Abstract:Physical activity plays an important role in preventing muscle atrophy and chronic diseases in adults and in the elderly. Calcium (Ca2+) cycling and activation of specific molecular pathways are essential in contraction-induced muscle adaptation. This study attains human muscle sections and total homogenates prepared from biopsies obtained before (control) and after 9 weeks of training by electrical stimulation (ES) on a group of volunteers. The aim of the study was to investigate about the molecular mechanism… Show more
“…Interestingly this was accompanied with the upregulation of Calsequestrin-1. In a recent study on humans, it was shown that these changes were reversed after 9 weeks of training by electrical stimulation [63] of the vastus lateralis muscle of sedentary senior volunteers. The decreased active SERCA, and thus insufficient SR Ca 2+ content, can also be explained by the findings of Boncompagni et al [64].…”
Section: Oxidative Stress and Ec-coupling Machinery In Agingmentioning
Reduction in muscle strength with aging is due to both loss of muscle mass (quantity) and intrinsic force production (quality). Along with decreased functional capacity of the muscle, age-related muscle loss is associated with corresponding comorbidities and healthcare costs. Mitochondrial dysfunction and increased oxidative stress are the central driving forces for age-related skeletal muscle abnormalities. The increased oxidative stress in the aged muscle can lead to altered excitation-contraction coupling and calcium homeostasis. Furthermore, apoptosis-mediated fiber loss, atrophy of the remaining fibers, dysfunction of the satellite cells (muscle stem cells), and concomitant impaired muscle regeneration are also the consequences of increased oxidative stress, leading to a decrease in muscle mass, strength, and function of the aged muscle. Here we summarize the possible effects of oxidative stress in the aged muscle and the benefits of physical activity and antioxidant therapy.
“…Interestingly this was accompanied with the upregulation of Calsequestrin-1. In a recent study on humans, it was shown that these changes were reversed after 9 weeks of training by electrical stimulation [63] of the vastus lateralis muscle of sedentary senior volunteers. The decreased active SERCA, and thus insufficient SR Ca 2+ content, can also be explained by the findings of Boncompagni et al [64].…”
Section: Oxidative Stress and Ec-coupling Machinery In Agingmentioning
Reduction in muscle strength with aging is due to both loss of muscle mass (quantity) and intrinsic force production (quality). Along with decreased functional capacity of the muscle, age-related muscle loss is associated with corresponding comorbidities and healthcare costs. Mitochondrial dysfunction and increased oxidative stress are the central driving forces for age-related skeletal muscle abnormalities. The increased oxidative stress in the aged muscle can lead to altered excitation-contraction coupling and calcium homeostasis. Furthermore, apoptosis-mediated fiber loss, atrophy of the remaining fibers, dysfunction of the satellite cells (muscle stem cells), and concomitant impaired muscle regeneration are also the consequences of increased oxidative stress, leading to a decrease in muscle mass, strength, and function of the aged muscle. Here we summarize the possible effects of oxidative stress in the aged muscle and the benefits of physical activity and antioxidant therapy.
“…The conclusions were that neuromuscular ES applied to Vastus lateralis muscle of sedentary seniors combines fiber remodeling with activation of Ca 2+ -Calmodulin molecular pathways and modulation of the key Ca 2+ -handling proteins. 80 Collagen expression was also reported to be remodelled during both volitional physical exercise and ES; indeed, expression of three different forms of collagen was upregulated in electrically stimulated muscle. 30 However, the increase in collagen expression seems not to stimulate fibrosis as is shown by both morphological evidence and at the level of important fibrosis modulators, namely the increase in expression of miR29.…”
Section: Role Of Myokines In Volitional Physical Activity and Hbfes Tmentioning
confidence: 99%
“…30 In addition, with ES an increase in expression of IGF-1 factors as well as markers of both satellite cell proliferation and extracellular matrix remodeling was detected along with downregulation in the expression of proteases just as occurs during volitional physical exercise. 31 Furthermore, Mosole et al, 80 recently demonstrated that ES modulate also the Calcium (Ca 2+) -handling proteins, NFAT, and related proteases. The aims were to study the molecular mechanisms that support functional muscle improvement by ES.…”
Section: Role Of Myokines In Volitional Physical Activity and Hbfes Tmentioning
Neuromuscular disorders, disuse, inadequate nutrition, metabolic diseases, cancer and aging produce muscle atrophy and this implies that there are different types of molecular triggers and signaling pathways for muscle wasting. Exercise and muscle contractions may counteract muscle atrophy by releasing a group of peptides, termed myokines, to protect the functionality and to enhance the exercise capacity of skeletal muscle. In this review, we are looking at the role of myokines in the recovery of permanent denervated and elderly skeletal muscle tissue. Since sub-clinical denervation events contribute to both atrophy and the decreased contractile speed of aged muscle, we saw a parallel to spinal cord injury and decided to look at both groups together. The muscle from lifelong active seniors has more muscle bulk and more slow fiber-type groupings than those of sedentary seniors, demonstrating that physical activity maintains slow motoneurons that reinnervate the transiently denervated muscle fibers. Furthermore, we summarized the evidence that muscle degeneration occur with irreversible Conus and Cauda Equina syndrome, a spinal cord injury in which the human leg muscles may be permanently disconnected from the peripheral nervous system. In these patients, suffering with an estreme case of muscle disuse, a complete loss of muscle fibers occurs within five to ten years after injury. Their recovered tetanic contractility, induced by home-based Functional Electrical Stimulation, can restore the muscle size and function in compliant Spinal Cord Injury patients, allowing them to perform electrical stimulation-supported stand-up training. Myokines are produced and released by muscle fibers under contraction and exert both local and systemic effects. Changes in patterns of myokine secretion, particularly of IGF-1 isoforms, occur in long-term Spinal Cord Injury persons and also in very aged people. Their modulation in Spinal Cord Injury and late aging are also key factors of home-based Functional Electrical Stimulation - mediated muscle recovery. Thus, Functional Electrical Stimulation should be prescribed in critical care units and nursing facilities, if persons are unable or reluctant to exercise. This will result in less frequent hospitalizations and a reduced burden on patients’ families and public health services.
“…ES treatment in old sedentary people improved muscle performance, increasing fiber size, stimulating satellite cells and modulating the degeneration of the mitochondrial apparatus [106,107]. Moreover, it has been reported that ES treatment increases the number of fast twitch fibers [108] and counteracts neuromuscular disabilities from age related NMJ degeneration in paraplegic patients [109,110]. At molecular level ES treatment activates signaling pathways that decode for a specific calcium signaling involved in metabolic and structural adaptation of muscle fibers, such as the Calcineurin-NFAT and CamKII pathways that control the maintenance or switching of muscle fiber type [108].…”
Section: Als and Aging As Paradigmatic Examples Of Altered Nerve-mmentioning
confidence: 99%
“…Moreover, it has been reported that ES treatment increases the number of fast twitch fibers [108] and counteracts neuromuscular disabilities from age related NMJ degeneration in paraplegic patients [109,110]. At molecular level ES treatment activates signaling pathways that decode for a specific calcium signaling involved in metabolic and structural adaptation of muscle fibers, such as the Calcineurin-NFAT and CamKII pathways that control the maintenance or switching of muscle fiber type [108]. Moreover, it has been described that biphasic electrical stimulation significantly increases the number and size of AChRs clusters available for NMJ formation during innervation [105] and that electrical stimulation promotes axonal growth and sensorimotor functional recovery after injury [106].…”
Section: Als and Aging As Paradigmatic Examples Of Altered Nerve-mmentioning
One of the crucial systems severely affected in several neuromuscular diseases is the loss of effective connection between muscle and nerve, leading to a pathological non-communication between the two tissues. The neuromuscular junction (NMJ) represents the critical region at the level of which muscle and nerve communicate. Defects in signal transmission between terminal nerve endings and muscle membrane is a common feature of several physio-pathologic conditions including aging and Amyotrophic Lateral Sclerosis (ALS). Nevertheless, controversy exists on whether pathological events beginning at the NMJ precede or follow loss of motor units. In this review, the role of NMJ in the physio-pathologic interplay between muscle and nerve is discussed.
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