Perfused skeletal muscle contraction and metabolism improved by angiotensin II-mediated vasoconstriction

Abstract

In the present study, the effects of angiotensin II (ANG II) on tension development and associated metabolism during twitch and tetanic stimulation via the sciatic nerve of the gastrocnemius-plantaris-soleus muscle group of the perfused rat hindlimb were investigated. Rat hindlimbs were perfused at constant flow with an erythrocyte-containing medium equilibrated with 95% air-5% CO2 at 37 degrees C, and determinations of oxygen and glucose uptake, lactate and glycerol release, and 2-deoxy-D-[1-3H]glucose uptake (Rg') into individual muscles were carried out. ANG II (1 nM) infusion alone caused vasoconstriction with increased oxygen (55%) and glucose (98%) uptake and lactate (37%) and glycerol (64%) release. ANG II infusion during muscle contraction gave less vasoconstriction but increased the tension development during tetanic stimulation by 80% and increased the contraction-induced oxygen uptake and Rg' by plantaris and gastrocnemius red and white muscles. These effects of ANG II may have been due to increased nutritive flow to contracting muscles or to redirection of flow from noncontracting and type I fiber muscles to the type II fiber contracting muscles in the hindlimb. The results indicate that the regulation of flow by the vasculature is an important regulator of muscle contraction and metabolism.

ACE Genotype May Have an Effect on Single versus Multiple Set Preferences in Strength Training

“…Inhibition of vasodilatation restricts local blood flow and lipolysis in skeletal muscle tissue (Goossens et al 2004) and glucose oxidation exceeds uptake (Townsend and DiPette, 1993) in those subjects. Elevated plasma and tissue angiotensin II levels in this genotype may facilitate the redirection of blood flow from type I muscle fibres to the type II fibres (Rattigan et al 1996) that are favoured in power performance. Greater plasma and tissue angiotensin II causes a reduction in mitochondrial density (Drexler et al 1992), reduces muscle oxidative capacity (Drexler et al 1992;Mettauer et al 2001) and increases the proportion of fatigue-sensitive fast type II fibres and consequently decreases proportion of slow-twitch, fatigue-resistant type I fibres (De Sousa et al 2000).…”

Skeletal muscle dysfunction in COPD: clinical and laboratory observations

“…Local AngII is necessary both for angiogenesis [104] and for optimal muscle trophic response to loading [105], and may therefore be necessary for skeletal muscle growth. AngII has been shown to increases muscle strength in rat hindlimb preparations [106]. Our laboratory has shown that, in a cohort of 103 COPD patients, those with the I/I polymorphism of the ACE gene had reduced quadriceps strength compared with those with the D/D polymorphism [107] (Figure 6).…”

Review of genetic research and testing in sport

“…A kutatók kimutatták, hogy a quadriceps ereje nagyobb mértékben növeke-dett a tréning hátasára a D allélt hordozóknál [17]. Az angiotenzin-II a vér I-es típusú rostok felől a II-es típusú rostok felé történő redisztribúcióját is előidéz-heti [18], amely szintén magyarázatul szolgálhat a D allél és az erőorientált sportágak asszociációjára.…”