Oxygen uptake, acid-base status, and performance with varied inspired oxygen fractions

Abstract

Six subjects rode a bicycle ergometer on three occasions breathing 17, 21, or 60% oxygen. In addition to rest and recovery periods, each subject worked for 10 min at 55% of maximal oxygen uptake (VO2 max) and then to exhaustion at approximately 90% VO2 max. Performance time, inspired and expired gas fractions, ventilation, and arterialized venous oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, and pH were measured. VO2, carbon dioxide output, [H+]a, and [HCO3-]a were calculated. Performance times were longer in hyperoxia than in normoxia or hypoxia. However, VO2 was not different at exhaustion in normoxia compared with hypoxia or hyperoxia. During exercise, hypoxia was associated with increased lactate levels and decreased [H+]a, PCO2, and [HCO3-]a. The opposite trends were generally associated with hyperoxia. At exhaustion, [H+]a was not different under any inspired oxygen fraction. These results support the contention that oxygen is not limiting for exercise of this intensity and duration. The results also suggest that [H+] is a possible limiting factor and that the effect of oxygen on performance is perhaps related to control of [H+].

No effect of glutamine supplementation and hyperoxia on oxidative metabolism and performance during high-intensity exercise

“…Therefore the decrease in plasma glutamine concentration from 30 min post-ingestion to the onset of exercise suggests that a significant amount of glutamine entered the muscle (Varnier, Leese, Thompson, & Rennie, 1995). Hence it is likely that in the present study glutamine ingestion The lack of any effect of hyperoxia on plasma lactate concentration during maximal exercise was perhaps not surprising since a number of previous studies have found similar results (Linnarsson et al 1974;Adams & Welch, 1980;Knight et al 1993;Hogan et al 1999;Linossier et al 2000;Savasi et al 2002) suggesting that whilst exercise performance is enhanced in hyperoxia, fatigue occurs at the same intracellular concentrations of potential fatiguing metabolites (H + , AMP, IMP, Pi).…”

“…In contrast performance was enhanced by ~ 6% in hyperoxia, with a concomitant significant increase in  2 o V  . Hyperoxia has previously been shown to result in enhanced performance during high intensity exercise (Linnarsson, et al 1974;Adams & Welch, 1980;Knight et al 1993;Hogan et al 1999;Richardson et al 1999a,b;Linossier et al 2000). The mechanism by which hyperoxia exerts this effect appears to be via facilitation of oxygen consumption compared to normoxic conditions, resulting in a delay before the accumulation of metabolic by-products (H + , AMP, IMP, Pi) to fatiguing levels (Linnarsson, et al 1974;Adams & Welch, 1980;Knight et al 1993;Hogan et al 1999;Linossier et al 2000;Prieur et al 2006) Glutamine ingestion conferred no main effect on any measured parameter.…”

“…oxygen delivery, enzyme activation), which prevent enhancement of oxidative metabolism (Tschakovsky & Hughson, 1999;Gurd et al 2006). We therefore hypothesised that any glutamine-mediated enhancement of TCA cycle flux, and hence NADH & FADH production, would exacerbate the oxygen delivery limitation found during high intensity exercise (Linnarsson, Karlsson, Fagraeus & Saltin, 1974;Adams & Welch, 1980;Knight et al 1993;Hogan, Richardson & Haseler, 1999;Richardson et al 1999a;Richardson, Leigh, Wagner & Noyszewski, 1999b;Linossier et al 2000). Therefore a second aim of this experiment was to compare the separate and combined effects of glutamine supplementation and hyperoxia on performance and oxidative metabolism during maximal aerobic exercise.…”

Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise

“…In healthy subjects and in patients with peripheral vascular disease, muscle ischaemia is a potent stimulus for improving endurance exercise [36]. Since supplemental oxygen abolishes the desaturation and reduces lactate levels during exercise [4,37], it might also have reduced the training stimulus in these patients.…”

Cerebral perturbations during exercise in hypoxia

“…This limitation has been attributed to a lowered O 2 partial pressure in arterial blood (Pa O 2 ) reducing arterial O 2 content and O 2 delivery to tissues with critical consequences on muscle metabolism and contraction (1,46). Magnetic nerve stimulation has confirmed the effects of reduced arterial oxygenation on dynamic (12,111) and static (54) exercise-induced alterations in muscle contractility.…”