Exercise and endothelial function.
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Acetylcholine↗
Biomedical subjects
B A Kingwell
Publications and source records attributed to B A Kingwell.
Nitric oxide as a metabolic regulator during exercise: effects of training in health and disease.
1. Accumulating animal and human data suggest that nitric oxide (NO) is important for both coronary and peripheral haemodynamic control and metabolic regulation during performance of exercise. 2. While still controversial, NO of endothelial origin is thought to potentiate exercise-induced hyperaemia, both in the peripheral and coronary circulations. The mechanism of release may include both acetylcholine derived from the neuromuscular junction and vascular shear stress. 3. A splice variant of neuronal nitric oxide synthase (NOS), nNOSmicro, incorporating an extra 34 amino acids, is expressed in human skeletal muscle. In addition to being a potential modulator of blood flow, skeletal muscle-derived NO is an important regulator of muscle contraction and metabolism. In particular, recent human data indicate that NO modulates muscle glucose uptake during exercise, independently of blood flow. 4. Exercise training in healthy individuals promotes adaptations in the various NO systems, which can increase NO bioavailability through a variety of mechanisms, including increased NOS enzyme expression and activity. Such adaptations likely contribute to increased exercise capacity and protection from cardiovascular events. 5. Cardiovascular risk factors, including hypercholesterolaemia, hypertension, diabetes and smoking, as well as established disease, are associated with impairment of the various NO systems. Given that NO is an important signalling mechanism during exercise, such impairment may contribute to limitations in exercise capacity through inadequate coronary or peripheral blood delivery and via metabolic effects. 6. 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 provides benefit in the setting of secondary prevention.
Animals↗
Nitric oxide-mediated metabolic regulation during exercise: effects of training in health and cardiovascular disease.
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.
Cardiovascular Diseases↗
Supplemental oxygen does not modulate responses to acetylcholine or ascorbic acid in the forearm of patients with congestive heart failure.
Despite providing symptomatic relief in patients with congestive heart failure (CHF), supplemental oxygen (O(2)) has been demonstrated to increase total peripheral resistance. The present study investigated the possibility that O(2) inhalation reduces nitric oxide (NO) bioavailability, using endothelium-dependent (acetylcholine) and -independent (phentolamine) vasodilators, and the antioxidant ascorbic acid. Ten patients (nine male and one female) with primary left ventricular failure participated in the study. Forearm venous occlusion plethysmography was used to study blood flow responses to acetylcholine and the alpha-adrenergic antagonist phentolamine during inhalation of either room air or 100% O(2), with and without the simultaneous infusion of ascorbic acid. Neither O(2) inhalation (3.9+/-0.4 compared with 3.8+/-0.3 ml.min(-1).100 ml(-1)) nor ascorbic acid infusion (5.2+/-0.4 compared with 5.5+/-0.4 ml.min(-1).100 ml(-1)) affected resting forearm blood flow. The percentage increase from basal blood flow after acetylcholine infusion was not altered by either O(2) inhalation or ascorbic acid infusion (room air, 140+/-55%; O(2), 118+/-46%; ascorbic acid, 147+/-39%; ascorbic acid+O(2), 109+/-31%). O(2) inhalation did, however, reduce the dilation induced by phentolamine (room air, 131+/-24%; O(2), 80+/-14%; P<0.05). These data indicate that oxygen inhalation does not increase forearm vascular resistance. Secondly, preservation of reactivity to acetylcholine during O(2) inhalation suggests that degradation of NO by O(2)-derived free radicals is not enhanced. Attenuation of phentolamine-induced vasodilation during O(2) inhalation, however, implies increased adrenergic activity, which may possibly exacerbate the detrimental effects of elevated sympathetic activity in CHF.
Acetylcholine↗
Effects of heart rate on arterial compliance in men.
1. Arterial compliance is a major determinant of left ventricular afterload. In keeping with earlier experimental data obtained in isolated arterial segments, it has recently been shown in the rat that arterial compliance decreases with an increase in heart rate (HR) induced by atrial pacing. 2. To elucidate the potential relevance of this effect in humans, we investigated nine male volunteers (age 20-30 years; mean 26 years). Systemic arterial compliance (SAC) was measured with the diastolic area method and carotid-to-femoral and femoral-to-dorsalis pedis pulse wave velocities (PWV) were measured to determine regional changes in compliance. Heart rate was first lowered with intravenous metoprolol to 56 +/- 2 b.p.m. and then increased by transoesophageal atrial pacing to 80 and 100 b.p.m. 3. Increasing HR from 56 +/- 2 to 80 b.p.m. by pacing increased mean arterial pressure (MAP) from 78 +/- 2 to 98 +/- 1 mmHg (P < 0.001) and then to 102 +/- 2 mmHg (P = NS). Systemic arterial compliance fell from 0.48 +/- 0.06 to 0.33 +/- 0.04 arbitrary compliance units (ACU; P < 0.01), carotid-to-femoral PWV increased from 6.1 +/- 0.3 to 6.8 +/- 0.4 m/s (P < 0.001) and femoral-to-dorsalis pedis PWV increased from 8.9 +/- 0.4 to 10.1 +/- 0.5 m/s (P < 0.001). Pacing at 100 b.p.m did not change MAP, but did lead to a further decrease in SAC (to 0.24 +/- 0.03 ACU; P < 0.05) and further increases in carotid-to-femoral (7.3 +/- 0.4 m/s; P = NS) and femoral-to-dorsalis pedis PWV (11.3 +/- 0.4 m/s; P < 0.001). 4. We conclude that systemic, central and peripheral compliances decrease in vivo with an increase in HR induced by atrial pacing.
Adrenergic beta-Antagonists↗
Withdrawal of hormonal therapy for 4 weeks decreases arterial compliance in postmenopausal women.
BACKGROUND: We demonstrated in a previous cross-sectional study that arterial compliance is elevated in postmenopausal women taking estrogen-containing hormonal therapy, which may partially account for the reduction in cardiovascular risk observed. OBJECTIVE: To investigate the effects of withdrawal and recommencement of hormonal therapy, each for 4 weeks, on arterial compliance. METHODS: Seventeen postmenopausal women [aged 56 +/- 4 years (mean +/- SD)] taking long-term hormonal therapy (+HT group) were studied at baseline, 4 weeks after withdrawal of hormonal therapy and again 4 weeks after recommencement. Systemic arterial compliance (SAC), pulse wave velocity (PWV) in the aorto-femoral and femoral-dorsalis pedis regions, and hemodynamic variables were measured at baseline, and at the end of each study intervention. As a time-control, seventeen postmenopausal women (aged 63 +/- 7 years) not taking hormonal therapy (-HT group) were also investigated. RESULTS: SAC significantly decreased from 0.47 +/- 0.06 to 0.40 +/- 0.05 arbitrary compliance units (mean +/- SEM; P < 0.05) after 4 weeks withdrawal from hormonal therapy. PWV in the femoral-dorsalis pedis region was elevated significantly by the withdrawal of hormonal therapy (8.4 +/- 0.4 to 9.4 +/- 0.5 m/s; P < 0.05), but PWV in the aortofemoral region did not change. After therapy had been recommenced for 4 weeks, SAC and PWV in the femoral-dorsalis pedis region were restored to baseline values. The -HT group showed no difference in SAC or PWV, and mean arterial pressure did not change in either group throughout the study period. CONCLUSION: These data suggest that hormonal modulation of distal arterial vascular tone may account for short-term changes in arterial compliance associated with estrogen-containing hormonal therapy.
Aorta, Thoracic↗
Targets in hypertension. Going nowhere or gone as far as we can go?
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Blood Pressure↗
Higher systemic arterial compliance is associated with greater exercise time and lower blood pressure in a young older population.
OBJECTIVES: Arterial compliance is an important therapeutic target in older individuals in whom stiffening of the proximal arterial circulation is thought to underlie systolic hypertension and increased cardiac work. We have shown previously that arterial compliance is related to aerobic fitness and that it is increased in young (20 to 35 years old), previously sedentary individuals by a 4-week period of moderate aerobic training. The extent to which compliance relates to exercise performance in a random selection of young older patients has not been reported previously. Therefore, we examined the interrelationship between systemic arterial compliance (SAC) and time to cessation of exercise during a standard treadmill exercise test in an older population. DESIGN: A cross-sectional survey. METHODS: SAC was estimated at rest using simultaneous recordings of ascending aortic flow and carotid applanation tonometry in 43 subjects aged 67 +/- 7 years (mean +/- SD; 24 men and 19 women). Treadmill exercise testing was performed using a modified Bruce protocol. Aerobic capacity was assessed as Heart Rate-Blood Pressure product and exercise tolerance as total treadmill time. RESULTS: SAC and exercise tolerance were related to gender, with men exhibiting greater exercise reserve and higher SAC than women. There was a significant positive correlation between SAC and time to cessation of exercise (r = .34; P = .03), with a negative correlation between SAC and resting heart rate-blood pressure product (r = -.66; P < .001). SAC was correlated with height and blood pressure. Exercise tolerance was related to height (P < .02). CONCLUSIONS: These data indicate a positive association between SAC and fitness level in healthy older people and an inverse association between SAC and systolic blood pressure. Our findings are consistent with either (1) acquisition of a more compliant circulation and lower blood pressure through more physical activity or (2) that a more compliant arterial circulation and lower blood pressure permit greater athletic performance.
Aged↗
Exercise training increases basal nitric oxide production from the forearm in hypercholesterolemic patients.
The objective of this study was to investigate the effects of cycle training on basal nitric oxide (NO) production and endothelium-dependent dilator capacity in hypercholesterolemic patients in whom acetylcholine responsiveness is impaired. Nine sedentary hypercholesterolemic volunteers (total plasma cholesterol >6.0 mmol/L; 2 female) aged 44+/-3 years (mean+/-SEM) participated in the study. Subjects remained sedentary for 4 weeks and performed 4 weeks of home-based cycle training (3 x 30 minutes/week at 65% maximum oxygen consumption [VO(2)max]) in a randomized order. Arteriovenous nitrate/nitrite (NO(x)) gradient was assessed and plethysmography was used to measure the forearm blood flow responses to arterial infusions of acetylcholine, sodium nitroprusside, and N(G)mono methyl L-arginine. Training increased VO(2)max from 30.4+/-1.9 to 34.3+/-1.4 mL x kg(-1) x min(-1) (P=0.01). Intrabrachial diastolic blood pressure was reduced from 70+/-3 to 68+/-3 mm Hg (P=0.02) with training, whereas systolic pressure did not change. Plasma triglycerides and total, LDL, and HDL cholesterol were not different between interventions. In the sedentary state, there was a positive forearm arteriovenous difference in plasma NO(x) indicating net extraction (6.8+/-4.0 nmol x 100 mL(-1) x min(-1)), whereas in the trained state this difference was negative, indicating net production (-5.8+/-5.8 nmol x 100 mL(-1) x min(-1); P=0.03). N(G)mono methyl L-arginine, at a dose of 4 micromol/min, caused a greater vasoconstriction after training (79.6+/-3.4% versus 69.9+/-6.8%; P=0.05). Acetylcholine and sodium nitroprusside induced dose-dependent elevations in forearm blood flow that were unaffected by training. These data suggest that basal release of endothelium-derived NO is increased with 4 weeks of home based training in hypercholesterolemic patients, independently of lipid profile modification. This may contribute to the cardiovascular protective effects of exercise training, including reduced blood pressure.
Acetylcholine↗
Muscular strength training is associated with low arterial compliance and high pulse pressure.
Aerobic exercise training increases arterial compliance and reduces systolic blood pressure, but the effects of muscular strength training on arterial mechanical properties are unknown. We compared blood pressure, whole body arterial compliance, aortic impedance, aortic stiffness (measured by beta-index and carotid pulse pressure divided by normalized systolic expansion [Ep]), pulse wave velocity, and left ventricular parameters in 19 muscular strength-trained athletes (mean+/-SD age, 26+/-4 years) and 19 sedentary controls (26+/-5 years). Subjects were healthy, non-steroid-using, nonsmoking males, and athletes had been engaged in a strength-training program with no aerobic component for a minimum of 12 months. There was no difference in maximum oxygen consumption between groups, but handgrip strength (mean+/-SEM, 44+/-2 versus 56+/-2 kg; P<0.01) and left ventricular mass (168+/-8 versus 190+/-8 g; P<0.05) were greater in athletes. Arterial stiffness was higher in athletes, as evidenced by lower whole body arterial compliance (0.40+/-0.04 versus 0.54+/-0.04 arbitrary compliance units; P=0.01), higher aortic characteristic impedance (1.55+/-0.13 versus 1.18+/-0.08 mm Hg. s. cm-1; P<0.05), beta-index (4.6+/-0.2 versus 3.8+/-0.4; P<0. 05), and ln Ep (10.86+/-0.06 versus 10.60+/-0.08; P<0.01). Femoral-dorsalis pedis pulse wave velocity was also higher in the athletes, but carotid-femoral pulse wave velocity was not different. Furthermore, both carotid (56+/-3 versus 44+/-2 mm Hg; P<0.001) and brachial (60+/-3 versus 50+/-2 mm Hg; P<0.01) pulse pressures were higher in the athletes, but mean arterial pressure and resting heart rate did not differ between groups. These data indicate that both the proximal aorta and the leg arteries are stiffer in strength-trained individuals and contribute to a higher cardiac afterload.
Adult↗
Nitric oxide synthase inhibition reduces leg glucose uptake but not blood flow during dynamic exercise in humans.
Nitric oxide (NO) appears to play a role in contraction-stimulated glucose uptake in isolated rodent skeletal muscle; however, no studies have examined this question in humans. Seven healthy men completed two 30-min bouts of supine cycling exercise at 60 +/- 2% peak pulmonary oxygen uptake (VO2 peak), separated by 90 min of rest. The NO synthase inhibitor N(G)-monomethyl-L-arginine ([L-NMMA]; total dose 5 mg/kg body weight) or saline (control) were administered via the femoral artery for the final 20 min of exercise in a randomized blinded crossover design. L-Arginine (5 mg/kg body weight) was co-infused during the final 5 min of each exercise bout. Leg blood flow (LBF) was measured by thermodilution in the femoral vein, and leg glucose uptake was calculated as the product of LBF and femoral arteriovenous (AV) glucose difference. L-NMMA infusion significantly (P < 0.05) reduced leg glucose uptake compared with control (48 +/- 12% lower at 15 min, mean +/- SE). The reduction in glucose uptake was due solely to a decrease in AV glucose difference, as there was no effect of L-NMMA infusion on LBF during exercise. Co-infusion of L-arginine restored glucose uptake during L-NMMA infusion to levels similar to control. These results indicate that NO production contributes substantially to exercise-mediated skeletal muscle glucose uptake in humans independent of skeletal muscle blood flow.
Adult↗
Effect of fish oil supplementation on aortic compliance in rats: role of the endothelium.
Arterial compliance improves with dietary fish oils in patients with high cardiovascular risk. Since fish oils alter prostaglandin metabolism and the L-arginine-nitric oxide pathway, and since compliance may be modified by vasoactive substances, the effect of the endothelium and some of its derivatives on aortic complaince were examined. Rats were randomly allocated to four groups, the first of which fed only the regular chow. The remaining three groups were fed the chow supplemented by daily gavage with either coconut, fish or safflower oil for 8 weeks. The thoracic aorta was removed and six 2 mm rings obtained. Rings were paired and one from each pair treated with either N(W)-nitro-L-arginine, indomethacin or de-endothelialized. A diameter-tension curve was initiated from wire touch position using incremental increases in wire distance until no further response observed. The data was transformed to a diameter-pressure relationship and fitted with a linear equation, the slope of which related directly to compliance. De-endothelialization (slopes: control vs de-endothelialized: 9.05+/-0.15 vs 8.31+/-0.24; P< 0.05) and indomethacin (slopes: control vs indomethacin: 9.11+/-0.15 vs 7.76+/-0.37; P< 0.05) significantly decreased arterial compliance as did dietary fish oils (slopes: control vs n-3: 9.16+/-0.11 vs 7.84+/-0.39; P< 0.05). No further effect was seen with indomethacin in the fish oil treated group. It is concluded that the endothelium and in particular, endothelium derived prostanoids, contribute to vessel compliance. We also conclude that fish oils have a similar action to indomethacin, leading to the increase in aortic stiffness observed.
Animals↗
The effects of voluntary running on cardiac mass and aortic compliance in Wistar-Kyoto and spontaneously hypertensive rats.
OBJECTIVE: To investigate the effects of voluntary running exercise from 4-20 weeks of age on aortic compliance in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). DESIGN: For each species we made comparisons between rats housed with an exercise wheel locked (10 rats) and unlocked (10 rats). METHODS: Rats were killed using CO2 asphyxia and the aorta and heart of each rat were rapidly removed. The heart was dissected and weighed. A 4 mm descending proximal aortic ring was mounted on wires in an organ bath for determination of static compliance from the slope of the diameter-pressure relationship derived using Laplace's equation. RESULTS: During the final 2 weeks of training WKY rats ran an average of 7.9 +/- 1.0 km/24 h compared with 1.0 +/- 0.2 km/24 h for SHR. Body weights of WKY rats and SHR and of animals housed with locked and unlocked exercise wheels did not differ. The septum, left ventricle and total heart weights and left ventricular:body weight ratios of sedentary SHR were greater than those of sedentary WKY rats. Trained WKY rats had significantly higher atrial, left and right ventricular and total heart weights and left ventricular:body weight ratios than did untrained WKY rats. Aortic compliance was higher in trained than it was in sedentary WKY rats (12.3 +/- 0.4 versus 14.2 +/- 0.5 microm/mmHg, P < 0.05). There was no difference between heart weights and aortic compliances of SHR housed with exercise wheels locked and unlocked. CONCLUSION: Exercise-trained WKY rats had greater intrinsic aortic compliance when it was measured statically in vitro, which supports results of previous human work revealing a blood-pressure-independent component in the elevation of arterial compliance with training. The lower physical activity of the SHR strain used in this study could contribute to their higher blood pressures and lack of change in aortic compliance with exercise training.
Animals↗
Relation between coronary artery disease, aortic stiffness, and left ventricular structure in a population sample.
To elucidate the relationship between coronary artery disease (CAD), aortic stiffness, and left ventricular structure, we recruited 55 subjects (33 men; average age, 63+/-1 years) with previously unknown CAD from a healthy general population sample, as well as 55 control subjects matched for gender, age, and serum cholesterol level. We measured arterial blood pressure and the systolic expansion of the transverse aorta and left ventricular structure by echocardiography. Aortic stiffness was higher in CAD patients than in controls, with a brachial pulse pressure of 59+/-3 versus 52+/-2 mm Hg and stiffness indices of Ep=212+/-26 versus 123+/-13 kN/m2 and beat=16+/-2 versus 9+/-1 (all P<0.01). Mean arterial pressure was similar in both groups during the measurements (95+/-2 versus 93+/-2 mm Hg, P=NS). Most CAD patients (61%) were in the highest stiffness quartile defined by the normal control values (P<0.05 versus control). Left ventricular mass index was also higher in CAD patients than in matched controls (139+/-5 versus 123+/-4 g/m2, P<0.05). We conclude that aortic stiffness and left ventricular mass are increased in subjects newly diagnosed as having CAD. This might explain previously reported associations of an increased mortality, particularly from CAD, found among subjects with elevated pulse pressures.
Aged↗
Spontaneous running increases aortic compliance in Wistar-Kyoto rats.
OBJECTIVE: Previous studies in humans have found, using non-invasive methodology, that arterial compliance is elevated with exercise training. Forced exercise in animals has corroborated these findings, but the association of this type of exercise with psychological stressors limits its relevance to humans. We have investigated the effects of spontaneous running exercise from 4-20 weeks of age on aortic and mesenteric compliance and vascular reactivity in Wistar-Kyoto (WKY) rats. METHODS: Animals were killed using CO2 asphyxia and the aorta, mesentery and heart rapidly removed. The heart was dissected and weighed. The aorta was separated into 3 4-mm rings which were mounted on wires in organ baths for determination of compliance and vascular reactivity to noradrenaline, acetylcholine and sodium nitroprusside. The slope of diameter-pressure relationship derived using Laplace's equation was used as an index of compliance. RESULTS: During the final 2 weeks of training WKY rats ran an average of 7.9 +/- 1.0 km/24 h. Body weight was not affected by training. Training significantly increased the weight of the atria, left and right ventricles as well as total heart weight and left ventricular/body weight ratio. Aortic compliance was increased from 12.3 +/- 0.4 to 14.2 +/- 0.5 microns/mmHg (P < 0.05) after training. There was no effect of training on aortic reactivity to noradrenaline, acetylcholine or sodium nitroprusside. CONCLUSION: Exercise training increased intrinsic aortic compliance in WKY rats which provides evidence for a structural basis for the elevated compliance reported previously with 4 weeks of aerobic exercise in man.
Acetylcholine↗
Hormonal therapy increases arterial compliance in postmenopausal women.
OBJECTIVES: This study investigated the effects of hormonal therapy on large arterial properties. BACKGROUND: Arterial stiffness is an emerging risk marker for coronary heart disease and is potentially modifiable. Postmenopausal use of hormonal therapy is associated with a lower risk of coronary heart disease. METHODS: Total systemic arterial compliance (SAC) and pulse wave velocity (PWV) were determined in 26 premenopausal and 52 postmenopausal women, 26 of whom were taking hormonal therapy. RESULTS: Arterial compliance was greater in the premenopausal group (mean +/- SEM 0.57 +/- 0.04 arbitrary compliance units [ACU]) than in the postmenopausal group not taking hormonal therapy (0.26 +/- 0.02 ACU, p = 0.001). Postmenopausal women taking hormonal therapy had a significantly increased total SAC compared with women not taking hormonal therapy (0.43 +/- 0.02 vs. 0.26 +/- 0.02 ACU, p = 0.001). PWV in the aortofemoral region in the premenopausal women was 6.0 +/- 0.2 vs. 8.9 +/- 0.3 m/s (p < 0.001) in untreated postmenopausal women. However, postmenopausal women taking hormonal therapy had a significantly lower PWV than those not taking hormonal therapy (7.9 +/- 0.2 vs. 8.9 +/- 0.3 m/s, p = 0.01). Eleven postmenopausal women had their hormone replacement therapy withdrawn for 4 weeks, resulting in a significant decrease in SAC and a significant increase in aortofemoral PWV. CONCLUSIONS: The increased SAC and decreased PWV in women receiving hormonal therapy suggest that such therapy may decrease stiffness of the aorta and large arteries in postmenopausal women, with potential benefit for age-related cardiovascular disorders. The reduction of arterial compliance with age appears to be altered with hormonal therapy.
Adolescent↗
Four weeks of cycle training increases basal production of nitric oxide from the forearm.
The purpose of this study was to determine whether nontrained vascular beds might contribute to the beneficial effects of exercise, including reduced blood pressure by enhanced nitric oxide production. Thirteen healthy, sedentary male volunteers performed 4 wk of normal sedentary activity and 4 wk of cycle training in a randomized order. At the end of each intervention, venous occlusion plethysmography was used to study the forearm blood flow responses to intra-arterial infusions of the nitric oxide synthase inhibitor N(G)-monomethyl-L-arginine (L-NMMA), acetylcholine, and sodium nitroprusside. Training increased the maximal work-load and maximal oxygen consumption, whereas intrabrachial blood pressure was reduced. L-NMMA caused a greater vasoconstriction after training (P = 0.004). Net nitrate and nitrite consumption by the forearm was less after training both before and after administration of L-NMMA (P = 0.04), consistent with increased nitrate and nitrite production from nitric oxide metabolism. There was no difference in the response to acetylcholine or sodium nitroprusside between the two states. Preliminary studies showed an increase in forearm blood flow and blood viscosity after cycling, suggesting that elevated shear stress in this vascular bed may contribute to endothelial adaptation and the cardiovascular protective effects of exercise training.
Acetylcholine↗
Arterial compliance increases after moderate-intensity cycling.
Exercise training elevates arterial compliance at rest, but the effects of acute exercise in this regard are unknown. This study investigated the effects of a single, 30-min bout of cycling exercise at 65% of maximal oxygen consumption on indexes of arterial compliance. Whole body arterial compliance determined noninvasively from simultaneous measurements of aortic flow and carotid pressure was elevated (66 +/- 26%) at 0.5 h postexercise (P = 0.04), followed by a decline to baseline 1 h after exercise. Aortic pulse-wave velocity, which is inversely related to compliance, was reduced (4 +/- 2%; P = 0.04) at 0.5 h postexercise. Pulse-wave velocity in the leg decreased by 10 +/- 4% at this time (P = 0.01). Mean arterial pressure was unchanged; however, central systolic blood pressure was reduced postexercise (P = 0.03). Cardiac output was elevated after exercise (P = 0.007) via heart rate elevation (P = 0.001), whereas stroke volume was unchanged. Total peripheral resistance was therefore reduced (P = 0.01) and would be expected to contribute to an elevation in arterial compliance. In conclusion, a single bout of cycling exercise increased whole body arterial compliance by mechanisms that may relate to vasodilation.
Adult↗