scholarly journals THE ROLE OF PHYSICAL FITNESS IN DETECTING AGE-RELATED DIFFERENCES IN SKELETAL MUSCLE OXIDATIVE FUNCTION DURING WHOLE-BODY AND ISOLATED MUSCLE WORK

2021 ◽  
Vol 53 (8S) ◽  
pp. 108-108
Author(s):  
Mireille van Beekvelt ◽  
Sigve Bakken Bolme ◽  
Martine Berg
2018 ◽  
Vol 28 (12) ◽  
pp. 2494-2504 ◽  
Author(s):  
Sune Dandanell ◽  
Anne-Kristine Meinild-Lundby ◽  
Andreas B. Andersen ◽  
Paul F. Lang ◽  
Laura Oberholzer ◽  
...  

Author(s):  
Yan Zhao ◽  
Jason Cholewa ◽  
Huayu Shang ◽  
Yueqin Yang ◽  
Xiaomin Ding ◽  
...  

Skeletal muscle anabolic resistance (i.e., the decrease in muscle protein synthesis (MPS) in response to anabolic stimuli such as amino acids and exercise) has been identified as a major cause of age-related sarcopenia, to which blunted nutrition-sensing contributes. In recent years, it has been suggested that a leucine sensor may function as a rate-limiting factor in skeletal MPS via small-molecule GTPase. Leucine-sensing and response may therefore have important therapeutic potential in the steady regulation of protein metabolism in aging skeletal muscle. This paper systematically summarizes the three critical processes involved in the leucine-sensing and response process: (1) How the coincidence detector mammalian target of rapamycin complex 1 localizes on the surface of lysosome and how its crucial upstream regulators Rheb and RagB/RagD interact to modulate the leucine response; (2) how complexes such as Ragulator, GATOR, FLCN, and TSC control the nucleotide loading state of Rheb and RagB/RagD to modulate their functional activity; and (3) how the identified leucine sensor leucyl-tRNA synthetase (LARS) and stress response protein 2 (Sestrin2) participate in the leucine-sensing process and the activation of RagB/RagD. Finally, we discuss the potential mechanistic role of exercise and its interactions with leucine-sensing and anabolic responses.


2020 ◽  
Vol 21 (15) ◽  
pp. 5236 ◽  
Author(s):  
Evelyn Ferri ◽  
Emanuele Marzetti ◽  
Riccardo Calvani ◽  
Anna Picca ◽  
Matteo Cesari ◽  
...  

Skeletal muscle aging is associated with a significant loss of skeletal muscle strength and power (i.e., dynapenia), muscle mass and quality of life, a phenomenon known as sarcopenia. This condition affects nearly one-third of the older population and is one of the main factors leading to negative health outcomes in geriatric patients. Notwithstanding the exact mechanisms responsible for sarcopenia are not fully understood, mitochondria have emerged as one of the central regulators of sarcopenia. In fact, there is a wide consensus on the assumption that the loss of mitochondrial integrity in myocytes is the main factor leading to muscle degeneration. Mitochondria are also key players in senescence. It has been largely proven that the modulation of mitochondrial functions can induce the death of senescent cells and that removal of senescent cells improves musculoskeletal health, quality, and function. In this review, the crosstalk among mitochondria, cellular senescence, and sarcopenia will be discussed with the aim to elucidate the role that the musculoskeletal cellular senescence may play in the onset of sarcopenia through the mediation of mitochondria.


2020 ◽  
Vol 319 (1) ◽  
pp. H192-H202
Author(s):  
Alexander B. Hansen ◽  
Gilbert Moralez ◽  
Steven A. Romero ◽  
Christopher Gasho ◽  
Michael M. Tymko ◽  
...  

Sympathetic restraint of vascular conductance to inactive skeletal muscle is critical to maintain blood pressure during moderate- to high-intensity whole body exercise. This investigation shows that cycle exercise-induced restraint of inactive skeletal muscle vascular conductance occurs primarily because of activation of α-adrenergic receptors. Furthermore, exercise-induced vasoconstriction restrains the subsequent vasodilatory response to hand-grip exercise; however, the restraint of active skeletal muscle vasodilation was in part due to nonadrenergic mechanisms. We conclude that α-adrenergic receptors are the primary but not exclusive mechanism by which sympathetic vasoconstriction restrains blood flow in humans during whole body exercise and that metabolic activity modulates the contribution of α-adrenergic receptors.


1982 ◽  
Vol 62 (1) ◽  
pp. 123-132 ◽  
Author(s):  
V. A. GREGG ◽  
L. P. MILLIGAN

The role of Na+, K+-ATPase in the energy expenditure of sheep skeletal muscle and the influence of exposure to cold on this role were studied. An in vitro preparation of muscle was developed that achieved O2 availability and a functional membrane potential. A 10−6 M concentration of ouabain yielded a maximum inhibition of respiration of 38.9 ± 1.8% using muscle preparations from a random group of sheep. Whole body and muscle O2 consumptions and ouabain-sensitive muscle respiration were measured for warm- and cold-exposed sheep fed at maintenance or 1150 g of alfalfa pellets per day. Cold exposure increased whole body and muscle O2 consumption. Inhibition of respiration by ouabain was 37.6 ± 1.2% and 41.0 ± 3.6% for warm- and cold-exposed sheep fed at maintenance, and 28.5 ± 4.0% and 45.0 ± 4.0% for warm- and cold-exposed sheep fed 1150 g of alfalfa pellets per day. The increase in the ouabain-sensitive component of respiration accounted for 48–79% of the increased O2 consumption of muscle from cold-exposed sheep. It was concluded that the Na+, K+-ATPase of sheep muscle is a major means of energy expenditure and has an important role in the increased thermogenesis resulting from cold exposure. Key words: Skeletal muscle, Energy expenditure, muscle respiration, cold thermogenesis, sodium-potassium transport


2014 ◽  
Vol 128 (3) ◽  
pp. 213-223 ◽  
Author(s):  
Gwenael Layec ◽  
Corey R. Hart ◽  
Joel D. Trinity ◽  
Yann Le Fur ◽  
Eun-Kee Jeong ◽  
...  

This study suggests that the excessive cost associated with ion transport, potentially mediated by chronic oxidative stress, is an important mechanism contributing to the decline in muscle efficiency with age and probably compromises functional capacity in older adults.


2005 ◽  
Vol 35 (6) ◽  
pp. 473-483 ◽  
Author(s):  
Amie J Dirks ◽  
Christiaan Leeuwenburgh

2009 ◽  
Vol 297 (3) ◽  
pp. R546-R555 ◽  
Author(s):  
Gary J. Hodges ◽  
Dwayne N. Jackson ◽  
Louis Mattar ◽  
John M. Johnson ◽  
J. Kevin Shoemaker

Neuropeptide Y (NPY) is a ubiquitous peptide with multiple effects on energy metabolism, reproduction, neurogenesis, and emotion. In addition, NPY is an important sympathetic neurotransmitter involved in neurovascular regulation. Although early studies suggested that the vasoactive effects of NPY were limited to periods of high stress, there is growing evidence for the involvement of NPY on baseline vasomotor tone and sympathetically evoked vasoconstriction in vivo in both skeletal muscle and the cutaneous circulation. In Sprague-Dawley rat skeletal muscle, Y1-receptor activation appears to play an important role in the regulation of basal vascular conductance, and this effect is similar in magnitude to the α1-receptor contribution. Furthermore, under baseline conditions, agonist and receptor-based mechanisms for Y1-receptor-dependent control of vascular conductance in skeletal muscle are greater in male than female rats. In skin, there is Y1-receptor-mediated vasoconstriction during whole body, but not local, cooling. As with the NPY system in muscle, this neural effect in skin differs between males and females and in addition, declines with aging. Intriguingly, skin vasodilation to local heating also requires NPY and is currently thought to be acting via a nitric oxide pathway. These studies are establishing further interest in the role of NPY as an important vasoactive agent in muscle and skin, adding to the complexity of neurovascular regulation in these tissues. In this review, we focus on the role of NPY on baseline vasomotor tone in skeletal muscle and skin and how NPY modulates vasomotor tone in response to stress, with the aim of compiling what is currently known, while highlighting some of the more pertinent questions yet to be answered.


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