Autophagy During and Following Dynamic Exercise in Young Adults: Influence of Exercise Intensity

Abstract

Autophagy plays a critical role in the cell’s response to exercise-induced cell stress. Exercise intensity and elevations in tissue temperature are known to modulate autophagic activation, however, the relationship is still unclear. Thus, we investigated the effect of increasing intensities of exercise, as well as evaluated high intensity exercise performed in a hot environment on autophagy and associated cellular stress pathways (the heat shock response [HSR], apoptosis, and the acute inflammatory response). To evaluate the hypothesis that greater autophagic activation occurs with increasing exercise intensity, which is be exacerbated by exercise performed in the heat, 9 young men (mean [SD]; 23 [2] years) cycled for 30 minutes at 40, 55 and 70% of VO2max at an ambient temperature of 25°C and at 70% of VO2max at an ambient temperature of 40°C. Peripheral blood mononuclear cells were harvested before exercise, as well as at 0, 3 and 6 hours post-exercise. Changes in protein content were analyzed via Western blotting. With each increase in exercise intensity, there was a concomitant increase in mean body temperature and heart rate, both of which were further increased in the heated condition. A significant increase (p≤0.05) in LC3-II and LC3-II/I protein expression was observed immediately post high-, but not low- or moderate-intensity exercise. Additionally, elevations in LC3-II immediately following high intensity exercise in a hot environment were significantly greater than those in the non-heat stress environment. Taken together, this may indicate a threshold volume of exercise- and heat-induced cellular stress required to stimulate elevations in autophagic activity.