bims-exemet 2021-07-04 papers

Issue of 2021–07–04
six papers selected by
Javier Botella Ruiz, Victoria University

Exp Physiol. 2021 Jul 01.

Repeated bouts of resistance exercise in rats alter mTORC1 activity and ribosomal capacity but not muscle protein synthesis.

Takaya Kotani, Junya Takegaki, Yuki Tamura, Karina Kouzaki, Koichi Nakazato, Naokata Ishii.

NEW FINDINGS: What is the central question of this study? Is muscle protein synthesis (MPS) additionally activated following exercise when ribosomal capacity is increased after repeated bouts of resistance exercise (RE)? What is the main finding and its importance? Skeletal muscles with increased ribosome content by repeated RE bouts showed sufficient activation of MPS with lower mTORC1 signaling. Thus, repeated bouts of RE possibly change the translational capacity and efficiency to optimize translation activation following RE.
ABSTRACT: Resistance exercise (RE) activates ribosome biogenesis and increases ribosome content in skeletal muscles. However, it is unclear whether the increase in ribosome content subsequently causes an increase in RE-induced muscle protein synthesis (MPS) activation. Thus, this study aimed to investigate the relationship between ribosome content and MPS after exercise using a rat RE model. Male Sprague-Dawley rats were categorized into three groups (n = 6 for each group): sedentary (SED), RE trained with one bout (1B) and three bouts (3B). The RE stimulus was applied to the right gastrocnemius muscle by transcutaneous electric stimulation under isoflurane anaesthesia. The 3B group underwent stimulation every other day. Our results revealed that 6 h after the last bout of RE, muscles in the 3B group showed an increase in total RNA and 18S + 28S rRNA content per muscle weight than in the SED and 1B groups. In both the 1B and 3B groups, MPS, estimated by puromycin incorporation in proteins, was higher than that in the SED group 6 h after exercise; however, no significant difference was observed between the 1B and 3B groups. In the 1B and 3B groups, phosphorylated p70S6K at Thr-389 increased, indicating mTORC1 activity. p70S6K phosphorylation level was lower in the 3B group than in the 1B group. Lastly, protein synthesis per ribosome (indicator of translation efficiency) was lower in the 3B group than in the 1B group. Thus, three bouts of RE changed the ribosome content and mTORC1 activation, however, not the degree of RE-induced global MPS activation. This article is protected by copyright. All rights reserved.

Keywords: mTORC1, SUnSET; translation efficiency, translation capacity, rRNA

DOI: https://doi.org/10.1113/EP089699

Int J Mol Sci. 2021 Jun 17. pii: 6479. [Epub ahead of print]22(12):

The Muscle-Brain Axis and Neurodegenerative Diseases: The Key Role of Mitochondria in Exercise-Induced Neuroprotection.

Johannes Burtscher, Grégoire P Millet, Nicolas Place, Bengt Kayser, Nadège Zanou.

Regular exercise is associated with pronounced health benefits. The molecular processes involved in physiological adaptations to exercise are best understood in skeletal muscle. Enhanced mitochondrial functions in muscle are central to exercise-induced adaptations. However, regular exercise also benefits the brain and is a major protective factor against neurodegenerative diseases, such as the most common age-related form of dementia, Alzheimer's disease, or the most common neurodegenerative motor disorder, Parkinson's disease. While there is evidence that exercise induces signalling from skeletal muscle to the brain, the mechanistic understanding of the crosstalk along the muscle-brain axis is incompletely understood. Mitochondria in both organs, however, seem to be central players. Here, we provide an overview on the central role of mitochondria in exercise-induced communication routes from muscle to the brain. These routes include circulating factors, such as myokines, the release of which often depends on mitochondria, and possibly direct mitochondrial transfer. On this basis, we examine the reported effects of different modes of exercise on mitochondrial features and highlight their expected benefits with regard to neurodegeneration prevention or mitigation. In addition, knowledge gaps in our current understanding related to the muscle-brain axis in neurodegenerative diseases are outlined.

Keywords: brain; exercise; mitochondria; muscle; myokines; neurodegeneration

DOI: https://doi.org/10.3390/ijms22126479

Compr Physiol. 2021 Jun 30. 11(3): 2249-2278

Resistance Exercise, Aging, Disuse, and Muscle Protein Metabolism.

James McKendry, Tanner Stokes, Jonathan C Mcleod, Stuart M Phillips.

Skeletal muscle is the organ of locomotion, its optimal function is critical for athletic performance, and is also important for health due to its contribution to resting metabolic rate and as a site for glucose uptake and storage. Numerous endogenous and exogenous factors influence muscle mass. Much of what is currently known regarding muscle protein turnover is owed to the development and use of stable isotope tracers. Skeletal muscle mass is determined by the meal- and contraction-induced alterations of muscle protein synthesis and muscle protein breakdown. Increased loading as resistance training is the most potent nonpharmacological strategy by which skeletal muscle mass can be increased. Conversely, aging (sarcopenia) and muscle disuse lead to the development of anabolic resistance and contribute to the loss of skeletal muscle mass. Nascent omics-based technologies have significantly improved our understanding surrounding the regulation of skeletal muscle mass at the gene, transcript, and protein levels. Despite significant advances surrounding the mechanistic intricacies that underpin changes in skeletal muscle mass, these processes are complex, and more work is certainly needed. In this article, we provide an overview of the importance of skeletal muscle, describe the influence that resistance training, aging, and disuse exert on muscle protein turnover and the molecular regulatory processes that contribute to changes in muscle protein abundance. © 2021 American Physiological Society. Compr Physiol 11:2249-2278, 2021.

DOI: https://doi.org/10.1002/cphy.c200029

Nurs Womens Health. 2021 Jun 25. pii: S1751-4851(21)00125-2. [Epub ahead of print]

Exercise and the Prevention of Gestational Diabetes Mellitus.

Ashley Woodside, Heather Bradford.

Gestational diabetes mellitus (GDM) is associated with pregnancy complications and fetal complications, as well as long-term health consequences for pregnant people and their offspring. Pregnancy is a pseudodiabetogenic state of increasing insulin resistance and decreasing insulin sensitivity, which places an individual at increased risk for GDM. Exercise facilitates the uptake of blood glucose into cells to be used for energy, making exercise a potential strategy in preventing GDM. Extensive evidence has found an association between consistent moderate to vigorous exercise in pregnancy and the prevention of GDM. With close attention to risk factors, maternity care nurses and other health care providers can play an important role in educating pregnant people on exercise recommendations to help them achieve optimal health and wellness.

Keywords: exercise; gestational diabetes; glucose; insulin resistance; physical activity; prenatal care; prevention; pseudodiabetogenic

DOI: https://doi.org/10.1016/j.nwh.2021.05.009

J Physiol. 2021 Jun 30.

Intermittent cold exposure improves glucose homeostasis despite exacerbating diet-induced obesity in mice housed at thermoneutrality.

Greg L McKie, Hesham Shamshoum, Kristin L Hunt, Hayley H A Thorpe, Hana A Dibe, Jibran Y Khokhar, Christine A Doucette, David C Wright.

KEY POINTS: Ambient cold exposure is often regarded as a promising anti-obesity treatment in mice. However, most preclinical studies aimed at treating obesity via cold-induced thermogenesis have been confounded by sub-thermoneutral housing temperatures. Therefore, the ability of ambient cold to combat diet-induced obesity in mice housed under humanized thermoneutral conditions is currently unknown. Moreover, mammals such as mice are rarely exposed to chronic ambient cold without reprieve, yet mice are often subjected to experimental conditions of chronic rather than intermittent cold exposure (ICE), despite ICE being more physiologically relevant. Having addressed these issues herein, we provide novel evidence that thermoneutral housing uncouples the effects of ICE on glucose and energy homeostasis suggesting that ICE, despite improving glucose tolerance, is not an effective obesity treatment when mice are housed under humanized thermoneutral conditions.
ABSTRACT: This study examined whether a physiologically relevant model of ambient cold exposure, intermittent cold exposure (ICE), could ameliorate the metabolic impairments of diet-induced obesity in male and female mice housed under humanized thermoneutral conditions. Male and female C57BL/6J mice housed at thermoneutrality (29 °C) were fed a low-fat diet (LFD) or high-fat diet (HFD) for 6 weeks before being weight matched into groups that remained unperturbed (CTRL) or underwent ICE for four weeks (4 °C for 60 min/day; 5 days/week) while being maintained on their respective diets. ICE induced rapid and persistent hyperphagia exacerbating rather than attenuating HFD-induced obesity over time. These ICE-induced increases in adiposity were found to be energy intake dependent via pair-feeding. Despite exacerbating HFD-induced obesity, ICE improved glucose tolerance, independent of diet, in a sex-specific manner. The effects of ICE on glucose tolerance were not attributed to improvements in whole-body insulin tolerance, tissue specific insulin action, nor to differences in markers of hepatic insulin clearance or pancreatic beta cell proliferation. Instead, ICE increased serum concentrations of insulin and C-peptide in response to glucose, suggesting that ICE may improve glucose tolerance by potentiating pancreatic glucose-stimulated insulin secretion. These data suggest that ICE, despite improving glucose tolerance, is not an effective obesity treatment in mice housed under humanized conditions. Greg L. McKie is a third year PhD Candidate in the Human Health and Nutritional Sciences Department at the University of Guelph, where he works under the supervision of Dr. David C. Wright. Greg's dissertation focuses on the effects of environmental perturbations, such as aerobic exercise and ambient cold exposure, on adipose tissue metabolism, specifically as it relates to promoting non-shivering thermogenesis under translationally relevant thermoneutral conditions. This article is a follow up to Greg's first PhD study, also published in The Journal of Physiology, which demonstrated that housing temperature affects the acute and chronic metabolic adaptations to aerobic exercise in mice. This article is protected by copyright. All rights reserved.

DOI: https://doi.org/10.1113/JP281774