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Journal of Experimental Biology, Vol 200, Issue 14 1975-1986, Copyright © 1997 by Company of Biologists
JOURNAL ARTICLES |
KE Korsmeyer, NC Lai, RE Shadwick and JB Graham
Center for Marine Biotechnology and Biomedicine, Scripps Institution of Oceanography, University of California San Diego, La Jolla 92093-0204, USA. mblkek@centrum.dk
Cardiac performance in the yellowfin tuna (Thunnus albacares, 673-2470 g, 33-53 cm fork length, FL) was examined in unanesthetized fish swimming in a large water tunnel. Yellowfin tuna were fitted with either electrocardiogram electrodes or a transcutaneous Doppler blood-flow probe over the ventral aorta and exposed to changes in swimming velocity (range 0.8-2.9 FLs-1) or to an acute change in temperature (18-28 degrees C). Heart rates (fH) at +/-1 degree C (30-130 beats min-1) were lower on average than previous measurements with non-swimming (restrained) tunas and comparable with those for other active teleosts at similar relative swimming velocities. Although highly variable among individuals, fH increased with velocity (U, in FLs-1) in all fish (fH = 17.93U + 49.93, r2 = 0.14, P < 0.0001). Heart rate was rapidly and strongly affected by temperature (Q10 = 2.37). Blood flow measurements revealed a mean increase in relative cardiac output of 13.6 +/- 3.0% with exercise (mean velocities 1.23-2.10 FLs-1) caused by an 18.8 +/- 5.4% increase in fH and a 3.9 +/- 2.3% decrease in stroke volume. These results indicate that, unlike most other fishes, cardiac output in yellowfin tuna is regulated primarily through increases in fH. Acute reductions in ambient temperature at slow swimming velocities resulted in decreases in cardiac output (Q10 = 1.52) and fH (Q10 = 2.16), but increases in stroke volume (Q10 = 0.78). This observation suggests that the lack of an increase in stroke volume during exercise is not due to the tuna heart operating at maximal anatomical limits.
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