Climate change-induced increases in summer water temperature have been associated with elevated mortality of adult sockeye salmon (Oncorhynchus nerka) during river migration. We show that cardiorespiratory physiology varies at the population level among Fraser River sockeye salmon and relates to historical environmental conditions encountered while migrating. Fish from populations with more challenging migratory environments have greater aerobic scope, larger hearts, and better coronary supply. Furthermore, thermal optima for aerobic, cardiac, and heart rate scopes are consistent with the historic river temperature ranges for each population. This study suggests that physiological adaptation occurs at a very local scale, with population-specific thermal limits being set by physiological limitations in aerobic performance, possibly due to cardiac collapse at high temperatures.
SUMMARY
As rainbow trout approach exhaustion during prolonged exercise, they maintain maximum cardiac output despite the fact their venous blood, which bathes the heart, becomes hypoxic, acidotic and hyperkalemic. Because these factors are individually recognized to have detrimental inotropic and chronotropic effects on cardiac performance, we hypothesized that adrenergic stimulation is critical in maintaining maximum cardiac performance under these collectively adverse conditions in vivo. To test this hypothesis,maximum cardiac performance in the presence and absence of maximal adrenergic stimulation was assessed with in situ rainbow trout hearts using relevant hyperkalemic (5.0 mmol l–1 K+), acidotic(pH 7.5) and hypoxic challenges. With tonic adrenergic stimulation (5.0 nmol l–1 adrenaline), hearts produced only 44.8±14.6% of their normal maximum cardiac output when exposed under normoxic conditions (20 kPa) to the hyperkalemic, acidotic perfusate, indicating that in vivothere was no refuge from cardiac impairment even if venous blood was fully oxygenated. By contrast, maximum adrenergic stimulation (500 nmol l–1 adrenaline), fully protected maximum cardiac performance under hyperkalemic and acidotic conditions over a wide range of oxygen availability, from normoxia to 2.0 kPa, a venous oxygen tension close to routine values in vivo. Extending the level of hypoxia to 1.3 kPa resulted in a 43.6±2.8% decrease in maximum cardiac output, with hearts failing when tested at 1.0 kPa. Our results suggest that adrenergic stimulation of the trout heart is critical in maintaining maximum performance during prolonged swimming tests, and probably during all forms of exhaustive activity and recovery, when venous blood is hyperkalemic, acidotic and hypoxic.
SUMMARYThe armoured catfish, Pterygoplichthys pardalis, is known to be extremely tolerant of environmental hypercarbia (elevated water CO 2 tensions), which occurs in their natural environment. In addition, previous studies have demonstrated that during exposure to hypercarbia, P. pardalis does not exhibit extracellular pH compensation and thus the heart and other organs must continue to function despite a severe extracellular acidosis. We used an in situ perfused heart preparation to determine the effects of an extracellular hypercapnic (elevated CO 2 in the animal) acidosis (1-7.5% CO 2 ) on heart function, specifically cardiac output, power output, heart rate and stroke volume. The present study is the first to comprehensively examine cardiac function in an acidosistolerant teleost. When compared with control conditions, maximum cardiac performance was unaffected at levels of CO 2 as high as 5%, far exceeding the hypercapnic tolerance of other teleosts. Moreover, P. pardalis exhibited only a moderate decrease (~35%) in cardiac performance when exposed to 7.5% CO 2 , and full cardiac performance was restored in six out of seven hearts upon return to control conditions. Myocardial intracellular pH (pH i ) was protected in situ, as has been found in vivo, and this protection extended to the highest level of CO 2 (7.5%) investigated. Thus, maintained heart function during a hypercapnic acidosis in P. pardalis is probably associated with preferential pH i regulation of the heart, but ultimately is not sufficient to prevent loss of cardiac function. Our findings suggest the need for further study to elucidate the mechanisms behind this remarkable cardiac hypercapnic tolerance.
Perfused rainbow trout Oncorhynchus mykiss hearts exposed to simulated exercise conditions (hypoxia, hyperkalemia and acidosis) at 18°C experienced complete failure of maximum cardiac performance at oxygen tensions <5Á6 kPa and partial failure at <6Á7 kPa. This hypoxic threshold, which occurred in the presence of maximal adrenergic stimulation (500 nM adrenaline), is unusually high compared with previous results at a colder acclimation temperature. Cardiac failure was primarily due to significant decreases (P < 0Á05) in heart rate rather than cardiac stroke volume at all hypoxia levels tested.
Using sharp electrode impalement, action potentials recorded from atrial and ventricular tissue of pink salmon Oncorhynchus gorbuscha generally decreased in duration with increasing test temperature (6, 10, 16 and 20° C). Stimulation of the tissue using 500 nM adrenaline had no significant effect on the duration of the atrial action potential at any test temperature but lengthened the ventricular action potential by ~17%.
This is an electronic version of an article that was published as: Baker, D.W., Hanson, L.M., Farrell, A.P., & Brauner, C.J. (2011). Exceptional CO2 tolerance in white sturgeon (Acipenser transmontanus) is associated with protection of maximum cardiac performance during hypercapnia in situ.
ABSTRACTWhite sturgeon rank among the most CO 2 -tolerant fish species examined to date. We investigated whether this exceptional CO 2 tolerance extended to the heart, an organ generally viewed as acidosis intolerant. Maximum cardiac output (Q max ) and maximum cardiac power output (PO max ) were assessed using a working, perfused, in situ heart preparation. Exposure to a Pco 2 of 3 kPa for 20 min had no significant effect on maximum cardiac performance, while exposure to 6-kPa Pco 2 reduced heart rate, Q max , PO max , and rate of ventricular force generation (F O ) by 23%, 28%, 26%, and 18%, respectively; however, full recovery was observed in all these parameters upon return to control conditions. These modest impairments during exposure to 6-kPa Pco 2 were associated with partially compensated intracellular ventricular acidosis. Maximum adrenergic stimulation (500 nmol L Ϫ1 adrenaline) during 6-kPa Pco 2 protected maximum cardiac performance via increased inotropy (force of contraction) without affecting heart rate. Exposure to higher CO 2 levels associated with morbidity in vivo (i.e., 8-kPa Pco 2 ) induced arrhythmia and a reduction in stroke volume during power assessment. Clearly, white sturgeon hearts are able to increase cardiac performance during severe hypercapnia that is lethal to other fishes. Future work focusing on atypical aspects of sturgeon cardiac function, including the lack of chronotropic response to adrenergic stimulation during hypercapnia, is warranted.
Background: Cognitive complaints involving problems with concentration, memory, decision-making and thinking are relatively common in the work force. The sensitivity of both subjective and objective cognitive functioning to common psychiatric conditions, stress levels and to cognitive load makes it plausible that psychosocial working conditions play a role in cognitive complaints. Thus, this study aimed to test the associations between psychosocial work factors and cognitive complaints in nationally representative samples of the Swedish work force. Cross-sectional (n = 9751) and prospective (n = 3644; two time points two years apart) sequential multiple regression analyses were run, adjusting for general confounders, depressive-and sleeping problems. Additional prospective analyses were run adjusting for baseline cognitive complaints.
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