Vitamin C and E supplementation does not affect heat shock proteins or endogenous antioxidants in trained skeletal muscles during 12 weeks of strength training.

BACKGROUND: Supplementation with large doses of antioxidants, such as vitamin C and E, has been shown to blunt some adaptations to endurance training. The effects of antioxidant supplementation on adaptations to strength training is sparsely studied. Herein we investigated the effects of vitamin C and E supplementation on acute stress responses to exercise and adaptation to traditional heavy load strength training. METHODS: In a double blind placebo-controlled design, twenty-eight, young, trained males and females were randomly assigned to receive either vitamin C and E (C: 1000 mg, E: 235 mg, per day) or placebo supplements, and underwent strength training for 10 weeks. After five weeks, a subgroup conducted a strength training session to investigate acute stress responses. Muscle samples were obtained to investigate changes in stress responses and in proteins and mRNA related to the heat shock proteins (HSPs) or antioxidant enzymes. RESULTS: The acute responses to the exercise session revealed activation of the NFκB pathway indicated by degradation of IκBα in both groups. Vitamin C and E supplementation had, however, no effects on the acute stress responses. Furthermore, ten weeks of strength training did not change muscle αB-crystallin, HSP27, HSP70, GPx1 or mnSOD levels, with no influence of supplementation. CONCLUSIONS: Our results showed that although vitamin C and E supplementation has been shown to interfere with training adaptations, it did not affect acute stress responses or long-term training adaptations in the HSPs or antioxidant enzymes in this study.

Role of exercise-induced reactive oxygen species in the modulation of heat shock protein response.

The multiple roles that have been associated with heat shock proteins (HSPs), inside and outside cells are remarkable. HSPs have been found to play a fundamental role in multiple stress conditions and to offer protection from subsequent insults. Exercise, because of the physiological stresses associated with it, is one of the main stimuli associated with a robust increase of different HSPs in several tissues. Given the combination of physiological stresses induced by exercise, and the 'cross-talk' that occurs between signaling pathways in different tissues, it is likely that exercise induces the HSP expression through a combination of 'stressors', among which reactive oxygen species (ROS) could play a major role. Indeed, although an imbalance between ROS production and antioxidant levels results in oxidative stress, causing damage to lipids, proteins, and nucleic acids with a possible activation of the programed cell death pathway, at moderate concentrations ROS play an important role as regulatory mediators in signaling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and re-establish redox homeostasis. The aim of this review is to provide a critical update on the role of exercise-induced ROS in the modulation of the HSP's response, focusing on experimental results from animal and human studies where the link between redox homeostasis and HSPs' expression in different tissues has been addressed.