Lymphocyte Redox Imbalance and Reduced Proliferation after a Single Session of High Intensity Interval Exercise

Abstract

This study investigated whether an acute session of high-intensity interval training (HIIT) is sufficient to alter lymphocyte function and redox status. Sixteen young healthy men underwent a HIIT session on a cycloergometer, consisting of eight bouts of 1 min at 90–100% of peak power, with 75 seconds of active recovery at 30 W between bouts. Venous blood was collected before, immediately after, and 30 minutes after the HIIT session. In response to Staphylococcus aureus superantigen B (SEB) stimulation, lymphocyte proliferation decreased and the IL-2 concentration increased after the HIIT session. However, the HIIT session had no effect on lymphocyte proliferation or IL-2 response to phytohemagglutinin stimulation. The HIIT session also induced lymphocyte redox imbalance, characterized by an increase in the concentration of thiobarbituric acid reactive substances and a decrease in the activity of the antioxidant enzyme catalase. Lymphocyte viability was not affected by the HIIT session. The frequencies of CD25+ and CD69+ T helper and B lymphocytes in response to superantigen stimulation were lower after exercise, suggesting that superantigen-induced lymphocyte activation was reduced by HIIT. However, HIIT also led to a reduction in the frequency of CD4+ and CD19+ cells, so the frequencies of CD25+ and CD69+ cells within the CD4 and CD19 cell populations were not affected by HIIT. These data indicate that the reduced lymphocyte proliferation observed after HIIT is not due to reduced early lymphocyte activation by superantigen. Our findings show that an acute HIIT session promotes lymphocyte redox imbalance and reduces lymphocyte proliferation in response to superantigenic, but not to mitogenic stimulation. This observation cannot be explained by alteration of the early lymphocyte activation response to superantigen. The manner in which lymphocyte function modulation by an acute HIIT session can affect individual immunity and susceptibility to infection is important and requires further investigation.

Late Neutrophil Priming Following a Single Session of High-intensity Interval Exercise

“…We and others have previously shown that a single HIIE session alters blood redox status [7,16,17,24]. We have also demonstrated that HIIE acutely disrupts lymphocyte proliferation and redox status [59], which supports the hypothesis that modification of cellular redox status contributes to the effects of exercise on immune cell function. However, despite the effect in f-MLP-induced ROS generation 30 min after the exercise, neutrophil redox status was not affected by HIIE in the same time frame.…”

“…How long do these changes last? To date, only Davison [17] and Tossige-Gomes et al [59] reported inhibitory effects of an acute HIIE session on the function of immune cells. However, neither of these studies investigated the duration of these effects.…”

“…Supernatant was used to determine SOD and CAT activity and TBARS concentration. The content of GSH was determined in intact cells, as described by Tossige-Gomes et al [59].…”

“…Thus, during HIIE sessions, neutrophils are exposed to great metabolic, endocrine and inflammatory demands compared to prolonged and continuous exercise, but only for a short period of time. Studies suggest that HIIE alters immune cell redox status and function as much as prolonged continuous exercise [16,17,59]. However, the duration of these changes is unknown.…”

Exercise-Induced Regulation of Redox Status in Cardiovascular Diseases: The Role of Exercise Training and Detraining

“…Similarly, another study also showed that a single bout of prolonged, moderate-intensity CVE (3-h walk at 30% of heart rate reserve) did not increase the lipid peroxidation levels, whereas an increase in the antioxidant defense was observed at the end of the exercise [166]. Furthermore, there has been reported that a single bout of high-intensity interval training (8x1min at 100% or 90% of Peak Power on a cycloergometer), promotes lymphocyte oxidative stress and reduces lymphocyte proliferation in response to super-antigenic stimulation [167].…”