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Fish Oil Reduces Heart Rate and Oxygen Consumption During Exercise - Source: Journal of Cardiovascular Pharmacology, Nov 19, 2008

  [ 18 votes ]   [ Discuss This Article ]
By GE Peoples, et al. • www.ProHealth.com • December 2, 2008


Dietary omega-3 polyunsaturated fatty acids (PUFAs) are readily incorporated into heart and skeletal muscle membranes where, in the heart, animal studies show they reduce O2 consumption.

To test the hypothesis that omega-3 PUFAs alter O2 efficiency in humans, the effects of fish oil (FO) supplementation on O2 consumption during exercise were evaluated.

Sixteen well-trained men (cyclists), randomly assigned to receive 8 x 1 g capsules per day of olive oil (control) or fish oil for 8 weeks in a double-blind, parallel design, completed the study (control: n = 7, age 27.1 +/- 2.7 years; FO: n = 9, age 23.2 +/- 1.2 years). Subjects used an electronically braked cycle ergometer to complete peak O2 consumption tests (VO2peak) and sustained submaximal exercise tests at 55% of peak workload (from the VO2peak test) before and after supplementation. Whole-body O2 consumption and indirect measurements of myocardial O2 consumption [heart rate and rate pressure product (RPP)] were assessed.

Fish oil supplementation increased omega-3 PUFA content of erythrocyte cell membranes. There were no differences in VO2peak (mL kg min) (control: pre 66.8 +/- 2.4, post 67.2 +/- 2.3; fish oil: pre 68.3 +/- 1.4, post 67.2 +/- 1.2) or peak workload after supplementation.

• The fish oil supplementation lowered heart rate (including peak heart rate) during incremental workloads to exhaustion (P < 0.05).

• In addition, the fish oil supplementation lowered steady-state submaximal exercise heart rate, whole-body O2 consumption, and RPP (P < 0.01).

• Time to voluntary fatigue was not altered by fish oil supplementation.

This study indicates that fish oils may act within the healthy heart and skeletal muscle to reduce both whole-body and myocardial O2 demand during exercise, without a decrement in performance.

Source: Journal of Cardiovascular Pharmacology, Nov 19, 2008. E-pub ahead of print. PMID: 19034030, by Peoples GE, McLennan PL, Howe PR, Groeller H. Human Performance Laboratories, School of Health Sciences, and Graduate School of Medicine, University of Wollongong, Wollongong, NSW, Australia.





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