scholarly journals Normoxic limitation of maximal oxygen consumption rate, aerobic scope and cardiac performance in exhaustively exercised rainbow trout (Oncorhynchus mykiss)

Author(s):  
T.J. McArley ◽  
D. Morgenroth ◽  
L.A. Zena ◽  
A.E. Ekström ◽  
E. Sandblom

In fish, maximum O2 consumption rate (MO2max) and aerobic scope can be expanded following exhaustive exercise in hyperoxia; however, the mechanisms explaining this are yet to be identified. Here, in exhaustively exercised rainbow trout (Oncorhynchus mykiss), we assessed the influence of hyperoxia on MO2max, aerobic scope, cardiac function and blood parameters to address this knowledge gap. Relative to normoxia, MO2max was 33% higher under hyperoxia, and this drove a similar increase in aerobic scope. Cardiac output, due to increased stroke volume, was significantly elevated under hyperoxia at MO2max indicating hyperoxia released a constraint on cardiac contractility apparent with normoxia. Thus, hyperoxia improved maximal cardiac performance, thereby enhancing tissue O2 delivery and allowing a higher MO2max. Venous blood O2 partial pressure (PvO2) was elevated in hyperoxia at MO2max, suggesting a contribution of improved luminal O2 supply in enhanced cardiac contractility. Additionally, despite reduced haemoglobin and higher PvO2, hyperoxia treated fish retained a higher arterio-venous O2 content difference at MO2max. This may have been possible due to hyperoxia offsetting declines in arterial oxygenation known to occur following exhaustive exercise in normoxia. If this occurs, increased contractility at MO2max with hyperoxia may also relate to an improved O2 supply to the compact myocardium via the coronary artery. Our findings show MO2max and aerobic scope may be limited in normoxia following exhaustive exercise due to constrained maximal cardiac performance and highlight the need to further examine whether or not exhaustive exercise protocols are suitable for eliciting MO2max and estimating aerobic scope in rainbow trout.

1994 ◽  
Vol 51 (3) ◽  
pp. 536-544 ◽  
Author(s):  
Rod W. Wilson ◽  
Harold L. Bergman ◽  
Chris M. Wood

Juvenile rainbow trout (Oncorhynchus mykiss, 5–13 g) were chronically exposed to sublethal Al (38 μg∙L−1) in acidified soft water (Na+ = 85, Ca2+ = 28 μEq∙L−1, pH 5.2–5.4) for 36 d. Acclimation (increased resistance to challenge with 162 μg Al∙L−1 Al at pH 5.2) occurred after 5 d and was associated with a fourfold increase in gill mucous cell density and reduction in apparent lamellar surface area; initially elevated blood–water diffusion distances returned to normal after 34 d, but the reduction in apparent surface area persisted. Chronic exposure to acid alone (pH 5.2, same water chemistry) caused no morphometric changes but resulted in persistent impairment of Ucrit (critical aerobic swimming speed) by about 10%. This was due to increased oxygen requirements at subcritical swimming speeds (loading stress) and was alleviated when trout were swum at pH 6.5 (zero Al) on day 36. In trout preexposed to sublethal Al, Ucrit was chronically impaired by approximately 16% due to loading stresses and reduction in the maximum rate of oxygen uptake, Mo2max (limiting stress); Ucrit and Mo2max remained depressed even when fish were swum at pH 6.5 (zero Al). Reduced gill area compromises the aerobic scope for activity but may be an unavoidable cost of acclimation to Al.


1994 ◽  
Vol 193 (1) ◽  
pp. 209-232 ◽  
Author(s):  
A Gamperl ◽  
A Pinder ◽  
R Grant ◽  
R Boutilier

To investigate the relationship between cardiac performance and coronary perfusion, cardiovascular variables (Q(dot), Vs, fh, Pda) and coronary blood flow (q·cor) were measured in rainbow trout (Oncorhynchus mykiss) (1.2­1.6 kg) before and after adrenergic stimulation (1.0 µg kg-1 adrenaline) under conditions of (1) normoxia, (2) hypoxia (approximate PwO2 12 kPa) and (3) 2.5 h after returning to normoxia. q·cor for resting fish under normoxic conditions was 0.14±0.02 ml min-1 kg-1 (approximately 0.85 % of Q(dot)). When exposed to hypoxia, although both resting Q(dot) and q·cor increased, q·cor increased to a greater degree (Q(dot) by 17 % and q·cor by 36 %). During hypoxia, maximum adrenaline-stimulated Q(dot) was comparable to that observed for normoxic fish. However, because Q(dot) was elevated in resting hypoxic fish, the capacity of hypoxic fish to increase Q(dot) above resting levels was 50 % lower than that measured in normoxic fish. Although maximum q·cor in adrenaline-injected hypoxic trout was greater than that measured in normoxic trout, post-injection increases in q·cor (above resting levels) were not different between the two groups. Two and a half hours after hypoxic exposure, resting Q(dot) was still elevated (11 %) above normoxic levels, and the ability to increase Q(dot) when adrenergically stimulated was not fully restored. These results suggest (1) that resting q·cor in salmonids is approximately 1 % of Q(dot), (2) that increases in q·cor may be important in maintaining cardiovascular performance during hypoxic conditions, (3) that interactions between alpha-adrenergic constriction and metabolically related vasodilation of the coronary vasculature are important in determining q·cor in fish, (4) that exposure of fish to moderate environmental hypoxia reduces the scope for adrenergically mediated increases in Q(dot), and (5) that periods of recovery in excess of several hours are required before cardiovascular performance returns to pre-hypoxic levels.


1991 ◽  
Vol 161 (1) ◽  
pp. 489-508 ◽  
Author(s):  
A. Pagnotta ◽  
C. L. Milligan

The role of blood-borne glucose in the restoration of white muscle glycogen following exhaustive exercise in the active, pelagic rainbow trout (Oncorhynchus mykiss) and the more sluggish, benthic winter flounder (Pseudopleuronectes americanus) were examined. During recovery from exhaustive exercise, the animals were injected with a bolus of universally labelled [14C]glucose via dorsal aortic (trout) or caudal artery (flounder) catheters. The bulk of the injected label (50–70%) remained as glucose in the extracellular fluid in both species. The major metabolic fates of the injected glucose were oxidation to CO2 (6–8%) and production of lactate (6–8%), the latter indicative of continued anaerobic metabolism post-exercise. Oxidation of labelled glucose could account for up to 40% and 15% of the post-exercise MO2 in trout and flounder, respectively. Exhaustive exercise resulted in a reduction of muscle glycogen stores and accumulation of muscle lactate. Glycogen restoration in trout began 2–4h after exercise, whereas in flounder, glycogen restoration began within 2h. Despite a significant labelling of the intramuscular glucose pool, less than 1% of the infused labelled glucose was incorporated into muscle glycogen. This suggests that blood-borne glucose does not contribute significantly to the restoration of muscle glycogen following exhaustive exercise in either trout or flounder and provides further evidence against a prominent role for the Cori cycle in these species.


1997 ◽  
Vol 2 (1) ◽  
pp. 1-10 ◽  
Author(s):  
S. F. Perry ◽  
C. J. Brauner ◽  
B. Tufts ◽  
K. M. Gilmour

Sign in / Sign up

Export Citation Format

Share Document