Key result
Exercise training increases basal coronary arteriole permeability by ~42% and alters adenosine-mediated changes.
Exercise training alters the basal and adenosine-mediated permeability of coronary arterioles to macromolecules in a size-dependent manner.
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May alter coronary microvascular function in exercise; leaves open translation to human disease.
Solute flux per unit surface area and concentration gradient, (JS/SΔC), was quantified in arterioles isolated from hearts of sedentary (SED) and exercise‐trained (EX) female Yucatan Miniature Swine. Apparent permeability (PS) was assessed from measures of JS/SΔC for two proteins, α‐lactalbumin (α‐lact) and porcine serum albumin (PSA), under basal conditions and following 5 min suffusion with 10−5M adenosine (ADO). Both proteins were labelled with the fluorescent dye tetramethyl rhodamine isothiocyanate. Basal Ps to α‐lact differed with exercise training ((Pα‐lacts)SED=5.2±1.8 (median±median absolute deviation (MAD), n=9 pigs) versus (Pα‐lacts)EX=7.4±1.1×10−7 cm s−1, n=9, P<0.05). For the larger protein PSA, basal Ps did not change with training ((PPSAs)SED=5.0±1.6, N=11 vs. (PPSAs)EX=4.1±1.2×10−7 cm s−1, N=11). Suffusion of the arterioles (33±4 μm diameter, n=18 vessels) from SED hearts (n=14) with 10−5M ADO decreased Pα‐lacts 15±8% relative to control and was without effect on PPSAs. By contrast, in arterioles (39±4 μm diameter, n=22 vessels) from EX hearts (n=14), ADO increased Pα‐lacts and PPSAs by 32 and 65% respectively, indicating that receptor‐mediated changes in permeability were also sensitive to exercise training. These data demonstrate that, for coronary arterioles, permeability to macromolecules adapts to exercise training. The adaptive mechanisms may involve more than one structural component of the vessel wall as the changes in permeability were size‐dependent.
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Huxley et al. (1997) studied this question. Exercise training vs. Sedentary was evaluated on Apparent permeability (Ps) to α-lactalbumin under basal conditions (p=<0.05). Exercise training increased basal coronary arteriole permeability to α-lactalbumin (7.4 vs 5.2 x 10‐7 cm s‐1, P<0.05) and altered adenosine-mediated permeability changes.
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