Effects of L-, D-, and DL-carnitine on morphometric parameters of skeletal muscle and exercise performance of laboratory animals receiving carnitine-deficient diet

2006 ◽  
Vol 142 (4) ◽  
pp. 458-460 ◽  
Author(s):  
A. A. Spasov ◽  
I. N. Iezhitsa ◽  
M. S. Kravchenko ◽  
V. B. Pisarev ◽  
G. L. Snigur
2012 ◽  
Vol 5 (6) ◽  
pp. 812-818 ◽  
Author(s):  
Stewart H. Lecker ◽  
Alexandra Zavin ◽  
Peirang Cao ◽  
Ross Arena ◽  
Kelly Allsup ◽  
...  

1959 ◽  
Vol 197 (2) ◽  
pp. 491-493 ◽  
Author(s):  
A. D. Bender ◽  
D. D. Schottelius ◽  
B. A. Schottelius

Myoglobin concentration was determined in gastrocnemius and masseter muscles of guinea pigs maintained up to 15 days on vitamin E-deficient and vitamin E-supplemented diets. A statistically significant increase in myoglobin was noted in muscles of animals on the deficient diet for 15 days. That the increase was real and not apparent was attested by studies of total nitrogen, noncollagen nitrogen, percentage of solids and muscle wet weight, all of which were the same in control and experimental muscles. Histological sections and creatine excretion studies confirmed the impression of mild, incipient nutritional dystrophy.


2019 ◽  
Vol 126 (2) ◽  
pp. 341-353 ◽  
Author(s):  
Margaret B. Bell ◽  
Zachary Bush ◽  
Graham R. McGinnis ◽  
Glenn C. Rowe

Endurance exercise has been shown to be a positive regulator of skeletal muscle metabolic function. Changes in mitochondrial dynamics (fusion and fission) have been shown to influence mitochondrial oxidative capacity. We therefore tested whether genetic disruption of mitofusins (Mfns) affected exercise performance in adult skeletal muscle. We generated adult-inducible skeletal muscle-specific Mfn1 (iMS-Mfn1KO), Mfn2 (iMS-Mfn2KO), and Mfn1/2 (iMS-MfnDKO) knockout mice. We assessed exercise capacity by performing a treadmill time to exhaustion stress test before deletion and up to 8 wk after deletion. Analysis of either the iMS-Mfn1KO or the iMS-Mfn2KO did not reveal an effect on exercise capacity. However, analysis of iMS-MfnDKO animals revealed a progressive reduction in exercise performance. We measured individual electron transport chain (ETC) complex activity and observed a reduction in ETC activity in both the subsarcolemmal and intermyofibrillar mitochondrial fractions specifically for NADH dehydrogenase (complex I) and cytochrome- c oxidase (complex IV), which was associated with a decrease in ETC subunit expression for these complexes. We also tested whether voluntary exercise training would prevent the decrease in exercise capacity observed in iMS-MfnDKO animals ( n = 10/group). However, after 8 wk of training we did not observe any improvement in exercise capacity or ETC subunit parameters in iMS-MfnDKO animals. These data suggest that the decrease in exercise capacity observed in the iMS-MfnDKO animals is in part the result of impaired ETC subunit expression and ETC complex activity. Taken together, these results provide strong evidence that mitochondrial fusion in adult skeletal muscle is important for exercise performance. NEW & NOTEWORTHY This study is the first to utilize an adult-inducible skeletal muscle-specific knockout model for Mitofusin (Mfn)1 and Mfn2 to assess exercise capacity. Our findings reveal a progressive decrease in exercise performance with Mfn1 and Mfn2 deletion. The decrease in exercise capacity was accompanied by impaired oxidative phosphorylation specifically for complex I and complex IV. Furthermore, voluntary exercise training was unable to rescue the impairment, suggesting that normal fusion is essential for exercise-induced mitochondrial adaptations.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Benjamin Leon ◽  
Andrea Carnie ◽  
Shannon Jenkins ◽  
Kevin Smith ◽  
Gloria Zalos ◽  
...  

Introduction Obesity is associated with many negative health impacts, including hyperinsulinemia and reduced exercise performance, despite being associated with greater lean skeletal mass which works as the insulin-targeting and exercising organ. Purpose of Study We delineated the associations amongst cardiorespiratory capacity, fat mass, skeletal mass distributions, and fasting plasma insulin in overweight, non-diabetic women. Methods One hundred and seventy-two sedentary women, age 22 to 68 years (range), body mass index (BMI) (34.2 ± 6.3 [mean ± SD]; range 25.3 to 57.6 kg/m 2 ), underwent dual energy x-ray absorptiometry for body composition, fasting insulin, and graded treadmill exercise test using the Bruce protocol with measurement of oxygen consumption (peak VO 2 ). Results After adjustment for age, fasting insulin (9.8 ± 8.1; range 1.9 to 47.6 mcU/ml) was positively associated with BMI (r = 0.43, p<0.001), fat mass (r = 0.41, p< 0.001), load-bearing skeletal muscle mass (lower extremity lean mass; r = 0.29, p< 0.001), and non-load-bearing skeletal muscle mass (upper extremity lean mass; Figure, Panel A). By multiple regression analysis with age, fat mass and lower and upper extremity lean masses as covariates, fat mass, age and upper extremity lean mass (Figure, Panel B) were independent negative predictors of peak VO 2 (all p< 0.01). Lower extremity, however, trended to be positively predictive of peak VO 2 (p = 0.067). Conclusions In non-load-bearing muscle, increased lean mass associated with elevated plasma insulin is predictive of reduced oxygen consumption during exercise, suggesting additional load that may diminish cardiorespiratory exercise performance or intrinsic impairment in skeletal muscle function. In load-bearing muscle, compensatory hypertrophy due to increased fat and lean mass loads may preserve exercise performance.


Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195 ◽  
Author(s):  
AC Chou ◽  
GO Jr Broun ◽  
CD Fitch

Abstract Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3–4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.


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