scholarly journals Lifelong physical activity prevents an age-related reduction in arterial and skeletal muscle nitric oxide bioavailability in humans

2012 ◽  
Vol 590 (21) ◽  
pp. 5361-5370 ◽  
Author(s):  
Michael Nyberg ◽  
James R. Blackwell ◽  
Rasmus Damsgaard ◽  
Andrew M. Jones ◽  
Ylva Hellsten ◽  
...  
2009 ◽  
Vol 106 (6) ◽  
pp. 2040-2048 ◽  
Author(s):  
René Koopman ◽  
Luc J. C. van Loon

Aging is accompanied by a progressive loss of skeletal muscle mass and strength, leading to the loss of functional capacity and an increased risk of developing chronic metabolic disease. The age-related loss of skeletal muscle mass is attributed to a disruption in the regulation of skeletal muscle protein turnover, resulting in an imbalance between muscle protein synthesis and degradation. As basal (fasting) muscle protein synthesis rates do not seem to differ substantially between the young and elderly, many research groups have started to focus on the muscle protein synthetic response to the main anabolic stimuli, i.e., food intake and physical activity. Recent studies suggest that the muscle protein synthetic response to food intake is blunted in the elderly. The latter is now believed to represent a key factor responsible for the age-related decline in skeletal muscle mass. Physical activity and/or exercise stimulate postexercise muscle protein accretion in both the young and elderly. However, the latter largely depends on the timed administration of amino acids and/or protein before, during, and/or after exercise. Prolonged resistance type exercise training represents an effective therapeutic strategy to augment skeletal muscle mass and improve functional performance in the elderly. The latter shows that the ability of the muscle protein synthetic machinery to respond to anabolic stimuli is preserved up to very old age. Research is warranted to elucidate the interaction between nutrition, exercise, and the skeletal muscle adaptive response. The latter is needed to define more effective strategies that will maximize the therapeutic benefits of lifestyle intervention in the elderly.


2011 ◽  
Vol 300 (4) ◽  
pp. H1434-H1441 ◽  
Author(s):  
Shawn B. Bender ◽  
Sean C. Newcomer ◽  
M. Harold Laughlin

Functional and structural heterogeneity exists among skeletal muscle vascular beds related, in part, to muscle fiber type composition. This study was designed to delineate whether the vulnerability to vascular dysfunction in insulin resistance is uniformly distributed among skeletal muscle vasculatures and whether physical activity modifies this vulnerability. Obese, hyperphagic Otsuka Long-Evans Tokushima fatty rats (20 wk old) were sedentary (OSED) or physically active (OPA; access to running wheels) and compared with age-matched sedentary Long-Evans Tokushima Otsuka (LSED) rats. Vascular responses were determined in isolated, pressurized feed arteries from fast-twitch gastrocnemius (GFAs) and slow-twitch soleus (SFAs) muscles. OSED animals were obese, insulin resistant, and hypertriglyceridemic, traits absent in LSED and OPA rats. GFAs from OSED animals exhibited depressed dilation to ACh, but not sodium nitroprusside, and enhanced vasoconstriction to endothelin-1 (ET-1), but not phenylephrine, compared with those in LSED. Immunoblot analysis suggests reduced endothelial nitric oxide synthase phosphorylation at Ser1177 and endothelin subtype A receptor expression in OSED GFAs. Physical activity prevented reduced nitric oxide-dependent dilation to ACh, but not enhanced ET-1 vasoconstriction, in GFA from OPA animals. Conversely, vasoreactivity of SFAs to ACh and ET-1 were principally similar in all groups, whereas dilation to sodium nitroprusside was enhanced in OSED and OPA rats. These data demonstrate, for the first time, that SFAs from insulin-resistant rats exhibit reduced vulnerability to dysfunction versus GFAs and that physical activity largely prevents GFA dysfunction. We conclude that these results demonstrate that vascular dysfunction associated with insulin resistance is heterogeneously distributed across skeletal muscle vasculatures related, in part, to muscle fiber type and activity level.


2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Kathryn Madren ◽  
Ian Bratz ◽  
Gregory Dick ◽  
Johnathan Tune ◽  
H. Glenn Bohlen ◽  
...  

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Trenton D. Colburn ◽  
Jesse C. Craig ◽  
Daniel M. Hirai ◽  
Ayaka Tabuchi ◽  
K. Sue Hageman ◽  
...  

2008 ◽  
Vol 40 (Supplement) ◽  
pp. S243
Author(s):  
Pedro A. Figueiredo ◽  
Rita M. Ferreira ◽  
Maria P. Mota ◽  
Hans J. Appell ◽  
José A. Duarte

2021 ◽  
Vol 163 ◽  
pp. 116-124
Author(s):  
Laura Leite-Almeida ◽  
Manuela Morato ◽  
Dina Cosme ◽  
Joana Afonso ◽  
José C. Areias ◽  
...  

2008 ◽  
Vol 105 (6) ◽  
pp. 1889-1896 ◽  
Author(s):  
Kyle F. Herspring ◽  
Leonardo F. Ferreira ◽  
Steven W. Copp ◽  
Brian S. Snyder ◽  
David C. Poole ◽  
...  

Aged rats exhibit a decreased muscle microvascular O2 partial pressure (PmvO2) at rest and during contractions compared with young rats. Age-related reductions in nitric oxide bioavailability due, in part, to elevated reactive O2 species, constrain muscle blood flow (Q̇m). Antioxidants may restore nitric oxide bioavailability, Q̇m, and ameliorate the reduced PmvO2. We tested the hypothesis that antioxidants would elevate Q̇m and, therefore, PmvO2 in aged rats. Spinotrapezius muscle PmvO2 and Q̇m were measured, and oxygen consumption (V̇mO2) was estimated in anesthetized male Fisher 344 × Brown Norway hybrid rats at rest and during 1-Hz contractions, before and after antioxidant intravenous infusion (76 mg/kg vitamin C and 52 mg/kg tempol). Before infusion, contractions evoked a biphasic PmvO2 that fell from 30.6 ± 0.9 Torr to a nadir of 16.8 ± 1.2 Torr with an “undershoot” of 2.8 ± 0.7 Torr below the subsequent steady-state (19.7 ± 1.2 Torr). The principal effect of antioxidants was to elevate baseline PmvO2 from 30.6 ± 0.9 to 35.7 ± 0.8 Torr ( P < 0.05) and reduce or abolish the undershoot ( P < 0.05). Antioxidants reduced Q̇m and V̇mO2 during contractions ( P < 0.05), while decreasing force production 16.5% ( P < 0.05) and elevating the force production-to-V̇mO2 ratio (0.92 ± 0.03 to 1.06 ± 0.6, P < 0.05). Thus antioxidants increased PmvO2 by altering the balance between muscle O2 delivery and V̇mO2 at rest and during contractions. It is likely that this effect arose from antioxidants reducing myocyte redox below the level optimal for contractile performance and directly (decreased tension) or indirectly (altered balance of vasoactive mediators) influencing O2 delivery and V̇mO2.


Sign in / Sign up

Export Citation Format

Share Document