News & Views from the Editor-in-Chief - L. Bruce Gladden
My attention is drawn to several articles in this month's issue, but as usual, I am highlighting three of them. First, cancer patient fatigue contributes to loss of functional independence and reduced life quality. Therapy development to combat this fatigue requires an improved mechanistic understanding of the skeletal muscle alterations and functional deficits linked to this condition. VanderVeen et al. examined the effects of increased physical activity on the functional decrements occurring during the initiation and progression of cachexia (detrimental, unintentional body weight, and muscle loss) using a preclinical mouse model of intestinal tumor development. Before and during cachexia initiation, these tumor-bearing mice exhibited decreased daily activity in the cage accompanied by muscular fatigue and reduced mitochondrial content. However, volitional wheel-running activity improved treadmill run time to exhaustion, grip strength, and direct muscle function measurements. These results align with a growing body of research suggesting that maintaining physical activity levels following a cancer diagnosis is vital for maintaining muscle function in cancer patients.
Second, Fulton et al. investigated the impact of sensory feedback from the respiratory system on exercise performance by inducing respiratory muscle fatigue prior to a self-paced cycling time trial. Importantly, power output during the time trial was free to vary thus allowing for examination of self-regulation of exercise performance. They found that preexisting respiratory muscle fatigue altered perceptions of breathing effort during exercise and caused a reduction in power output that impaired overall exercise performance. Furthermore, the reduction in power output coincided with less locomotor muscle fatigue. Together, these findings indicate that the respiratory system is an integral component in a global sensory feedback loop that regulates exercise performance and the development of locomotor muscle fatigue.
Third, Vellers et al. have established a pipeline of laboratory techniques and bioinformatic methods that enables complete and accurate assessment of the mitochondrial genome. These methods also provide the means to assess mitochondrial DNA (mtDNA) heteroplasmy or change in sequence variants across mtDNA copies. For the current investigation, they implemented the pipeline to determine the contribution of the mitochondrial genome to aerobic capacity trainability. They found that the mtDNA haplogroup known as J1c (defined by a similar set of mtDNA variants), was associated with individuals who were categorized by low aerobic exercise trainability. They also found 13 mtDNA sequence variants that occurred more frequently in low- versus high-responders. These results suggest that the mitochondrial genome may have important implications for exercise trainability.
L. Bruce Gladden
School of Kinesiology