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Effect of dietary omega-3 polyunsaturated Fatty acids on heart rate and heart rate variability in animals susceptible or resistant to ventricular fibrillation.

Billman GE - Front Physiol (2012)

Bottom Line: The consumption of omega-3 polyunsaturated fatty acids (n-3 PUFAs) has been reported to reduce cardiac mortality following myocardial infarction as well as to decrease resting heart rate (HR) and increase HR variability (HRV).However, it has not been established whether n-3 PUFAs exhibit the same actions on HR and HRV in individuals known to be either susceptible or resistant to ventricular fibrillation (VF).These data demonstrate that dietary n-3 PUFA decreased HR and increased HRV to a similar extent in animals known to be prone to or resistant to malignant cardiac tachyarrhythmias.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Cell Biology, The Ohio State University Columbus, OH, USA.

ABSTRACT
The consumption of omega-3 polyunsaturated fatty acids (n-3 PUFAs) has been reported to reduce cardiac mortality following myocardial infarction as well as to decrease resting heart rate (HR) and increase HR variability (HRV). However, it has not been established whether n-3 PUFAs exhibit the same actions on HR and HRV in individuals known to be either susceptible or resistant to ventricular fibrillation (VF). Therefore, HR and HRV (high frequency and total R-R interval variability) were evaluated before and 3 months after n-3 PUFA treatment in dogs with healed myocardial infarction that were either susceptible (VF+, n = 31) or resistant (VF-, n = 31) to ventricular tachyarrhythmias induced by a 2-min coronary artery occlusion during the last minute of a submaximal exercise test. HR and HRV were evaluated at rest, during submaximal exercise and in response to acute myocardial ischemia at rest before and after either placebo (1 g/day, corn oil, VF+, n = 9; VF- n = 8) or n-3 PUFA (docosahexaenoic acid + eicosapentaenoic acid ethyl esters, 1-4 g/day, VF+, n = 22; VF-, n = 23) treatment for 3 months. The n-3 PUFA treatment elicited similar increases in red blood cell membrane, right atrial, and left ventricular n-3 PUFA levels in both the VF+ and VF- dogs. The n-3 PUFA treatment also provoked similar reductions in baseline HR and increases in baseline HRV in both groups that resulted in parallel shifts in the response to either exercise or acute myocardial ischemia (that is, the change in these variables induced by physiological challenges was not altered after n-3 PUFA treatment). These data demonstrate that dietary n-3 PUFA decreased HR and increased HRV to a similar extent in animals known to be prone to or resistant to malignant cardiac tachyarrhythmias.

No MeSH data available.


Related in: MedlinePlus

Effect of omega-3 polyunsaturated fatty acids (n− 3 PUFAs) on the heart rate and heart rate variability response to submaximal exercise in dogs susceptible to ventricular fibrillation. Dietary n−3 PUFA, but not the placebo, produced a significant downward shift of the heart rate (HR) response curve that was accompanied by an upward shift in the high frequency (HF) component of the R–R interval variability (vagal tone index 0.24–1.04 Hz; i.e., significant pre–post effect: HR, P < 0.04; HF, P < 0.02). Despite the shifts in the curves, the absolute change in these variables induced by the exercise was not altered before or after the treatment (i.e., there were no significant pre–post-treatment × exercise interactions: HR, P = 0.68; HF, P = 0.45). The data were averaged over the last 30 s of given exercise level. Exercise levels are as follows: 1 = 0 kph and 0% grade; 2 = 4.8 kph and 0% grade; 3 = 6.4 kph and 0% grade; 4 = 6.4 kph and 4% grade; 5 = 6.4 kph and 8% grade; 6 = 6.4 kph and 12% grade; 7 = 6.4 kph and 16% grade. Pre = before placebo (n = 9) or n−3 PUFA (1–4 g/day, n = 22) treatment began, post = after 3 months of treatment.
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Figure 3: Effect of omega-3 polyunsaturated fatty acids (n− 3 PUFAs) on the heart rate and heart rate variability response to submaximal exercise in dogs susceptible to ventricular fibrillation. Dietary n−3 PUFA, but not the placebo, produced a significant downward shift of the heart rate (HR) response curve that was accompanied by an upward shift in the high frequency (HF) component of the R–R interval variability (vagal tone index 0.24–1.04 Hz; i.e., significant pre–post effect: HR, P < 0.04; HF, P < 0.02). Despite the shifts in the curves, the absolute change in these variables induced by the exercise was not altered before or after the treatment (i.e., there were no significant pre–post-treatment × exercise interactions: HR, P = 0.68; HF, P = 0.45). The data were averaged over the last 30 s of given exercise level. Exercise levels are as follows: 1 = 0 kph and 0% grade; 2 = 4.8 kph and 0% grade; 3 = 6.4 kph and 0% grade; 4 = 6.4 kph and 4% grade; 5 = 6.4 kph and 8% grade; 6 = 6.4 kph and 12% grade; 7 = 6.4 kph and 16% grade. Pre = before placebo (n = 9) or n−3 PUFA (1–4 g/day, n = 22) treatment began, post = after 3 months of treatment.

Mentions: The HR and HRV response to submaximal exercise before and after 3 months of placebo or n−3 PUFA treatment are displayed in Figure 3 (VF+) and Figure 4 (VF−). As one would predict, exercise provoked large increases in HR (exercise level effect, P < 10−6) that were accompanied by large reductions in HRV (exercise level effect, P < 10−6) in all four groups. HR was significantly lower (pre–post effect: VF−, P < 0.05; VF+, P < 0.04), and both HF (pre–post: VF−, P < 0.02; VF+, P < 0.02) and SD (data not shown pre–post: VF−, P < 0.0004; VF+, P < 0.005) were higher during exercise after n−3 PUFA treatment as compared to values obtained prior to the treatment. In contrast, HR, HF, and SD were not altered (no significant pre–post effects) by the placebo treatment. The change in HR (VF−, pre-treatment 62.4 ± 6.7 vs. post-treatment 66.6 ± 5.5; VF+, pre 65.8 ± 5.3 vs. post 59.8 ± 6.3 beats/min), HF (VF−, pre −4.9 ± 0.3 vs. post −5.0 ± 0.2; VF+, pre −6.2 ± 0.5 vs. post −6.3 ± 0.5 ln ms2), and SD (VF−, pre −44.5 ± 4.2 vs. post 60.3 ± 9.3; VF+, −36.5 ± 4.7 vs. post −47.7 ± 6.3 ms) provoked by exercise were not affected by the n−3 PUFA treatment (i.e., there were no significant pre–post × exercise level interactions). Thus, n−3 PUFA produced a similar shift in the pre-exercise values of HR, HF, and SD in both VF+ and VF− animals and, further, the magnitude of the change in these variables that was induced by exercise was not altered by n−3 PUFA for either group. In other words, the response to exercise per se was not affected by the treatment.


Effect of dietary omega-3 polyunsaturated Fatty acids on heart rate and heart rate variability in animals susceptible or resistant to ventricular fibrillation.

Billman GE - Front Physiol (2012)

Effect of omega-3 polyunsaturated fatty acids (n− 3 PUFAs) on the heart rate and heart rate variability response to submaximal exercise in dogs susceptible to ventricular fibrillation. Dietary n−3 PUFA, but not the placebo, produced a significant downward shift of the heart rate (HR) response curve that was accompanied by an upward shift in the high frequency (HF) component of the R–R interval variability (vagal tone index 0.24–1.04 Hz; i.e., significant pre–post effect: HR, P < 0.04; HF, P < 0.02). Despite the shifts in the curves, the absolute change in these variables induced by the exercise was not altered before or after the treatment (i.e., there were no significant pre–post-treatment × exercise interactions: HR, P = 0.68; HF, P = 0.45). The data were averaged over the last 30 s of given exercise level. Exercise levels are as follows: 1 = 0 kph and 0% grade; 2 = 4.8 kph and 0% grade; 3 = 6.4 kph and 0% grade; 4 = 6.4 kph and 4% grade; 5 = 6.4 kph and 8% grade; 6 = 6.4 kph and 12% grade; 7 = 6.4 kph and 16% grade. Pre = before placebo (n = 9) or n−3 PUFA (1–4 g/day, n = 22) treatment began, post = after 3 months of treatment.
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Figure 3: Effect of omega-3 polyunsaturated fatty acids (n− 3 PUFAs) on the heart rate and heart rate variability response to submaximal exercise in dogs susceptible to ventricular fibrillation. Dietary n−3 PUFA, but not the placebo, produced a significant downward shift of the heart rate (HR) response curve that was accompanied by an upward shift in the high frequency (HF) component of the R–R interval variability (vagal tone index 0.24–1.04 Hz; i.e., significant pre–post effect: HR, P < 0.04; HF, P < 0.02). Despite the shifts in the curves, the absolute change in these variables induced by the exercise was not altered before or after the treatment (i.e., there were no significant pre–post-treatment × exercise interactions: HR, P = 0.68; HF, P = 0.45). The data were averaged over the last 30 s of given exercise level. Exercise levels are as follows: 1 = 0 kph and 0% grade; 2 = 4.8 kph and 0% grade; 3 = 6.4 kph and 0% grade; 4 = 6.4 kph and 4% grade; 5 = 6.4 kph and 8% grade; 6 = 6.4 kph and 12% grade; 7 = 6.4 kph and 16% grade. Pre = before placebo (n = 9) or n−3 PUFA (1–4 g/day, n = 22) treatment began, post = after 3 months of treatment.
Mentions: The HR and HRV response to submaximal exercise before and after 3 months of placebo or n−3 PUFA treatment are displayed in Figure 3 (VF+) and Figure 4 (VF−). As one would predict, exercise provoked large increases in HR (exercise level effect, P < 10−6) that were accompanied by large reductions in HRV (exercise level effect, P < 10−6) in all four groups. HR was significantly lower (pre–post effect: VF−, P < 0.05; VF+, P < 0.04), and both HF (pre–post: VF−, P < 0.02; VF+, P < 0.02) and SD (data not shown pre–post: VF−, P < 0.0004; VF+, P < 0.005) were higher during exercise after n−3 PUFA treatment as compared to values obtained prior to the treatment. In contrast, HR, HF, and SD were not altered (no significant pre–post effects) by the placebo treatment. The change in HR (VF−, pre-treatment 62.4 ± 6.7 vs. post-treatment 66.6 ± 5.5; VF+, pre 65.8 ± 5.3 vs. post 59.8 ± 6.3 beats/min), HF (VF−, pre −4.9 ± 0.3 vs. post −5.0 ± 0.2; VF+, pre −6.2 ± 0.5 vs. post −6.3 ± 0.5 ln ms2), and SD (VF−, pre −44.5 ± 4.2 vs. post 60.3 ± 9.3; VF+, −36.5 ± 4.7 vs. post −47.7 ± 6.3 ms) provoked by exercise were not affected by the n−3 PUFA treatment (i.e., there were no significant pre–post × exercise level interactions). Thus, n−3 PUFA produced a similar shift in the pre-exercise values of HR, HF, and SD in both VF+ and VF− animals and, further, the magnitude of the change in these variables that was induced by exercise was not altered by n−3 PUFA for either group. In other words, the response to exercise per se was not affected by the treatment.

Bottom Line: The consumption of omega-3 polyunsaturated fatty acids (n-3 PUFAs) has been reported to reduce cardiac mortality following myocardial infarction as well as to decrease resting heart rate (HR) and increase HR variability (HRV).However, it has not been established whether n-3 PUFAs exhibit the same actions on HR and HRV in individuals known to be either susceptible or resistant to ventricular fibrillation (VF).These data demonstrate that dietary n-3 PUFA decreased HR and increased HRV to a similar extent in animals known to be prone to or resistant to malignant cardiac tachyarrhythmias.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology and Cell Biology, The Ohio State University Columbus, OH, USA.

ABSTRACT
The consumption of omega-3 polyunsaturated fatty acids (n-3 PUFAs) has been reported to reduce cardiac mortality following myocardial infarction as well as to decrease resting heart rate (HR) and increase HR variability (HRV). However, it has not been established whether n-3 PUFAs exhibit the same actions on HR and HRV in individuals known to be either susceptible or resistant to ventricular fibrillation (VF). Therefore, HR and HRV (high frequency and total R-R interval variability) were evaluated before and 3 months after n-3 PUFA treatment in dogs with healed myocardial infarction that were either susceptible (VF+, n = 31) or resistant (VF-, n = 31) to ventricular tachyarrhythmias induced by a 2-min coronary artery occlusion during the last minute of a submaximal exercise test. HR and HRV were evaluated at rest, during submaximal exercise and in response to acute myocardial ischemia at rest before and after either placebo (1 g/day, corn oil, VF+, n = 9; VF- n = 8) or n-3 PUFA (docosahexaenoic acid + eicosapentaenoic acid ethyl esters, 1-4 g/day, VF+, n = 22; VF-, n = 23) treatment for 3 months. The n-3 PUFA treatment elicited similar increases in red blood cell membrane, right atrial, and left ventricular n-3 PUFA levels in both the VF+ and VF- dogs. The n-3 PUFA treatment also provoked similar reductions in baseline HR and increases in baseline HRV in both groups that resulted in parallel shifts in the response to either exercise or acute myocardial ischemia (that is, the change in these variables induced by physiological challenges was not altered after n-3 PUFA treatment). These data demonstrate that dietary n-3 PUFA decreased HR and increased HRV to a similar extent in animals known to be prone to or resistant to malignant cardiac tachyarrhythmias.

No MeSH data available.


Related in: MedlinePlus