Respiration rates of ectothermic organisms are affected by environmental temperatures, and sustainable metabolism at high temperatures sometimes limits heat tolerance. Organisms are hypothesized to exhibit acclimatory metabolic compensation effects, decelerating their metabolic processes below Arrhenius expectations based on temperature alone. We tested the hypothesis that either heritable or plastic heat tolerance differences can be explained by metabolic compensation in the eurythermal freshwater zooplankton crustacean Daphnia magna. We measured respiration rates in a ramp-up experiment over a range of assay temperatures (5-37°C) in eight genotypes of D. magna representing a range of previously reported acute heat tolerances and, at a narrower range of temperatures (10-35°C), in D. magna with different acclimation history (either 10 or 25°C). We discovered no difference in temperature-specific respiration rates between heat-tolerant and heat-sensitive genotypes. In contrast, we observed acclimationspecific compensatory differences in respiration rates at both extremes of the temperature range studied. Notably, there was a deceleration of oxygen consumption at higher temperature in 25°Cacclimated D. magna relative to their 10°C-acclimated counterparts, observed in active animals, a pattern corroborated by similar changes in filtering rate and, partly, by changes in mitochondrial membrane potential. A recovery experiment indicated that the reduction of respiration was not caused by irreversible damage during exposure to a sublethal temperature. Response time necessary to acquire the respiratory adjustment to high temperature was lower than for low temperature, indicating that metabolic compensation at lower temperatures requires slower, possibly structural changes.

Historically, whole stream open channel metabolism has been measured over short periods in conjunction with nutrient injections to assess nutrient dynamics within streams. The purpose of my study was to understand the seasonal changes in metabolism within and among streams as well as the impacts of different land use. This was addressed by monitoring nine different watersheds in the Little Tennessee River watershed in southwestern North Carolina.  The nine study watersheds were selected to represent a gradient of forested, agricultural, and developed land use / land cover types. Data loggers were deployed to collect continuous oxygen, temperature, conductivity, and stage height data from 2010-2011. I used these data to estimate gross primary production (GPP) and ecosystem respiration (ER). GPP and ER were compared to stream chemistry, light, land cover, and storms. I found that there is greater influence of local riparian land cover than watershed land cover on GPP and ER. Streams had varying annual GPP, but generally the peak in GPP occurred in late winter- early spring with lows in fall. GPP was most strongly influenced by the amount of available light, which is directly related to the amount of canopy cover. ER was much more variable than GPP within and among streams but generally peaked in summer and was lowest in the winter. ER was most strongly related to the proportion of agricultural land cover in the local riparian area. My results suggest that local riparian vegetation may have a greater impact on metabolism than mountainside development. / Master of Science

For many years man has been searching for a cure for lime-induced chlorosis. This disease is prevalent throughout the entire western United States and is characterized by a yellowing of the leaves, destruction of the chlorophyll, and eventual death of the plant. It has brought devastation of fruit orchards in Utah, costing fruit producers millions of dollars. Hardly any county in Utah is free from this destructive nutritional disease.

Indiana University-Purdue University Indianapolis (IUPUI) / Huntington’s disease (HD) is an autosomal dominantly inherited, fatal neurodegenerative disorder for which there is no cure. HD is clinically characterized by progressively worsening motor, cognitive, and psychiatric disturbances. Currently available therapeutics for HD only treat symptoms, but do not address underlying disease pathology. HD pathogenesis is linked to a mutation in the huntingtin gene, which encodes a protein called huntingtin (Htt) that is normally involved in a variety of cellular processes. In healthy individuals, the N-terminus of huntingtin possesses a polyglutamine stretch containing less than 35 glutamines, however, the mutated huntingtin protein (mHtt) has an elongated polyglutamine tract that correlates with the development of HD. The mechanism of deleterious action by mHtt is unknown, but a major hypothesis postulates that mHtt may cause mitochondrial dysfunction. However, the data regarding involvement of mitochondrial impairment in HD pathology are contradictory. Some investigators previously reported, for example, that mHtt suppresses mitochondrial respiratory activity and decreases mitochondrial Ca2+ uptake capacity. However, other investigators found increased respiratory activity and augmented mitochondrial Ca2+ uptake capacity. We used transgenic mouse models of HD to investigate the effect of full-length and fragments of mHtt on oxidative metabolism and Ca2+ handling using a combination of isolated mitochondria, primary neurons, and whole-animal metabolic measurements. We evaluated the effect of full-length mHtt on isolated mitochondria and primary neurons from YAC128 mice. We found no alteration in respiratory activity or Ca2+ uptake capacity, indicative of mitochondrial damage, between mitochondria or neurons from YAC128 mice compared to wild-type (WT) mice. Furthermore, we measured whole animal oxidative metabolism and physical activity level and found that YAC128 mice do not display any decline in metabolic and physical activity. Although full-length mHtt expressing YAC128 mice may be a more faithful genetic recapitulation of HD, data suggests mHtt fragments may be more toxic. To assess the effect of mHtt fragments, we used isolated brain mitochondria and primary striatal neurons from the R6/2 mouse model and found no significant impairment in respiration or Ca2+ handling. Thus, our data strongly support the hypothesis that mHtt does not alter mitochondrial functions assessed either with isolated mitochondria, primary neurons, or whole animals.

It would facilitate the coaching process if coaches could compare the various levels of cardiovascular fitness that their swimmers have attained. The purpose of this study was to determine the relationship between maximum oxygen uptake and the 12, 9, 6 and 3 minute aerobic swim performance tests in intercollegiate male and female swimmers.

Controlled frequency breathing (CFB) is a training technique used by swimmers in an effort to limit oxygen availability to the body and stimulate anaerobic metabolism. During CFB, a swimmer restricts breathing to one breath every six, seven, or even eight strokes per breath. The purpose of this study was to determine tb.e influen<;:e of CFB on blood lactate, heart rate, and stroke rate during front crawl stroke swimming. A maximal exertion test was used to determine peak swimming velocity. Based on this maximal test, five different workloads were used to compare CFB and normal breathing (NB). Subjects swam three-minute workloads at 55%,65%,75%, 85%, and 95% of maximal effort with two minutes rest between each workload. Blood lactate and heart rate were measured immediately after each workload and stroke rate was counted manually. Subjects were assigned to breathe normally (NB) or to restrict their breathing to one breath every eight strokes (CFB). Breathing conditions were randomly assigned. Multivariate analysis was used to compare the blood lactate, heart rate, and stroke rate between NB and CFB. Tukey's post hoc test was used when F-values were significant (p<0.05). Twenty-eight subjects (18 females, 10 males) completed the entire protocol. As expected there were significant main effects for the heart rate and blood lactate responses to increasing workloads (p<0.01). However, CFB did not alter blood lactate levels when compared to NB. Interestingly, heart rate (p=0.014) was lower and stroke rate (p=0.011) was higher in the CFB condition when compared to N'B.

Among the basal bony fishes, the American paddlefish (Polyodon spathula) has a unique respiratory strategy of ram-ventilation. However, despite the increasing problems caused by hypoxia in natural habitats occupied by this species, little information exists about their response to hypoxia. Four studies were conducted to examine the physiological and biochemical responses of juvenile paddlefish (150-181 g) to acute and chronic hypoxia. Acute hypoxia tolerance, aerobic metabolic rates and swimming capabilities of paddlefish in an intermittent respirometer or swim flume were evaluated under normoxic (partial pressures of oxygen [pO2] =140 mm Hg) and hypoxic (pO2 =62 mm Hg) conditions at 18 °C and 26 °C. Additionally, blood oxygen transport, blood acid-base balance and metabolic stress were evaluated in paddlefish independently exposed to 4 different pO2s: normoxia =148 mm Hg, mild hypoxia =89 mm Hg, moderate hypoxia =59 mm Hg and extreme hypoxia =36 mm Hg, at 21°C. Blood samples were collected from paddlefish after they had been exposed to treatment pO2’s for 0.25, 2, 6, 24 and 72 hours, and analyzed for hematocrit, pO2, total oxygen content, pCO2, pH, hemoglobin, Na+, K+, Ca2+, Cl-, glucose, lactate, etc. A third study used 1-D and 2-D J-resolved 1H NMR to analyze metabolite changes in muscle tissue of paddlefish exposed to normoxia (148 mm Hg), or acute (0.25 h) or chronic (72 h) moderate hypoxia (59 mm Hg). The last study examined the effect of moderate hypoxia (pO2: 59 mm Hg) and subsequent recovery in normoxia (pO2: 148 mm Hg) on plasma cortisol, blood oxygen transport, blood acid-base balance, metabolic, ion-osmoregulation and enzyme parameters in paddlefish. The results indicate that paddlefish have a critical pO2 of 74 mm Hg at 18 °C and 89 mm Hg at 26 °C and a lethal oxygen threshold of ~2 mg/ L. Sensitive to moderate hypoxia, death occured after 3-8 hours of extreme hypoxia. Paddlefish have reduced capacity for metabolic depression and, as a result, survival in hypoxia is limited due to a reduction in both aerobic and anaerobic (glycogen and glucose) energy stores as well as the accumulations of toxic H+ and lactate. Nonetheless recovery is possible.

No description available.

No description available.

No description available.