We hypothesize that the V˙O2 time constant (τV˙O2) determines exercise tolerance by defining the power output associated with a "critical threshold" of intramuscular metabolite accumulation (e.g., inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V˙O2 "slow component" and its consequences (increased pulmonary, circulatory, and neuromuscular demands) determine performance limits.
The age-related decline in muscle function is aggravated by a high-fat diet (HFD)-induced increase in fat mass. The hypothesis is that an HFD leads to a faster accumulation of intramyocellular lipids (IMCL) and an earlier onset of muscle dysfunction in old than in young-adult individuals. The IMCL accumulation is attenuated in young-adult organisms by an elevated oxidative capacity. Methionine restriction enhances mitochondrial biogenesis and is promising to combat obesity across the ages.
This review explores the hypothesis that the repetitive contraction-relaxation that occurs during chronic exercise activates skeletal myocyte nuclear factor erythroid-derived 2-like 2 (Nrf2) to upregulate antioxidant enzymes. These proteins are secreted into the circulation within extracellular vesicles and taken up by remote cells, thus providing remote organs with cytoprotection against subsequent oxidative stress.
Patients with diabetes display heightened blood pressure response to exercise, but the underlying mechanism remains to be elucidated. There is no direct evidence that insulin resistance (hyperinsulinemia or hyperglycemia) impacts neural cardiovascular control during exercise. We propose a novel paradigm in which hyperinsulinemia or hyperglycemia significantly influences neural regulatory pathways controlling the circulation during exercise in diabetes.
Adipose tissue and arterial dysfunction are common in the obese state. Perivascular adipose tissue (PVAT) plays an important role in mediating arterial health, and with obesity, the PVAT dysfunction negatively affects arterial health. Exercise training exerts direct and beneficial effects on PVAT, providing an additional and novel pathway by which exercise can improve arterial health in diseased populations.
Although several methods have been used to estimate exercise-induced changes in human neuronal networks, there are growing doubts about the methodologies used. This review describes a single motor unit-based method that minimizes the errors inherent in classical methods. With this method, it is now possible to identify human neuronal networks' changes due to exercise.
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