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Abstract
Intense exercise is a physiological stress capable of inducing the interaction of neutrophils with muscle endothelial cells and their transmigration into tissue. Mechanisms driving this physiological inflammatory response are not known. Here, we investigate whether production of reactive oxygen species is relevant for neutrophil interaction with endothelial cells and recruitment into the quadriceps muscle in mice subjected to the treadmill fatiguing exercise protocol. Mice exercised until fatigue by running for 56.3±6.8 min on an electric treadmill. Skeletal muscle was evaluated by intravital microscopy at different time points after exercise, and then removed to assess local oxidative stress and histopathological analysis. We observed an increase in plasma lactate and creatine kinase (CK) concentrations after exercise. The numbers of monocytes, neutrophils, and lymphocytes in blood increased 12 and 24 hours after the exercise. Numbers of rolling and adherent leukocytes increased 3, 6, 12, and 24 hours post-exercise, as assessed by intravital microscopy. Using LysM-eGFP mice and confocal intravital microscopy technology, we show that the number of transmigrating neutrophils increased 12 hours post-exercise. Mutant gp91phox-/- (non-functional NADPH oxidase) mice and mice treated with apocynin showed diminished neutrophil recruitment. SOD treatment promoted further adhesion and transmigration of leukocytes 12 hours after the exercise. These findings confirm our hypothesis that treadmill exercise increases the recruitment of leukocytes to the postcapillary venules, and NADPH oxidase-induced ROS plays an important role in this process.
Highlights
Intense, unaccustomed, and eccentric exercise is associated with reactive skeletal muscle inflammatory responses [1,2]
Fatiguing exercise protocol induced a rapid increase in oxygen consumption (VO2) that indicates an enhancement of metabolic rate exercise-induced (Fig. 1B)
The serum creatine kinase (CK) activity, a specific muscle injury marker, was elevated at the 6 and 12 hours post-exercise (Fig. 1D) and the glucose level, that is an energetic substrate, was reduced in blood immediately after the fatiguing exercise protocol (Fig. 1E). These results indicate that our exercise protocol was at a high intensity level and induces skeletal muscle damage
Summary
Intense, unaccustomed, and eccentric exercise is associated with reactive skeletal muscle inflammatory responses [1,2]. These types of physical activity result in disruptions in the cytoskeleton and plasma membrane of skeletal muscle cells, which may occur because of the increased mechanical load [2]. This type of muscle damage is associated with an increase in circulating muscle proteins, such as creatine kinase and myoglobin, and a decrease in motor control [3]. These molecules may activate resident cells to release chemotactic mediators [6,7], which may act on leukocytes and make them adhere to, and transmigrate through, the endothelial wall [8]
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