Effect of 6-Week Sprint Training on Long-Distance Running Performance in Highly Trained Runners.

PURPOSE: Long-distance running performance has been reported to be associated with sprint performance in highly trained distance runners. Therefore, we hypothesized that sprint training could enhance distance running and sprint performance in long-distance runners. This study examined the effect of 6-week sprint training on long-distance running and sprint performance in highly trained distance runners. METHODS: Nineteen college runners were divided into control (n = 8) and training (n = 11) groups. Participants in the training group performed 12 sprint training sessions in 6 weeks, while those in the control group performed 12 distance training sessions. Before and after the interventions, maximal oxygen uptake (V˙O2max), O2 cost during submaximal running (290 m·min-1 and 310 m·min-1 of running velocity), and time to exhaustion (starting at 290 m·min-1 and increased 10 m·min-1 every minute) were assessed on a treadmill. Additionally, the 100-m and 400-m sprinting times and 3000-m running time were determined on an all-weather track. RESULTS: In the control group, no measurements significantly changed after the intervention. In the training group, the time to exhaustion, 100-m and 400-m sprinting times, and 3000-m running time improved significantly, while V˙O2max and O2 cost did not change. CONCLUSIONS: These results showed that 6-week sprint training improved both sprint and long-distance running performance in highly trained distance runners without a change in aerobic capacity. Improvement in the time to exhaustion without a change in V˙O2max suggests that the enhancement of long-distance running performance could be attributable to improved anaerobic capacity.

Interferon regulatory factor 7 mediates obesity-associated MCP-1 transcription.

Hypertrophy, associated with adipocyte dysfunction, causes increased pro-inflammatory adipokine, and abnormal glucose and lipid metabolism, leading to insulin resistance and obesity-related-health problems. By combining DNA microarray and genomic data analyses to predict DNA binding motifs, we identified the transcription factor Interferon Regulatory Factor 7 (IRF7) as a possible regulator of genes related to adipocyte hypertrophy. To investigate the role of IRF7 in adipocytes, we examined gene expression patterns in 3T3-L1 cells infected with a retrovirus carrying the IRF7 gene and found that enforced IRF7 expression induced the expression of monocyte chemoattractant protein-1 (MCP-1), a key initial adipokine in the chronic inflammation of obesity. CRISPR/Cas9 mediated-suppression of IRF7 significantly reduced MCP-1 mRNA. Luciferase assays, chromatin immunoprecipitation PCR analysis and gel shift assay showed that IRF7 transactivates the MCP-1 gene by binding to its proximal Interferon Stimulation Response Element (ISRE), a putative IRF7 binding motif. IRF7 knockout mice exhibited lower expression of MCP-1 in epidydimal white adipose tissue under high-fat feeding conditions, suggesting the transcription factor is physiologically important for inducing MCP-1. Taken together, our results suggest that IRF7 transactivates MCP-1 mRNA in adipocytes, and it may be involved in the adipose tissue inflammation associated with obesity.