scholarly journals Fish Oil for Healthy Aging: Potential Application to Master Athletes

2021 ◽  
Author(s):  
Caoileann H. Murphy ◽  
Chris McGlory
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Exercise Performance ◽  
Healthy Aging ◽  
Master Athletes ◽  
Pufa Supplementation ◽  
Pufa Intake ◽  
Clinical Literature ◽  
Oily Fish ◽  
Response To Exercise

AbstractMaster athletes perform high volumes of exercise training yet display lower levels of physical functioning and exercise performance when compared with younger athletes. Several reports in the clinical literature show that long chain n-3 polyunsaturated fatty acid (LC n-3 PUFA) ingestion promotes skeletal muscle anabolism and strength in untrained older persons. There is also evidence that LC n-3 PUFA ingestion improves indices of muscle recovery following damaging exercise in younger persons. These findings suggest that LC n-3 PUFA intake could have an ergogenic effect in master athletes. However, the beneficial effect of LC n-3 PUFA intake on skeletal muscle in response to exercise training in both older and younger persons is inconsistent and, in some cases, generated from low-quality studies or those with a high risk of bias. Other factors such as the choice of placebo and health status of participants also confound interpretation of existing reports. As such, when considered on balance, the available evidence does not indicate that ingestion of LC n-3 PUFAs above current population recommendations (250–500 mg/day; 2 portions of oily fish per week) enhances exercise performance or recovery from exercise training in master athletes. Further work is now needed related to how the dose, duration, and co-ingestion of LC n-3 PUFAs with other nutrients such as amino acids impact the adaptive response to exercise training. This work should also consider how LC n-3 PUFA supplementation may differentially alter the lipid profile of cellular membranes of key regulatory sites such as the sarcolemma, mitochondria, and sarcoplasmic reticulum.

scholarly journals Adult skeletal muscle deletion of Mitofusin 1 and 2 impedes exercise performance and training capacity

2019 ◽  
Vol 126 (2) ◽  
pp. 341-353 ◽  
Author(s):  
Margaret B. Bell ◽  
Zachary Bush ◽  
Graham R. McGinnis ◽  
Glenn C. Rowe
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Exercise Capacity ◽  
Exercise Performance ◽  
Complex I ◽  
Voluntary Exercise ◽  
Complex Activity ◽  
Complex Iv ◽  
Adult Skeletal Muscle ◽  
Subunit Expression

Endurance exercise has been shown to be a positive regulator of skeletal muscle metabolic function. Changes in mitochondrial dynamics (fusion and fission) have been shown to influence mitochondrial oxidative capacity. We therefore tested whether genetic disruption of mitofusins (Mfns) affected exercise performance in adult skeletal muscle. We generated adult-inducible skeletal muscle-specific Mfn1 (iMS-Mfn1KO), Mfn2 (iMS-Mfn2KO), and Mfn1/2 (iMS-MfnDKO) knockout mice. We assessed exercise capacity by performing a treadmill time to exhaustion stress test before deletion and up to 8 wk after deletion. Analysis of either the iMS-Mfn1KO or the iMS-Mfn2KO did not reveal an effect on exercise capacity. However, analysis of iMS-MfnDKO animals revealed a progressive reduction in exercise performance. We measured individual electron transport chain (ETC) complex activity and observed a reduction in ETC activity in both the subsarcolemmal and intermyofibrillar mitochondrial fractions specifically for NADH dehydrogenase (complex I) and cytochrome- c oxidase (complex IV), which was associated with a decrease in ETC subunit expression for these complexes. We also tested whether voluntary exercise training would prevent the decrease in exercise capacity observed in iMS-MfnDKO animals ( n = 10/group). However, after 8 wk of training we did not observe any improvement in exercise capacity or ETC subunit parameters in iMS-MfnDKO animals. These data suggest that the decrease in exercise capacity observed in the iMS-MfnDKO animals is in part the result of impaired ETC subunit expression and ETC complex activity. Taken together, these results provide strong evidence that mitochondrial fusion in adult skeletal muscle is important for exercise performance. NEW & NOTEWORTHY This study is the first to utilize an adult-inducible skeletal muscle-specific knockout model for Mitofusin (Mfn)1 and Mfn2 to assess exercise capacity. Our findings reveal a progressive decrease in exercise performance with Mfn1 and Mfn2 deletion. The decrease in exercise capacity was accompanied by impaired oxidative phosphorylation specifically for complex I and complex IV. Furthermore, voluntary exercise training was unable to rescue the impairment, suggesting that normal fusion is essential for exercise-induced mitochondrial adaptations.

Effect of exercise training on skeletal muscle histology and metabolism in peripheral arterial disease

1996 ◽  
Vol 81 (2) ◽  
pp. 780-788 ◽  
Author(s):  
W. R. Hiatt ◽  
J. G. Regensteiner ◽  
E. E. Wolfel ◽  
M. R. Carry ◽  
E. P. Brass
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Exercise Performance ◽  
Citrate Synthase ◽  
Normal Subjects ◽  
Arterial Occlusive Disease ◽  
Treadmill Training ◽  
Peak Exercise ◽  
Muscle Histology ◽  
Peripheral Arterial

Patients with symptomatic peripheral arterial occlusive disease have a claudication-limited peak exercise performance that is improved with exercise training. The effects of training on skeletal muscle metabolism were evaluated in 26 patients with claudication, randomized into a 12-wk program of treadmill training (enhances muscle metabolic activity in normal subjects), strength training (stimulates muscle hypertrophy in normal subjects), or a nonexercising control group. Gastrocnemius muscle biopsies were performed at rest and before and after training. After 12 wk, only treadmill training improved peak exercise performance and peak oxygen consumption. Treadmill training did not alter type I or type II fiber area and did not increase citrate synthase activity but was associated with an increase in the percentage of denervated fibers (from 7.6 +/- 5.4 to 15.6 +/- 7.5%, P < 0.05). Improvement in exercise performance with treadmill training was associated with a correlative decrease in the plasma (r = -0.67) and muscle (r = -0.59) short-chain acylcarnitine concentrations (intermediates of oxidative metabolism). Patients in the strength and control groups had no changes in muscle histology or carnitine metabolism, but strength-trained subjects had a decrease in citrate synthase activity. Thus treadmill training increased peak exercise performance, but this benefit was associated with skeletal muscle denervation and the absence of a "classic" mitochondrial training response (increase in citrate synthase activity). The present study confirms the relationship between skeletal muscle acylcarnitine content and function in peripheral arterial occlusive disease, demonstrating that the response to treadmill training was associated with parallel improvements in intermediary metabolism.

Angiogenic growth factor expression in rat skeletal muscle in response to exercise training

2003 ◽  
Vol 284 (5) ◽  
pp. H1668-H1678 ◽  
Author(s):  
Pamela G. Lloyd ◽  
Barry M. Prior ◽  
Hsiao T. Yang ◽  
Ronald L. Terjung
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Mrna Expression ◽  
Sedentary Control ◽  
Artery Ligation ◽  
Monocyte Chemoattractant Protein 1 ◽  
Cellular Events ◽  
Angiopoietin 2 ◽  
Response To Exercise ◽  
Endothelial Nitric Oxide

Angiogenesis occurs in skeletal muscle in response to exercise training. To gain insight into the regulation of this process, we evaluated the mRNA expression of factors implicated in angiogenesis over the course of a training program. We studied sedentary control ( n = 17) rats and both sedentary ( n = 18) and exercise-trained ( n = 48) rats with bilateral femoral artery ligation. Training consisted of treadmill exercise (4 times/day, 1–24 days). Basal mRNA expression in sedentary control muscle was inversely related to muscle vascularity. Angiogenesis was histologically evident in trained white gastrocnemius muscle by day 12. Training produced initial three- to sixfold increases in VEGF, VEGF receptors (KDR and Flt), the angiopoietin receptor (Tie-2), and endothelial nitric oxide synthase mRNA, which dissipated before the increase in capillarity, and a substantial (30- to 50-fold) but transient upregulation of monocyte chemoattractant protein 1 mRNA. These results emphasize the importance of early events in regulating angiogenesis. However, we observed a sustained elevation of the angiopoietin 2-to-angiopoietin 1 ratio, suggesting continued vascular destabilization. The response to exercise was (in general) tempered in high-oxidative muscles. These findings place importance on cellular events coupled to the onset of angiogenesis.

scholarly journals Impaired training-induced angiogenesis process with loss of pericyte-endothelium interactions is associated with an abnormal capillary remodelling in the skeletal muscle of COPD patients

2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Léo Blervaque ◽  
Emilie Passerieux ◽  
Pascal Pomiès ◽  
Matthias Catteau ◽  
Nelly Héraud ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Exercise Intolerance ◽  
Moderate Intensity ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Link Type ◽  
Copd Patients ◽  
Response To Exercise

Abstract Chronic obstructive pulmonary disease (COPD) is associated with exercise intolerance and limits the functional gains in response to exercise training in patients compared to sedentary healthy subjects (SHS). The blunted skeletal muscle angiogenesis previously observed in COPD patients has been linked to these limited functional improvements, but its underlying mechanisms, as well as the potential role of oxidative stress, remain poorly understood. Therefore, we compared ultrastructural indexes of angiogenic process and capillary remodelling by transmission electron microscopy in 9 COPD patients and 7 SHS after 6 weeks of individualized moderate-intensity endurance training. We also assessed oxidative stress by plasma-free and esterified isoprostane (F2-IsoP) levels in both groups. We observed a capillary basement membrane thickening in COPD patients only (p = 0.008) and abnormal variations of endothelial nucleus density in response to exercise training in these patients when compared to SHS (p = 0.042). COPD patients had significantly fewer occurrences of pericyte/endothelium interdigitations, a morphologic marker of capillary maturation, than SHS (p = 0.014), and significantly higher levels of F2-IsoP (p = 0.048). Last, the changes in pericyte/endothelium interdigitations and F2-IsoP levels in response to exercise training were negatively correlated (r = − 0.62, p = 0.025). This study is the first to show abnormal capillary remodelling and to reveal impairments during the whole process of angiogenesis (capillary creation and maturation) in COPD patients. Trial registration NCT01183039 & NCT01183052, both registered 7 August 2010 (retrospectively registered).

scholarly journals AMPK and PPARβ positive feedback loop regulates endurance exercise training-mediated GLUT4 expression in skeletal muscle

2019 ◽  
Vol 316 (5) ◽  
pp. E931-E939 ◽  
Author(s):  
Jin-Ho Koh ◽  
Chad R. Hancock ◽  
Dong-Ho Han ◽  
John O. Holloszy ◽  
K. Sreekumaran Nair ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Glut4 Expression ◽  
Amp Activated Protein Kinase ◽  
Response To Exercise ◽  
Glucose Transporter Type 4

The objective of this study is to determine whether AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma coactivator 1-α (PGC-1α), or peroxisome proliferator-activated receptor β (PPARβ) can independently mediate the increase of glucose transporter type 4 (GLUT4) expression that occurs in response to exercise training. We found that PPARβ can regulate GLUT4 expression without PGC-1α. We also found AMPK and PPARβ are important for maintaining normal physiological levels of GLUT4 protein in the sedentary condition as well following exercise training. However, AMPK and PPARβ are not essential for the increase in GLUT4 protein expression that occurs in response to exercise training. We discovered that AMPK activation increases PPARβ via myocyte enhancer factor 2A (MEF2A), which acted as a transcription factor for PPARβ. Furthermore, exercise training increases the cooperation of AMPK and PPARβ to regulate glucose uptake. In conclusion, cooperation between AMPK and PPARβ via NRF-1/MEF2A pathway enhances the exercise training mediated adaptive increase in GLUT4 expression and subsequent glucose uptake in skeletal muscle.

Master Athletes

2001 ◽  
Vol 11 (s1) ◽  
pp. S196-S207 ◽  
Author(s):  
Scott Trappe
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Fiber ◽  
Physiological Data ◽  
Sporting Events ◽  
Master Athletes ◽  
Cross Sectional ◽  
Recreational Athletes ◽  
Wide Range ◽  
Senior Athletes

Over the past 3 decades, there has been a continued increase in the number of “older” participants in sporting events such as running, swimming, cycling, rowing, and weightlifting. Some master athletes come from a background with years of training and competition experience, while others have only begun to compete as they approach middle-aged and older. The majority of what we currently know about master athletes and aging has been gained from both cross-sectional and longitudinal testing and re-testing master athletes and recreational athletes. The focus of this paper is on the physiological profile of athletes and individuals performing regular exercise training. Physiological data from elite and non-elite, recreational, sedentary, and senior athletes clearly indicate that human skeletal muscle has a high degree of plasticity that is maintained late into life. Muscle fiber protein expression and single muscle fiber contractile properties are greatly influenced by exercise training. It appears that skeletal muscle can quickly adapt to accommodate a wide range of functionality to meet the demands (or lack of demands) placed upon it.

Oral quercetin supplementation hampers skeletal muscle adaptations in response to exercise training

2013 ◽  
Vol 24 (6) ◽  
pp. 920-927 ◽  
Author(s):  
R. A. Casuso ◽  
E. J. Martínez-López ◽  
N. B. Nordsborg ◽  
F. Hita-Contreras ◽  
R. Martínez-Romero ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Muscle Adaptations ◽  
Response To Exercise ◽  
Skeletal Muscle Adaptations
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