Increase Mitochondrial Mass for a Hotter, Healthier Metabolic Rate

Walking is a vagal tone relaxing endeavor that does not increase mitochondrial mass.

Mitochondrial mass is higher in professional athletes than moderately activated amateurs.

Why this is important?

Lower mitochondrial mass persons with activity reach their lactate threshold earlier in exercise.  

Lactate inhibits fat burning relative to carbohydrate metabolism.

The goal is to burn more fat per day or fat per time whether one is resting (basal metabolic rate) or exercising (activity metabolic rate maximum.)

In effect, more mitochondria raises both metabolic rates and eliminates STORED ENERGY FAT and a high fat western diet fat content.

Higher metabolism, higher fat burning, lower BMI AT THE SAME LIFESTYLE.

One makes more antioxidant enzymes or bullets whenever one is burning fat.

Mitochondrial biogenesis is increased relatively by the following.

Exercise where high intensity interval exercise is better than steady state exercise.

Diet where Mediterranean diet food supplements INCREASE ANTIOXIDANT ENZYMES, because they are like "young cells" which make more antioxidant enzymes because they contain more chemical signals that produce them.

(Antioxidant enzymes are directly related to mitochondrial biogenesis.)

Heat as in sauna, climate, hot tubs and exercise which activate heat shock proteins which are directly related to mitochondria and is an exercise mimetic.

Thinner persons have higher mitochondrial mass and or better lower lactate producing diets (Carbohydrate).

HIIE increases mitochondrial mass 14% and jogging 60 minutes aerobically 9% and walking 0 to less.

Are women "hotter" before or after sauna, Mediterranean diet and high intensity exercise?

I know they are "healthier" and with intermittent fasting able to maintain high metabolic rate and burn faster excessive fat stores.

The above discussion is also relevant to the single cell and cell biology.

Exercise related lactate threshold, like aerobic exercise testing, indicates ability to burn fats and not produce lactate from carbohydrates.

Metabolic rates directly correlate to aerobic fitness and mitochondrial mass.

Paradoxically lactate also signals the muscles to increase mitochondrial mass.  This occurs because 30% of lactate produced by type 2 muscle fibers engaged in high intensity exercise is converted into pyruvate and acetylCoA which signals mitochondrial biogenesis.

https://link.springer.com/article/10.1007/s40279-017-0751-x

Assessment of Metabolic Flexibility by Means of Measuring Blood Lactate, Fat, and Carbohydrate Oxidation Responses to Exercise in Professional Endurance Athletes and Less-Fit Individuals

February 2018

Abstract

Background

Increased muscle mitochondrial mass is characteristic of elite professional endurance athletes (PAs), whereas increased blood lactate levels (lactatemia) at the same absolute submaximal exercise intensities and decreased mitochondrial oxidative capacity are characteristics of individuals with low aerobic power. In contrast to PAs, patients with metabolic syndrome (MtS) are characterized by a decreased capacity to oxidize lipids and by early transition from fat to carbohydrate oxidation (FATox/CHOox), as well as elevated blood lactate concentration [La⁻] as exercise power output (PO) increases, a condition termed ‘metabolic inflexibility’.

Objective

The aim of this study was to assess metabolic flexibility across populations with different metabolic characteristics.

Methods

We used indirect calorimetry and [La⁻] measurements to study the metabolic responses to exercise in PAs, moderately active individuals (MAs), and MtS individuals.

Results

FATox was significantly higher in PAs than MAs and patients with MtS (p < 0.01), while [La⁻] was significantly lower in PAs compared with MAs and patients with MtS. FATox and [La⁻] were inversely correlated in all three groups (PA: r = −0.97, p < 0.01; MA: r = −0.98, p < 0.01; MtS: r = −0.92, p < 0.01). The correlation between FATox and [La⁻] for all data points corresponding to all populations studied was r = −0.76 (p < 0.01).

Conclusions

Blood lactate accumulation is negatively correlated with FATox and positively correlated with CHOox during exercise across populations with widely ranging metabolic capabilities. Because both lactate and fatty acids are mitochondrial substrates, we believe that measurements of [La⁻] and FATox rate during exercise provide an indirect method to assess metabolic flexibility and oxidative capacity across individuals of widely different metabolic capabilities

Preventing and Reversing Aging 1,2,3

Is anything more quintessential of aging as sensory loss of hearing (and vision?)

Here age related decline in Nrf2 expression (lack of bullets) leads to cortical auditory degeneration.

Step 1.  More  antioxidant enzyme bullets.  Step 2.  Increase Vagal tone, calm down microglia.  Step 3.  BrainHQ.com to increase BDNF  and rebuild a parallel processing auditory cortex.

This is something I literally did in a study N of 1.

This statistically valid research of step 3 alone produces a 135% increase in auditory processing speed and 230% increase in visual processing speed.  

Why is the processing speed so important?. The sharp  area of central focal vision is small, like a flashlight beam, that uses scanning and processing to see the bigger picture.  PROCESSING, important for seeing, hearing, comprehending and remembering.  Auditory sampling speed determines processing speed and accuracy.

Bullets, Vagal tone and BDNF build.   Age related Epigenetic switching off of Nrf2, alpha 7 Nicotinic acetylcholine receptors and BDNF CpG gene promoter sites is directly correlated to aging and disease in cells, tissues, organs and people.

https://europepmc.org/abstract/med/30272261

Age-associated decline in Nrf2 signaling and associated mtDNA damage may be involved in the degeneration of the auditory cortex: Implications for central presbycusis.

Europe PMC

Central presbycusis is the most common sensory disorder in the elderly population, however, the underlying molecular mechanism remains unclear. NF‑E2‑related factor 2 (Nrf2) is a key transcription factor in the cellular response to oxidative stress, however, the role of Nrf2 in central presbycusis remains to be elucidated. The aim of the present study was to investigate the pathogenesis of central presbycusis using a mimetic aging model induced by D‑galactose (D‑gal) in vivo and in vitro. The degeneration of the cell was determined with transmission electron microscopy, terminal deoxynucleotidyl transferase‑mediated deoxyuridine 5'‑triphosphate nick‑end labeling staining, and senescence‑associated β‑galactosidase staining. The expression of protein was detected by western blotting and immunofluorescence. The quantification of the mitochondrial DNA (mtDNA) 4,834‑base pair (bp) deletion and mRNA was detected by TaqMan quantitative polymerase chain reaction (qPCR) and reverse transcription‑qPCR respectively. Cell apoptosis and intracellular ROS in vitro were determined with flow cytometry. The levels of nuclear Nrf2, and the mRNA levels of Nrf2‑regulated antioxidant genes, were downregulated in the auditory cortex of aging rats, which was accompanied by an increase in 8‑hydroxy‑2'‑deoxyguanosine formation, an accumulation of mtDNA 4,834‑bp deletion, and neuron degeneration. In addition, oltipraz, a typical Nrf2 activator, was found to protect cells against D‑gal‑induced mtDNA damage and mitochondrial dysfunction by activating Nrf2 target genes in vitro. It was also observed that activating Nrf2 with oltipraz inhibited cell apoptosis and delayed senescence. Taken together, the data of the present study suggested that the age‑associated decline in Nrf2 signaling activity and the associated mtDNA damage in the auditory cortex may be implicated in the degeneration of the auditory cortex. Therefore, the restoration of Nrf2 signaling activity may represent a potential therapeutic strategy for central presbycusis.

Joseph Thomas (Tony) Liverma