ELN and endothelial dysfunction: We openly acknowledge that the actual cellular/molecular mechanisms driving acute and training responses to exercise may differ from those contributing to physiological changes with aging/age-related chronic disease (e.g., exercise and the cardiovascular demands required to meet metabolic output for musculoskeletal movement are fundamentally different mechanisms than those governing increases in blood pressure with aging such as degradation of elastin, microvascular rarefaction, endothelial dysfunction etc.).