This one suggests that the neuromuscular mechanisms of exercise-induced muscle fatigue are predominantly central (i.e., neural) factors.
- Healthy and physically active men performed two intermittent isometric handgrip exercise protocols to failure, 72 hours apart, combined with either blood flow restriction or without.
- Electromechanical delay, the rate of force development and time to peak force were used to investigate whether the source of performance decline in those exercise protocols performed to failure was central or peripheral.
In plain english, central is the brain and spinal cord, therefore the capacity of the central nervous system to activate muscles, while peripheral is about processes distal to the neuromuscular junction, therefore we're talking about impaired muscle function per se.
Electromechanical delay corresponds to the time lag between the beginning of muscle electrical activity and the beginning of muscle force production.
The rate of force development is how fast an individual can develop force.
Time to peak force is the elapsed time between the beginning of force production and the maximum force obtained during a resisted muscle contraction.
- Impairments in muscle performance (peak force and rate of force development), with no difference between conditions was observed.
- Electromechanical delay was not altered after exercise in either condition.
- On the contrary, time to peak force increased, but only after exercise without blood flow restriction.
- Taken together, these findings suggest the predominance of fatigue-related central (i.e., neural) factors, in the applied exercise protocol, at least.
Effects of Blood Flow Restricted Exercise on Electromechanical Delay and Time to Peak Force after Task Failure: A Randomized Crossover Trial (open access)
This one in individuals at clinical high-risk for psychosis suggests that the beneficial impact of omega-3 PUFAs on clinical symptoms in psychosis is mediated, at least in part, through the complement and coagulation pathway proteins.
- The complement system is a network of proteins that play an important role in host defense and inflammation.
- The coagulation system, you guessed it, is the good ol' system that is made up of blood cells and proteins, responsible for creating blood clots to allow for rapid healing and prevention of excessive bleeding.
Here, 4000 IU/day vitamin D supplementation in older adults aged 50–80 years with overweight or obesity and vitamin D deficiency had no effect on gait speed either with or without exercise, but combined with exercise, it was more likely to result in decreased waist circumference.
- Further, Vitamin D supplementation taken alone also reduced stair climb times, an effect not observed in combination with exercise, but had no beneficial effects on any other biochemical, body composition or physical function parameters.
- Finally, vitamin D supplementation increased muscle density during exercise, but only in men and "however, this finding should be interpreted with caution given the low numbers in our subgroups".
Here, physically inactive primary care patients aged between 19 and 80 years living in Spain, were more likely to have a reduced risk of mortality by increasing their physical activity, even in doses below the recommended levels.
- Physical activity levels in this inactive population of primary care patients translated into risk reductions in mortality.
- These benefits followed a clear dose–response relationship, in which mortality started to fall even with only small increases in physical activity.
In this one in mice, branched-chain amino acid (BCAA) ingestion suppressed chronic detraining-induced reductions of skeletal muscle mitochondrial content.
- The BCAA dose was 0.6 mg/g of body weight twice daily for 2 mouse weeks of detraining, which translates roughly into ~50 mg/kg of body weight for 560 human days of detraining.
- BCAA supplementation suppressed the reduction of mitochondrial enzyme activities and protein content in skeletal muscle.
In this one, Lawrence Mandarino and colleagues clearly show that fuel choice during mild exercise is unaffected by insulin resistance, doing away with the notion that insulin resistant muscle may use and sometimes prefer lipid oxidation.
- There is evidence that resting, insulin-resistant skeletal muscle prefers to oxidize carbohydrate. This contrasts with a preference for lipid oxidation in skeletal muscle from active, fit, healthy individuals.
- This preference for carbohydrate in resting muscle has been proposed to be responsible for insulin resistance in skeletal muscle, at least in part.
In this one in mice, branched-chain amino acid (BCAA) ingestion suppressed chronic detraining-induced reductions of skeletal muscle mitochondrial content.
- The BCAA dose was 0.6 mg/g of body weight twice daily for 2 mouse weeks of detraining, which translates roughly into ~50 mg/kg of body weight for 560 human days of detraining.
- BCAA supplementation suppressed the reduction of mitochondrial enzyme activities and protein content in skeletal muscle.