Epinephrine and norepinephrine mediate interactions between the neuroendocrine and the immune systems to alter immune cell activity. Although both systems respond to exercise stress, less is known about how they interact in response to such stress. The purpose of this investigation was to examine β2-adrenergic receptor (β2-ADR) expression on circulating leukocytes to an acute bout of resistance exercise in men and women.
Resistance-trained men (n = 8; mean ± SD age = 24.63 ± 5.07 yr, body mass index = 26.09 ± 2.21 kg·m−2) and women (n = 7; age = 22.13 ± 3.09 yr, body mass index = 22.63 ± 2.03 kg·m−2) performed an acute resistance exercise protocol (six sets of five-repetition maximum heavy squats) and a control test (i.e., identical conditions with no exercise) in a balanced, randomized order. Using a within-subject design, β2-ADR expressions on circulating leukocytes were evaluated with flow cytometry, and plasma epinephrine and norepinephrine were evaluated with high-performance liquid chromatography.
Plasma epinephrine and norepinephrine increased during the exercise bout and returned to baseline during recovery. β2-ADR expression on monocytes was elevated in anticipation of the exercise protocol. β2-ADR expression on monocytes and granulocytes decreased during the exercise. β2-ADR expression on lymphocytes was elevated during the recovery time points.
In conclusion, β2-ADR expression on leukocyte subpopulations changes in response to acute heavy resistance exercise protocol. The present findings provide insights into the potential temporal interactions between the neuroendocrine and the immune systems in response to the physiological stress of acute heavy resistance exercise in men and women.
1Human Performance Laboratory, Department of Kinesiology, University of Connecticut, Storrs, CT; 2Center for Aging, Division of Geriatric Medicine, University of Connecticut Health Center, Farmington, CT; 3Department of Physiology and Neurobiology, University of Connecticut, Storrs, CT; 4Department of Microbiology and Cell Biology, The Pennsylvania State University, University Park, PA; and 5Department of Biology of Physical Activity & Neuromuscular Research Center, University of Jyväskylä, Jyväskylä, FINLAND
Address for correspondence: William J. Kraemer, Ph.D., Kinesiology, Physiology and Neurobiology, Human Performance Laboratory, Department of Kinesiology, 2095 Hillside Rd., Unit-1110, University of Connecticut, Storrs, CT 06269-1110; E-mail: William.email@example.com.
Submitted for publication October 2010.
Accepted for publication December 2010.