Publications by authors named "Joshua Lonthair"

Declining body size in fishes and other aquatic ectotherms associated with anthropogenic climate warming has significant implications for future fisheries yields, stock assessments and aquatic ecosystem stability. One proposed mechanism seeking to explain such body-size reductions, known as the gill oxygen limitation (GOL) hypothesis, has recently been used to model future impacts of climate warming on fisheries but has not been robustly empirically tested. We used brook trout (Salvelinus fontinalis), a fast-growing, cold-water salmonid species of broad economic, conservation and ecological value, to examine the GOL hypothesis in a long-term experiment quantifying effects of temperature on growth, resting metabolic rate (RMR), maximum metabolic rate (MMR) and gill surface area (GSA).

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Respiratory acidosis and subsequent metabolic compensation are well-studied processes in fish exposed to elevated CO (hypercapnia). Yet, such exposures in the marine environment are invariably accompanied by a return of environmental CO to atmospheric baselines. This understudied phenomenon has the potential to cause a respiratory alkalosis that would necessitate base excretion.

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The neurochemical serotonin (5-HT) is involved in stimulating pulsatile urea excretion in Gulf toadfish (Opsanus beta) through the 5-HT receptor; however, it is not known if (1) the 5-HT signal originates from circulation or if (2) additional 5-HT receptor subtypes are involved. The first objective was to test whether 5-HT may be acting as a hormone in the control of pulsatile urea excretion by measuring potential fluctuations in circulating 5-HT corresponding with a urea pulse, which would suggest circulating 5-HT may be involved with urea pulse activation. We found that plasma 5-HT significantly decreased by 38% 1 h after pulse detection when branchial urea excretion was significantly elevated and then returned to baseline.

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