In this one, swedish men that had high fitness at ∼18 years of age (early adulthood) had a lower prevalence of atherosclerotic plaques 40 years later (later adulthood), independent of muscle strength.
- This cohort study that followed men for approximately 40 years from early adulthood, found that exercise capacity at early adulthood was consistently associated with lower prevalence of carotid plaques at later adulthood independent of muscle strength.
- This beneficial association of exercise capacity on the presence of plaques was mediated through the combination of later, but not early, adulthood CVD risk factors.
The protective association between higher exercise capacity and presence of plaques in this study, was mediated by later adulthood BMI, systolic blood pressure, glucose tolerance status, non-HDL cholesterol and triglycerides.
- However, the associations of exercise capacity with and muscle strength with measures of subclinical atherosclerosis were inconsistent.
- Finally, no association between muscle strength and the presence of plaques was observed.
These findings may suggest that exercise capacity at early adulthood may have some beneficial effects on atherosclerosis, but they are not as important as traditional risk factors.
Early adulthood exercise capacity, but not muscle strength, associates with subclinical atherosclerosis 40 years later in Swedish men (open access)
The findings of this one support the hypothesis of a compensatory upregulation of autophagy in the setting of deterioration of tissue composition and muscle dysfunction, as seen in ageing.
- "In contrast to what has been observed in preclinical models... in our study, the protein content of the lysosomal mediators TFEB, vATPase, and LAMP1 was not different between age groups".
- "Therefore, upregulation of upstream autophagy and mitophagy proteins in muscle of older adults not accompanied by increased expression of lysosomal markers may indicate greater autophagic signaling with no actual disposal of damaged mitochondria."
The findings of this one may suggest that as physical activity energy expenditure decreases, the importance of nutrition and body fat and their impact on blood lipids concentration increases.
- The present study aimed to examine whether nutrition, body composition and physical activity energy expenditure have diverse impact on lipidemic blood profiles among young female Caucasian females (~ 20 years of age) with different blood cholesterol concentrations.
- Participants were categorized into three groups according to the newest guidelines for blood Cholesterol concentrations:
In this one, breaking up prolonged sitting with regular bouts of light intensity physical activity was associated with reductions in glucose and blood pressure in middle- and older-aged adults.
- Only sedentary breaks that were high in frequency and duration (every 30 min for 5 min) yielded statistically significant reductions in glucose relative to a control condition.
Low frequency (every 60 min) did not yield such reductions in glucose.
Here, prolonged β2-agonist treatment at a somewhat moderate dose was associated with improvements in insulin sensitivity, plasma triglyceride concentrations, plasma amino acid concentrations, arterial blood flow velocity and increases in basal and sleeping metabolic rate.
- A two-week treatment with the selective β2-AR agonist clenbuterol enhances insulin sensitivity, mainly via increased insulin-stimulated non-oxidative glucose disposal in healthy young males.
- These beneficial effects were accompanied by increases in sleeping metabolic rate, improvements in plasma triglyceride concentrations, reductions in plasma amino acid concentrations, and increases in arterial blood flow velocity.
The findings of this one suggest that BDNF responses to low-intensity endurance exercise are mediated by increased circulating platelets, and increasing exercise duration, and to a greater extent, intensity, is required to liberate free, unbound BDNF in circulation.
- Intermittent fasting and exercise provide neuroprotection from age-related cognitive decline.
- A link between these two seemingly distinct stressors is their capability to steer the brain away from exclusively glucose metabolism.