Bigger tank faster growth?

[peewee]

i don't think so. it's in the fishes genes weather it would grow fast or slow. also care and feeding has a role to play.

 

[frontosablkrhom]

i think it has alot to do with water changes, but having a big tank means more swim room and exercise space so im going to have to say. yes having a big tank will really help with growth.

 

[Peanut_Power]

They will grow faster in a larger tank. More room, more area to dissolve wastes and dilute growth inhibitors possibly released by other fish.

I tested this out too btw. Got some juv. H. nicaraguensis, which aren't really fast growers per say, and grew them up in seperate tanks.

I kept four in a 29gal tank, and four in a 300gal tank. They were all approximately the same size, fed the same foods, same water and temp. Only difference was I did three 30% w/c on the 29gal, and only one 30% w/c on the 300gal a week.

After a month, the fish in the 300gal were between a 1/4 to 1/2" larger.

Again, just what I observed. Perhaps it was a one time thing.

 

[tcarswell]

Isn't there also speculation that the fish release hormones that can stunt growth during times of stress from bad water quality and or inadequate swimming area? I can't say for sure but I have heard that.

Truth is the bigger tank the better IMO because no matter if your keeping neon tetra's in a 500 gallon its still a puddle compared to their natural habitat. But its best to do all you can to give them more than adequate space and water quality.

 

[Lupin]

I would not call it speculation short of "proven study". Being a goldfish enthusiast myself, I ventured some of the scientific abstracts for goldfish and found this one about growth regulations and inhibitions.

If you're not into scientific terms nor can understand the abstract fully, read the last quote which is a summary of the above two quotes.

http://www.ingentaconnect.com/content/bsc/jneur/2000/00000012/00000004/art00006

Norepinephrine Regulation of Growth Hormone Release from Goldfish Pituitary Cells. I. Involvement of α2 Adrenoreceptor and Interactions With Dopamine and Salmon Gonadotropin-Releasing Hormone
Authors: Lee1; Chan1; Chang2; Yunker2; Wong1
Source: Journal of Neuroendocrinology, Volume 12, Number 4, April 2000 , pp. 311-322(12)
Publisher: Blackwell Publishing

Abstract:
Adrenergic regulation of growth hormone (GH) release in the goldfish was examined in vitro using dispersed goldfish pituitary cells under column perifusion. Norepinephrine and epinephrine suppressed basal GH release from goldfish pituitary cells in a reversible and dose-dependent manner. At high doses, a transient rebound of GH release was observed after termination of norepinephrine and epinephrine treatment. In this study, the dose-dependence of adrenergic inhibition on basal GH release was mimicked by the α2 agonists clonidine and UK14304. Basal GH secretion, however, was not affected by the β agonist isoproterenol and α1 agonist methoxamine. In addition, the inhibitory actions of norepinephrine and clonidine on basal GH release were blocked by the α2 antagonists yohimbine and RX821002. The β antagonist propranolol and α1 antagonists prasozin and benoxathian were not effective in this respect. Salmon gonadotropin-releasing hormone (sGnRH) and dopamine, two known GH-releasing factors in fish, stimulated GH release from goldfish pituitary cells and their GH-releasing actions were inhibited by simultaneous treatment with norepinephrine. Furthermore, the GH rebound after norepinephrine treatment was significantly enhanced by prior exposure to sGnRH and this effect was not observed with dopamine treatment. These results, taken together, suggest that in the goldfish adrenergic input at the pituitary level inhibit basal GH release through activation of α2 adrenoreceptors. This α2 inhibitory influence may interact with dopaminergic and GnRH input to regulate GH secretion from goldfish pituitary cells. The `post-inhibition' GH rebound after NE treatment and its sensitivity to sGnRH potentiation may also represent a novel mechanism for GH regulation in fish.
Keywords: growth hormone; α2 adrenoreceptor; norepinephrine; epinephrine; dopamine; gonadotropin-releasing hormone; goldfish pituitary cells
Document Type: Research article
DOI: 10.1046/j.1365-2826.2000.00455.x
Affiliations: 1: Department of Zoology, University of Hong Kong, Hong Kong., 2: Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada.

http://www.ingentaconnect.com/content/bsc/jneur/2000/00000012/00000004/art00007

Norepinephrine Regulation of Growth Hormone Release from Goldfish Pituitary Cells. II. Intracellular Sites of Action

Authors: Yunker1; Lee2; Wong2; Chang1
Source: Journal of Neuroendocrinology, Volume 12, Number 4, April 2000 , pp. 323-333(11)
Publisher: Blackwell Publishing

Abstract:
Previous results suggest that norepinephrine decreases growth hormone (GH) release in goldfish by means of α-2 adrenoceptor activation. The intracellular mechanisms by which norepinephrine inhibits GH release were examined in the present study using dispersed goldfish pituitary cells. In 2-h static incubation experiments, norepinephrine and the α-2 agonist clonidine decreased basal GH release and the GH responses to stimulation by the dopamine D1 agonist SKF38393 and two native gonadotropin-releasing hormones (GnRH). Norepinephrine also reduced GH responses to the adenylate cyclase activator forskolin, two protein kinase C (PKC) activators (phorbol ester and synthetic diacylglycerol), and two Ca2+ ionophores (ionomycin and A23187). Similarly, norepinephrine applied as a 1-h pulse in cell column perifusion experiments reduced basal GH release and abolished the GH response to a 5-min pulse of arachidonic acid. In goldfish, D1-stimulated GH release is mediated by AC-, arachidonic acid-and Ca2+-dependent pathways, whereas GnRH action is coupled to PKC-and Ca2+-dependent mechanisms. These results suggest that norepinephrine activation of α-2 receptors inhibits ligand-induced GH secretion by actions subsequent to activation of these second messenger cascades. To further characterize norepinephrine mechanisms of action on unstimulated hormone release, the ability of norepinephrine and an α-2 agonist to affect activation of two second messenger cascades under basal conditions was also investigated. Static incubation with clonidine reduced cAMP production in a time-and dose-dependent manner, suggesting that norepinephrine inhibitory action can also be expressed at the level of cAMP production. Resting intracellular free calcium levels in single, identified goldfish somatotropes was unaffected by norepinephrine. However, the inhibitory effects of norepinephrine on basal GH secretion was not observed in the presence of a voltage-sensitive Ca2+ channel agonist. Whether these channels are targets for norepinephrine action on unstimulated GH release requires further investigation.
Keywords: α-2 adrenoceptor action; [Ca2+]i in identified goldfish somatotropes; voltage-sensitive Ca2+ channel; cAMP; protein kinase C; arachidonic acid
Document Type: Research article
DOI: 10.1046/j.1365-2826.2000.00456.x
Affiliations: 1: Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada., 2: Department of Zoology, University of Hong Kong, Hong Kong.

A summary by Dataguru of Thegab.org in response to two abstracts above.
http://72.36.167.186/~thegab/forum/viewtopic.php?f=8&t=2347&hilit=hormone

Norepinephrine and epinephrine are hormones released in response to stress. They are a big part of the fight or flight response and affect all sorts of things like increasing blood sugar for energy, vasoconstriction to the organs and vasodilation to the muscles, immunosupression, etc. I think in fish it also causes them to take on too much fluid via the gills and lose solutes (e.g. sodium, chloride, etc).

Norepinephrine and epinephrine reduce growth hormone released from the pituitary gland and there is a rebound effect of releasing more GH afterwards. It means that chronically stressed fish will grow less than they should and that there should be increased growth for a time after an acute stressor goes away.

 

[Peanut_Power]

To sum that up, more water changes, more water, less inhibitor. Less inhibitor = faster growth.

 

[Noto]

A clarification may be in order: the papers Lupin linked are about what happens to a fish's growth when that fish is stressed. They say nothing about effects on other fish.

 

[siebertn]

It's the water quality not the size of the tank. There are those who raise discus and recommend against the larger tanks. The though being the fish will burn more energy swimming about, instead of bulking up.

Warmer water and multiple smaller frrding will also increase growth along with the cleaner water.

agree

 

[brianp]

First, let me say that I have absolutely no scientific data to back up anything that I'm about to say. My comments are based on "informed speculation" and empirical observation. Basically, I agree with those who say that wcs are an important factor in promoting fish growth. If for no other reason than routine wcs promote general fish health, reduce stress and this can only be good for fish growth. Having a larger tank would also tend to dilute whatever metabolites and contaminants are being diluted by the wcs, so the two should operate in a mutually supportive manner. Empirically, I had 5 STs in a 150 gallon tank for about three years. When I transferred them to a 350, they all seemed to grow at a much faster rate and in fact, the largest has exhibited phenomenal growth compared to the previous rate. Again, this is all empirical observation...BUT...I pay pretty close attention to what is going on in my tanks and it seems to me that the move to the larger tank accelerated the rate of growth. Of course, it is also true that wcs are a religion with me. For what it's worth.