Psychological Stress and Oxidative Damage in Lymphocytes of Aerobically Fit and Unfit Individuals¹

Abstract

Habitual aerobic exercise has a beneficial effect on many systems of the body, and psychological stress has a negative influence on several of the same systems. One possible pathway is through those systems that account for the detrimental effects of stress; by buffering these harmful effects, exercise may reduce the consequences of stress. This study examined increased resistance of cells to stress-induced oxidative damage as a result of fitness. Forty healthy participants were assigned to either a stress group or a no-stress control group, and measures of stress and oxidative damage were collected. Variation in fitness level across participants was also measured. Oxidative damage increased as a function of stress, but this was not buffered by fitness level. These results should be interpreted with caution because of the small sample size and the limited variability of cardiorespiratory fitness levels in the sample.

Chronic stress exposure and daily stress appraisals relate to biological aging marker p16INK4a

“…In addition, murine cells exposed to physiological concentrations of catecholamines (i.e., epinephrine, norepinephrine) or cortisol showed five-fold increases in DNA damage compared to untreated cells (Flint et al, 2007). In a human study, young adults that participated in an acute stressor task had greater oxidative damage than those in the control group (Knickelbein et al, 2008). Another study found that postmenopausal women's cortisol reactivity in response to an acute stressor task mediated the association between perceived stress and oxidative damage for those undergoing chronic caregiving stress but not age-matched controls (Aschbacher et al, 2013).…”

“…Another important hallmark of biological aging is cellular senescence, a permanent state of cell cycle arrest (López-Otín et al, 2013). A growing literature links stress exposure to the secretion of catecholamines, which can lead to increased production of oxidants and DNA damage (Aschbacher et al, 2013;Flint et al, 2007Flint et al, , 2005Hara et al, 2011;Knickelbein et al, 2008). DNA damage serves an important role in biological aging as excess levels of DNA damage can initiate cellular senescence (Campisi, 2005).…”

Chronic stress increases transcriptomic indicators of biological aging in mouse bone marrow leukocytes

“…For instance, research with mice and rats has linked stress exposure to elevated markers of cell stress, including lower Nrf2 translocation to the nucleus and increased heat shock proteins ( Bouvier et al., 2017 ; Fleshner et al., 2004 ; Johnson et al., 2005 ). Other research has demonstrated that mice exposed to chronic stress and humans exposed to an acute laboratory stressor showed increased DNA damage and decreased DNA repair processes ( Aschbacher et al., 2013 ; Nishio et al., 2007 ; Consiglio et al., 2010 ; Hara et al., 2013 ; Forsberg et al., 2015 ; Flint et al., 2005 ; Knickelbein et al., 2008 ). To our knowledge, only two studies have examined links between chronic stress and cellular senescence.…”