scholarly journals Vascular Effects of Exercise: Endothelial Adaptations Beyond Active Muscle Beds

Physiology ◽  
2011 ◽  
Vol 26 (3) ◽  
pp. 132-145 ◽  
Author(s):  
Jaume Padilla ◽  
Grant H. Simmons ◽  
Shawn B. Bender ◽  
Arturo A. Arce-Esquivel ◽  
Jeffrey J. Whyte ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Chronic Exercise ◽  
Active Muscle ◽  
Vascular Effects ◽  
The Impact

Endothelial adaptations to exercise training are not exclusively conferred within the active muscle beds. Herein, we summarize key studies that have evaluated the impact of chronic exercise on the endothelium of vasculatures perfusing nonworking skeletal muscle, brain, viscera, and skin, concluding with discussion of potential mechanisms driving these endothelial adaptations.

Prenatal exercise and cardiovascular health (PEACH) study: impact of acute and chronic exercise on cerebrovascular hemodynamics and dynamic cerebral autoregulation

2021 ◽  
Author(s):  
Rachel J. Skow ◽  
Lawrence Labrecque ◽  
Jade A. Rosenberger ◽  
Patrice Brassard ◽  
Craig D. Steinback ◽  
...  
Keyword(s):  
Exercise Training ◽  
Gestational Age ◽  
Cerebral Autoregulation ◽  
Acute Exercise ◽  
Controlled Trial ◽  
Moderate Intensity ◽  
Chronic Exercise ◽  
Arterial Blood ◽  
The Impact ◽  
Dynamic Cerebral Autoregulation

We performed a randomised controlled trial measuring dynamic cerebral autoregulation (dCA) using a sit-to-stand maneuver before (SS1) and following (SS2) an acute exercise test at 16-20 weeks gestation (trimester 2; TM2) and then again at 34-37 weeks gestation (third trimester; TM3). Following the first assessment, women were randomised into exercise training or control (standard care) groups; women in the exercise training group were prescribed moderate intensity aerobic exercise for 25-40 minutes on 3-4 days per week for 14±1weeks. Resting seated mean blood velocity in the middle cerebral artery (MCAvmean) was lower in TM3 compared to TM2 but not impacted by exercise training intervention. dCA was not impacted by gestational age, or exercise training during SS1. During SS2, dCA was altered such that there were greater absolute and relative decreases in mean arterial blood pressure (MAP) and MCAvmean, but this was not impacted by the intervention. There was also no difference in the relationship between the decrease in MCAvmean compared to the decrease in MAP (%/%), or the onset of the regulatory response with respect to acute exercise, gestational age, or intervention; however, rate of regulation was faster in women in the exercise group following acute exercise (interaction effect, p=0.048). These data highlight the resilience of the cerebral circulation in that dCA was well maintained or improved in healthy pregnant women between TM2 and TM3. However, future work addressing the impact of acute and chronic exercise on dCA in women who are at risk for cardiovascular complications during pregnancy is needed.

The impact of acute and chronic exercise on Nrf2 expression in relation to markers of mitochondrial biogenesis in human skeletal muscle

2019 ◽  
Vol 120 (1) ◽  
pp. 149-160 ◽  
Author(s):  
Hashim Islam ◽  
Jacob T. Bonafiglia ◽  
Patrick C. Turnbull ◽  
Craig A. Simpson ◽  
Christopher G. R. Perry ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Human Skeletal Muscle ◽  
Chronic Exercise ◽  
The Impact ◽  
Nrf2 Expression

scholarly journals The historical context and scientific legacy of John O. Holloszy

2019 ◽  
Vol 127 (2) ◽  
pp. 277-305 ◽  
Author(s):  
James M. Hagberg ◽  
Edward F. Coyle ◽  
Kenneth M. Baldwin ◽  
Gregory D. Cartee ◽  
Luigi Fontana ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Caloric Restriction ◽  
Exercise Physiology ◽  
Historical Context ◽  
Cross Sectional ◽  
Insulin Metabolism ◽  
Scientific Legacy ◽  
Muscle Plasticity ◽  
The Impact

John O. Holloszy, as perhaps the world’s preeminent exercise biochemist/physiologist, published >400 papers over his 50+ year career, and they have been cited >41,000 times. In 1965 Holloszy showed for the first time that exercise training in rodents resulted in a doubling of skeletal muscle mitochondria, ushering in a very active era of skeletal muscle plasticity research. He subsequently went on to describe the consequences of and the mechanisms underlying these adaptations. Holloszy was first to show that muscle contractions increase muscle glucose transport independent of insulin, and he studied the mechanisms underlying this response throughout his career. He published important papers assessing the impact of training on glucose and insulin metabolism in healthy and diseased humans. Holloszy was at the forefront of rodent studies of caloric restriction and longevity in the 1980s, following these studies with important cross-sectional and longitudinal caloric restriction studies in humans. Holloszy was influential in the discipline of cardiovascular physiology, showing that older healthy and diseased populations could still elicit beneficial cardiovascular adaptations with exercise training. Holloszy and his group made important contributions to exercise physiology on the effects of training on numerous metabolic, hormonal, and cardiovascular adaptations. Holloszy’s outstanding productivity was made possible by his mentoring of ~100 postdoctoral fellows and substantial NIH grant funding over his entire career. Many of these fellows have also played critical roles in the exercise physiology/biochemistry discipline. Thus it is clear that exercise biochemistry and physiology will be influenced by John Holloszy for numerous years to come.

scholarly journals N2A Titin: Signaling Hub and Mechanical Switch in Skeletal Muscle

2020 ◽  
Vol 21 (11) ◽  
pp. 3974 ◽  
Author(s):  
Kiisa Nishikawa ◽  
Stan L. Lindstedt ◽  
Anthony Hessel ◽  
Dhruv Mishra
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mechanics ◽  
Active Muscle ◽  
Small Deletion ◽  
Calcium Dependent ◽  
Hypertrophic Signaling ◽  
Pevk Region ◽  
Mechanical Switch ◽  
The Impact ◽  
Muscle Calcium

Since its belated discovery, our understanding of the giant protein titin has grown exponentially from its humble beginning as a sarcomeric scaffold to recent recognition of its critical mechanical and signaling functions in active muscle. One uniquely useful model to unravel titin’s functions, muscular dystrophy with myositis (mdm), arose spontaneously in mice as a transposon-like LINE repeat insertion that results in a small deletion in the N2A region of titin. This small deletion profoundly affects hypertrophic signaling and muscle mechanics, thereby providing insights into the function of this specific region and the consequences of its dysfunction. The impact of this mutation is profound, affecting diverse aspects of the phenotype including muscle mechanics, developmental hypertrophy, and thermoregulation. In this review, we explore accumulating evidence that points to the N2A region of titin as a dynamic “switch” that is critical for both mechanical and signaling functions in skeletal muscle. Calcium-dependent binding of N2A titin to actin filaments triggers a cascade of changes in titin that affect mechanical properties such as elastic energy storage and return, as well as hypertrophic signaling. The mdm phenotype also points to the existence of as yet unidentified signaling pathways for muscle hypertrophy and thermoregulation, likely involving titin’s PEVK region as well as the N2A signalosome.

scholarly journals Effects of short-term endurance exercise training on acute doxorubicin-induced FoxO transcription in cardiac and skeletal muscle

2014 ◽  
Vol 117 (3) ◽  
pp. 223-230 ◽  
Author(s):  
Andreas N. Kavazis ◽  
Ashley J. Smuder ◽  
Scott K. Powers
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Skeletal Muscles ◽  
Target Genes ◽  
Ring Finger ◽  
Peroxisome Proliferator ◽  
Short Term ◽  
Peroxisome Proliferator Activated Receptor ◽  
The Impact

Doxorubicin (DOX) is a potent antitumor agent used in cancer treatment. Unfortunately, DOX can induce myopathy in both cardiac and skeletal muscle, which limits its clinical use. Importantly, exercise training has been shown to protect against DOX-mediated cardiac and skeletal muscle myopathy. However, the mechanisms responsible for this exercise-induced muscle protection remain elusive. These experiments tested the hypothesis that short-term exercise training protects against acute DOX-induced muscle toxicity, in part, due to decreased forkhead-box O (FoxO) transcription of atrophy genes. Rats ( n = 6 per group) were assigned to sedentary or endurance exercise-trained groups and paired with either placebo or DOX treatment. Gene expression and protein abundance were measured in both cardiac and skeletal muscles to determine the impact of DOX and exercise on FoxO gene targets. Our data demonstrate that DOX administration amplified FoxO1 and FoxO3 mRNA expression and increased transcription of FoxO target genes [i.e., atrogin-1/muscle atrophy F-box (MaFbx), muscle ring finger-1 (MuRF-1), and BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3)] in heart and soleus muscles. Importantly, exercise training protected against DOX-induced increases of FoxO1 and MuRF-1 in cardiac muscle and also prevented the rise of FoxO3, MuRF-1, and BNIP3 in soleus muscle. Furthermore, our results indicate that exercise increased peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α) in both the heart and soleus muscles. This is important because increased PGC-1α expression is known to suppress FoxO activity resulting in reduced expression of FoxO target genes. Together, these results are consistent with the hypothesis that exercise training protects against DOX-induced myopathy in both heart (FoxO1 and MuRF-1) and skeletal muscles (FoxO3, MuRF-1, and BNIP3).

scholarly journals Aerobic Exercise Training and In Vivo Akt Activation Counteract Cancer Cachexia by Inducing a Hypertrophic Profile through eIF-2α Modulation

Cancers ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 28
Author(s):  
Marcelo G. Pereira ◽  
Vanessa A. Voltarelli ◽  
Gabriel C. Tobias ◽  
Lara de Souza ◽  
Gabriela S. Borges ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Cancer Cachexia ◽  
Aerobic Exercise Training ◽  
Akt Activation ◽  
The Impact

Cancer cachexia is a multifactorial and devastating syndrome characterized by severe skeletal muscle mass loss and dysfunction. As cachexia still has neither a cure nor an effective treatment, better understanding of skeletal muscle plasticity in the context of cancer is of great importance. Although aerobic exercise training (AET) has been shown as an important complementary therapy for chronic diseases and associated comorbidities, the impact of AET on skeletal muscle mass maintenance during cancer progression has not been well documented yet. Here, we show that previous AET induced a protective mechanism against tumor-induced muscle wasting by modulating the Akt/mTORC1 signaling and eukaryotic initiation factors, specifically eIF2-α. Thereafter, it was determined whether the in vivo Akt activation would induce a hypertrophic profile in cachectic muscles. As observed for the first time, Akt-induced hypertrophy was able and sufficient to either prevent or revert cancer cachexia by modulating both Akt/mTORC1 pathway and the eIF-2α activation, and induced a better muscle functionality. These findings provide evidence that skeletal muscle tissue still preserves hypertrophic potential to be stimulated by either AET or gene therapy to counteract cancer cachexia.

scholarly journals Exercise and insulin resistance in PCOS: muscle insulin signalling and fibrosis

2020 ◽  
Vol 9 (4) ◽  
pp. 346-359 ◽  
Author(s):  
N K Stepto ◽  
D Hiam ◽  
M Gibson-Helm ◽  
S Cassar ◽  
C L Harrison ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Transforming Growth Factor ◽  
Insulin Signalling ◽  
Tissue Fibrosis ◽  
Overweight Women ◽  
The Impact ◽  
Specific Insulin

Objective Mechanisms of insulin resistance in polycystic ovary syndrome (PCOS) remain ill defined, contributing to sub-optimal therapies. Recognising skeletal muscle plays a key role in glucose homeostasis we investigated early insulin signalling, its association with aberrant transforming growth factor β (TGFβ)-regulated tissue fibrosis. We also explored the impact of aerobic exercise on these molecular pathways. Methods A secondary analysis from a cross-sectional study was undertaken in women with (n = 30) or without (n = 29) PCOS across lean and overweight BMIs. A subset of participants with (n = 8) or without (n = 8) PCOS who were overweight completed 12 weeks of aerobic exercise training. Muscle was sampled before and 30 min into a euglycaemic-hyperinsulinaemic clamp pre and post training. Results We found reduced signalling in PCOS of mechanistic target of rapamycin (mTOR). Exercise training augmented but did not completely rescue this signalling defect in women with PCOS. Genes in the TGFβ signalling network were upregulated in skeletal muscle in the overweight women with PCOS but were unresponsive to exercise training except for genes encoding LOX, collagen 1 and 3. Conclusions We provide new insights into defects in early insulin signalling, tissue fibrosis, and hyperandrogenism in PCOS-specific insulin resistance in lean and overweight women. PCOS-specific insulin signalling defects were isolated to mTOR, while gene expression implicated TGFβ ligand regulating a fibrosis in the PCOS-obesity synergy in insulin resistance and altered responses to exercise. Interestingly, there was little evidence for hyperandrogenism as a mechanism for insulin resistance.

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