Physiological and biochemical correlates of increased work in trained iron-deficient rats

We investigated physiological and biochemical factors associated with the improved work capacity of trained iron-deficient rats. Female 21-day-old rats were assigned to one of four groups, two dietary groups (50 and 6 ppm dietary iron) subdivided into two levels of activity (sedentary and treadmill trained). Iron deficiency decreased hemoglobin (61%), maximal O2 uptake. (VO2max) (40%), skeletal muscle mitochondrial oxidase activities (59-90%), and running endurance (94%). In contrast, activities of tricarboxylic acid (TCA) cycle enzymes in skeletal muscle were largely unaffected. Four weeks of mild training in iron-deficient rats resulted in improved blood lactate homeostasis during exercise and increased VO2max (15%), TCA cycle enzymes of skeletal muscle (27-58%) and heart (29%), and liver NADH oxidase (34%) but did not affect any of these parameters in the iron-sufficient animals. In iron-deficient rats training affected neither the blood hemoglobin level nor any measured iron-dependent enzyme pathway of skeletal muscle but substantially increased endurance (230%). We conclude that the training-induced increase in endurance in iron-deficient rats may be related to cardiovascular improvements, elevations in liver oxidative capacity, and increases in the activities of oxidative enzymes that do not contain iron in skeletal and cardiac muscle.

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Work performance in the iron-deficient rat: improved endurance with exercise training

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1985.249.3.e306 ◽

1985 ◽

Vol 249 (3) ◽

pp. E306-E311 ◽

Cited By ~ 2

Author(s):

M. V. Perkkio ◽

L. T. Jansson ◽

S. Henderson ◽

C. Refino ◽

G. A. Brooks ◽

...

Keyword(s):

Skeletal Muscle ◽

Endurance Training ◽

Oxidase Activity ◽

Work Performance ◽

Maximal Oxygen Consumption ◽

Treadmill Running ◽

Oxidative Enzymes ◽

Sprague Dawley ◽

Iron Deficient ◽

Type Of Exercise

The effect of an endurance training regimen on muscle oxidative enzymes and work performance was studied in iron-deficient and -sufficient rats. Three-week-old male Sprague-Dawley rats (n = 40) were randomly assigned to diets containing either 6 mg iron/kg (iron deficient) or 50 mg iron/kg (iron sufficient). After 2 wk, each group of rats was further divided into untrained or endurance-trained subgroups. Training consisted of daily treadmill running of gradually increasing duration for a 1-mo period. After the training period, sedentary and endurance-trained iron-deficient rats were anemic (Hgb approximately 8 g/dl compared with 16 g/dl in the 2 control groups) and had significantly lower skeletal muscle cytochrome c concentration, cytochrome oxidase activity, and succinic oxidase activity compared with the iron-sufficient groups. In response to training iron-deficient rats also generally had a substantial increase in skeletal muscle oxidative enzymes (P less than 0.05), in contrast to iron-sufficient animals, in which there was little or no training effect. Work performance in response to training in the iron-deficient rats improved more than sixfold in an endurance type of exercise (P less than 0.05), but maximal oxygen consumption during a brief, intense type of exercise was not significantly affected. The results suggest that endurance training of iron-deficient rats results in a milder anemia and less drastic reduction of skeletal muscle oxidative enzymes which in turn allows better performance in an endurance type of exercise.

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THE RELATIONSHIP BETWEEN CYTOCHONDRIA AND MYOFIBRILS IN PIGEON SKELETAL MUSCLE

Journal of Experimental Medicine ◽

10.1084/jem.98.1.81 ◽

1953 ◽

Vol 98 (1) ◽

pp. 81-98 ◽

Cited By ~ 21

Author(s):

John W. Harman ◽

Ursula H. Osborne

Keyword(s):

Skeletal Muscle ◽

Oxidative Phosphorylation ◽

Oxidative Metabolism ◽

Krebs Cycle ◽

Oxidative Capacity ◽

Breast Muscle ◽

Oxidative Enzymes ◽

Mitochondrial Oxidative Capacity ◽

The Relationship ◽

Oxidative Rate

In pigeon breast muscle the mitochondria are the principal site of oxidative metabolism, whereas the myofibrils are incapable of oxidizing intermediates of the Krebs cycle. The mitochondria contain the oxidative enzymes, and the sarcosomes are associated with a factor which accelerates the mitochondrial oxidative rate. The maintenance of myofibrillar contractility and structure is closely correlated with preservation of mitochondrial oxidative capacity and structure. By use of fluoride and dinitrophenol the connection between mitochondrial metabolism and myofibrillar behavior is shown to occur through the process of oxidative phosphorylation.

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5'-Aminolevulinate synthase activity is decreased in skeletal muscle of anemic rats

AJP Cell Physiology ◽

10.1152/ajpcell.1992.263.2.c429 ◽

1992 ◽

Vol 263 (2) ◽

pp. C429-C435 ◽

Cited By ~ 40

Author(s):

L. A. McNabney ◽

D. A. Essig

Keyword(s):

Skeletal Muscle ◽

Enzyme Activity ◽

Citrate Synthase ◽

Muscle Growth ◽

Biosynthetic Enzyme ◽

Deficient Diet ◽

Aminolevulinate Synthase ◽

Iron Deficient ◽

Old Rats ◽

Rate Limiting

Expression of the rate-limiting heme biosynthetic enzyme 5'-aminolevulinate synthase (ALAS) was investigated in skeletal muscle of 3-wk-old rats fed an iron-deficient diet. After 14 days, ALAS activity had declined 70% relative to control (2.1 +/- 0.2 vs. 0.6 +/- 0.1 nmol.h-1.g-1; P less than 0.005). Similar decreases were observed for blood hemoglobin (11.4 +/- 0.2 vs. 3.9 +/- 0.3 g/dl; P less than 0.005) and muscle cytochrome c (14.5 +/- 1.3 vs. 7.1 +/- 0.6 nmol/g; P less than 0.005). An iron-deficient diet decreased body and skeletal muscle growth by 15 (P less than 0.005) and 10% (P less than 0.05), respectively, whereas concentrations of protein, RNA, ALAS mRNA, and citrate synthase activity in muscle were not different from control. One mechanism by which heme biosynthesis may be slowed in muscle of young anemic rats is a decrease in ALAS activity. At a time when enzyme activity was decreased, ALAS mRNA expression was not affected by an iron-deficient diet, suggesting that steps after transcription of the ALAS gene may regulate the decrease in activity.

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Lower oxygen consumption and Complex I activity in mitochondria isolated from skeletal muscle of fetal sheep with intrauterine growth restriction

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00057.2020 ◽

2020 ◽

Vol 319 (1) ◽

pp. E67-E80

Author(s):

Alexander L. Pendleton ◽

Andrew T. Antolic ◽

Amy C. Kelly ◽

Melissa A. Davis ◽

Leticia E. Camacho ◽

...

Keyword(s):

Skeletal Muscle ◽

Oxygen Consumption ◽

Intrauterine Growth Restriction ◽

Complex I ◽

Tca Cycle ◽

Growth Restriction ◽

Fetal Sheep ◽

Intrauterine Growth ◽

Tca Cycle Enzymes ◽

Complex I Activity

Fetal sheep with placental insufficiency-induced intrauterine growth restriction (IUGR) have lower hindlimb oxygen consumption rates (OCRs), indicating depressed mitochondrial oxidative phosphorylation capacity in their skeletal muscle. We hypothesized that OCRs are lower in skeletal muscle mitochondria from IUGR fetuses, due to reduced electron transport chain (ETC) activity and lower abundances of tricarboxylic acid (TCA) cycle enzymes. IUGR sheep fetuses ( n = 12) were created with mid-gestation maternal hyperthermia and compared with control fetuses ( n = 12). At 132 ± 1 days of gestation, biceps femoris muscles were collected, and the mitochondria were isolated. Mitochondria from IUGR muscle have 47% lower State 3 (Complex I-dependent) OCRs than controls, whereas State 4 (proton leak) OCRs were not different between groups. Furthermore, Complex I, but not Complex II or IV, enzymatic activity was lower in IUGR fetuses compared with controls. Proteomic analysis ( n = 6/group) identified 160 differentially expressed proteins between groups, with 107 upregulated and 53 downregulated mitochondria proteins in IUGR fetuses compared with controls. Although no differences were identified in ETC subunit protein abundances, abundances of key TCA cycle enzymes [isocitrate dehydrogenase (NAD+) 3 noncatalytic subunit β (IDH3B), succinate-CoA ligase ADP-forming subunit-β (SUCLA2), and oxoglutarate dehydrogenase (OGDH)] were lower in IUGR mitochondria. IUGR mitochondria had a greater abundance of a hypoxia-inducible protein, NADH dehydrogenase 1α subcomplex 4-like 2, which is known to incorporate into Complex I and lower Complex I-mediated NADH oxidation. Our findings show that mitochondria from IUGR skeletal muscle adapt to hypoxemia and hypoglycemia by lowering Complex I activity and TCA cycle enzyme concentrations, which together, act to lower OCR and NADH production/oxidation in IUGR skeletal muscle.

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β-Alanine Supplementation Does Not Augment the Skeletal Muscle Adaptive Response to 6 Weeks of Sprint Interval Training

International Journal of Sport Nutrition and Exercise Metabolism ◽

10.1123/ijsnem.2015-0046 ◽

2015 ◽

Vol 25 (6) ◽

pp. 541-549 ◽

Cited By ~ 17

Author(s):

Andrew J.R. Cochran ◽

Michael E. Percival ◽

Sara Thompson ◽

Jenna B. Gillen ◽

Martin J. MacInnis ◽

...

Keyword(s):

Skeletal Muscle ◽

Exercise Performance ◽

Training Stimulus ◽

Training Session ◽

Time Trial ◽

Interval Training ◽

Work Capacity ◽

Oxidative Capacity ◽

Sprint Interval Training ◽

Repeated Sprint

Sprint interval training (SIT), repeated bouts of high-intensity exercise, improves skeletal muscle oxidative capacity and exercise performance. β-alanine (β-ALA) supplementation has been shown to enhance exercise performance, which led us to hypothesize that chronic β-ALA supplementation would augment work capacity during SIT and augment training-induced adaptations in skeletal muscle and performance. Twenty-four active but untrained men (23 ± 2 yr; VO2peak = 50 ± 6 mL·kg−1·min−1) ingested 3.2 g/day of β-ALA or a placebo (PLA) for a total of 10 weeks (n = 12 per group). Following 4 weeks of baseline supplementation, participants completed a 6-week SIT intervention. Each of 3 weekly sessions consisted of 4–6 Wingate tests, i.e., 30-s bouts of maximal cycling, interspersed with 4 min of recovery. Before and after the 6-week SIT program, participants completed a 250-kJ time trial and a repeated sprint test. Biopsies (v. lateralis) revealed that skeletal muscle carnosine content increased by 33% and 52%, respectively, after 4 and 10 weeks of β-ALA supplementation, but was unchanged in PLA. Total work performed during each training session was similar across treatments. SIT increased markers of mitochondrial content, including cytochome c oxidase (40%) and β-hydroxyacyl-CoA dehydrogenase maximal activities (19%), as well as VO2peak (9%), repeated-sprint capacity (5%), and 250-kJ time trial performance (13%), but there were no differences between treatments for any measure (p < .01, main effects for time; p > .05, interaction effects). The training stimulus may have overwhelmed any potential influence of β-ALA, or the supplementation protocol was insufficient to alter the variables to a detectable extent.

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Endotoxin Alteration of the Mucopolysaccharide Blood Vessel Coating in Rats

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100050755 ◽

1974 ◽

Vol 32 ◽

pp. 148-149

Author(s):

D. E. Philpott ◽

A. Takahashi

Keyword(s):

Skeletal Muscle ◽

Endothelial Cells ◽

Salivary Gland ◽

Carotid Artery ◽

Basement Membrane ◽

Coronary Vessels ◽

Ruthenium Red ◽

E Coli ◽

Old Rats ◽

The Brain

Two month, eight month and two year old rats were treated with 10 or 20 mg/kg of E. Coli endotoxin I. P. The eight month old rats proved most resistant to the endotoxin. During fixation the aorta, carotid artery, basil arartery of the brain, coronary vessels of the heart, inner surfaces of the heart chambers, heart and skeletal muscle, lung, liver, kidney, spleen, brain, retina, trachae, intestine, salivary gland, adrenal gland and gingiva were treated with ruthenium red or alcian blue to preserve the mucopolysaccharide (MPS) coating. Five, 8 and 24 hrs of endotoxin treatment produced increasingly marked capillary damage, disappearance of the MPS coating, edema, destruction of endothelial cells and damage to the basement membrane in the liver, kidney and lung.

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