Seasonal changes in enzymes of aerobic heat production in the white-footed mouse

1981 ◽  
Vol 240 (5) ◽  
pp. R289-R294 ◽  
Author(s):  
S. J. Wickler
Keyword(s):  
Skeletal Muscle ◽  
Heat Production ◽  
Cardiac Tissue ◽  
Citrate Synthase ◽  
Whole Body ◽  
Primary Role ◽  
Beta Oxidation ◽  
Brown Adipose ◽  
Cyt C ◽  
Hydroxyacyl Coa Dehydrogenase

During seasonal acclimatization in white-footed mice (Peromyscus leucopus), there is a substantial increase in the capacity for aerobic heat production under cold stress (Mmax) in winter animals. The possibility that increases in levels of enzymes involved in aerobic heat production could be responsible for the increase in Mmax was investigated in mice captured in summer and winter. Activities of citrate synthase (CS) and beta-hydroxyacyl-CoA dehydrogenase (HOAD) and concentrations of cytochrome c (cyt c) were measured in the two primary thermogenic tissues of small mammals, skeletal muscle and brown adipose tissue (BAT). Additionally, cyt c was measured in heart, liver, and whole-body samples. CS and cyt c were used as indicators of aerobic capacity, and HOAD was used to indicate the capacity for beta-oxidation. In winter CS, cyt c, and HOAD increased (expressed per g wet mass) in skeletal muscle and BAT. There was an increase in cyt c of whole-body samples, liver, and skeletal muscle of between 55 and 78%, but no change was observed in cardiac tissue. There was an approximately 80% increase in CS and HOAD in skeletal muscle. The highly aerobic nature of BAT and its primary role in heat production are supported by the high activities in summer animals and the increase observed in winter (200, 1,570, and 220% increase in CS, HOAD, and cyt c, respectively).

scholarly journals Muscle Oxidative Capacity Is a Better Predictor of Insulin Sensitivity than Lipid Status

2003 ◽  
Vol 88 (11) ◽  
pp. 5444-5451 ◽  
Author(s):  
Clinton R. Bruce ◽  
Mitchell J. Anderson ◽  
Andrew L. Carey ◽  
David G. Newman ◽  
Arend Bonen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Citrate Synthase ◽  
Oxidative Capacity ◽  
Fatty Acyl ◽  
Whole Body ◽  
Before And After ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Long Chain

Abstract We determined whole-body insulin sensitivity, long-chain fatty acyl coenzyme A (LCACoA) content, skeletal muscle triglyceride (TGm) concentration, fatty acid transporter protein content, and oxidative enzyme activity in eight patients with type 2 diabetes (TYPE 2); six healthy control subjects matched for age (OLD), body mass index, percentage of body fat, and maximum pulmonary O2 uptake; nine well-trained athletes (TRAINED); and four age-matched controls (YOUNG). Muscle biopsies from the vastus lateralis were taken before and after a 2-h euglycemic-hyperinsulinemic clamp. Oxidative enzyme activities, fatty acid transporters (FAT/CD36 and FABPpm), and TGm were measured from basal muscle samples, and total LCACoA content was determined before and after insulin stimulation. Whole-body insulin-stimulated glucose uptake was lower in TYPE 2 (P < 0.05) than in OLD, YOUNG, and TRAINED. TGm was elevated in TYPE 2 compared with all other groups (P < 0.05). However, both basal and insulin-stimulated skeletal muscle LCACoA content were similar. Basal citrate synthase activity was higher in TRAINED (P < 0.01), whereas β-hydroxyacyl CoA dehydrogenase activity was higher in TRAINED compared with TYPE 2 and OLD. There was a significant relationship between the oxidative capacity of skeletal muscle and insulin sensitivity (citrate synthase, r = 0.71, P < 0.001; β-hydroxyacyl CoA dehydrogenase, r = 0.61, P = 0.001). No differences were found in FAT/CD36 protein content between groups. In contrast, FABPpm protein was lower in OLD compared with TYPE 2 and YOUNG (P < 0.05). In conclusion, despite markedly elevated skeletal muscle TGm in type 2 diabetic patients and strikingly different levels of whole-body glucose disposal, both basal and insulin-stimulated LCACoA content were similar across groups. Furthermore, skeletal muscle oxidative capacity was a better predictor of insulin sensitivity than either TGm concentration or long-chain fatty acyl CoA content.

Metabolic organization of muscle and brown fat of normal and dystrophic hamsters

1983 ◽  
Vol 244 (3) ◽  
pp. R407-R411
Author(s):  
S. J. Wickler ◽  
B. A. Horwitz
Keyword(s):  
Cardiac Tissue ◽  
Citrate Synthase ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Brown Fat ◽  
Nonshivering Thermogenesis ◽  
Beta Oxidation ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Metabolic Organization ◽  
Thermogenic Response

The thermogenic response to catecholamines, i.e., regulatory nonshivering thermogenesis (NST), is significantly reduced in dystrophic hamsters (BIO 14.6) compared with age-matched normals. The possibility that this reduction reflects, in part, lower levels of enzymes in those tissues implicated in NST has been examined by assaying citrate synthase (CS), beta-hydroxyacyl CoA dehydrogenase (HOAD), and phosphofructokinase (PFK), enzymes whose activity reflect the potential flux of substrates through the tricarboxylic acid cycle, beta-oxidation, and glycolysis, respectively. Each enzyme was assayed in brown fat, heart, gastrocnemius, and semitendinosus of 3-mo-old normal (n = 15) and dystrophic (n = 18) hamsters. Brown fat masses from interscapular, cervical, and scapular-axillary regions of dystrophics averaged only 50% those of normals (424 vs. 890 mg). Additionally, markers of aerobic metabolism (CS and HOAD) were significantly reduced in the brown fat from dystrophic animals. (CS activities averaged 59% of normal, whereas HOAD activities averaged 75% of normal). In dystrophic animals CS and HOAD levels were similar to those of normals in cardiac tissue but were significantly elevated in skeletal muscle samples. Tissue PFK activities were reduced only in cardiac tissue of the more affected dystrophics. Thus decreased NST capacity in dystrophic hamsters is accompanied by reduced masses and CS values in brown fat but not by decreases in the aerobic markers in skeletal or cardiac muscle.

Influence of training on skeletal muscle enzymatic adaptations in normal and diabetic rats

1985 ◽  
Vol 249 (4) ◽  
pp. E360-E365 ◽  
Author(s):  
E. G. Noble ◽  
C. D. Ianuzzo
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Citrate Synthase ◽  
Diabetic Rats ◽  
Muscle Fiber Types ◽  
Fiber Types ◽  
Marker Enzymes ◽  
Oxidative Potential ◽  
Hydroxyacyl Coa Dehydrogenase ◽  
Fast Twitch

Muscle homogenates representing slow-twitch oxidative, fast-twitch oxidative-glycolytic, fast-twitch glycolytic, and mixed fiber types were prepared from normal, diabetic, and insulin-treated diabetic rats. Diabetes was induced by injection of 80 mg . kg-1 of streptozotocin. The activities of citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were employed as markers of oxidative potential, whereas phosphorylase, hexokinase, and phosphofructokinase activities were used as an indication of glycolytic capacity. Diabetes was associated with a general decrement in the activity of oxidative marker enzymes for all fiber types except the fast-twitch glycolytic fiber. In contrast, the fast-twitch glycolytic fibers demonstrated the greatest decline in glycolytic enzymatic activity. Insulin-treated animals, either trained or untrained, exhibited enzyme activities similar to their normal counterparts. Exercise training of diabetic rats mimicked the effect of insulin treatment and caused a near normalization of the activity of the marker enzymes. These findings suggest that the enzymatic potential of all skeletal muscle fiber types of diabetic rats may be normalized by exercise training even in the absence of significant amounts of insulin.

scholarly journals Whole body and muscle energy metabolism in preruminant calves: effects of nutrient synchrony and physical activity

2007 ◽  
Vol 97 (4) ◽  
pp. 667-675 ◽  
Author(s):  
Joost J. G. C. van den Borne ◽  
Jean-François Hocquette ◽  
Martin W. A. Verstegen ◽  
Walter J. J. Gerrits
Keyword(s):  
Physical Activity ◽  
Heat Production ◽  
Enzyme Activities ◽  
Citrate Synthase ◽  
Human Subjects ◽  
Fat Content ◽  
Oxidative Enzyme ◽  
Whole Body ◽  
Muscle Energy ◽  
Body Heat

The effects of asynchronous availability of amino acids and glucose on muscle composition and enzyme activities in skeletal muscle were studied in preruminant calves. It was hypothesized that decreased oxidative enzyme activities in muscle would explain a decreased whole body heat production with decreasing nutrient synchrony. Preruminant calves were assigned to one of six degrees of nutrient synchrony, step-wise separating the intake of protein and lactose over the two daily meals. Calves at the most synchronous treatment received two identical meals daily. At the most asynchronous treatment, 85 % of the daily protein and 20 % of the daily lactose supply were fed in one meal and the remainder in the other meal. Daily intakes of all dietary ingredients were identical for all treatments. Oxidative enzyme activities and fat content increased with decreasing nutrient synchrony inM. Rectus Abdominis(RA), but not inM. Semitendinosus. Cytochrome-c-oxidase activity was positively correlated with fat content in RA (r0·49;P < 0·01). Oxidative enzyme activities in both muscles were not correlated with average daily heat production, but citrate synthase activity in RA was positively correlated (P < 0·01) with the circadian amplitude (r0·53) and maximum (r0·61) of heat production associated with physical activity. In conclusion, this study indicates that muscle energy stores are regulated by nutrient synchrony. The lack of correlation between muscle oxidative enzyme activities and average daily heat production was in contrast with findings in human subjects. Therefore, oxidative enzyme activity in muscle should not be used as an indicator for whole body heat production in growing calves.

scholarly journals Malleability of the system in overcoming limitations: functional elements

1985 ◽  
Vol 115 (1) ◽  
pp. 345-354
Author(s):  
B. Saltin
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Uptake ◽  
Maximal Oxygen Uptake ◽  
Mean Transit Time ◽  
The Body ◽  
Whole Body ◽  
Limiting Factor ◽  
Primary Role ◽  
Pump Function ◽  
Cardiac Pump Function

Three different views can be found in the literature concerning the classical question in exercise physiology: what limits maximal oxygen uptake in man? Some authors believe that the limitation is the maximal rate of oxygen delivery by the cardiovascular system. Others argue that oxygen uptake is limited by the capillary bed or metabolic capacity of skeletal muscle, and the third line of thought is that no single factor can be found to be directly limiting as all links in the oxygen transport are so closely matched. The stand taken in this paper is that the skeletal muscle of man can be excluded as a limiting factor for maximal oxygen uptake in whole body exercise. It can be shown, by direct measurements, that in sedentary and in trained man maximal perfusion and oxygen utilization of skeletal muscle is so high that if all muscles in the body were engaged in intense exercise, the cardiac pump function would have to be 2–3 fold larger than it is. What happens in whole body exercise is that each muscle group receives only a fraction of the blood it can accommodate. The primary role for a larger capillary network observed in trained muscles is to keep or extend mean transit time. Elevated mitochondrial enzyme activities affect the metabolic response (i.e. lipid oxidation is elevated in trained muscles). However, these adaptations are not necessary for increasing the maximal oxygen uptake of man, as the capacity of the heart is limiting. Improved training techniques (which induce even larger improvements in cardiac pump function) may reveal that pulmonary diffusion capacity is the limiting factor.

Effects of age and gender on brown fat and skeletal muscle metabolic responses to cold in F344 rats

1995 ◽  
Vol 268 (4) ◽  
pp. R931-R941 ◽  
Author(s):  
A. M. Gabaldon ◽  
M. L. Florez-Duquet ◽  
J. S. Hamilton ◽  
R. B. McDonald ◽  
B. A. Horwitz
Keyword(s):  
Skeletal Muscle ◽  
Core Temperature ◽  
Cold Exposure ◽  
Citrate Synthase ◽  
Uncoupling Protein ◽  
Plasma Norepinephrine ◽  
Interscapular Brown Adipose Tissue ◽  
Brown Adipose ◽  
F344 Rats ◽  
Older Males

Older male Fischer 344 (F344) rats do not maintain core temperature as well as do older females during cold exposure. To elucidate factors contributing to the decreased thermoregulatory ability of older males, the metabolic potentials of interscapular brown adipose tissue (IBAT) and skeletal muscle were evaluated at rest (26 degrees C) and during 4 h of cold (6 degrees C) in male and female F344 rats, aged 6, 12, and 26 mo. Compared with 26-mo-old females, cold-exposed 26-mo-old males exhibited a greater drop in core temperature and lower amounts of IBAT mitochondrial uncoupling protein (UCP) and IBAT thyroxine 5'-deiodinase (T5'D) activity. Unlike females, 26-mo-old males showed no cold-induced increase in total IBAT UCP or T5'D activity. In contrast, plasma norepinephrine was higher in cold-exposed 26-mo-old males vs. females, whereas plasma insulin and thyroxine did not differ with gender. Skeletal muscle oxidative capacity (measured by citrate synthase activity) and carbohydrate availability (measured by muscle glycogen and plasma glucose levels) did not differ between the 26-mo-old males and females. Our data suggest that altered regulation of IBAT UCP levels during cold exposure of aged rats, due at least in part to attenuated cold-induced IBAT T5'D activity, contributes to the gender difference in thermoregulatory ability of older males vs. females.

Muscle respiratory capacity and VO2 max in identically trained young and old rats

1987 ◽  
Vol 63 (1) ◽  
pp. 257-261 ◽  
Author(s):  
G. D. Cartee ◽  
R. P. Farrar
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Treadmill Running ◽  
Whole Body ◽  
Vo2 Max ◽  
Respiratory Enzymes ◽  
Respiratory Capacity ◽  
Palmitate Oxidation ◽  
Age Related ◽  
Old Rats

Old rats have a decreased hindlimb muscle respiratory capacity and whole-body maximal O2 consumption (VO2 max). The decline in spontaneous physical activity in old rats might contribute to these age-related changes. The magnitude of the age-related decline is not uniform in all skeletal muscle respiratory enzymes, and the decrease in palmitate oxidation is particularly great. This study was designed to determine if young and old rats subjected to the same exercise-training protocol would attain similar values for VO2 max and several markers of muscle respiratory capacity. Four- and 18-mo-old Fischer 344 rats underwent an identical 6-mo program of treadmill running. After training, both age groups had increased VO2 max above sedentary age-matched controls. However, the old trained rats had a lower VO2 max than identically trained young rats. In contrast to VO2 max, the two trained groups attained similar values for gastrocnemius citrate synthase, cytochrome oxidase, 3-hydroxyacyl-CoA dehydrogenase, palmitate oxidation, and total carnitine concentration. Thus, when the young and old rats performed an identical exercise protocol within the capacity of the old animals, differences in skeletal muscle respiratory capacity were eliminated. The dissimilarity in VO2 max between the identically trained groups was apparently caused by age-related differences in factors other than muscle respiratory capacity.

scholarly journals Enhanced cardiac protein glycosylation (O-GlcNAc) of selected mitochondrial proteins in rats artificially selected for low running capacity

2013 ◽  
Vol 45 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Virginia L. Johnsen ◽  
Darrell D. Belke ◽  
Curtis C. Hughey ◽  
Dustin S. Hittel ◽  
Russell T. Hepple ◽  
...  
Keyword(s):  
Protein Modification ◽  
Cardiac Tissue ◽  
Citrate Synthase ◽  
Specific Protein ◽  
Protein Glycosylation ◽  
Whole Body ◽  
Glucose Disposal ◽  
Insulin Resistant ◽  
Specific Proteins ◽  
Response To Stress

O-linked β-N-acetyl glucosamine (O-GlcNAc) is a posttranslational modification consisting of a single N-acetylglucosamine moiety attached by an O-β-glycosidic linkage to serine and threonine residues of both nuclear and cytosolic proteins. Analogous to phosphorylation, the modification is reversible and dynamic, changing in response to stress, nutrients, hormones, and exercise. Aims of this study were to examine differences in O-GlcNAc protein modification in the cardiac tissue of rats artificially selected for low (LCR) or high (HCR) running capacity. Hyperinsulinemic-euglycemic clamps in conscious animals assessed insulin sensitivity while 2-[14C] deoxyglucose tracked both whole body and tissue-specific glucose disposal. Immunoblots of cardiac muscle examined global O-GlcNAc modification, enzymes that control its regulation (OGT, OGA), and specific proteins involved in mitochondrial oxidative phosphorylation. LCR rats were insulin resistant disposing of 65% less glucose than HCR. Global tissue O-GlcNAc, OGT, OGA, and citrate synthase were similar between groups. Analysis of cardiac proteins revealed enhanced O-GlcNAcylation of mitochondrial Complex I, Complex IV, VDAC, and SERCA in LCR compared with HCR. These results are the first to establish an increase in specific protein O-GlcNAcylation in LCR animals that may contribute to progressive mitochondrial dysfunction and the pathogenesis of insulin resistance observed in the LCR phenotype.

scholarly journals Quantification in vivo of the effects of insulin on glucose utilization in individual tissues of warm- and cold-acclimated rats

1986 ◽  
Vol 237 (3) ◽  
pp. 789-795 ◽  
Author(s):  
S A Smith ◽  
P Young ◽  
M A Cawthorne
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Acclimation ◽  
Glucose Utilization ◽  
Insulin Treatment ◽  
Glucose Production ◽  
Whole Body ◽  
Metabolic Index ◽  
Brown Adipose

Cold-acclimation of rats (3 weeks, 4 degrees C) had no effect on basal rates of glucose production or utilization. Under euglycaemic-clamp conditions, in which the circulating insulin concentration was increased by approx. 50 microunits/ml, cold-acclimated rats showed a greater increase in glucose utilization and a greater suppression of endogenous glucose production. Tissue sites of glucose utilization were investigated by using a tracer dose of 2-deoxy-D-[14C]glucose and a glucose metabolic index determined for each tissue. In 5 h-starved warm-acclimated rats, heart had the highest glucose metabolic index. This was increased further by both cold-acclimation and insulin treatment. The glucose metabolic index of skeletal muscle was 3.5-14-fold lower than that of heart, but, as a result of the large muscle mass, skeletal muscle made the largest contribution to whole-body glucose utilization. White and brown adipose tissue had low glucose metabolic indices in warm-acclimated rats under basal conditions, and the indices were not increased by the insulin treatment. However, cold-acclimation produced a significant increase in the glucose metabolic index of brown adipose tissue, but not of white adipose tissue. In contrast with the warm-acclimated rats, insulin treatment of cold-acclimated rats resulted in a marked increase in the glucose metabolic index of brown adipose tissue. The results provide evidence that cold-acclimation produces a selective alteration in the insulin-sensitivity of brown adipose tissue.

scholarly journals New records in aerobic power among octogenarian lifelong endurance athletes

2013 ◽  
Vol 114 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Scott Trappe ◽  
Erik Hayes ◽  
Andrew Galpin ◽  
Leonard Kaminsky ◽  
Bozena Jemiolo ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Aerobic Capacity ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Endurance Athletes ◽  
Whole Body ◽  
Oxidative Enzymes ◽  
Vastus Lateralis Muscle ◽  
Peroxisome Proliferator ◽  
Mrna Targets

We examined whole body aerobic capacity and myocellular markers of oxidative metabolism in lifelong endurance athletes [ n = 9, 81 ± 1 yr, 68 ± 3 kg, body mass index (BMI) = 23 ± 1 kg/m2] and age-matched, healthy, untrained men ( n = 6; 82 ± 1 y, 77 ± 5 kg, BMI = 26 ± 1 kg/m2). The endurance athletes were cross-country skiers, including a former Olympic champion and several national/regional champions, with a history of aerobic exercise and participation in endurance events throughout their lives. Each subject performed a maximal cycle test to assess aerobic capacity (V̇o2max). Subjects had a resting vastus lateralis muscle biopsy to assess oxidative enzymes (citrate synthase and βHAD) and molecular (mRNA) targets associated with mitochondrial biogenesis [peroxisome proliferator-activated receptor-γ coactivator 1α (PGC-1α) and mitochondrial transcription factor A (Tfam)]. The octogenarian athletes had a higher ( P < 0.05) absolute (2.6 ± 0.1 vs. 1.6 ± 0.1 l/min) and relative (38 ± 1 vs. 21 ± 1 ml·kg−1·min−1) V̇o2max, ventilation (79 ± 3 vs. 64 ± 7 l/min), heart rate (160 ± 5 vs. 146 ± 8 beats per minute), and final workload (182 ± 4 vs. 131 ± 14 W). Skeletal muscle oxidative enzymes were 54% (citrate synthase) and 42% (βHAD) higher ( P < 0.05) in the octogenarian athletes. Likewise, basal PGC-1α and Tfam mRNA were 135% and 80% greater ( P < 0.05) in the octogenarian athletes. To our knowledge, the V̇o2max of the lifelong endurance athletes is the highest recorded in humans >80 yr of age and comparable to nonendurance trained men 40 years younger. The superior cardiovascular and skeletal muscle health profile of the octogenarian athletes provides a large functional reserve above the aerobic frailty threshold and is associated with lower risk for disability and mortality.

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