Dietary Flavanols: A Review of Select Effects on Vascular Function, Blood Pressure, and Exercise Performance.

An individual's diet affects numerous physiological functions and can play an important role in reducing the risk of cardiovascular disease. Epidemiological and clinical studies suggest that dietary flavanols can be an important modulator of vascular risk. Diets and plant extracts rich in flavanols have been reported to lower blood pressure, especially in prehypertensive and hypertensive individuals. Flavanols may act in part through signaling pathways that affect vascular function, nitric oxide availability, and the release of endothelial-derived relaxing and constricting factors. During exercise, flavanols have been reported to modulate metabolism and respiration (e.g., maximal oxygen uptake, O2 cost of exercise, and energy expenditure), and reduce oxidative stress and inflammation, resulting in increased skeletal muscle efficiency and endurance capacity. Flavanol-induced reductions in blood pressure during exercise may decrease the work of the heart. Collectively, these effects suggest that flavanols can act as an ergogenic aid to help delay the onset of fatigue. More research is needed to better clarify the effects of flavanols on vascular function, blood pressure regulation, and exercise performance and establish safe and effective levels of intake. Flavanol-rich foods and food products can be useful components of a healthy diet and lifestyle program for those seeking to better control their blood pressure or to enhance their physical activity. Key teaching points • Epidemiological and clinical studies indicate that dietary flavanols can reduce the risk of vascular disease. • Diets and plant extracts rich in flavanols have been reported to lower blood pressure and improve exercise performance in humans. • Mechanisms by which flavanols may reduce blood pressure function include alterations in signaling pathways that affect vascular function, nitric oxide availability, and the release of endothelial-derived relaxation and constriction factors. • Mechanisms by which flavanols may enhance exercise performance include modulation of metabolism and respiration (e.g., maximal oxygen uptake, O2 cost of exercise, and energy expenditure) and reduction of oxidative stress and inflammation. These effects can result in increased skeletal muscle efficiency and endurance capacity. • Further research is needed to clarify the amount, timing, and frequency of flavanol intake for blood pressure regulation and exercise performance.

Grape Seed Extract Supplementation Attenuates the Blood Pressure Response to Exercise in Prehypertensive Men.

We tested the hypothesis that exaggerated pressor responses observed in prehypertensive males (N = 9) during dynamic exercise are attenuated following acute dietary supplementation with grape seed extract (GSE) (i.e., a single dose). Effects of placebo and GSE (300 mg) on systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), cardiac output (CO), stroke volume (SV), total vascular conductance (TVC), and rate × pressure product (RPP) in response to two submaximal cycling workloads (40% and 60% VO2peak) were compared 2 h after ingestion of GSE or placebo on different days, 1 week apart. Endothelial function was also evaluated using flow-mediated dilation (FMD). Placebo treatment had no effect on any of the variables. GSE supplementation attenuated MAP at both workloads (40% VO2peak: 115 ± 1 vs. 112 ± 2 mmHg; 60% VO2peak: 126 ± 2 vs. 123 ± 2 mmHg) and RPP at the lower workload. Conversely, SV, CO, and TVC were augmented during both workloads. FMD was augmented by GSE (18.9 ± 2.0 vs. 12.4% ± 2.0%). These findings indicate that in exercising prehypertensive males, a single dose of GSE reduces blood pressure, peripheral vasoconstriction, and work of the heart and enhances O2 delivery; effects that may be due, in part, to endothelium-dependent vasodilation. We propose that acute GSE treatment represents an intervention that may minimize potential increases in the risk of cardiovascular events during dynamic exercise in prehypertensives.

Histamine H2 receptor blockade augments blood pressure responses to acute submaximal exercise in males.

Histamine is a potent vasodilator that has been found to increase during exercise. We tested the hypothesis that histamine would attenuate blood pressure (BP), cardiac output (CO), and vascular resistance responses to short-term, submaximal dynamic exercise during H2 receptor blockade. Fourteen healthy men (20-29 years of age) were studied. Systolic (SBP), diastolic (DBP), and mean arterial (MAP) BP and heart rate (HR) were assessed at rest and during the last minute of 10 min of submaximal cycling exercise (60% of peak oxygen consumption) in the absence and presence of histamine H2 receptor blockade (ranitidine, 300 mg). Stroke volume (SV) (impedance cardiography) and plasma norepinephrine (NE) were measured, and CO, rate × pressure product (RPP), and total peripheral resistance (TPR) were calculated. Plasma levels of histamine were also measured. H2 blockade had no effects on any variables at rest. During exercise, SBP (184 ± 3 mm Hg vs. 166 ± 2 mm Hg), MAP (121 ± 2 mm Hg vs. 112 ± 5 mm Hg), and RPP (25.9 ± 0.8 × 10(3) mm Hg·beats/min vs. 23.5 ± 0.8 × 10(3) mm Hg/beats·min) were greater during blocked conditions (P < 0.05), and an interaction was observed for TPR. SV, DBP, HR, and NE levels were unaffected by blockade. Plasma histamine increased from 1.83 ± 0.14 ng/mL at rest to 2.33 ± 0.23 ng/mL during exercise (P < 0.05) and was not affected by H2 blockade (1.56 ± 0.23 ng/mL vs. 1.70 ± 0.24 ng/mL). These findings suggest that, during submaximal exercise, histamine attenuates BP, vascular resistance, and the work of the heart via activation of H2 receptors and that these effects occurred primarily in the vasculature and not in the myocardium.

Effects of chronic dietary nitrate supplementation on the hemodynamic response to dynamic exercise.

While acute treatment with beetroot juice (BRJ) containing nitrate (NO3 (-)) can lower systolic blood pressure (SBP), afterload, and myocardial O2 demand during submaximal exercise, effects of chronic supplementation with BRJ (containing a relatively low dose of NO3 (-), 400 mg) on cardiac output (CO), SBP, total peripheral resistance (TPR), and the work of the heart in response to dynamic exercise are not known. Thus, in 14 healthy males (22 ± 1 yr), we compared effects of 15 days of both BRJ and nitrate-depleted beetroot juice (NDBRJ) supplementation on plasma concentrations of NOx (NO3 (-)/NO2 (-)), SBP, diastolic blood pressure (DBP), mean arterial pressure (MAP), CO, TPR, and rate pressure product (RPP) at rest and during progressive cycling exercise. Endothelial function was also assessed via flow-mediated dilation (FMD). BRJ supplementation increased plasma NOx from 83.8 ± 13.8 to 167.6 ± 13.2 µM. Compared with NDBRJ, BRJ reduced SBP, DBP, MAP, and TPR at rest and during exercise (P < 0.05). In addition, RPP was decreased during exercise, while CO was increased, but only at rest and the 30% workload (P < 0.05). BRJ enhanced FMD-induced increases in brachial artery diameter (pre: 12.3 ± 1.6%; post: 17.8 ± 1.9%). We conclude that 1) chronic supplementation with BRJ lowers blood pressure and vascular resistance at rest and during exercise and attenuates RPP during exercise and 2) these effects may be due, in part, to enhanced endothelium-induced vasodilation in contracting skeletal muscle. Findings suggest that BRJ can act as a dietary nutraceutical capable of enhancing O2 delivery and reducing work of the heart, such that exercise can be performed at a given workload for a longer period of time before the onset of fatigue.

Mechanisms Underlying Exaggerated Metaboreflex Activation in Prehypertensive Men.

PURPOSE: Previously, we found that the pressor response to muscle metaboreflex activation is enhanced in prehypertension and associated with peripheral vasoconstriction. However, mechanisms underlying this exaggerated response are not clear. Therefore, we tested the hypothesis that activation of this reflex is augmented owing to increased production of muscle metabolites (i.e., lactate, K, and H). METHODS: Twenty-two men (11 normotensive and 11 prehypertensive) were studied. Changes in cardiac output (Q˙), mean arterial pressure (MAP), and total peripheral resistance (TPR) were compared between the two groups during static exercise (SE) and postexercise muscular ischemia (PEMI). Subjects completed 2 min of SE at 50% of maximal voluntary contraction (MVC) followed by 2 min of PEMI. Venous blood samples for determination of metabolites and hormones (catecholamines, vasopressin, and plasma renin activity) were taken from the exercising and nonexercising arm, respectively. RESULTS: Mean arterial pressure responses to SE (39 ± 3 vs 31 ± 2 mm Hg) and PEMI (24 ± 3 vs 19 ± 3 mm Hg) were significantly higher in the prehypertensive group. Increases in lactate and decreases in pH during PEMI were seen in both groups. However, changes in these variables were greater in the prehypertensive group (lactate, 50.1 ± 6.2 vs 32.8 ± 7.6 mg·dL; pH, -0.06 ± 0.02 vs -0.01 ± 0.01) (P < 0.05). Postexercise muscular ischemia did not evoke increases in hormones in either group. CONCLUSIONS: Compared to the normotensive group, the augmented pressor response to the metaboreflex in the prehypertensive group was associated with greater production of muscle metabolites that activate its afferent arm. The augmented response was not associated with activation of the vasopressin and renin-angiotensin systems and greater activation of the sympathetic nervous system was not apparent. Consequently, additional factors specific to prehypertension, such as arterial stiffness, may have been involved.

The effects of dietary fish oil on exercising skeletal muscle vascular and metabolic control in chronic heart failure rats.

Impaired vasomotor control in chronic heart failure (CHF) is due partly to decrements in nitric oxide synthase (NOS) mediated vasodilation. Exercising muscle blood flow (BF) is augmented with polyunsaturated fatty acid (PUFA) supplementation via fish oil (FO) in healthy rats. We hypothesized that FO would augment exercising muscle BF in CHF rats via increased NO-bioavailability. Myocardial infarction (coronary artery ligation) induced CHF in Sprague-Dawley rats which were subsequently randomized to dietary FO (20% docosahexaenoic acid, 30% eicosapentaenoic acid, n = 15) or safflower oil (SO, 5%, n = 10) for 6-8 weeks. Mean arterial pressure (MAP), blood [lactate], and hindlimb muscles BF (radiolabeled microspheres) were determined at rest, during treadmill exercise (20 m·min(-1), 5% incline) and exercise + N(G)-nitro-l-arginine-methyl-ester (l-NAME) (a nonspecific NOS inhibitor). FO did not change left ventricular end-diastolic pressure (SO: 14 ± 2; FO: 11 ± 1 mm Hg, p > 0.05). During exercise, MAP (SO: 128 ± 3; FO: 132 ± 3 mm Hg) and blood [lactate] (SO: 3.8 ± 0.4; FO: 4.6 ± 0.5 mmol·L(-1)) were not different (p > 0.05). Exercising hindlimb muscle BF was lower in FO than SO (SO: 120 ± 11; FO: 93 ± 4 mL·min(-1)·100 g(-1), p < 0.05) but was not differentially affected by l-NAME. Specifically, 17 of 28 individual muscle BF's were lower (p < 0.05) in FO demonstrating that PUFA supplementation with FO in CHF rats does not augment muscle BF during exercise but may lower metabolic cost.

Effects of cadence on aerobic capacity following a prolonged, varied intensity cycling trial.

We determined if high cadences, during a prolonged cycling protocol with varying intensities (similar to race situations) decrease performance compared to cycling at a lower, more energetically optimal, cadence. Eight healthy, competitive male road cyclists (35 ± 2 yr) cycled for 180 min at either 80 or 100 rpm (randomized) with varying intensities of power outputs corresponding to 50, 65 and 80% of VO2max. At the end of this cycling period, participants completed a ramped exercise test to exhaustion at their preferred cadence (90 ± 7 rpm). There were no cadence differences in blood glucose, respiratory exchange ratio or rate of perceived exertion. Heart Rate, VO2 and blood lactate were higher at 100 rpm vs. 80 rpm. The total energy cost while cycling during the 65% and 80% VO2max intervals at 100 rpm (15.2 ± 2.7 and 19.1 ± 2.5 kcal∙min(-1), respectively) were higher than at 80 rpm (14.3 ± 2.7 and 18.3± 2.2 kcal∙min(-1), respectively) (p < 0.05). Gross efficiency was higher at 80 rpm vs. 100 rpm during both the 65% (22.8 ± 1.0 vs. 21.3 ± 4.5%) and the 80% (23.1 vs. 22.1 ± 0.9%) exercise intensities (P< 0.05). Maximal power during the performance test (362 ± 38 watts) was greater at 80 rpm than 100 rpm (327 ± 27 watts) (p < 0.05). Findings suggest that in conditions simulating those seen during prolonged competitive cycling, higher cadences (i.e., 100 vs. 80 rpm) are less efficient, resulting in greater energy expenditure and reduced peak power output during maximal performance. Key PointsWhen competitive cyclists perform prolonged exercise that simulates racing conditions (i.e., variable, low-moderate submaximal cycling), a higher cadence results in excess energy expenditure and lower gross efficiency compared to a lower cadence at the same power output.Consequently, maximal power output is reduced during a subsequent exercise bout to exhaustion after using a higher cadence.Selection of a lower, more energetically optimal cadence during prolonged cycling exercise may allow competitive cyclists to enhance maximal performance later in a race.

Augmentation of the exercise pressor reflex in prehypertension: roles of the muscle metaboreflex and mechanoreflex.

This study investigated the hemodynamic mechanisms underlying the exaggerated blood pressure response to muscle contraction in prehypertensive humans and the potential role of skeletal muscle metabo- and mechanoreceptors in this response. To accomplish this, changes in peak mean arterial blood pressure (ΔMAP), cardiac output, and total peripheral resistance (ΔTPR) were compared between prehypertensive (n = 23) and normotensive (n = 19) male subjects during 2 min of static contraction (at 50% of maximal tension), 2 min of postexercise muscle ischemia (metaboreflex), and 1 min of passive dorsiflexion of the foot (tendon stretch, mechanoreceptor reflex). These variables were assessed before and during the interventions. Percentage increases from baseline in MAP and TPR in response to the exercise pressor reflex were augmented in the prehypertensives, compared with the normotensives (44% ± 5% vs. 33% ± 4% and 34% ± 15% vs. 2% ± 8%, respectively) (p < 0.05). Metaboreflex-induced increases in MAP and TPR were also augmented in the prehypertensives (28% ± 5% vs. 14% ± 4% and 36% ± 12% vs. 14% ± 9%, respectively) (p < 0.05). In response to the mechanoreflex, no differences in the percentage increase in MAP or TPR were seen between groups. The results indicate that the reflex pressor response to static contraction is augmented in prehypertension and suggest that this phenomenon is due, at least in part, to enhanced activation of metaboreceptors.

Effects of Ovarian Cycle on Hemodynamic Responses during Dynamic Exercise in Sedentary Women.

This study tested the hypothesis that effects of the menstrual cycle on resting blood pressure carry over to dynamic exercise. Eleven healthy females were studied during the early (EP; low estrogen, low progesterone) and late follicular (LP; high estrogen, low progesterone) menstrual phases. Stroke volume (SV), heart rate (HR), cardiac output (CO), systolic blood pressure (SBP), diastolic blood pressure (DBP), and total vascular conductance (TVC) were assessed at rest and in response to mild and moderate cycling exercise during EP and LP. During EP, compared to LP, baseline SBP (111±1 vs. 103±2 mmHg), DBP (71±2 vs. 65±2 mmHg) and mean arterial pressure (MAP) (84±2 vs. 78±1 mmHg) were higher and TVC (47.0±1.5 vs. 54.9±4.2 ml/min/mmHg) was lower (p<0.05). During exercise, absolute values of SBP (Mild: 142±4 vs. 127±5 mmHg; Moderate: 157±4 vs. 144±5 mmHg) and MAP (Mild: 100±3 vs. 91±3 mmHg; Moderate: 110±3 vs. 101±3 mmHg) were also higher, while TVC was lower (Mild: 90.9±5.1 vs. 105.4±5.2 ml/min/mmHg; Moderate: 105.4±5.3 vs. 123.9±8.1 ml/min/mmHg) during EP (p<0.05). However, exercise-induced increases in SBP, MAP and TVC at both work intensities were similar between the two menstrual phases, even though norepinephrine concentrations were higher during LP. Results indicate that blood pressure during dynamic exercise fluctuates during the menstrual cycle. It is higher during EP than LP and appears to be due to additive effects of simultaneous increases in baseline blood pressure and reductions in baseline TVC.

Skeletal muscle metaboreflex is enhanced in postmenopausal women.

This study determined whether an elevated muscle metaboreflex contributes to the excessive blood pressure response to exercise in postmenopausal women. Thirty healthy female volunteers were studied (15 postmenopausal and 15 premenopausal). Stroke volume, heart rate, cardiac output (CO), systolic blood pressure, diastolic blood pressure, and total vascular conductance (TVC) were continuously assessed throughout the experiment. To activate the muscle metaboreflex, occlusion of the vasculature was induced via inflation of a blood pressure cuff (2 min) on the upper arm following static handgrip exercise. Muscle metaboreflex activation increased mean arterial pressure (MAP) in both groups. However, this pressor response was greater in the postmenopausal women (ΔMAP: 21.4 ± 3 vs. 14.5 ± 2 mmHg) (P < 0.05) even though the corresponding increase in CO was less (ΔCO: 0.0 ± 0.2 vs. 0.3 ± 0.2 l/min) (P < 0.05). TVC decreased in both the groups but was more pronounced in the postmenopausal group (ΔTVC: -10.7 ± 2.6 vs. -17.1 ± 3.6 ml/min/mmHg) (P < 0.05). In conclusion, the exaggerated blood pressure response to exercise in postmenopausal women is mediated, in part, by an overactive metaboreflex that is associated with enhanced peripheral vasoconstriction.

Effects of dynamic exercise on plasma arachidonic acid epoxides and diols in human volunteers.

Metabolites of the cytochrome P450 (CYP) pathway may contribute to vasodilation of the vasculature. However, it is not known whether exercise affects their circulating concentrations. The authors determined effects of exercise intensity and duration on plasma concentrations of epoxy and dihydroxy metabolites of arachidonic acid. Their goal was to delineate the threshold workload, optimal workload, and duration required to produce increases in plasma concentrations of these vasoactive substances. Healthy volunteers (N = 14) performed maximal exercise testing on a bicycle ergometer during Visit 1. On separate days, subjects cycled for 20 min at 30%, 60%, and 80% of their maximal exercise intensity. The last day consisted of 40 min of exercise at 60% of maximal exercise intensity. Venous blood was obtained before, during, and after exercise for analysis. Compared with rest, increases were observed during the 80% workload at 20 min postexercise -14,15-DHET (0.77 ± 0.21 vs. 0.93 ± 0.27 nM) - and at 2 min postexercise: 11,12-DHET (0.64 ± 0.22 vs. 0.71 ± 0.24 nM; p < .05). Also compared with rest, 40-min values during the 60% workload were 14,15-DHET 0.79 ± 0.22 vs. 0.91 ± 0.31 nM and at 2 min post 14,15 EET 0.12 ± 0.06 vs. 0.21 ± 0.16 nM (p < .05). Results suggest the CYP metabolites (i.e., DHETs) are released during short-term high-intensity and long-term moderate-intensity exercise.

Taekwondo training and fitness in female adolescents.

In this study, we determined the specificity of a low frequency taekwondo training programme on physical fitness levels in adolescent females who receive limited physical education instruction (i.e. 2 days per week). Major components of physical fitness assessed were: skeletal muscle fitness (hand grip strength, bent arm hang, standing long jump, and isokinetic strength), flexibility (sit-and-reach test), speed and agility (10 × 5-m shuttle run), and cardiovascular fitness (VO(2max) and 20-m shuttle run). Changes in body composition were also assessed (dual X-ray absorptiometry, DXA). Participants were divided into two groups, a taekwondo training group (n = 21), which trained 50 min a day, 2 days per week for 12 weeks, and a control group (n = 10). Taekwondo training improved isokinetic strength, standing long jump, and sit-and-reach performance. Body fat mass and percent body fat were reduced. No changes in grip strength, bent arm hang time, speed and agility, or cardiorespiratory fitness were observed. Results indicate that low frequency taekwondo training in adolescent females produces beneficial changes in skeletal muscle fitness, flexibility, and body composition in a relatively short period of time. Consequently, this specific type of training can be useful to female adolescents in structured school environments where physical education classes are limited and there is little free time for physical activity.

Effects of dietary omega-3 polyunsaturated Fatty acids on the skeletal-muscle blood-flow response to exercise in rats.

The polyunsaturated fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) affect vascular relaxation and involve factors (e.g., nitric oxide) that contribute to exercise-induced increases in skeletal-muscle blood flow (Q). The authors investigated whether DHA and EPA supplementation augments skeletal-muscle Q and vascular conductance (VC) and attenuates renal and splanchnic Q and VC in exercising rats. Rats were fed a diet of 5% lipids by weight, of which 20% was DHA and 30% EPA (PUFA group, n = 9), or 5% safflower oil (SO group, n = 8) for 6 wk. Heart rate (HR), blood pressure (MAP), and hind-limb, renal, and splanchnic Q were measured at rest and during moderate treadmill running. MAP, HR, and renal and splanchnic Q and VC were similar between the 2 groups at rest and during exercise. In the PUFA group, Q (158 ± 27 vs. 128 ± 28 ml × min⁻¹ × 100 g⁻¹) and VC (1.16 ± 0.21 vs. 0.92 ± 0.23 ml × min⁻¹ × 100 g⁻¹ × mm Hg⁻¹) were greater in the exercising hind-limb muscle. Q and VC were also higher in 8 of 28 and 11 of 28 muscles and muscle parts, respectively. These increases were positively correlated to the percent sum of Types I and IIa fibers. Results suggest that DHA+EPA (a) enhances Q and VC in active skeletal muscle (especially Type I and IIa fibers) and that the increase in Q is due to an increase in cardiac output secondary to increases in VC and (b) has no apparent influence on vasoconstriction in renal and splanchnic tissue.

Effects of dietary decosahexaenoic acid (DHA) on eNOS in human coronary artery endothelial cells.

Endothelial dysfunction occurs in heart disease and may reduce functional capacity via attenuations in peripheral blood flow. Dietary decosahexaenoic acid (DHA) may improve this dysfunction, but the mechanism is unknown. This study determined if DHA enhances expression and activity of eNOS in cultured human coronary artery endothelial cells (HCAEC). HCAEC from 4 donors were treated with 5 nM, 50 nM, or 1 microM DHA for 7 days to model chronic DHA exposure. A trend for increased expression of endothelial nitric oxide synthase (eNOS) and phospho-eNOS was observed with 5 and 50 nM DHA. DHA also enhanced expression of 2 proteins instrumental in activation of eNOS: phospho-Akt (5 and 50 nM) and HSP90 (50 nM and 1 microM). Vascular endothelial growth factor-induced activation of Akt increased NOx in treated (50 nM DHA) versus untreated HCAEC (9.2 +/- 1.0 vs 3.3 +/- 1.1 micromol/microg protein/microL). Findings suggest that DHA enhances eNOS and Akt activity, augments HSP90 expression, and increases NO bioavailability in response to Akt kinase activation.

Omega-3 fatty acid supplementation enhances stroke volume and cardiac output during dynamic exercise.

Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have beneficial effects on cardiovascular function. We tested the hypotheses that dietary supplementation with DHA (2 g/day) + EPA (3 g/day) enhances increases in stroke volume (SV) and cardiac output (CO) and decreases in systemic vascular resistance (SVR) during dynamic exercise. Healthy subjects received DHA + EPA (eight men, four women) or safflower oil (six men, three women) for 6 weeks. Both groups performed 20 min of bicycle exercise (10 min each at a low and moderate work intensity) before and after DHA + EPA or safflower oil treatment. Mean arterial pressure (MAP), heart rate (HR), SV, CO, and SVR were assessed before exercise and during both workloads. HR was unaffected by DHA + EPA and MAP was reduced, but only at rest (88 +/- 5 vs. 83 +/- 4 mm Hg). DHA + EPA augmented increases in SV (14.1 +/- 6.3 vs. 32.3 +/- 8.7 ml) and CO (8.5 +/- 1.0 vs. 10.3 +/- 1.2 L/min) and tended to attenuate decreases in SVR (-7.0 +/- 0.6 vs. -10.1 +/- 1.6 mm Hg L(-1) min(-1)) during the moderate workload. Safflower oil treatment had no effects on MAP, HR, SV, CO or SVR at rest or during exercise. DHA + EPA-induced increases in SV and CO imply that dietary supplementation with these fatty acids can increase oxygen delivery during exercise, which may have beneficial clinical implications for individuals with cardiovascular disease and reduced exercise tolerance.

Supplementation with omega-3 polyunsaturated fatty acids augments brachial artery dilation and blood flow during forearm contraction.

Omega-3 polyunsaturated fatty acids such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) have beneficial effects on the heart and vasculature. We tested the hypothesis that 6 weeks of dietary supplementation with DHA (2.0 g/day) and EPA (3.0 g/day) enhances exercise-induced increases in brachial artery diameter and blood flow during rhythmic exercise. In seven healthy subjects, blood pressure, heart rate and brachial artery diameter, blood flow, and conductance were assessed before and during the last 30 s of 90 s of rhythmic handgrip exercise (30% of maximal handgrip tension). Blood pressure (MAP), heart rate (HR), and brachial artery vascular conductance were also determined. This paradigm was also performed in six other healthy subjects who received 6 weeks of placebo (safflower oil). Placebo treatment had no effect on any variable. DHA and EPA supplementation enhanced contraction-induced increases in brachial artery diameter (0.28+/-0.04 vs. 0.14+/-0.03 mm), blood flow (367+/-65 vs. 293+/-55 ml min-1) and conductance (3.86+/-0.71 vs. 2.89+/-0.61 ml min-1 mmHg-1) (P<0.05). MAP and HR were unchanged. Results indicate that treatment with DHA and EPA enhances brachial artery blood flow and conductance during exercise. These findings may have implications for individuals with cardiovascular disease and exercise intolerance (e.g., heart failure).

Heart rate recovery in heart failure patients after a 12-week cardiac rehabilitation program.

Heart rate recovery (HRR) after maximal exercise is a predictor of all-cause mortality. It was hypothesized that aerobic exercise training would increase HRR in patients with heart failure (HF), because it has been shown to be accelerated in athletes and improved in patients with coronary artery disease after cardiac rehabilitation. To date, no study has examined the effects of exercise training on HRR in HF. This was a retrospective study of patients with HF who had completed a phase II aerobic cardiac rehabilitation program with entry and exit maximal stress tests (n = 46). Thirty-five patients exhibited a training effect, 18 had abnormal HRR of < or =12 beats/min and the lowest initial functional capacity (L12), and 17 had HRR of >12 beats/min before training (G12). A group of 11 other patients did not achieve a training effect. After training, the L12 and G12 groups improved their estimated peak oxygen uptake (by 6.7 +/- 3.1 and 8.6 ml/kg/min, respectively) and treadmill time (by 117 +/- 62 and 181 +/- 108 seconds, respectively) compared with the no-training effect group (p <0.05). Only the L12 group demonstrated improvement in HRR (7 +/- 1 to 12 +/- 2 beats/min). In conclusion, the results indicate that short-term aerobic training can favorably modify HRR in patients with HF with low exercise capacity.

Topical analgesics and blood pressure during static contraction in humans.

PURPOSE: In decerebrate cats, topical application of analgesic balm (AB) can attenuate the pressor response to electrically induced static contraction. We examined the possibility that this phenomenon also occurs in humans and determined whether such effects were limited to a local action on the contracting muscle (e.g., attenuations of the action of groups III and IV muscle afferents that cause the exercise pressor reflex) or whether they also may have affected active muscle blood flow and/or central command. METHODS: Blood pressure (mean arterial pressure (MAP)), heart rate (HR), brachial artery blood flow (BABF), and relative perceived exertion (RPE) were assessed at rest and during 90 s of static handgrip contraction before and 50 min after application of a commercially available AB (1% capsaicin, 12.5% methyl salicylate) to the skin of the forearm muscles. RESULTS: AB attenuated the MAP response to contraction (19 +/- 3 vs 27 +/- 5 mm Hg) but had no effect on the HR response. Absolute BABF was enhanced at rest and during contraction, but absolute (118 +/- 47 vs 114 +/- 47 mL x min) and percent increases (83 +/- 31 vs 55 +/-19%) were not statistically different between conditions. AB appeared to slightly enhance RPE, but this was also the case in a control protocol where only the vehicle (petroleum jelly) was used and no change in the blood pressure response was seen. CONCLUSIONS: AB attenuates contraction-induced increases in MAP that do not seem to be related to alterations in perfusion of active muscle or central command. Effects appear to be localized to the active skeletal muscle and likely involve reductions in sensitivity of groups III and IV muscle afferents to local chemical and/or mechanical stimulation.

Endogenous prostaglandins limit angiotensin-II induced regional vasoconstriction in conscious rats.

In conscious rats, we tested the hypothesis that prostaglandins attenuate regional vasoconstriction caused by acute infusion of angiotensin II. Mean arterial pressure, regional blood flow, and vascular conductance in response to 2-minute infusions of 0.05 or 1 microg/kg/min Ang II were assessed before and during indomethacin treatment (5 mg/kg). Effects of the lower dose of Ang II (n=8) on regional blood flow were not altered by indomethacin, but conductance in the kidney (2.98+/-0.35 vs. 2.19+/-0.32), stomach (1.15+/-0.13 vs. 0.83+/-0.13), and white gastrocnemius muscle (0.11+/-0.02 vs. 0.07+/-0.01 mL/min/100g/mm Hg) were reduced. Changes in conductance were not seen in the pancreas or spleen. In response to the higher dose of Ang II (n=7), indomethacin reduced blood flow in the kidney, red and white gastrocnemius, and soleus muscles. Reductions in conductance were found in the kidney, stomach and small intestine, and in the red and white gastrocnemius, and soleus muscles (2.27+/-0.9 vs. 1.79+/-0.14, 0.44+/-0.07 vs. 0.27+/-0.03, 0.68+/-0.11 vs. 0.60+/-0.07, 0.43+/-0.08 vs. 0.16+/-0.03, 0.10+/-0.02 vs. 0.05+/-0.01, and 0.26+/-0.03 vs. 0.15+/-0.02 mL/min/100g, respectively). No changes occurred in the pancreas and spleen. Indomethacin had no effect on baseline blood flow or conductance in any of these organs. These results suggest that prostaglandins attenuate vasoconstriction caused by Ang II in a manner that is organ-specific and dependent on the dose of Ang II. Consequently, prostaglandins may limit vasoconstriction and potential ischemia caused by elevated levels of this hormone.

Cardiovascular responses to static and dynamic contraction during comparable workloads in humans.

Previous studies suggest that the blood pressure response to static contraction is greater than that caused by dynamic exercise. In anesthetized cats, however, pressor responses to electrically induced static and dynamic contraction of the same muscle group are similar during equivalent workloads and peak tension development [i.e., similar tension-time index (TTI)]. To determine if the same relationship exists in humans, where contraction is voluntary and central command is present, dynamic (180 s; 1/s) and static (90 s) contractions at 30% of maximal voluntary contraction (MVC) were performed. Dynamic contraction also was repeated at the same TTI for 90 s at 60% MVC. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), MAP during postexercise arterial occlusion (an index of the metaboreceptor-induced activation of the exercise pressor reflex), and relative perceived exertion (RPE) (an index of central command) were assessed. No differences in these variables were found between static and dynamic contraction at a tension of 30% MVC. During dynamic contraction at 60% MVC, changes in MAP (16 +/- 3 vs. 19 +/- 4 mmHg) and absolute HR (92 +/- 6 vs. 69 +/- 5 beats/min), CO (7.9 +/- 0.4 vs. 6.3 +/- 0.3 l/min), RPE (16 +/- 1 vs. 13 +/- 1), and MAP during postexercise arterial occlusion (115 +/- 3 vs. 100 +/- 4 mmHg) were greater than during static contraction (P < 0.05). Thus increases in MAP and HR, activation of central command, and muscle metabolite-induced stimulation of the exercise pressor reflex during static and dynamic contraction in humans seem to be similar when peak tension and TTI are equal. Augmented responses to dynamic contraction at 60% MVC are likely related to greater activation of these two mechanisms.