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Special Issue Editor

Dr. Robert A. Jacobs

Human Physiology & Nutrition Program, Department of Biology, University of Colorado Colorado Springs, CO, USA
Interests: mitochondria; aging; insulin resistance; redox; human performance; bioenergetics; hypoxia

Special Issue Information

Dear Colleagues,

Skeletal muscle accounts for ~40% of total body mass and ~75% of variability in the basal metabolic rate, which is, on average, the largest component of total daily energy expenditure, and is the only tissue in the human body capable of increasing metabolic demand >1,000-fold in response to extreme metabolic stress. Whole-body health tracks with skeletal muscle function, and skeletal muscle health is reliant on the maintenance of mitochondrial function. Diminished skeletal muscle and mitochondrial function is now evident in the etiology and/or pathology of many diseases and disorders, especially metabolic disease. Moreover, biological decrements concomitant to aging are complementary to diminished skeletal muscle and mitochondrial function. The direction that these relationships take is largely attributed to the regularity and magnitude of energetic flux through skeletal muscle. Exercise is a necessary strategy to stimulate and/or maintain skeletal muscle and mitochondrial function across the lifespan. Accordingly, it is paramount to identify the physiology of skeletal muscle and mitochondrial function vs. dysfunction, and discuss how energetic flux relates to both. Therefore, the aim of this Special Issue is to discuss the biological relationship between skeletal muscle as well as mitochondrial function in relation to whole-body health.

Dr. Robert A. Jacobs
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

mitochondria
aging
insulin resistance
redox
contraction
exercise

Published Papers (2 papers)

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Review

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18 pages, 1275 KiB

Open AccessFeature PaperReview

Exercise-Induced Mitohormesis for the Maintenance of Skeletal Muscle and Healthspan Extension

by Robert V. Musci, Karyn L. Hamilton and Melissa A. Linden

Sports 2019, 7(7), 170; https://0-doi-org.brum.beds.ac.uk/10.3390/sports7070170 - 11 Jul 2019

Cited by 38 | Viewed by 7289

Abstract

Oxidative damage is one mechanism linking aging with chronic diseases including the progressive loss of skeletal muscle mass and function called sarcopenia. Thus, mitigating oxidative damage is a potential avenue to prevent or delay the onset of chronic disease and/or extend healthspan. Mitochondrial hormesis (mitohormesis) occurs when acute exposure to stress stimulates adaptive mitochondrial responses that improve mitochondrial function and resistance to stress. For example, an acute oxidative stress via mitochondrial superoxide production stimulates the activation of endogenous antioxidant gene transcription regulated by the redox sensitive transcription factor Nrf2, resulting in an adaptive hormetic response. In addition, acute stresses such as aerobic exercise stimulate the expansion of skeletal muscle mitochondria (i.e., mitochondrial biogenesis), constituting a mitohormetic response that protects from sarcopenia through a variety of mechanisms. This review summarized the effects of age-related declines in mitochondrial and redox homeostasis on skeletal muscle protein homeostasis and highlights the mitohormetic mechanisms by which aerobic exercise mitigates these age-related declines and maintains function. We discussed the potential efficacy of targeting the Nrf2 signaling pathway, which partially mediates adaptation to aerobic exercise, to restore mitochondrial and skeletal muscle function. Finally, we highlight knowledge gaps related to improving redox signaling and make recommendations for future research. Full article

(This article belongs to the Special Issue Biological Relationship Between Skeletal Muscle and Whole-Body Health)

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Other

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12 pages, 630 KiB

Open AccessCommentary

Cardiovascular Consequences of Skeletal Muscle Impairments in Breast Cancer

by Gabriel H. Zieff, Chad W. Wagoner, Craig Paterson, Patricia Pagan Lassalle and Jordan T. Lee

Sports 2020, 8(6), 80; https://0-doi-org.brum.beds.ac.uk/10.3390/sports8060080 - 31 May 2020

Cited by 6 | Viewed by 3110

Abstract

Breast cancer survivors suffer from disproportionate cardiovascular disease risk compared to age-matched controls. Beyond direct cardiotoxic effects due to treatments such as chemotherapy and radiation, breast-cancer-related reductions in skeletal muscle mass, quality and oxidative capacity may further contribute to cardiovascular disease risk in this population by limiting the ability to engage in aerobic exercise—a known promoter of cardiovascular health. Indeed, 20–30% decreases in peak oxygen consumption are commonly observed in breast cancer survivors, which are indicative of exercise intolerance. Thus, breast-cancer-related skeletal muscle damage may reduce exercise-based opportunities for cardiovascular disease risk reduction. Resistance training is a potential strategy to improve skeletal muscle health in this population, which in turn may enhance the capacity to engage in aerobic exercise and reduce cardiovascular disease risk. Full article

(This article belongs to the Special Issue Biological Relationship Between Skeletal Muscle and Whole-Body Health)

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