There are a number of supposed mechanisms whereby T2 is believed to
increase mitochondrial energy production rates, resulting in increased ATP levels.
These include an increased influx of Ca++ into the mitochondria, with a resulting
increase in mitochondrial dehydrogenases. This leads to an increase in reduced
substrates available for oxidation. Also if there is an increase in cytochrome oxidase
activity this would hastens the reduction of O2, speeding up respiration. Scientists
looking for the mechanism of increased ATP production in kundalini might like
to consider the influence of T2.
HYPertHYroiDism
catabolic—During fasting or when carbohydrate intake is reduced the conversion
of T4 to the physiologically active T3 is reduced in order to lower the basal metabolic
rate to preserve fat and muscle. Long-term hyperthyroidism with excessive T3
production is catabolic to bone as well as muscle.
overworked heart—The increased work of the heart puts the greatest single
demand on ATP usage, with increased heart rate and force of contraction
accounting for up to 30% to 40% of ATP usage in hyperthyroidism.
increased oxidative energy metabolism—T3 and T2 increase the flux of
nutrients into the mitochondria as well as the rate at which they are oxidized,
by increasing the activities of the enzymes involved in the oxidative metabolic
pathway. The increased rate of oxidation is reflected by an increase in oxygen
consumption by the body.
Hyperthyroidism increases ATP production and thereby increases metabolic activity in
the following ways:
increased na+/K+atPase: This is the enzyme responsible for controlling the Na/
K pump, which regulates the relative intracellular and extracellular concentrations
of these ions, maintaining the normal transmembrane ion gradient. It has estimated
this effect may account for up to 10% of the increased ATP usage.
increased ca++-dependent atPase: The intracellular concentration of calcium
must be kept lower than that outside the cell to maintain normal cellular function.
ATP is required to pump out excess calcium. It has been estimated that 10% of a
cell’s energy expenditure is used just to maintain Ca++ homeostasis.
Futile cycling: Hyperthyroidism induces a futile cycle of lipogenesis/lipolysis in
fat cells. The stored triglycerides are broken down into free fatty acids and glycerol,
then reformed back into triglycerides again. This is an energy dependent process
that utilizes some of the excess ATP produced in the hyperthyroid state. Futile
cycling has been estimated to use approximately 15% of the excess ATP created
during hyperthyroidism.
Heat Production: T3, has the ability to uncouple oxidation of substrates from
ATP production. Resulting in reduced ATP production and an astounding
production of heat. Such uncoupling occurs in skeletal muscle, contributing to