We tested the hypothesis that adaptations in peripheral arterial vasoreactivity are induced by exercise training. Male rats were trained to run on a treadmill at 30 m/min (15 degrees incline) for 1 h/day 5 days/wk for 10-12 wk. Efficacy was indicated by a 51% increase (P < 0.05) in citrate synthase activity in soleus muscle of exercise-trained (ET) rats compared with that of sedentary (SED) control rats. Responses to vasoactive compounds were examined in vitro using rings of abdominal aorta. Maximal isometric contractile tension evoked by KCl, norepinephrine (NE), and phenylephrine were not different between groups; sensitivity to phenylephrine was also not different between groups. However, sensitivity was lower for both KCl and NE in vessels from ET animals. Endothelium removal did not influence KCl sensitivity but did abolish the difference in NE sensitivity of vessel segments between ET and SED animals. Maximal vasodilator responses induced by acetylcholine (ACh; NE or prostaglandin F2 alpha preconstriction) were greater in vessel rings from ET rats. However, dilatory responses by sodium nitroprusside (NE or prostaglandin F2 alpha preconstriction) and forskolin (NE preconstriction) were not different between groups, indicating that the augmented ACh-induced dilatory response resulted from an adaptation of the endothelium. Blockade of nitric oxide synthase activity diminished ACh-induced vasodilation by 79 and 100% in SED and ET rats, respectively. These results indicate that training alters vasomotor function in rat abdominal aortas through adaptations of both endothelium and smooth muscle.

Aerobic exercise training induces an increase in coronary vascular transport capacity. This increased transport capacity is the result of increases in both blood flow capacity and capillary exchange capacity. These functional changes are the result of two major types of adaptive responses, structural vascular adaptation and altered control of vascular resistance. Structural vascular adaptation occurs in response to exercise training in at least two forms, increases in the cross-sectional area of the proximal coronary arteries and angiogenesis. Angiogenesis has been demonstrated in that training causes moderate cardiac hypertrophy while maintaining or increasing capillary density and increasing arteriolar density. Training-induced changes in coronary vascular control have been shown to include altered coronary responses to vasoactive substances, changes in endothelium-mediated vasoregulation, and alterations in the cellular-molecular control of intracellular free Ca2+ in both endothelial and vascular smooth muscle cells isolated from coronary arteries of exercise-trained animals. The signal or signals for these adaptive responses remain unknown. The hypothesis that the adaptive strategy entails maintenance of normal shear stress in coronary arterial vessels is discussed. We propose that as a result of training-induced structural vascular adaptations and alterations in the control of vascular resistance, shear stress throughout the coronary vasculature is returned to the level present in sedentary animals. The signal for adaptation may be peak shear stress during exercise and/or average shear stress over a 24-h period of time.

The primary purpose of this study was to test the hypothesis that short-term exercise training enhances endothelium-dependent relaxation of porcine femoral and brachial arteries. Miniature swine ran on a treadmill for 1 h at 3.5 miles/h, twice daily, for 7 consecutive days (Trn; n = 8). Compared with sedentary controls (Sed; n = 7), Trn swine exhibited increased skeletal muscle citrate synthase activity (P < 0.05). Vascular rings approximately 3 mm in axial length were prepared from segments of femoral and brachial arteries, and responses to vasoactive agents were determined in vitro. Sensitivity to bradykinin (BK) was enhanced in brachial vascular rings from Trn swine compared with those from Sed swine, as indicated by lower concentration of vasorelaxing agent eliciting 50% of maximal response values [Sed, 8.63 +/- 0.09 (-log M); Trn, 9.07 +/- 0.13; P < 0.05]. This difference between groups was preserved in brachial rings in which formation of nitric oxide and vasodilator prostaglandins were inhibited [Sed, 8.57 +/- 0.17 (-log M); Trn, 8.97 +/- 0.13; P < 0.05]. Sensitivity to BK was not different between Sed and Trn in femoral arterial rings. Relaxation responses to the calcium ionophore A-23187 and sodium nitroprusside were not altered with training. Femoral and brachial arterial rings from Trn swine, compared with those from Sed swine, exhibited augmented vasocontraction across a range of concentrations and increased sensitivity to norepinephrine (all P < 0.05). These findings indicate that responses of porcine femoral and brachial arteries change in response to short-term training. Together with findings from previous studies involving longer term training, our data suggest that vascular adaptations may differ at different time points during long-term endurance exercise training.

Endurance exercise training (Ex) has been shown to increase maximal skeletal muscle blood flow. The purpose of this study was to test the hypothesis that increased endothelium-dependent vasodilation is associated with the Ex-induced increase in muscle blood flow. Furthermore, we hypothesized that enhanced endothelium-dependent dilation is confined to vessels in high-oxidative muscles that are recruited during Ex. To test these hypotheses, sedentary (Sed) and rats that underwent Ex (30 m/min x 10% grade, 60 min/day, 5 days/wk, 8-12 wk) were studied using three experimental approaches. Training effectiveness was evidenced by increased citrate synthase activity in soleus and vastus lateralis (red section) muscles (P < 0.05). Vasodilatory responses to the endothelium-dependent agent acetylcholine (ACh) in situ tended to be augmented by training in the red section of gastrocnemius muscle (RG; Sed: control, 0.69 +/- 0.12; ACh, 1.25 +/- 0.15; Ex: control, 0.86 +/- 0.17; ACh, 1.76 +/- 0.27 ml x min(-1) x 100 g(-1) x mmHg(-1); 0.05 < P < 0.10 for Ex vs. Sed during ACh). Responses to ACh in situ did not differ between Sed and Ex for either the soleus muscle or white section of gastrocnemius muscle (WG). Dilatory responses of second-order arterioles from the RG in vitro to flow (4-8 microl/min) and sodium nitroprusside (SNP; 10(-7) through 10(-4) M), but not ACh, were augmented in Ex (vs. Sed; P < 0.05). Dilatory responses to ACh, flow, and SNP of arterioles from soleus and WG muscles did not differ between Sed and Ex. Content of the endothelial isoform of nitric oxide synthase (eNOS) was increased in second-order, fourth-order, and fifth-order arterioles from the RG of Ex; eNOS content was similar between Sed and Ex in vessels from the soleus and WG muscles. These findings indicate that Ex induces endothelial adaptations in fast-twitch, oxidative, glycolytic skeletal muscle. These adaptations may contribute to enhanced skeletal muscle blood flow in endurance-trained individuals.