Oxidative stress responses to a graded maximal exercise test in older adults following explosive-type resistance training

Abstract

We recently demonstrated that low frequency, moderate intensity, explosive-type resistance training (EMRT) is highly beneficial in elderly subjects towards muscle strength and power, with a systemic adaptive response of anti-oxidant and stress-induced markers. In the present study, we aimed to evaluate the impact of EMRT on oxidative stress biomarkers induced in old people (70–75 years) by a single bout of acute, intense exercise. Sixteen subjects randomly assigned to either a control, not exercising group (n=8) or a trained group performing EMRT protocol for 12-weeks (n=8), were submitted to a graded maximal exercise stress test (GXT) at baseline and after the 12-weeks of EMRT protocol, with blood samples collected before, immediately after, 1 and 24 h post-GXT test. Blood glutathione (GSH, GSSG, GSH/GSSG), plasma malonaldehyde (MDA), protein carbonyls and creatine kinase (CK) levels, as well as PBMCs cellular damage (Comet assay, apoptosis) and stress–protein response (Hsp70 and Hsp27 expression) were evaluated. The use of multiple biomarkers allowed us to confirm that EMRT per se neither affected redox homeostasis nor induced any cellular and oxidative damage. Following the GXT, the EMRT group displayed a higher GSH/GSSG ratio and a less pronounced increase in MDA, protein carbonyls and CK levels compared to control group. Moreover, we found that Hsp70 and Hsp27 proteins were induced after GXT only in EMRT group, while any significant modification within 24 h was detected in untrained group. Apoptosis rates and DNA damage did not show any significant variation in relation to EMRT and/or GXT.In conclusion, the adherence to an EMRT protocol is able to induce a cellular adaptation allowing healthy elderly trained subjects to cope with the oxidative stress induced by an acute exercise more effectively than the aged-matched sedentary subjects.

Resistance Training and Redox Homeostasis: Correlation with Age-Associated Genomic Changes

“…Recently we have conducted a controlled trial in which elderly subjects (70-75 years) were randomly divided into training and control group, to evaluate the effect of an EMRT protocol for 12 weeks on muscle strength, power and functional performance, as well as the adaptive response to oxidative stress induced by an acute exercise [11,6]. The study has been expanded utilizing subjects from both the trained group (TR: n¼ 10) and from the control group (CTRL: n ¼10), successfully able to complete the blood samplings at baseline and after the EMRT protocol period.…”

“…Indeed, EMRT not only enhanced the muscle strength, power, and functional performance without detrimental effects on cardiovascular and inflammatory parameters [6], but improved the general adaptive response to oxidative stress related to intense acute exercise [11].…”

Influence of the PDE5 inhibitor tadalafil on redox status and antioxidant defense system in C2C12 skeletal muscle cells

“…Glutathione is the primary antioxidant responsible for maintaining a reduced intracellular microenvironment. When ROS production is accelerated to the point that it overwhelms ROS scavenging capacity, GSH/GSSG ratio, a well-known marker of oxidative stress, decreases in significant manner (Towsend et al 2003;Ceci et al 2014). Indeed, a reduction in GSH/GSSG reflects a reduced antioxidant capacity and increased vulnerability to oxidative damage to macromolecules (Jones 2006).…”

Regular exercise participation improves genomic stability in diabetic patients: an exploratory study to analyse telomere length and DNA damage

“…Nevertheless, the training regime produced a decrease, although not significant, in spontaneous DNA damage in both trained groups, possibly due to a decrease of the pro-oxidant cellular environment and increase of endogenous antioxidant defences induced in both diabetic and non-diabetic subjects by this type of exercise, as recently demonstrated by our group 20 . Physical activity has demonstrated an induction of an adaptive response of several stress-proteins/molecules (anti-oxidants, heat shock proteins) [38][39][40][41][42] , and thereby could modify the susceptibility to subsequent pro-oxidant stimuli 14,28,43 . Our results from ex vivo treatment with exogenous hydrogen peroxide seem to verify the hypothesis that telomere attrition is dependent upon oxidative damage.…”