Recovery from an activity-induced metabolic acidosis in the American alligator, Alligator mississippiensis

The metabolic acidosis resulting from an intense exercise bout is large in crocodilians. Here we studied recovery from this pH perturbation in the American alligator. Metabolic rate, minute ventilation, arterial pH and gases, and strong ion concentration were measured for 10 h after exhaustion to elucidate the mechanisms and time course of recovery. Exhaustion resulted in a significant increase in lactate, metabolic rate, and ventilation, and a decrease in arterial PCO2), pH and bicarbonate. By 15 min after exhaustion, oxygen consumption returned to rest though carbon dioxide excretion remained elevated for 30 min. Arterial PO2), [Na+], and [K+], increased following exhaustion and recovered by 30 min post-exercise. Minute ventilation, tidal volume, [Cl-], and respiratory exchange ratio returned to resting values by 1 h. The air convection requirement for oxygen was elevated between 15 and 60 min of recovery. Breathing frequency and pH returned to resting values by 2 h of recovery. Lactate levels remained elevated until 6 h post-exercise. Arterial PCO2) and [HCO3-] were depressed until 8 h post-exercise. Compensation during recovery of acid-base balance was achieved by altering ventilation: following the initial metabolic acidosis and titration of bicarbonate, a relative hyperventilation prevented a further decrease in pH.     

Acid-base balance and plasma glutamine concentration in man

Plasma glutamine concentrations were measured in chronic metabolic acidosis and alkalosis in healthy male volunteers. Metabolic acidosis resulted in a significant drop in glutamine concentration while metabolic alkalosis significantly elevated glutamine levels. These changes in glutamine concentration correlated with both the bicarbonate and PCO2 levels. To determine whether bicarbonate or PCO2 levels influence the glutamine concentrations, respectively acidosis was induced by respiring 5% CO2. This resulted in a significant elevation in both PCO2 and glutamine while bicarbonate levels remained unchanged. The results demonstrate an effect of acid-base alterations upon plasma glutamine concentration mediated by PCO2.     

Physiological responses to emersion in the intertidal green crab,Carcinus maenas (L.)

The green shore crab, Carcinus maenas, undergoes on average 6?h periods of emersion during each low-tide cycle during the summer months. Under those conditions, the crab is cut off from its normal water environment and is exposed to potential stress from a suite of environmental and physiological changes: dehydration, compromised gas exchange and resultant internal hypoxia and hypercapnia, thermal stress, and ammonia toxicity. This study examined the comprehensive responses of the green crab in water and to a 6?h emersion period laboratory simulation of a tidal cycle followed by a 1?h re-immersion period, measuring indicators of dehydration, hemolymph osmolality, oxygen uptake, hemolymph acid–base status, heart and ventilatory rate, and hemolymph ammonia and ammonia excretion. Green crabs showed physiological responses of varying magnitude to 6?h of emersion. Individuals were found in the field exclusively under rocks and large clumps of seaweed where temperatures were approximately half those of exposed surfaces and relative humidity was about twice as high as ambient air. During emersion, crabs lost less than 5% of their wet weight, and hemolymph osmolality did not increase significantly. Oxygen uptake continued in air at about 50% of the control, aquatic values; and the gills continued to be ventilated by the scaphognathite, albeit at lower rates. Hemolymph lactate concentrations increased, indicating a shift to a greater reliance on anaerobic metabolism to support energetic needs. A slight acidosis developed in the hemolymph after 1?h of emersion, but it did not increase thereafter. Ammonia concentrations in the hemolymph were unchanged, as ammonia was volatilized by the gills and excreted into the air as NH₃ gas. These results show that the green crab copes with emersion by seeking refuge in microhabitats that mitigate the changes in the physical parameters of intertidal emersion. Physiologically, desiccation is avoided, cardio-respiratory processes are maintained at reduced levels, and hemolymph acid–base balance is minimally affected. Ammonia toxicity appears to be avoided by a shift to excreting NH₃ gas directly or indirectly to air.     

Active ammonia excretion in the giant mudskipper, Periophthalmodon schlosseri (Pallas), during emersion

The main objective of this study was to determine whether active NH(4) (+) excretion occurred in the giant mudskipper, Periophthalmodon schlosseri, during emersion. Our results demonstrated that continual ammonia excretion in P. schlosseri during 24 hr of emersion resulted in high concentrations ( approximately 30 mmol l(-1)) of ammonia in fluid collected from the branchial surface. For fish injected intraperitoneally with 8 mumol g(-1) ammonium acetate (CH3COONH4) followed by 24 hr of emersion, the cumulative ammonia excreted was significantly greater than that of the control injected with sodium acetate. More importantly, the ammonia excretion rate at hour 2 in fish injected with CH3COONH4 followed by emersion was greater than that in fish immersed in water as reported elsewhere, with the greatest change in the ammonia excretion rate occurring at hour 2. Assuming that the rate of endogenous ammonia production remained unchanged, 33% of the exogenous ammonia was excreted through the head region, presumably through the gills, during the first 6 hr of emersion. Indeed, at hour 6, the ammonia concentration in the branchial fluid increased to an extraordinarily high concentration of >90 mmol l(-1). Therefore, our results confirm for the first time that P. schlosseri can effectively excrete a high load of ammonia on land, and corroborate the proposition that active NH(4) (+) excretion through its gills contributes in part to its high tolerance of aerial exposure. Only 4.6% of the exogenous ammonia was detoxified to urea. The glutamate contents in the muscle and liver also increased significantly, but the glutamine contents remained unchanged.     

Effect of air breathing on acid-base and ion regulation after exhaustive exercise and during low pH exposure in the bowfin, Amia calva.

To explore a potential conflict between air breathing and acid-base regulation in the bowfin (Amia calva), we examined how individuals with access to air differed from fish without air access in their response to acidosis. After exhaustive exercise, bowfin with access to air recovered significantly more slowly from the acidosis than fish without air access. While arterial blood pH (pH(a)) of fish without air access recovered to resting levels by 8 h, pH(a) was still significantly depressed in fish having access to air. In addition, Pco(2) was slightly more elevated in fish having air access than those without it. Fish with access to air still had a significant metabolic acid load after 8-h recovery, while those without air access completely cleared the load within 4 h. These results suggest that bowfin with access to air were breathing air and, consequently, were less able to excrete CO(2) and H(+) and experienced a delayed recovery. In contrast, during exposure to low pH, air breathing seemed to have a protective effect on acid-base status in bowfin. During exposure to low pH water, bowfin with access to air developed a much milder acidosis than bowfin without air access. The more severe acidosis in fish without air access was caused by an increased rate of lactic acid production. It appears that enhanced O(2) delivery allowed air-breathing bowfin to avoid acidosis-induced anaerobic metabolism and lactic acid production. In addition, during low pH exposure, plasma Na(+) and Cl(-) concentrations of fish without air access fell slightly more rapidly than those in fish with air access, indicating that the branchial ventilatory changes associated with air breathing limited, to some degree, ion losses associated with low pH exposure.     

Cerebrospinal fluid ions in metabolic acidosis in dogs: effects of acetazolamide

We hypothesized that, during isosmotic isonatremic HCl acidosis with maintained isocapnia in cisternal cerebrospinal fluid (CSF), acetazolamide, by inhibiting carbonic anhydrase (CA) in the central nervous system (CNS), should produce an isonatric hyperchloric metabolic acidosis in CSF. Blood and CSF ions and acid-base variables were measured in two groups of anesthetized and paralyzed dogs with bilateral ligation of renal pedicles during 5 h of HCl acidosis (plasma [HCO3-] = 11 meq/l). Mechanical ventilation was regulated such that arterial PCO2 dropped and CSF Pco2 remained relatively constant. In group I (control group, n = 6), CSF [Na+] remained unchanged, [HCO3-] and strong ions difference (SID) fell, respectively, 6.1 and 5 meq/l, and [Cl-] rose 3.5 meq/l after 5 h of acidosis. In acetazolamide-treated animals, (group II, n = 7), CSF [Na+] remained unchanged, [HCO3-], and SID fell 11 and 7.1 meq/l, respectively, and [Cl-] rose 7.1 meq/l. We conclude that during HCl acidosis inhibition of CNS CA by acetazolamide induces an isonatric hyperchloric metabolic acidosis in CSF, which is more severe than that observed in controls.     

Effect of air exposure on nitrogen metabolism in the crab Cancer pagurus.

In C. pagurus exposed to air for 18 h, blood ammonia content decreased within the 2 first hours, then increased at a relatively constant rate (25 microM/h); blood urate content increased at a lower rate (10 microM/h) and a classical blood acidosis was observed. In the cheliped muscle, a transient 22% decrease in GDH activity for ammonia formation and a 48% increase in GDH activity in the reverse reaction (glutamate synthesis) occurred following 6 and 12 h of emersion, respectively. Changes in LDH activity, used as an indicator of anaerobic potential of muscle, were not observed, except for an 18% increase in crabs exposed to air for 24 h. The increase in blood urate content, not known as a response to emersion in decapods, appeared to be different from that observed in response to hypoxia. The relatively low blood ammonia overload and the GDH increased activity for glutamate synthesis suggested that part of the produced ammonia was stored under a bound form in some tissues. The response of C. pagurus to air exposure is discussed on account of the Storey and Storey ('90) theory.     

Cerebral metabolic and pressure-flow responses during sustained hypoxia in awake sheep.

Conscious sheep (n = 6), exposed to 3.5 h of normobaric hypoxia (arterial PO2 = 40 Torr) while allowed varying arterial PCO2, showed striking early increments of cerebral blood flow (CBF; +200-250%, by radiolabeled microspheres) and decrements of cerebral vascular resistance (CVR) in association with an early temporary elevation of cerebral O2 consumption (CMRO2; +25-60%). After 2 h, CMRO2 returned to normoxic levels, while CBF declined to a lower but still elevated level (+150%). CBF/CMRO2 increased twofold, while cerebral fractional extraction of O2 was unchanged. Mean arterial pressure was unchanged, but cerebral venous pressure rose (+11 mmHg) in a stable fashion such that cerebral perfusion pressure declined by 13%. Cerebral venous hematocrit and hemoglobin concentration were both elevated (+2.2-2.7% Hct units; +1.0-1.3 g/dl, respectively) above the corresponding arterial values between 150 and 210 min of hypoxia, suggesting venous hemoconcentration in possible association with a transcapillary fluid shift. CBF, and especially CVR, were well correlated with arterial O2 content.     

Urinary-blood delta PCO2 in renal tubular acidosis (author's transl)

A state of renal tubular acidosis has been produced in rats by the administration of sodium maleate or acetazolamide (proximal tubular acidosis) and of lithium chloride of amiloride (distal tubular acidosis). During progressive alkaline diuresis, delta PCO2 (urine minus blood PCO2) increases significantly in rats presenting proximal tubular acidosis. Delta PCO2 is significantly depressed in rats presenting distal tubular acidosis. In well defined conditions of bicarbonate or phosphate excretion, delta PCO2 is a valuable index of distal ion secretion.     

Effect of pH on metabolic and cardiorespiratory responses during progressive exercise

Six healthy male subjects performed three exercise tests in which the power output was increased by 100 kpm/min each minute until exhaustion. The studies were carried out after oral administration of CaCO3 (control), NH4Cl (metabolic acidosis), and NaHCO3 (metabolic alkalosis). Ventilation (VE), O2 intake (VO2), and CO2 output (VCO2) were monitored continuously. Arterialized-venous blood samples were drawn at specific times and analyzed for pH, PCO2, and lactate concentration. Resting pH (mean +/- SE) was lowest in acidosis (7.29 +/- 0.01) and highest in alkalosis (7.46 +/- 0.02). A lower peak power output (kpm/min) was achieved in acidosis (1,717 +/- 95) compared with control (1,867 +/- 120) alkalosis (1,867 +/- 125). Submaximal VO2 and VCO2 were similar, but peak VO2 and VCO2 were lower in acidosis. Plasma lactate concentration was lower at rest and during exercise in acidosis. Although lactate accumulation was reduced in acidosis, increases in hydrogen ion concentration were similar in the three conditions. We conclude that acid-base changes influence the maximum power output that may be sustained in incremental dynamic exercise and modify plasma lactate appearance, but have little effect on hydrogen ion appearance in plasma.     

Newborn puppy cerebral acid-base regulation in experimental asphyxia and recovery

We hypothesized that part of the newborn tolerance of asphyxia involves strong ion changes that minimize the cerebral acidosis and hasten its correction in recovery. After exposure of newborn puppies to 15 or 30 min experimental asphyxia (inhalation of gas with fractional concentration of CO2 and of O2 in inspired gas = 0.07-0.08 and 0.02-0.03, respectively), blood lactate increased to 13.2 and 23.4 mmol/l, respectively, brain tissue lactate increased to 14.4 and 19.7 mmol/kg, and cerebrospinal fluid (CSF) lactate increased to 7.6 and 14.4 mmol/l. We presume that the tissue lactate increase reflects increases in brain cell and extracellular fluid lactate concentration. The lactate increase, a change that will decrease the strong ion difference (SID), [HCO3-], and pH, was accompanied by increases in Na+ (plasma, CSF, brain), K+ (plasma, CSF), and osmolality without change in Cl-. After 60-min recovery, plasma and brain lactate decreased significantly, but CSF lactate remained unchanged. [H+] recovery was more complete than that of the strong ions due to hyperventilation-induced hypocapnia. We conclude that during asphyxia-induced lactic acidosis, changes in strong ions occur that lessen the decrease in SID and minimize the acidosis in plasma and CSF. To the extent that the increase in brain tissue sodium reflects increases in intra-and extracellular fluid sodium concentration, the decrease in SID will be less in these compartments as well. In recovery, CSF ionic values change little; plasma and brain tissue lactate decrease with a similar time course, and the [H+] is rapidly returned toward normal by hypocapnia even while the SID is below normal.     

Mechanisms of respiratory response to isoproterenol in glomectomized cats

Effects of intravenous isoproterenol (2-3 micrograms) on arterial pressure, end-tidal CO2 partial pressure (PCO2), medullary extracellular fluid (ECF) pH, and phrenic activity were studied in 13 anesthetized paralyzed cats whose vagi and carotid sinus nerves were cut. The cats were servo-ventilated to keep PCO2 relatively constant. Injections of Ringer solution were without effect. Isoproterenol caused arterial pressure to fall, a transient small (1 Torr) increase of PCO2, increased venous CO2 return to the lungs, a medullary ECF acidosis, and a stimulation of respiration that continued to be elevated after arterial pressure, PCO2, and medullary ECF pH had returned to control. We show that the ECF acidosis is minimally due to the hypotension and to the small transient rise of PCO2. We also show that the respiratory response cannot be explained solely by the ECF acidosis. We conclude that, in addition to its known stimulation of peripheral chemoreceptors, isoproterenol causes medullary ECF to become acidic probably due to metabolic effects on neural tissue and has a separate direct stimulating effect on neurons in the brain.     

Effects of acute hypobaric hypoxia on acid-base status of fowl blood

Arterial blood Po/, Pco2, lactate levels and Cl- ion concentration as well as pH were measured on the time course in chickens (Gallus domesticus) as they settled in normoxic conditions and during exposure to acute hypobaric hypoxia (Pb = 450 Torr). Hypoxia provoked at first a CO2 increased output from blood and a brief stage of deep metabolic acidosis during which lactate levels suddenly increased. This acidosis was then compensated producing a return to the initial pH and a decrease in [HCO3-] + [CO3(2-)] after 60 min. Subsequently respiratory alkalosis associated with an increase in [HCO-3] + [CO3(2-)], a decrease in cl- ion concentration and a small decrease in lactate levels were observed. Prolonged exposure to hypoxia (16 h) resulted in a new return to the initial pH, a decrease in concentration of [HCO3-] + [CO3(2-)] and a high lactate level. The hematocrit value, the Hb concentration, and the plasma Na+, K+, Ca++ and Mg++ ion concentration did not change significantly.     

Onset of and recovery from physiological stress in <Emphasis Type="Italic">Liocarcinus depurator</Emphasis> after trawling and air exposure under different seasonal conditions

The onset of and recovery from physiological stress in Liocarcinus depurator (Decapoda: Portunidae), that were trawled and subjected to emersion during fishing activities, was analysed in a field study in the Northern Adriatic Sea. Our working hypothesis intended to assess the development of physiological impairment due to air exposure during sorting operations, and the possible recovery trajectories after the return to sea of this by-caught species. The protocol we used included experimental trawling and quantification of physiological stress indicators (haemolymph concentrations of l-lactate, d-glucose, ammonia and pH) under different seasonal conditions. Immediately after being caught, when the fishing net was emptied on board, L. depurator showed higher physiological imbalance in the summer vs. winter experiments, highlighting the immediate effect of temperature shock due to the difference in temperature between the sea bottom and the deck (15–18 and 2°C in summer and winter, respectively). Experimental animals in the permanently emersed condition exhibited a progressive disruption of homeostasis in both seasons, as confirmed by a significant increase in lactate and a decrease in the pH of the haemolymph as a function of the emersion time. Ammonia levels were almost stable in the summer, when the physiological limits of this metabolite were reached immediately after animals were caught. In the winter, a significant increase in ammonia was observed over the time. This pattern can be attributed to the impairment of gill function, resulting in suffocation (manifested by marked haemolymph acidosis) and reduced ammonia excretion. Glucose concentration was revealed to be stable during air exposure in both seasons, though a higher concentration was recorded in the summer compared to the winter. The recovered individuals tended to return to pre-caught values for all of the haemolymph parameters we measured, though with different trajectories in the two seasons. From these results, we conclude that temperature shock, coupled with air exposure, influenced the ultimate stress level of this species to a greater extent than other effects of fishing.     

Monocyte-conditioned medium, interleukin-1, and tumor necrosis factor stimulate the acute phase response in human hepatoma cells in vitro

Human hepatoma cells mimic the acute phase response after treatment with monocyte-conditioned medium. Levels of secreted fibrinogen, alpha-1 acid glycoprotein, C-reactive protein, haptoglobin, and the third component of complement were elevated compared with control levels after 48 h of incubation with conditioned supernatant medium from an enriched fraction of normal peripheral monocytes. Albumin levels declined and alpha-1 antitrypsin remained unchanged. Levels of specific mRNA were measured by hybridization to slot blots and Northern blots and changed in correspondence with protein alterations. Interleukin-1 and tumor necrosis factor stimulated the third component of complement, but did not elevate any other member of the acute phase group and were therefore only partially active in this system. The identification of an in vitro model of the human acute phase response will permit analysis of the molecular basis for coordinate regulation of this group of facultative genes.     

Stress effect of different temperatures and air exposure during transport on physiological profiles in the American lobster Homarus americanus

Homarus americanus is an important commercial species that can survive 2-3 days out of water if kept cool and humid. Once caught for commercial purpose and shipped around the world, a lobster is likely to be subjected to a number of stressors, including emersion and air exposure, hypoxia, temperature changes and handling. This study focused on the effect of transport stress and specifically at different animal body temperature (6 and 15 degrees C) and air exposure during commercial transport and recovery process in water. Animals were monitored, by hemolymph bleeding, at different times: 0 h (arrival time at plant) 3 h, 12 h, 24 h and 96 h after immersion in the stocking tank with a water temperature of 6.5+/-1.5 degrees C. We analysed the effects by testing some physiological variables of the hemolymph: glucose, cHH, lactate, total protein, cholesterol, triglycerides, chloride and calcium concentration, pH and density. All these variables appeared to be influenced negatively by high temperature both in average of alteration from the physiological value and in recovering time. Blood glucose, lactate, total protein, cholesterol were significantly higher in the group with high body temperature compared to those with low temperature until 96 h after immersion in the recovery tank.     

Permeability of epidural somatostatin and morphine into the intrathecal space of dogs

In an in vivo saline perfusate of the intrathecal space of 6 dogs, the concentration of somatostatin was determined by radioimmunoassay before and over 2 h after epidural administration of 3 mg somatostatin. The total recovered amount of somatostatin was negligible, about 0.02%. However, within 50 min after the bolus epidural injection of somatostatin, the concentration per ml perfusate increased from 0.1 +/- 0.02 ng/ml to 138 +/- 102 ng/ml (P less than 0.001) and declined to 4 +/- 1.7 ng/ml after 120 min. This increase of the somatostatin concentration by 3 orders of magnitude might explain why epidurally administered somatostatin is effective in treatment of acute and chronic pain. In a control investigation with epidural morphine in another 6 dogs to prove the feasibility of the method, the total recovered amount of morphine in the intrathecal perfusate over 2 h was about 12%.     

Mitigation of chlorine-induced lung injury by low-molecular-weight antioxidants

Chlorine (Cl(2)) is a highly reactive oxidant gas used extensively in a number of industrial processes. Exposure to high concentrations of Cl(2) results in acute lung injury that may either resolve spontaneously or progress to acute respiratory failure. Presently, the pathophysiological sequelae associated with Cl(2)-induced acute lung injury in conscious animals, as well as the cellular and biochemical mechanisms involved, have not been elucidated. We exposed conscious Sprague-Dawley rats to Cl(2) gas (184 or 400 ppm) for 30 min in environmental chambers and then returned them to room air. At 1 h after exposure, rats showed evidence of arterial hypoxemia, respiratory acidosis, increased levels of albumin, IgG, and IgM in bronchoalveolar lavage fluid (BALF), increased BALF surfactant surface tension, and significant histological injury to airway and alveolar epithelia. These changes were more pronounced in the 400-ppm-exposed rats. Concomitant decreases of ascorbate (AA) and reduced glutathione (GSH) were also detected in both BALF and lung tissues. In contrast, heart tissue AA and GSH content remained unchanged. These abnormalities persisted 24 h after exposure in rats exposed to 400 ppm Cl(2). Rats injected systemically with a mixture of AA, deferoxamine, and N-acetyl-L-cysteine before exposure to 184 ppm Cl(2) had normal levels of AA, lower levels of BALF albumin and normal arterial Po(2) and Pco(2) values. These findings suggest that Cl(2) inhalation damages both airway and alveolar epithelial tissues and that resulting effects were ameliorated by prophylactic administration of low-molecular-weight antioxidants.     

The Relation between Accumulation of Abscisic Acid and Proline in Detached Rice Leaves

The relation between abscisic acid (ABA) and proline accumulation was investigated in detached rice (Oryza sativa L.) leaves. In darkness, proline content increased about 2-, 2,5- and 6-fold after 24, 48 and 72 h. ABA content reached maximum after 48 h. In the light, proline content remained almost unchanged until 48 h and subsequently increased slightly. ABA content in the light was lower than in darkness, but the maximum was also after 48 h. During 12-h exposure to decreased air humidity, proline content gradually increased, but ABA content increased about 25-fold after 4 h and declined thereafter. Exogenous application of ABA resulted in an increase in proline content in detached rice leaves under both light and darkness.     

Physiological changes in the Norway lobster Nephrops norvegicus (L.) escaping and discarded from commercial trawls on the West Coast of Scotland: II. Disturbances in haemolymph respiratory gases, tissue metabolites and swimming performance after capture and during recovery

The physiological states of trawled and creel-caught (control) Norway Lobsters (Nephrops norvegicus (L.)) captured on grounds off the West Coast of Scotland (120–150 m) were compared. Undersized “discards” (<25–35 mm carapace length) were sampled directly from the cod-end and following recovery in underwater (u/w) cages at a mean depth of 24 m. “Escaped” animals which had passed through the cod-end meshes and collected in a small-meshed net “cover” were transferred without emersion (air-exposure) for sampling on-board. Some of these individuals were also transferred by SCUBA divers to u/w cages. Haemolymph PO₂, PCO₂ and pH measurements showed that both discarded and escaped animals experienced moderate internal hypoxia, hypercapnia and acidosis which became severe after 1 h emersion of the former on deck. A marked handling effect was evident in which haemolymph PO₂ declined and PCO₂ became elevated in both controls and recovering trawled animals. In both discarded and escaped animals haemolymph l-lactate and d-glucose concentrations were high compared to controls, but with levels significantly lower in escapes suggesting less tail-flip swimming activity within the cod-end cover. Further emersion had little effect on haemolymph l-lactate in discards. Recovery to control levels of both metabolites occurred within 24 h in u/w cages but the exercising of captured individuals (by tactile stimulation) produced further significant increases. Abdominal flexor muscle concentrations of l-lactate were also elevated in discards and escapes and positively correlated with haemolymph levels. Muscle glycogen showed severe depletion in both groups compared to unexercised controls and 1 h emersion reduced levels drastically (to 20% of normal concentrations). High haemolymph ammonia (T_amm) was characteristic of both trawled groups but was reduced rapidly during recovery. These metabolite changes were accompanied by reductions in the number of escape swimming tail-flips that could be elicited before exhaustion, particularly in discards. This reduction in performance was evident in discards even after 24 h recovery, but escapes showed almost normal responses. The severity of the physiological stresses experienced during trawling, and to a lesser extent in escaped animals, and their effects on recovery of undersized discards regaining the seabed, is discussed. These findings may help us predict the survival, longer-term recovery and fitness of fished N. norvegicus, and their potential contribution to the regeneration of exploited populations.