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.
- This cerebral substrate switch has been implicated in upregulating brain-derived neurotrophic factor (BDNF), a protein involved in neuroplasticity, learning and memory, and may underlie some of these neuroprotective effects.
- Switching the brain’s fuel source from glucose to either ketone bodies or lactate, i.e. a cerebral substrate switch, has been shown to promote BDNF production in the rodent brain.
- This study investigated how circulating BDNF is affected by: (1) fasting for 20 h, (2) light, prolonged exercise, (3) short duration, high-intensity interval exercise, and (4) combined fasting and exercise.
- Despite a shift in energy substrate delivery to the brain, fasting for 20 hours did not affect peripheral circulating BDNF at rest, or BDNF responses to exercise.
Note that fasting for 20 hours reduced circulating glucose by 0.7 mmol/l, insulin by 110 pmol/l and increased βHB by 0.5 mmol/l.
- Increases in circulating BDNF within 30 minutes of beginning light exercise were due exclusively to exercise-mediated increased platelet concentration, which itself appeared to be accounted for by plasma volume contraction.
- Prolonged (90 minute) light cycling exercise was sufficient to increase plasma-derived BDNF, which represents an unbound, bioavailable source of BDNF independent of elevated platelet concentration.
- 6 minutes of high-intensity cycling intervals increased every metric of BDNF by 4- to 5-fold more than prolonged exercise did.
- There was no relationship between cerebral shear stress and BDNF release during exercise or in the isolated, larger-magnitude shear-altering interventions.
Altogether, these data may suggest that BDNF responses to exercise are mediated by increased circulating platelets, and either increasing exercise duration or particularly exercise intensity are required to liberate free, bioavailable BDNF...
...while fasting for days, plural, may be required to increase BDNF.
Fasting for 20 h does not affect exercise-induced increases in circulating BDNF in humans…

#exercise #fitness #fit #FitFam #FitLife #FitnessAddict #Workout #TrainHard #GymLife #GymTime #muscle #strength #lift #GetStrong #cardio #hiit

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More from @nick_krontiris

Jan 15
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."
Read 4 tweets
Jan 15
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:
Read 18 tweets
Jan 15
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.
Read 8 tweets
Jan 15
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.
Read 7 tweets
Jan 14
This a great review from George Brooks that examines the various roles of lactate as a myokine and exerkine.
A few nice excerpts from the conclusion:
- "Certainly, lactate is not the only myokine of exerkine, but lactate has important signaling functions to be considered...
Read 8 tweets
Jan 14
The findings of this one may suggest that, in the context of a ketogenic diet, the two major sources of cardiovascular risk stemming from aldosterone elevations (hypertension and inflammation) are inhibited, potentially due to elevated chronic βOHB concentrations.
- The renin-angiotensin-aldosterone system (RAAS) is a central regulator of cardiac output, blood pressure, sodium, and potassium homeostasis.
- Aldosterone, the end effector of the RAAS, activates mineralocorticoid receptors causing cardiac inflammation and fibrosis as well as the remodeling of arteries, veins, and capillaries.
Read 15 tweets

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