EHS 385 Lecture Notes - Lecture 13: Tachycardia, Cellular Respiration, Oxidative Phosphorylation

• School: UMass Boston
• Department: Exercise and Health Science
• Course: EHS 385
• Professor: Rachel Drew

Document Summary

O2 consumption = measure of aerobic metabolism. Resting o2 consumption: 0. 24 l/min or 3. 5 ml/kg/min (measured from indirect calorimetry) Atp production/o2 uptake increases immediately: steady state 1-4 mins, after atp requirement met through aerobic atp production. Oxygen deficit: period when o2 uptake below necessary to supply atp aerobically, lag in o2 uptake at beginning of exercise. Atp production initially through anaerobic pathway (atp-pc system and glycolysis) O2 uptake = direct indicator of energy supplied by aerobic pathway of oxidative phosphorylation. Trained have lower o2 deficit: better aerobic bioenergetic capacity from cellular adaptations from training, cardiovascular/muscular adaptions, rapid increase cardiac output, larger percentage of blood direct to muscle, reach steady state faster (smaller o2 deficit, less production lactate/h+ Lag in oxygen consumption at start of exercise. O2 uptake elevated above resting level during recovery from exercise. Hill: repayment for o2 deficit at onset of exercise.