Respiratory Muscle and Function Decline Of Aging Reversible?

Aging, Pneumonia, Exercise Shortness of Breath and BDNF

This article is relevant to aging, pneumonia, exercise dyspnea and BDNF.

The lifestyle changes that increase BDNF preserves diaphragm innervation and type 2 fibers required for explosive movements such as clearing the airway of secretions or aspiration. One can measure inspiratory and expiratory force, timing of cough to irritants (a proxy for aspiration). Exertional dyspnea correlates with peak inspiratory and expiratory force, inspiratory force/vital capacity ratio and 6 minute walk in COPD patients. (Shortness of breath with exercise improves with measures of strength of lung muscles to breathe in and breathe out, lung inspiratory strength to lung volume or size ratio, and the distance walked in 6 minutes in lung disease patients.)

BDNF likely improves presbyesophagous, epiglottis dysfunction and pharyngoesophageal dysphagia in the aging sarcopenic patient. I.e. Neuromuscular function and integrity. BDNF reverses aging of swallowing in patients losing muscle due to inflamaging. 

The heart and respiratory muscles are crucial to human power production.  Their poor performance is associated with increased IL-6 an inflammatory marker.  In effect poor muscle function of the heart and lungs produces waste or exhausts like a car with a poorly functioning power plant.

Could interventions that increase BDNF increase 6 minute walk times? Reverse loss of respiratory muscle loss and function loss?

Weekly Intermittent fasting?

Resistance breathing training?

Slow paced breathing 2 minutes twice daily?

Antidepressant medications?

4 minute HIIE?

Is the diaphragm/lung or heart/circulatory system the stronger limiting factor for functional performance?  Doesn't BDNF improve both and all?

http://www.sciencedirect.com/science/article/pii/S1569904815300550

Melatonin strengthens bone, Synergy with Vitamins D and K2

Why does Melatonin increase bone strength, cartilage and collagen quality?

Consistent with my recent post about collagen cross linking and osteoporosis is this article showing antioxidants reduce non-enzymatic weak collagen cross linking in connective tissue including bone.

Collagen cross links are trivalent strong or bivalent weaker forms from enzymatic activity;  respectfully (the product of cellular activity requiring ATP) and non-enzymatic from AGP advanced glycosylated products (diabetes and aging) and Reactive Oxygen Species (aging).

Here Melatonin reduces the products that increase weak cross linkages thereby strengthening bone both in the cell and extra cellular matrix.  The quality of bone with strong cross linkages is independent of calcification or mineral content!  Ideally, one with/or at risk of osteoporosis will have both.  I also note that Melatonin is unique in its ability to reduce the rate of neurodegenerative brain changes by reducing activation of the inflamasome or innate cellular immune "autoimmunity."

Also note that Alpha Lipoic acid an antioxidant has also made bone stronger likely through the same mechanism of melatonin.

http://www.omicsgroup.org/journals/an-early-development-budget-impact-model-for-the-use-of-melatonin-in-the-treatment-and-prevention-of-osteoporosi-2167-065X-1000132.pdf

Vitamin D3 K2 Synergy Reduces Aging in Collagen-Cross Lnking?

How does Vitamin K2 improve cartilage, bone and reduce fractures?  

Conjecture: Vitamin K2 and Vitamin D synergy reduces Collagen Cross-Links through 2 mechanisms;  

1. increased energy production during connective tissue use, and 

2. improved structure, architecture and calcification  during bone formation.

Vitamin K2 can substitute for coenzyme Q10 in the electron transport system in mitochondrial energy production.  Vitamin K2 is also the essential cofactor for matrix gla protein which removes calcium deposits from soft tissue to sequester calcium in bone and other vitamin k dependent proteins that produce healthy cartilage and well formed matrix for bone trabecular formation.

In this article below, age related collagen cross linkages affect bone quality independent of bone density.  

Vitamin K2 potentially reduces collagen cross linkages by providing more ATP energy, more antioxidant activity during the bone formation interval AND also makes well formed bone forming matrix and delays calcification until well formed even in the presence of hypomagnesemia which is notorious for premature calcification and poor quality bone. One may remember that magnesium is required for each Mg-ATP energy molecule.  Without energy from Mg-ATP to ACTIVELY form bone INACTIVE calcification occurs even of soft tissue or poorly formed bone matrix. 

The Bone constantly remodels and is effectively replaced every 7 years.

If during this seven year cycle of bone turn over and replacement vitamin k2 and vitamin D3 levels (which promotes vitamin k2 dependent proteins production) are normal or sufficient, one could form better quality bone and higher bone density thereby reducing fragility and fracture risk.  

It might also allow regeneration of better quality bone cartilage interface and better cartilage during that interval.

How does these functions of K2 relate to my DrLiverman.blogspot.com about BDNF increasing improving metabolic health of body brain function reciprocity?  In case I lost you, performing body and brain functions at their limits of low energy supply or high energy demand is the stimulus to increase BDNF (brain derived neurotrophic factor) allowing the individual to optimum energy production via somatic fat burning and cerebral glucose and beta hydroxybutyrate burning.  

Energy can be further amplified in every cell and all cells by higher BDNF levels from a metabolic healthy lifestyle of intermittent fasting, slow paced breathing, lactate producing high intensity interval exercise, resistance training or Prolonged steady state endurance exercise, BrainHQ sub cortical brain speed training that increases BDNF, increases synapticity or nerve connections allowing sensory imputs to parallel process and perceive and encode faster into the CPU or hippocampus while simultaneously increasing synapticity or nerve network capacity and storage down from the cortex processing neurons focused by attentional states.  

A maintained faster brain body is the end result of metabolic Heath.  In effect metabolic health speeds up the network of sensory imputs to the CPU of the brain and memory and meaning storage imputs gated by ATTENTION from the CPU.  Attentional states are convergent or divergent or some combination of both at all times.  Highly educated brain networks appear, to me, to expand convergent networks into more divergent metaphorical, virtual and multiple meanings for each convergent symbol.  E.g.  In the hippocampal processing interval that the slow learner processes three real symbols, ball flag and tree, the medium fast learner can also process a golf ball on a green with a flag in the hole and a green side tree, and the fast learner can also process a virtual tree with flags replacing leaves and balls replacing seeds falling from the tree!  For expansion on this discussion of the brain as an organ for improvement and the model of top down bottom up see my Livermanlearnngtolearn.blogspot.com and start at the beginning with increasing bandwidth.

http://link.springer.com/chapter/10.1007/978-4-431-55778-4_3

Collagen Cross-Links as a Determinant of Bone Quality

Aging, Disconnection Syndrome and Brain Network Weakening for Lack of BDNF

Here is the concept of disconnection syndrome related to aging and directly proportional to peripheral BDNF.  I recently blogged that decreased BDNF first resulted in loss of connections or synapticity first, neuron function second and neuron integrity last.

Peripheral levels of BDNF directly correlate to network or synaptic connectivity .

Raise peripheral BDNF levels and preserve motor function by preserving nerve connections or brain synapticity or network health first, neuron health second and neuron integrity last.

This study uses fMRI to show the direct correlation of BDNF and Connectivity.

Babies walk slowly and with poor balance.

Elders walk slowly and with declining balance.

Both are respectfully due to immature networks with high BDNF and mature networks with low BDNF.

Babies gain and elders lose network connectivity in relation to BDNF and synapticity or  brain network connection strength.

Would elders reduce falls and increase their timed walking distance with cognitive brain speed training?  This has been confirmed as superior to leg strengthening and gait training, the usual recommended treatment to prevent falls.

What if the goal was redirected to maximize BDNF?  

BDNF is a bio marker that directly correlates to "connectivity" and function should follow the peripheral level of BDNF  and the restoration of brain body learning as in post stroke motor rehabilitation.

http://www.sciencedirect.com/science/article/pii/S0197458015005552

Serum BDNF correlates with connectivity in the (pre)motor hub in the aging human brain—a resting-state fMRI pilot study