Glucocorticoid Receptor Expression on Human B Cells in Response to Acute Heavy Resistance Exercise

Abstract

Objective: To examine glucocorticoid receptor (GCR) expression on B lymphocytes in response to an acute bout of resistance exercise. Methods: Using a within-subject design, resistance-trained women (n = 7; age: 22.13 ± 3.09 years; height: 1.69 ± 0.084 m; body weight: 65.60 ± 10.01 kg; body mass index: 22.63 ± 2.03 kg/m²; means ± SD) and men (n = 8; age: 23.28 ± 4.26 years; height: 1.73 ± 0.086 m; body weight: 73.93 ± 12.71 kg; body mass index: 24.51 ± 2.61 kg/m²; means ± SD) performed an acute resistance exercise protocol (6 sets of 5 repetition maximum heavy squats) and a control test in a balanced, randomized order. Blood samples were obtained before, during, and immediately after exercise, and after 1, 6, and 24 h of recovery. GCR expression on circulating B lymphocytes was evaluated with flow cytometry, and circulating cortisol was assayed. Results: Resting GCR expression on B lymphocytes was similar between men and women. GCR expression was elevated in anticipation of exercise (p = 0.047), decreased during exercise (p = 0.049), and increased during recovery (p = 0.05 and p = 0.03 after 1 and 6 h of recovery, respectively). Trends for gender differences were apparent before and during exercise, and after 6 h of recovery. Men had significantly higher cortisol responses during (p = 0.002) and after exercise (p = 0.094) compared to before exercise. In women, however, circulating cortisol concentrations did not significantly increase in response to the squat exercise protocol. Conclusions: GCR expression on B lymphocytes decreased during resistance exercise and increased during recovery. Circulating cortisol increased during exercise in men only. Responses were attenuated in women compared to men. Our data provide insights into the temporal interactions between the endocrine and immune systems in response to acute heavy resistance exercise in men and women.

Growth Hormone(s), Testosterone, Insulin-Like Growth Factors, and Cortisol: Roles and Integration for Cellular Development and Growth With Exercise

“…On the other hand, agents that increase GRα expression sensitize cells to glucocorticoids (204). Exercise affects receptor expression (205) and relative expression of receptor isoforms; athletes show less GRα mRNA expression in peripheral blood mononuclear cells than do untrained controls, indicating reduced sensitivity (206). Yet, GR-β does not appear involved in exercise adaptations in peripheral blood mononuclear cells of athletes (206).…”

The Effects of Cold Exposure on Leukocytes, Hormones and Cytokines during Acute Exercise in Humans

“…Studies examining immuno-endocrine modulations have investigated the implications of the sympathetic nervous system (SNS) (norepinephrine [NE] and epinephrine [Epi]), and the hypothalamic-pituitary-adrenal axis (HPA) (cortisol [COR] and adrenocorticotropic hormone [ACTH]) to explain the variance in cytokine and leukocyte responses [3] , [14] , [25] . The control mechanisms of these hormones on the immune system have been well studied [3] , [14] , [26] , [27] , [28] , [29] . Nonetheless, immune responses are further modulated by the hypothalamic-pituitary-thyroid axis (HPT) and the hypothalamic-pituitary-gonadal axis (HPG) [30] , [31] .…”

Impact of Adiposity and Fat Distribution, Rather Than Obesity, on Antibodies as an Illustration of Weight-Loss-Independent Exercise Benefits

“…Exercise (combined or not with diet and/or pharmacological therapies) is among the most widely accepted approaches to controlling body weight and managing obesity [ 29 , 30 , 31 ]. Exercise has known benefits and effects on the immunity system [ 32 , 33 ] including antibodies [ 34 ], B lymphocytes [ 35 ], cytokines such as Interleukin-6 [ 36 ], antioxidant effects [ 37 ], regeneration adjuvants [ 38 , 39 , 40 ], and improved immunosurveillance and immunocompetence with an anti-inflammatory effects [ 41 ] via macrophage infiltration suppression [ 42 ]. Importantly, as illustrated above, the antibody-related immunity decline with obesity would be associated with the adiposity and its distribution rather than body weight [ 17 ].…”