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.
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
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
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