News & Views from the Editor-in-Chief - L. Bruce Gladden
I am drawing attention to three unique papers in this month's journal. First, Farber and colleagues examined the effects of diet-induced obesity and/or exercise training on cancer incidence and health span in a mouse model of radiation-induced cancer. Their results showed that diet-induced obesity increased long-term cancer incidence and reduced overall health span as determined from measures of physical performance, metabolic health, and anxiety/depression in irradiated mice. Intriguingly, life-long exercise training reduced cancer incidence and improved health span in irradiated lean mice. Further, life-long exercise training in diet-induced obese mice restored cancer incidence and health span to levels observed in sedentary, lean mice following radiation exposure. For the approximately 18 million cancer survivors in North America, these results provide important preclinical evidence that modifiable host factors, such as diet-induced obesity, and participation in exercise training modify cancer incidence and other key metrics related to long-term health.
On a different topic, Nagelkirk and coworkers examined the effects of an 8-week resistance training program on thrombotic potential. Participants performed moderate intensity weight-lifting exercises (60%–80% of one repetition maximum) that targeted all major muscle groups 3 days per week. Plasma concentration of pro-thrombotic proteins like fibrinogen and coagulation factors VII and VIII were not affected by training. However, fibrinolytic activity, the process of dissolving blood clots, was significantly higher after the 8-week regimen. Markers of fibrinolytic potential are independently associated with CVD, risk of heart attack, stroke, and a host of other thrombotic complications. Thus, this study suggests that regular resistance exercise may reduce risk of thrombotic and cardiovascular diseases, and their associated sequelae. This is one of the first longitudinal studies to explore adaptations in thrombotic potential after regular resistance training.
Finally, in a unique case study, Marchant et al. investigated the effects of an extreme bout of exercise (pace-matched 100-km run) on skeletal muscle mitochondrial function in a pair of genetically identical twins. The twins were also extremely well-matched in physical fitness (V̇O2max), body composition, and training load. Furthermore, calorie and macronutrient intake were matched during training, and the 100-km run, except for 2 days per week in which one twin consumed a calorie-matched, glycogen-depleting diet, while the other maintained a high-carbohydrate diet. The most novel finding was that mitochondrial proteins and function were reduced post-run, regardless of diet. Following 2 days of recovery, nearly all measures of mitochondrial function and content recovered. These results suggest that the mitochondria in trained muscle have an immense capacity to recover following damaging ultra-endurance activity.
L. Bruce Gladden
School of Kinesiology