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G B McClelland

Publications and source records attributed to G B McClelland.

9 recordsLinked to original sources
PubMed2006

Lifetime performance in foraging honeybees: behaviour and physiology.

Honeybees, Apis mellifera, gradually increase their rate of forage uptake as they gain foraging experience. This increase in foraging performance has been proposed to occur as a result of learning; however, factors affecting flight ability such as changes in physiological components of flight metabolism could also contribute to this pattern. Thus, the purpose of this study was to assess the contribution of physiological changes to the increase in honeybee foraging performance. We investigated aspects of honeybee flight muscle biochemistry throughout the adult life, from non-foraging hive bees, through young and mature foragers, to old foragers near the end of their lifespan. Two-dimensional gel proteomic analysis on honeybee thorax muscle revealed an increase in several proteins from hive bees to mature foragers including troponin T 10a, aldolase and superoxide dismutase. By contrast, the activities (V(max)) of enzymes involved in aerobic performance, phosphofructokinase, hexokinase, pyruvate kinase and cytochrome c oxidase, did not increase in the flight muscles of hive bees, young foragers, mature foragers and old foragers. However, citrate synthase activity was found to increase with foraging experience. Hence, our results suggest plasticity in both structural and metabolic components of flight muscles with foraging experience.

Age Factors↗
PubMed2005

Muscle remodeling in relation to blood supply: implications for seasonal changes in mitochondrial enzymes.

We investigated if seasonal changes in rainbow trout muscle energetics arise in response to seasonal changes in erythrocyte properties. We assessed if skeletal muscle mitochondrial enzymes changed (1) acutely in response to changes in erythrocyte abundance, or (2) seasonally when we altered the age profile of erythrocytes. Rainbow trout were treated with pheynylhydrazine, causing a 75% reduction in hematocrit within 4 days. After erythropoiesis had returned hematocrit to normal, treated and control fish were subjected to a seasonal cold acclimation regime to assess the impact of erythrocyte age on skeletal muscle remodeling. Anemia (i.e. phenylhydrazine treatment) did not alter the specific activities (U g(-1) tissue) of mitochondrial enzymes in white or red muscle. Anemic pretreatment did not alter the normal pattern of cold-induced mitochondrial proliferation in skeletal muscle, suggesting erythrocyte age was not an important influence on seasonal remodeling of muscle. Anemia and cold acclimation both induced a 25-30% increase in relative ventricular mass. The increase in relative ventricular mass with phenylhydrazine treatment was accompanied by a 35% increase in DNA content (mg DNA per ventricle), suggesting an increase in number of cells. In contrast, the increase in ventricular mass with cold temperature acclimation occurred without a change in DNA content (mg DNA per ventricle), suggesting an increase in cell size. Despite the major increases in relative ventricular mass, neither anemia nor seasonal acclimation had a major influence on the specific activities of a suite of mitochondrial enzymes in heart. Collectively, these studies argue against a role for erythrocyte dynamics in seasonal adaptive remodeling of skeletal muscle energetics.

Acclimatization↗
PubMed2004

Leptin and the control of respiratory gene expression in muscle.

Leptin plays a central role in the regulation of fatty acid homeostasis, promoting lipid storage in adipose tissue and fatty acid oxidation in peripheral tissues. Loss of leptin signaling leads to accumulation of lipids in muscle and loss of insulin sensitivity secondary to obesity. In this study, we examined the direct and indirect effects of leptin signaling on mitochondrial enzymes including those essential for peripheral fatty acid oxidation. We assessed the impact of leptin using the JCR:LA-cp rat, which lacks functional leptin receptors. The activities of marker mitochondrial enzymes citrate synthase (CS) and cytochrome oxidase (COX) were similar between wild-type (+/?) and corpulent (cp/cp) rats. In contrast, several tissues showed variations in the fatty acid oxidizing enzymes carnitine palmitoyltransferase II (CPT II), long-chain acyl-CoA dehydrogenase (LCAD) and 3-hydroxyacyl-CoA dehydrogenase (HOAD). It was not clear if these changes were due to loss of leptin signaling or to insulin insensitivity. Consequently, we examined the effects of leptin on cultured C(2)C(12) and Sol8 cells. Leptin (3 days at 0, 0.2, or 2.0 nM) had no direct effect on the activities of CS, COX, or fatty acid oxidizing enzymes. Leptin treatment did not affect luciferase-based reporter genes under the control of transcription factors involved in mitochondrial biogenesis (nuclear respiratory factor-1 (NRF-1), nuclear respiratory factor-2 (NRF-2)) or fatty acid enzyme expression (peroxisome proliferator-activated receptors (PPARs)). These studies suggest that leptin exerts only indirect effects on mitochondrial gene expression in muscle, possibly arising from insulin resistance.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed2001

High-altitude acclimation increases the triacylglycerol/fatty acid cycle at rest and during exercise.

High-altitude acclimation alters lipid metabolism during exercise, but it is unknown whether this involves changes in rates of lipolysis or reesterification, which form the triacylglycerol/fatty acid (TAG/FA) cycle. We combined indirect calorimetry with [2-(3)H]glycerol and [1-(14)C]palmitate infusions to simultaneously measure total lipid oxidation, lipolysis, and rate of appearance (R(a)) of nonesterified fatty acids (NEFA) in high-altitude-acclimated (HA) rats exercising at 60% maximal O(2) uptake (VO(2 max)). During exercise, relative total lipid oxidation (%VO(2)) equaled sea-level control (SL) values; however, acclimation greatly stimulated lipolysis (+75%) but had no effect on R(a) NEFA. As a result, TAG/FA cycling increased (+119%), due solely to an increase in recycling (+144%) within adipocytes. There was no change in either group in these variables with the transition from rest to exercise. We conclude that, in HA, 1) acclimation is a potent stimulator of lipolysis; 2) rats do not modify TAG/FA cycling with the transition to exercise; and 3) in normoxia, HA and SL derive the same fraction of their total energy from lipids and carbohydrates.

Acclimatization↗
PubMed2000

Effect of brood size manipulation on offspring physiology: an experiment with passerine birds.

The environment experienced during ontogeny has a significant impact on the physiological condition of offspring. This, in turn, forecasts survival probabilities and future reproductive potential. Despite the prominent role that the concept of condition plays in evolutionary studies, the physiological and biochemical characters that define it remain relatively unexplored. In this study, we quantified the impact of brood size manipulations on the physiology and biochemistry of nestling tree swallows (Tachycineta bicolor) shortly before they fledged. Over two breeding seasons, we either increased or decreased the number of individuals in a brood by a single nestling. Every 2-4 days, we determined the resting rate of oxygen consumption [V(O(2))] of individuals in each brood. Growth was followed until 16 days of age, at which time, to look for potential trade-offs in energy allocation, we measured total lipid mass, skeletal muscle and organ mass, indices of blood oxygen-carrying capacity and the activities of key metabolic enzymes in various tissues. Surprisingly, there was a minimal response of most characters to brood manipulation, suggesting that physiological and biochemical development is relatively invariant except perhaps under extreme conditions. Individuals reared in artificially enlarged broods, however, had a significantly lower body mass, body-size-adjusted [V(O(2))], gizzard mass and total lipid mass. These individuals also had decreased activity of cardiac 3-hydroxyacyl CoA dehydrogenase, suggesting a decreased capacity for oxidation of fatty acids. How these characters affect survival or the future adult phenotype remains unknown.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1999

Effect of high-altitude acclimation on NEFA turnover and lipid utilization during exercise in rats.

Relative exercise intensity (or %maximum O(2) consumption, VO(2 max)) controls fuel selection at sea level (SL) and after high-altitude acclimation (HA) in rats. In this context we used indirect calorimetry, [1-(14)C]palmitate infusions, and muscle triacylglycerol (TAG) measurements to determine 1) total lipid oxidation, 2) the relationship between circulatory nonesterified fatty acid (NEFA) flux and concentration, and 3) muscle TAG depletion after exercise in HA-acclimated rats. Aerobic capacity is decreased in trained rats after 10 wk of acclimation. Both SL and HA showed the same relative use of lipids at 60% [62 +/- 5% (HA) and 61 +/- 3% (SL) of O(2) consumption (VO(2))] and 80% [46 +/- 6% (HA) and 47 +/- 5% (SL) of VO(2)] of their respective VO(2 max). At 60% VO(2 max), plasma [NEFA] were higher in HA, but rate of appearance was essentially the same in both groups (at 30 min, 38 +/- 9 vs. 49 +/- 6 micromol. kg(-1). min(-1) in HA and SL, respectively). At this intensity SL showed no significant decrease in muscle TAG, but in HA it decreased by 64% in soleus and by 90% in red gastrocnemius. We conclude that 1) the relative contributions of total lipid are the same in SL and HA, contrary to differences in [NEFA], because the relationship between flux rate and [NEFA] is modified after acclimation, and 2) muscle TAG may play a more important role at HA.

Acclimatization↗
PubMed1998

Carbohydrate utilization during exercise after high-altitude acclimation: a new perspective.

At high altitude (HA), carbohydrate (CHO) is thought to be the preferred fuel because of its higher yield of ATP per mole of O2. We used indirect calorimetry and D-[6-3H]glucose infusions to determine total CHO and circulatory glucose utilization during exercise in HA-acclimated and sea level (SL) rats. We hypothesized that the percent contribution of CHO to total metabolism (VO2) is determined by exercise intensity relative to an aerobic maximum (% VO2max). HA rats run under hypoxia (FIO2 = 0.12) showed a decrease in VO2max compared with SL (67.55 +/- 1.26 vs. 89.30 +/- 1.23 ml kg-1 min-1). When exercised at 60% of their respective VO2max, both groups showed the same relative use of CHO (38 +/- 3% and 38 +/- 5% of VO2, at the beginning of exercise, in HA and SL, respectively). In both HA and SL, circulatory glucose accounted for approximately 20% of VO2, the balance was provided by muscle glycogen (approximately 18% of VO2). After 20 min at a higher intensity of 80% VO2max, 54 +/- 5% (HA) and 59 +/- 4% (SL) of VO2 was accounted for by CHO. We conclude the following: (i) the relative contributions of total CHO, circulatory glucose, and muscle glycogen do not increase after HA acclimation because the O2-saving advantage of CHO is outweighed by limited CHO stores; and (ii) relative exercise intensity is the major determinant of metabolic fuel selection at HA, as well as at SL.

Acclimatization↗
PubMed1997

Cellular metabolic homeostasis during large-scale change in ATP turnover rates in muscles.

The term homeostasis traditionally refers to the maintenance of a relatively constant internal milieu in the face of changing environmental conditions or changing physiological function. Tissues such as skeletal and cardiac muscles must sustain very large-scale changes in ATP turnover rate during equally large changes in work. In many skeletal muscles, these changes can exceed 100-fold. In unique biological circumstances (for example, during periods of oxygen limitation, vasoconstriction and hypometabolism), tissues such as skeletal muscles may be obliged to sustain further decreases in ATP turnover rates and operate for varying periods at seriously suppressed ATP turnover rates. Examination of a number of cellular and whole-organism systems identifies ATP concentration as a key parameter of the interior milieu that is nearly universally "homeostatic'; it is common to observe no change in ATP concentration even while the change in its turnover rate can increase or decrease by two orders of magnitude. A large number of other intermediates of cellular metabolism are also regulated within narrow concentration ranges, but none seemingly as precisely as is [ATP]. In fact, the only other metabolite in aerobic energy metabolism that is seemingly as "homeostatic' is oxygen-at least in working muscles. The central regulatory question is how such homeostasis of key intermediates in pathways of energy supply and energy demand is achieved.

Adenosine Triphosphate↗