Atrial Fibrillation : Effects of Aging and Endurance Sports

ATRIAL FIBRILLATION (AF) is the most common arrhythmia of the heart and is caused when the atrial contraction becomes out of sync with the ventricle due to dysfunctional electrical signaling. The result is the ineffective movement of blood through the body. Atrial fibrillation may result in a fast fluttering heartbeat, which is a common characteristic. Because the blood is not being pumped through the body properly, atrial fibrillation increases risk of heart failure and the pooling of blood in the heart, which increases chances of blood clot formation. Blood clots which travel to the brain may cause a stroke.

Risk of atrial fibrillation increases with age which coincides with increased oxidative stress, where excessive free radicals exceed the body’s ability to protect against them. Oxidative stress activates inflammatory pathways and chronic inflammation. Mitochondrial production of free radicals is a major source of oxidative stress in the atrial cells. Onset of atrial fibrillation includes changes to the atrial myocardium which includes inflammation and fibrosis which effects changes to the electrical properties and loss of synchronization. Therefore, research suggests two important factors may play a role in the alteration of the atrial cells and electrical impulse: Oxidative stress and inflammation.

AGING AND ENDURANCE EXERCISE

• AGING: A prominent risk factor for atrial fibrillation is aging. Aging is correlated with increased levels of systemic oxidative stress and inflammation.
• ENDURANCE EXERCISE: AF has an increased occurrence in athletes, in particular those involved in endurance exercise (e.g. long distance running). The frequency of AF in endurance athletes is most notable in veteran endurance athletes (from ages 45 and higher). (1,2)
• During endurance exercise, versus moderate exercise, repeated strenuous overloads of the atria result in microtears and consequently inflammation and fibrosis.(2)

NATURAL SUPPORT:

Inhibition of oxidative stress and inflammation of the artrial myocardial tissue, which reduces potential for fibrosis in the atria, are key in reducing the risk for atrial fibrillation. Beneficial steps:

• INCREASING NRF2 – Nrf2 is a transcription factor which regulates the expression of proteins involved with cellular protection. Deficiency of Nrf2 reduces levels of protective proteins and facilitates the pathogenesis of structural changes to the atrial tissue, including fibrosis.(3-6) The condition of AF continues the cycle of oxidative stress, further altering the atrial tissue.
• INHIBITION OF INFLAMMATION. TNF-alpha and NK-BKappa are signaling proteins which are central to the inflammatory pathway activation. TNF-alpha plays an important role in the pathogenesis of atrial structural changes and atrial fibrillation.(6)
• ROLE OF NRF2 ACTIVATORS such as sulforaphane (and precursor glucoraphanin), supports the reduction of the tissue oxidative state while concurrently reducing the activation of the formation of fibrotic atrial tissue.(3-6) The Nrf2 activators, as powerful cell protectors, also support inflammation reduction and decrease expression of proinflammatory TNF-Alpha and NF-KappaB,
• RESVERATROL may also have direct effects on cardiac function and the pathways that affect the structural changes to the atria. Recent research indicates that resveratrol may inhibit changes to the atria with decreased atrial fibrosis formation.(7-8)

XGEVITY    (Glucoraphanin / Sulforaphane plus other Nrf2 activators)

PURPLE LONGEVITY    (Resveratrol plus Nrf2 activators)

REFERENCES:

(1) Laszio R, et al. Atrial fibrillation and physical activity: An overview. Herz. 2015 Sept.
(2) Redpath CJ, et al. Atrial fibrillation and the athletic heart. Curr Opin Cardiol. 2015 Jan.
(3) Hecker L, et al. Reversal of persistent fibrosis in aging by targeting Nox4-Nrf2 redox imbalance. Sci Transl Med. 2014 Apr
(4) Wolke C, et al. Redox control of cardiac remodeling in atrial fibrillation. Biochim Biophys Acta. 2015 Aug;
(5) Yeh YH, et al. Rosuvastatin suppresses atrial tachycardia-induced cellular remodeling via Akt/Nrf2/heme oxygenase-1 pathway. J Mol Cell Cardiol. 2015 May.
(6) Ren M, et al. Role of tumor necrosis factor alpha in the pathogenesis of atrial fibrillation: A novel potential therapeutic target? Ann Med. 2015 Jun
(7) Baczkó I, et al. Resveratrol and derivatives for the treatment of atrial fibrillation. Ann N Y Acad Sci. 2015 Aug
(8) Chong E, et al. Resveratrol, a red wine antioxidant, reduces atrial fibrillation susceptibility in the failing heart by PI3K/AKT/eNOS signaling pathway activation. Heart Rhythm. 2015 May