Question

3) In what ways do aerobic training adaptations lead to glucose sparing as well as preferential fat oxidation at sub- maximal workloads? 4) How do acrobic training adaptations lead to faster transition from rest to steady state (less oxygen deficit) as well as less production of lactate? 5) During Aerobic exercise there are increases in intracellular Ca2+, increased AMP/ATP ratio, as well as oxidative stress (free radicals). These are primary signals within the muscle cells. What are the secondary signals that respond to each, and what are the end results from the gene transcription and translation (ie, what training adaptations do these lead to)? 6) During Resistance training mechanical stretch and strairn lead to the accumulation of phosphatidic acid (PA) and allow Rheb to be disinhibited (activated). What do these signals lead to, and what is the end result (adaptation)?

Answer 1

1. In aerobic training, there is maximal use of energy by oxidation of carbohydrates or fats. With continuous exercise, all the Glucose gets utilised but the energy demand doesn't get fulfilled. In this case, body shifts to oxidation of fatty acids because in this case there is production of 108 ATPs in one cycle.

2. In aerobic respiration, there is maximal use of oxygen for more energy production. We know, that in anaerobic respiration, only 2 ATPs are formed which is not sufficient to fulfil energy demands. So, there is less production of lactate and more use of oxygen.

3. Aerobic exercise leads to change in calcium homeostasis. Increase in intracellular Ca ion leads to vesicular transport. AMP level increases which leads to increase in activity of AMP kinase which activates the sensors to sense low fuel state. Ros Accumulation also states that cell is in stress condition.

During aerobic training, following gene expressions are regulated: I) decreased expression of FOXO1.

II) increased expression of CaMK2, CREB1, complex I to V.

III) increase in translation of various regulators like TEAM, NR4A3, CRTC2 etc.

4. Accumulation of phosphatidic acid and hence activation of Rheb leads to unregulated mTOR signalling which is a key regulator of cell metabolism and survival. ( protein synthesis and transcription also)