Metabolic recovery in goldfish: A comparison of recovery from severe hypoxia exposure and exhaustive exercise

2008 ◽  
Vol 148 (4) ◽  
pp. 332-338 ◽  
Author(s):  
Milica Mandic ◽  
Gigi Y. Lau ◽  
Manu M.S. Nijjar ◽  
Jeffrey G. Richards
Keyword(s):  
Exhaustive Exercise ◽  
Severe Hypoxia ◽  
Hypoxia Exposure ◽  
Metabolic Recovery

Superoxide scavengers augment contractile but not energetic responses to hypoxia in rat diaphragm

2005 ◽  
Vol 98 (5) ◽  
pp. 1753-1760 ◽  
Author(s):  
V. P. Wright ◽  
P. F. Klawitter ◽  
D. F. Iscru ◽  
A. J. Merola ◽  
T. L. Clanton
Keyword(s):  
Contractile Function ◽  
Force Production ◽  
Creatine Phosphate ◽  
High Energy ◽  
Diaphragm Muscle ◽  
Severe Hypoxia ◽  
High Energy Phosphates ◽  
Rat Diaphragm ◽  
Tetanic Force ◽  
Hypoxia Exposure

Acute exposure to severe hypoxia depresses contractile function and induces adaptations in skeletal muscle that are only partially understood. Previous studies have demonstrated that antioxidants (AOXs) given during hypoxia partially protect contractile function, but this has not been a universal finding. This study confirms that specific AOXs, known to act primarily as superoxide scavengers, protect contractile function in severe hypoxia. Furthermore, the hypothesis is tested that the mechanism of protection involves preservation of high-energy phosphates (ATP, creatine phosphate) and reductions of Pi. Rat diaphragm muscle strips were treated with AOXs and subjected to 30 min of hypoxia. Contractile function was examined by using twitch and tetanic stimulations and the degree of elevation in passive force occurring during hypoxia (contracture). High-energy phosphates were measured at the end of 30-min hypoxia exposure. Treatment with the superoxide scavengers 4,5-dihydroxy-1,3-benzenedisulfonic acid (Tiron, 10 mM) or Mn(III)tetrakis(1-methyl-4-pyridyl) porphyrin pentachloride (50 μM) suppressed contracture during hypoxia and protected maximum tetanic force. N-acetylcysteine (10 or 18 mM) had no influence on tetanic force production. Contracture during hypoxia without AOXs was also shown to be dependent on the extracellular Ca2+ concentration. Although hypoxia resulted in only small reductions in ATP concentration, creatine phosphate concentration was decreased to ∼10% of control. There were no consistent influences of the AOX treatments on high-energy phosphates during hypoxia. The results demonstrate that superoxide scavengers can protect contractile function and reduce contracture in hypoxia through a mechanism that does not involve preservation of high-energy phosphates.

Excess posthypoxic oxygen consumption in rainbow trout (Oncorhynchus mykiss): recovery in normoxia and hypoxia

2012 ◽  
Vol 90 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Jon Christian Svendsen ◽  
John Fleng Steffensen ◽  
Kim Aarestrup ◽  
Michael Frisk ◽  
Anne Etzerodt ◽  
...  
Keyword(s):  
Oxygen Consumption ◽  
Rainbow Trout ◽  
Oncorhynchus Mykiss ◽  
Metabolic Rate ◽  
Oxygen Content ◽  
Standard Metabolic Rate ◽  
Oxygen Availability ◽  
Severe Hypoxia ◽  
Rainbow Trout Oncorhynchus Mykiss ◽  
Metabolic Recovery

Under certain conditions, a number of fish species may perform brief excursions into severe hypoxia and return to water with a higher oxygen content. The term severe hypoxia describes oxygen conditions that are below the critical oxygen saturation (Scrit), defined here as the oxygen threshold at which the standard metabolic rate becomes dependent upon the ambient oxygen content. Using rainbow trout ( Oncorhynchus mykiss (Walbaum, 1792), this study quantified the excess posthypoxic oxygen consumption (EPHOC) occurring after exposure to oxygen availability below Scrit. Tests showed that Scrit was 13.5% air saturation (O2sat). Fish were exposed to 10% O2sat for 0.97 h, and the EPHOC was quantified in normoxia (≥95% O2sat) and hypoxia (30% O2sat) to test the hypothesis that reduced oxygen availability would decrease the peak metabolic rate (MO2peak) and prolong the duration of the metabolic recovery. Results showed that MO2peak during the recovery was reduced from 253 to 127 mg O2·kg–1·h–1 in hypoxia compared with normoxia. Metabolic recovery lasted 5.2 h in normoxia and 9.8 h in hypoxia. The EPHOC, however, did not differ between the two treatments. Impeded metabolic recovery in hypoxia may have implications for fish recovering from exposure to oxygen availability below Scrit.

scholarly journals Severe hypoxia exposure inhibits larval brain development but does not affect the capacity to mount a cortisol stress response in zebrafish

2021 ◽  
Author(s):  
Kristina V. Mikloska ◽  
Zoe A. Zrini ◽  
Nicholas J. Bernier
Keyword(s):  
Stress Response ◽  
Brain Development ◽  
Hypoxia Tolerance ◽  
Severe Hypoxia ◽  
Whole Body ◽  
Hypoxic Exposure ◽  
Larval Brain ◽  
Fish Nursery ◽  
Hypoxia Exposure ◽  
The Impact

Fish nursery habitats are increasingly hypoxic and the brain is recognized as highly hypoxia-sensitive, yet there is a lack of information on the effects of hypoxia on the development and function of the larval fish brain. Here, we tested the hypothesis that by inhibiting brain development, larval exposure to severe hypoxia has persistent functional effects on the cortisol stress response in zebrafish (Danio rerio). Exposing 5 days post-fertilization (dpf) larvae to 10% dissolved O2 (DO) for 16 h only marginally reduced survival, but it decreased forebrain neural proliferation by 55%, and reduced the expression of neurod1, gfap, and mbpa, markers of determined neurons, glia, and oligodendrocytes, respectively. The 5 dpf hypoxic exposure also elicited transient increases in whole body cortisol and in crf, uts1, and hsd20b2 expression, key regulators of the endocrine stress response. Hypoxia exposure at 5 dpf also inhibited the cortisol stress response to hypoxia in 10 dpf larvae and increased hypoxia tolerance. However, 10% DO exposure at 5 dpf for 16h did not affect the cortisol stress response to a novel stressor in 10 dpf larvae or the cortisol stress response to hypoxia in adult fish. Therefore, while larval exposure to severe hypoxia can inhibit brain development, it also increases hypoxia tolerance. These effects may transiently reduce the impact of hypoxia on the cortisol stress response but not its functional capacity to respond to novel stressors. We conclude that the larval cortisol stress response in zebrafish has a high capacity to cope with severe hypoxia-induced neurogenic impairment.

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