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).

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.

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.