P < 0.05), with no differences between treatments. Whole body carbohydrate utilization was greater with sucrose (2.03 ± 0.43 g/min) vs. glucose (1.66 ± 0.36 g/min; P < 0.05) ingestion. Both liver (from 454 ± 33 to 283 ± 82 mmol/l; P < 0.05) and muscle (from 111 ± 46 to 67 ± 31 mmol/l; P < 0.01) glycogen concentrations declined during exercise when only water was ingested. Both glucose and sucrose ingestion prevent liver glycogen depletion during prolonged endurance-type exercise. Sucrose ingestion does not preserve liver glycogen concentrations more than glucose ingestion. However, sucrose ingestion does increase whole body carbohydrate utilization compared with glucose ingestion. This trial was registered at https://www.clinicaltrials.gov as NCT02110836.


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