Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Accumulating data suggest that nitric oxide (NO) is important for both coronary and peripheral hemodynamic control and metabolic regulation during exercise. Although still controversial, NO of endothelial origin may potentiate exercise-induced hyperemia. Mechanisms of release include both acetylcholine derived from the neuromuscular junction and elevation in vascular shear stress. A splice variant of neuronal nitric oxide synthase (NOS), nNOSmu, is expressed in human skeletal muscle. In addition to being a potential modulator of blood flow, NO from skeletal muscle regulates muscle contraction and metabolism. In particular, recent human data indicate that NO plays a role in muscle glucose uptake during exercise independently of blood flow. Exercise training in healthy individuals elevates NO bioavailability through a variety of mechanisms including increased NOS enzyme expression and activity. Such adaptations likely contribute to increased exercise capacity and cardiovascular protection. Cardiovascular risk factors including hypercholesterolemia, hypertension, diabetes, and smoking as well as established disease are associated with impairment of the various NO systems. Given that NO is an important signaling mechanism during exercise, such impairment may contribute to limitations in exercise capacity through inadequate coronary or peripheral perfusion and via metabolic effects. Exercise training in individuals with elevated cardiovascular risk or established disease can increase NO bioavailability and may represent an important mechanism by which exercise training conveys benefit in the setting of secondary prevention.
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PMID:Nitric oxide-mediated metabolic regulation during exercise: effects of training in health and cardiovascular disease. 1097 17

The systemic and nonmuscular adaptive response to moderate exercise is reviewed and compared with muscle responses to moderate and exhaustive exercise. Rats participating in voluntary wheel running and mice subjected to treadmill exercise on a lifelong basis showed 10-19% increased median life span. Mice also showed improved neurological functions, such as better (35-216%) neuromuscular coordination (tightrope test) and better (11-27%) exploratory activity (T maze). These effects are consistent with the systemic effects of moderate exercise lowering hyperglycemia, hypercholesterolemia, and hypertension. Mitochondria isolated from brain, liver, heart, and kidney of exercised mice show a 12-32% selectively increased complex IV activity, with a significant correlation between complex IV activity and performance in the tightrope test. Chronic exercise decreases (10-20%) the mitochondrial content of TBARS and protein carbonyls in the four organs after 24 weeks of training. Protein carbonyls were linearly and negatively related to complex IV activity. Exercise increased the levels of nNOSmu in human muscle and of nNOS in mouse brain. It is concluded that chronic moderate exercise exerts a whole-body beneficial effect that exceeds muscle adaptation, likely through mechanosensitive afferent nerves and beta-endorphin release to brain and plasma that promote mitochondrial biogenesis in distant organs.
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PMID:Systemic and mitochondrial adaptive responses to moderate exercise in rodents. 1819 58