Effects of oxygen fraction in inspired air on force production and electromyogram activity during ergometer rowing

Abstract

Six male rowers rowed maximally for 2500 m in ergometer tests during normoxia (fractional concentration of oxygen in inspired air, F(I)O2 0.209), in hyperoxia (F(I)O2 0.622) and in hypoxia (F(I)O2 0.158) in a randomized single-blind fashion. Oxygen consumption (VO2), force production of strokes as well as integrated electromyographs (iEMG) and mean power frequency (MPF) from seven muscles were measured in 500-m intervals. The iEMG signals from individual muscles were summed to represent overall electrical activity of these muscles (sum-iEMG). Maximal force of a stroke (Fmax) decreased from the 100% pre-exercise maximal value to 67 (SD 12)%, 63 (SD 15)% and 76 (SD 13)% (P < 0.05 to normoxia, ANOVA) and impulse to 78 (SD 4)%, 75 (SD 14)% and 84 (SD 7)% (P < 0.05) in normoxia, hypoxia and hyperoxia, respectively. A strong correlation between Fmax and VO2 was found in normoxia but not in hypoxia and hyperoxia. The mean sum-iEMG tended to be lower (P < 0.05) in hypoxia than in normoxia but hyperoxia had no significant effect on it. In general, F(I)O2 did not affect MPF of individual muscles. In conclusion, it was found that force output during ergometer rowing was impaired during hypoxia and improved during hyperoxia when compared with normoxia. Moreover, the changes in force output were only partly accompanied by changes in muscle electrical activity as sum-iEMG was affected by hypoxic but not by hyperoxic gas. The lack of a significant correlation between Fmax and VO2 during hypoxia and hyperoxia may suggest a partial uncoupling of these processes and the existence of other limiting factors in addition to VO2.

Cardiorespiratory responses to exercise in acute hypoxia, hyperoxia and normoxia

“…Noakes' suggestion is that the oxygen tension in the coronary vascular bed would be the monitored variable to prevent the development of a progressive myocardial ischemia. Alternatively, the evidence of the previous studies (Harik et al 1996;Kayser et al 1994;Kjaer et al 1999;Koller et al 1991;Peltonen et al 1997) and the ®nding that peak exercise f c can be higher in silent ischemia than in symptomatic ischemia (Visser et al 1990) can be interpreted such that the signals that inhibit the increase of f c in acute hypoxia may arise somewhere else, or at least also somewhere else than in the myocardium itself, possibly in the central nervous system. The notion that the level of sympathetic activity at a given f c is the same under normoxic and hypoxic conditions (Rowell 1986) suggests that the reduced f cmax in hypoxia is due to reduced sympathetic stimulation, which provides further support for the central governor hypothesis.…”

“…This suggestion is supported by several ®ndings. Firstly, the typical signs of neuromuscular fatigue (i.e., an increase in the integrated electromyogram signal) are missing during chronic (Kayser et al 1994) and acute (Peltonen et al 1997) hypoxia. Secondly, the hypoxia-induced enhancement of systemic adaptations to exercise is not mediated by neural feedback from working muscles, suggesting that the limitations in exercise performance are of central origin (Kjaer et al 1999).…”

Mechanisms of Improved Exercise Performance under Hyperoxia

“…These findings support the notion that in normoxia, reduced cerebral O 2 availability contributes to termination of exercising via reduced neural muscle activation [11], while hyperoxia improves exercise performance by increasing CTO. Since hyperoxia diminished the perception of dyspnea at maximal exercise despite a V•E similar to that in normoxia (Table 2), we propose that the greater availability of O 2 to both sensory and motor neurons plays a role in enhancing exercise performance with hyperoxia [35,36,37]. …”

Modulation of exercise-induced spinal loop properties in response to oxygen availability

“…Although V-wave assessment is less unsettling/painful than transcranial or cervicomedular stimulation techniques (McNeil et al 2013), V-waves have been used only rarely to investigate exercise-induced fatigue (Racinais et al 2007) and never under hypoxic conditions. Hypoxia is, however, known to impair in vitro CNS function (cerebral neuron excitability, ion channels, signaling pathways, synaptic neurotransmission) (Cater et al 2003;Hong et al 2004;Lopez-Barneo et al 2001), and evidence demonstrating that hypoxiainduced cerebral perturbations strongly contribute to exercise performance limitation are growing (Amann et al 2006;Peltonen et al 1997) despite conflicting results in studies that investigated in vivo corticospinal excitability (for a review see Verges et al 2012).…”