Abstract
CD4+ T cells are sensitive to peripheral changes of cytokine levels and metabolic substrates such as glucose and lactate. This study aimed to analyze whether factors released after exercise alter parameters of human T cell metabolism, specifically glycolysis and oxidative phosphorylation. We used primary human CD4+ T cells activated in the presence of autologous serum, which was collected before (CO) and after a 30-min exercise intervention (EX). In the course of activation, cells and supernatants were analyzed for cell viability and diameter, real-time oxygen consumption by using PreSens Technology, mRNA expression of glycolytic enzymes and complexes of the electron transport chain by real-time PCR, glucose, and lactate levels in supernatants, and in vitro differentiation by flow cytometry. EX did not alter T cell phenotype, viability, or on-blast formation. Similarly, no difference between CO and EX were found for CD4+ T cell activation and cellular oxygen consumption. In contrast, higher levels of glucose were found after 48 h activation in EX conditions. T cells activated in autologous exercise serum expressed lower HK1 mRNA and higher IFN-γ receptor 1. We suggest that the exercise protocol used was not sufficient to destabilize the immune metabolism of T cells. Therefore, more intense and prolonged exercise should be used in future studies.
Highlights
Obesity, aging, and associated co-morbidities commonly lead to metabolic reprogramming of human cells [1]
Cell count did not vary between conditions, neither at t48 after activation of CD4+ T cells (p = 0.14) nor at 72 h after activation (t72, p = 0.14) (Figure 2b,c)
The selected parameters of CD4+ metabolism are marginally affected by incubation in exercise serum
Summary
Obesity, aging, and associated co-morbidities commonly lead to metabolic reprogramming of human cells [1]. It becomes more and more evident that metabolism tightly controls T cell effector function [2]. Targeting metabolic pathways of T cells is a promising therapeutic intervention [3]. The main focus lies on drugs that inhibit or enhance metabolic pathways to restore cellular homeostasis [4]. Exercise is known as an acute metabolic stressor for the human body that counteracts factors leading to metabolic reprogramming [5,6]. Exercise-induced changes such as increased production of reactive oxygen species or changes of the metabolic environment are known to modulate immune cell function, in particular those of CD4+ T cell [8,9,10,11]
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