scholarly journals Effects of long-term intradialytic oral nutrition and exercise on muscle protein homeostasis and markers of mitochondrial content in patients on hemodialysis

2020 ◽  
Vol 319 (5) ◽  
pp. F885-F894
Author(s):  
Jorge L. Gamboa ◽  
Serpil Muge Deger ◽  
Bradley W. Perkins ◽  
Cindy Mambungu ◽  
Feng Sha ◽  
...  

Patients with end-stage kidney disease on maintenance hemodialysis commonly develop protein-energy wasting, a syndrome characterized by nutritional and metabolic abnormalities. Nutritional supplementation and exercise are recommended to prevent protein-energy wasting. In a 6-mo prospective randomized, open-label, clinical trial, we reported that the combination of resistance exercise and nutritional supplementation does not have an additive effect on lean body mass measured by dual-energy X-ray absorptiometry. To provide more mechanistic data, we performed a secondary analysis where we hypothesized that the combination of nutritional supplementation and resistance exercise would have additive effects on muscle protein accretion by stable isotope protein kinetic experiments, muscle mass by MRI, and mitochondrial content markers in muscle. We found that 6 mo of nutritional supplementation during hemodialysis increased muscle protein net balance [baseline: 2.5 (−17.8, 13.0) µg·100 mL−1·min−1 vs. 6 mo: 43.7 (13.0, 98.5) µg·100 mL−1·min−1, median (interquartile range), P = 0.04] and mid-thigh fat area [baseline: 162.3 (104.7, 226.6) cm2 vs. 6 mo: 181.9 (126.3, 279.2) cm2, median (interquartile range), P = 0.04]. Three months of nutritional supplementation also increased markers of mitochondrial content in muscle. Although the study is underpowered to detected differences, the combination of nutritional supplementation and exercise failed to show further benefit in protein accretion or muscle cross-sectional area. We conclude that long-term nutritional supplementation increases the skeletal muscle anabolic effect, the fat cross-sectional area of the thigh, and markers of mitochondrial content in skeletal muscle.

2013 ◽  
Vol 24 (4) ◽  
pp. e260-e268 ◽  
Author(s):  
M. S. Kristiansen ◽  
A. Uhrbrand ◽  
M. Hansen ◽  
J. M. Shiguetomi-Medina ◽  
K. Vissing ◽  
...  

1981 ◽  
Vol 48 (1) ◽  
pp. 35-54
Author(s):  
C.R. Shear

The effects of long-term muscle inactivity, throughout post-hatching development, have been examined. Continuous immobilization of the chicken posterior latissimus dorsi (PLD) muscle from the first hour after hatching for varying periods up to 330 days, resulted in a significantly greater decrease in myofibre size (40-64% less than control) than occurred when adult muscles were immobilized for similar periods (20-40% less than control). The myofibre atrophy resulting from long-term immobilization of adult muscle is reversible, after removal of the plaster cast. In contrast, the myofibres immobilized immediately after hatching, for similar periods of time, were unable to recover one the casts were removed. On the basis of myofibre cross-sectional area, 2 populations of cells were seen in muscles immobilized during postnatal development: small myofibres of 0.5-200 micron 2 and larger myofibres of 500–800 micron 2. The distribution of fibre cross-sectional area within immobilized adult muscles was similar to controls, suggesting a uniform response (i.e. atrophy) by all of the myofibres within the muscle. Immobilization in both newly hatched and adult PLD muscles did not appear to alter the pattern of motor endplate distribution within the muscle. Small, multiple motor endplates were observed associated with immobilized and control myofibres near their terminal ends. This finding suggests that the embryonic pattern of myofibre innervation is not entirely lost from all the fibres during postnatal development.


2020 ◽  
Vol 128 (4) ◽  
pp. 1000-1011 ◽  
Author(s):  
Thomas M. Maden-Wilkinson ◽  
Thomas G. Balshaw ◽  
Garry J. Massey ◽  
Jonathan P. Folland

Here we demonstrate that the larger muscle strength (+60%) of a long-term (4+ yr) resistance-trained group compared with untrained controls was due to their similarly larger muscle volume (+56%), primarily due to a larger physiological cross-sectional area and modest differences in fascicle length, as well as modest differences in maximum voluntary specific tension and patella tendon moment arm. In addition, the present study refutes the possibility of regional hypertrophy, despite large differences in muscle volume.


2015 ◽  
Vol 308 (11) ◽  
pp. C932-C943 ◽  
Author(s):  
Damien M. Callahan ◽  
Timothy W. Tourville ◽  
Mark S. Miller ◽  
Sarah B. Hackett ◽  
Himani Sharma ◽  
...  

In older adults, we examined the effect of chronic muscle disuse on skeletal muscle structure at the tissue, cellular, organellar, and molecular levels and its relationship to muscle function. Volunteers with advanced-stage knee osteoarthritis (OA, n = 16) were recruited to reflect the effects of chronic lower extremity muscle disuse and compared with recreationally active controls ( n = 15) without knee OA but similar in age, sex, and health status. In the OA group, quadriceps muscle and single-fiber cross-sectional area were reduced, with the largest reduction in myosin heavy chain IIA fibers. Myosin heavy chain IIAX fibers were more prevalent in the OA group, and their atrophy was sex-specific: men showed a reduction in cross-sectional area, and women showed no differences. Myofibrillar ultrastructure, myonuclear content, and mitochondrial content and morphology generally did not differ between groups, with the exception of sex-specific adaptations in subsarcolemmal (SS) mitochondria, which were driven by lower values in OA women. SS mitochondrial content was also differently related to cellular and molecular functional parameters by sex: greater SS mitochondrial content was associated with improved contractility in women but reduced function in men. Collectively, these results demonstrate sex-specific structural phenotypes at the cellular and organellar levels with chronic disuse in older adults, with novel associations between energetic and contractile systems.


2007 ◽  
Vol 292 (1) ◽  
pp. C440-C451 ◽  
Author(s):  
Z. Ashley ◽  
H. Sutherland ◽  
H. Lanmüller ◽  
M. F. Russold ◽  
E. Unger ◽  
...  

Our understanding of the effects of long-term denervation on skeletal muscle is heavily influenced by an extensive literature based on the rat. We have studied physiological and morphological changes in an alternative model, the rabbit. In adult rabbits, tibialis anterior muscles were denervated unilaterally by selective section of motor branches of the common peroneal nerve and examined after 10, 36, or 51 wk. Denervation reduced muscle mass and cross-sectional area by 50–60% and tetanic force by 75%, with no apparent reduction in specific force (force per cross-sectional area of muscle fibers). The loss of mass was associated with atrophy of fast fibers and an increase in fibrous and adipose connective tissue; the diameter of slow fibers was preserved. Within fibers, electron microscopy revealed signs of ultrastructural disorganization of sarcomeres and tubular systems. This, rather than the observed transformation of fiber type from IIx to IIa, was probably responsible for the slow contractile speed of the muscles. The muscle groups denervated for 10, 36, or 51 wk showed no significant differences. At no stage was there any evidence of necrosis or regeneration, and the total number of fibers remained constant. These changes are in marked contrast to the necrotic degeneration and progressive decline in mass and force that have previously been found in long-term denervated rat muscles. The rabbit may be a better choice for a model of the effects of denervation in humans, at least up to 1 yr after lesion.


2000 ◽  
Vol 25 (6) ◽  
pp. 524-535 ◽  
Author(s):  
Martin J. Gibala

Many athletes and recreational weightlifters believe that dietary manipulations-either following a single bout of resistance exercise or during habitual training-may augment the normal gains in muscle fibre hypertrophy. Very few studies, however, have directly examined the effect of nutritional supplementation on muscle protein metabolism after resistance exercise. Ingestion of an amino acid and/or carbohydrate solution during the initial hours following a single bout of resistance exercise promotes an acute increase in protein net balance compared to the fasted state. The precise mechanism involved has not been elucidated but seems related to an increased availability of intracellular amino acids and/or an increase in plasma insulin concentration. As a practical recommendation, therefore, postexercise feeding appears to be very important. Recent evidence suggests that creatine supplementation in conjunction with resistance training may elicit larger increases in muscle fibre cross-sectional area compared to training alone. This intervention may be most beneficial in persons with "compromised" skeletal muscle. Key words: protein metabolism, amino acids, creatine, insulin, human


2018 ◽  
Vol 315 (5) ◽  
pp. C744-C756 ◽  
Author(s):  
Blas A. Guigni ◽  
Damien M. Callahan ◽  
Timothy W. Tourville ◽  
Mark S. Miller ◽  
Brad Fiske ◽  
...  

How breast cancer and its treatments affect skeletal muscle is not well defined. To address this question, we assessed skeletal muscle structure and protein expression in 13 women who were diagnosed with breast cancer and receiving adjuvant chemotherapy following tumor resection and 12 nondiseased controls. Breast cancer patients showed reduced single-muscle fiber cross-sectional area and fractional content of subsarcolemmal and intermyofibrillar mitochondria. Drugs commonly used in breast cancer patients (doxorubicin and paclitaxel) caused reductions in myosin expression, mitochondrial loss, and increased reactive oxygen species (ROS) production in C2C12 murine myotube cell cultures, supporting a role for chemotherapeutics in the atrophic and mitochondrial phenotypes. Additionally, concurrent treatment of myotubes with the mitochondrial-targeted antioxidant MitoQ prevented chemotherapy-induced myosin depletion, mitochondrial loss, and ROS production. In patients, reduced mitochondrial content and size and increased expression and oxidation of peroxiredoxin 3, a mitochondrial peroxidase, were associated with reduced muscle fiber cross-sectional area. Our results suggest that chemotherapeutics may adversely affect skeletal muscle in patients and that these effects may be driven through effects of these drugs on mitochondrial content and/or ROS production.


2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Zhifei Ke

Objective Insufficient physical activity, aerospace weight loss, and fixed treatment of fractures, tendons, and neuropathy, or the resulting muscle atrophy caused by reduced exercise, have become an urgent health problem. Exercise has received widespread attention as an effective means of preventing muscle atrophy. Through the literatures related to "sports and muscle atrophy" at home and abroad, the effects of exercise on muscle atrophy in simulated weightless rats were analyzed, in order to provide theoretical basis and guidance for exercise prevention and treatment of muscle atrophy. Methods The electronic databases PubMed, EMBASE and SPORTDiscus were searched for relevant studies reporting on the effects of physical exercise on muscle therapy. The keywords are: “aerobic exercise or resistance exercise”; "muscle atrophy"; "weightless or weightlessness"and the limitation period is 2013-2018. At the same time, the relevant literatures of the Chinese Journal Full-text Database were searched. The search terms were:“aerobic exercise; resistance exercise; muscle atrophy”, and the language of the article was limited to Chinese. Inclusion criteria: exercise and sarcopenia; effects of exercise on muscle atrophy; relationship between muscle atrophy and exercise. Exclusion criteria: repetitive studies. A total of 54 literature reviews were included in the literature. Results (1)The simulated weightless model is mainly for unloading and tail suspension. After the tail suspension, the soleus muscle becomes thinner and thinner, the elasticity decreases, the volume and mass decrease, the cross-sectional area of the muscle fiber decreases, and the cross-sectional area of the muscle fiber increases after exercise intervention. , suggesting that exercise can effectively slow down the quality of the soleus muscle caused by simulated weightlessness. (2)After 4 weeks of tail suspension, IGF-1 was found to change significantly. Exercise can stimulate the secretion of IGF-1, TESTO and myogenin to some extent, and promote the synthesis of muscle protein. At the same time, myogenin showed different expression under different exercise forms, suggesting myogenin. It may not be used as a predictor of muscle atrophy change. (3) Oxidative stress occurs after 4 weeks of tail suspension, aggravating muscle atrophy, and activity of SOD and GSH-Px is enhanced after exercise intervention. The possible mechanism is to exercise the body SOD and GSH-Px. Vitality, thereby reducing muscle atrophy caused by oxidative stress in the body. (4)Exercise to reduce muscle atrophy may be through down-regulation of atrogin-1 expression and reduction of Caspase-3 expression.  (5) Regardless of endurance exercise or resistance exercise, long-term low-intensity exercise or high-intensity exercise can down-regulate atrogin-1 expression in skeletal muscle. However, different exercise intensity and different exercise patterns have irregular expression of atrogin-1. The effects of different exercise patterns and exercise intensity on the expression of atrogin-1 under simulated weightlessness and its specific mechanism need to be further explored. Conclusions Exercise improves muscle atrophy by promoting the secretion of anabolic hormones in the body, increasing the antioxidant capacity in the body and inhibiting the expression of atrogin-1 protein in the ubiquitin proteasome pathway, which promotes the synthesis and inhibition of skeletal muscle protein to a certain extent. Decomposition of skeletal muscle proteins to reduce muscle atrophy caused by tail suspension.   


2000 ◽  
Vol 278 (3) ◽  
pp. R705-R711 ◽  
Author(s):  
T. A. McAllister ◽  
J. R. Thompson ◽  
S. E. Samuels

The effect of long-term cold exposure on skeletal and cardiac muscle protein turnover was investigated in young growing animals. Two groups of 36 male 28-day-old rats were maintained at either 5°C (cold) or 25°C (control). Rates of protein synthesis and degradation were measured in vivo on days 5, 10, 15, and 20. Protein mass by day 20 was ∼28% lower in skeletal muscle (gastrocnemius and soleus) and ∼24% higher in heart in cold compared with control rats ( P < 0.05). In skeletal muscle, the fractional rates of protein synthesis ( k syn) and degradation ( k deg) were not significantly different between cold and control rats, although k syn was lower (approximately −26%) in cold rats on day 5; consequent to the lower protein mass, the absolute rates of protein synthesis (approximately −21%; P < 0.05) and degradation (approximately −13%; P < 0.1) were lower in cold compared with control rats. In heart, overall, k syn(approximately +12%; P < 0.1) and k deg(approximately +22%; P < 0.05) were higher in cold compared with control rats; consequently, the absolute rates of synthesis (approximately +44%) and degradation (approximately +54%) were higher in cold compared with control rats ( P < 0.05). Plasma triiodothyronine concentration was higher ( P < 0.05) in cold compared with control rats. These data indicate that long-term cold acclimation in skeletal muscle is associated with the establishment of a new homeostasis in protein turnover with decreased protein mass and normal fractional rates of protein turnover. In heart, unlike skeletal muscle, rates of protein turnover did not appear to immediately return to normal as increased rates of protein turnover were observed beyond day 5. These data also indicate that increased rates of protein turnover in skeletal muscle are unlikely to contribute to increased metabolic heat production during cold acclimation.


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