LeuCAM and Reactive Oxygen Species during Long-Term Exercise Combined with Sleep and Energy Deficiency


Medicine & Science in Sports & Exercise: February 2007 - Volume 39 - Issue 2 - pp 275-282
doi: 10.1249/01.mss.0000241648.07382.7c
BASIC SCIENCES: Original Investigations

Introduction: During the Norwegian military ranger-training course, cadets are exposed to prolonged physical exercise combined with sleep-, energy-, and food deficiency. The open-window postexercise hypothesis indicates that after hard physical activity, there is an increased risk of contracting infectious diseases.

Purpose: The purpose of the present study was to determine leukocyte reactive oxygen species (ROS) levels, total antioxidant status (TAS), leukocyte expression of the cell adhesion molecules CD62L and CD11b, and plasma levels of soluble adhesion molecule L-selectin before, during, and in the recovery phase of a military ranger-training course.

Methods: Ten cadets from the Norwegian Military Academy were recruited to the study. Flow cytometry was used to study the intracellular levels of ROS in leukocytes (basally, as well as after in vitro stimulation with phorbol myristate acetate (PMA)), applying the probes dihydroethidium (DHE) and dihydrorhodamine 123 (DHR) and the leukocyte expression of adhesion molecules CD62L and CD11b. ELISA was used to assess the plasma levels of soluble L-selectin, and TAS in plasma was measured using the ABTS+ reduction assay kit.

Results: The basal levels of ROS as well as PMA-stimulated ROS in leukocytes declined gradually during the ranger-training course, being lowest on the last day (P < 0.05). The level of TAS increased (P < 0.01) during the course. A striking decrease (P < 0.001) was observed in leukocyte CD62L expression and was sustained even after 3 d of recovery. The leukocyte expression of CD11b remained unchanged.

Conclusion: The ranger-training course leads to a partial exhaustion of the leukocyte ROS-generating machinery and to a nearly total extinguishing of leukocyte CD62L expression. These changes may support the open-window hypothesis indicating reduced ability to combat microbial invasions before total restitution.

1Center for Clinical Research, Ullevaal University Hospital, Oslo, NORWAY; and 2Norwegian Defence Research Establishment, Kjeller, NORWAY

Address for correspondence: Hilde Grindvik Nielsen, Center for Clinical Research, Ullevaal University Hospital, N-0407 Oslo, Norway; E-mail: hdgn@c2i.net.

Submitted for publication January 2006.

Accepted for publication August 2006.

©2007The American College of Sports Medicine