Alterations in the oxygen deficit‐oxygen debt relationships with beta‐adrenergic receptor blockade in man.

Abstract

SUMMARY1. The effects of fi-adrenergic receptor blockade (100 mg oral metoprolol) or matched placebo on gas exchange kinetics were studied in six males. Ventilation and gas exchange were monitored in four transitions for each treatment from loadless pedalling (0 W) to a selected work rate (100 W) and back to 0 W. Breath-by-breath data were averaged for analysis.2. Oxygen uptake (Po.) kinetics were significantly slowed at the onset of exercise and recovery by fl-blockade. This resulted in larger oxygen deficit and oxygen debt (671 + 115, 586 ± 87 ml 02, respectively) for fl-blockade than for placebo (497 ± 87, 474+104 ml 02). In addition, oxygen deficit was significantly larger than oxygen debt during fl-blockade tests. These results can be explained by greater utilization of oxygen and creatine phosphate stores as well as anaerobic glycolysis at the onset of 100 W exercise with f-blockade.3. Carbon dioxide output ( rco,) kinetics were significantly slowed by fl-blockade only at the onset of exercise.4. Expired ventilation (VE) kinetics were not affected by f-blockade. At 0 W, )'E was significantly reduced by fl-blockade. Heart rate was lower at all times with fl-blockade. Kinetics of heart rate were not affected.5. These data for Po, kinetics at the start and end of exercise indicate that even in moderate-intensity exercise, lactic acid production can contribute significantly to energy supply. The use ofthe term 'alactic' to describe the deficit and debt associated with this exercise is not appropriate.

Effects of Age and Long-Term Endurance Training on V·O2 Kinetics

“…Beta-adrenergic receptor blockade slowed VO 2 kinetics in MOD by reducing heart rate and subsequently O 2 transport (Hughson, 1984). Several research groups have also slowed VO 2 kinetics with hypoxia (lower fraction of inspired O 2 (FiO 2 ) and thus reducing arterial partial pressure of oxygen (PaO 2 )) across varying work rates (DeLorey et al, 2004c;Hughson & Kowalchuk, 1995;Springer et al, 1991).…”

Oxygen Uptake Kinetics During Exercise

“…The authors suggested that the slower heart rate kinetics during work-to-work transition may be due to a reduced influence of parasympathetic neural activity on the control of heart rate at the onset of exercise. Furthermore, Hughson and his colleagues [48,49] found that V . O 2 kinetics during exercise were slowed by administration of β-blockers in healthy participants.…”

Biochemical Background of the VO2 On-Kinetics in Skeletal Muscles

“…The discussed findings indicate that the rate of oxygen uptake at the onset of exercise may be affected by the interventions contributing to oxygen delivery to the working muscles (especially at high-power output exercise) [37,38,40] and the factors affecting the rate of muscle metabolism [41][42][43][44]16].…”

“…An administration of β-adrenergic blockade slows down the O 2 on-kinetics in humans [41], whereas an administration of L-NAME, causing an inhibition of nitric oxide synthase, significantly accelerates the O 2 on-kinetics in a thoroughbred horse [42], as well as in humans [43,44]. The authors concluded that the intrinsic inertia of oxidative metabolism at the onset of heavy-intensity exercise may result from an inhibition of mitochondrial respiration by nitric oxide.…”