Effects of arterial oxygen content on peripheral locomotor muscle fatigue

Abstract

The effect of arterial O2 content (Ca(O2)) on quadriceps fatigue was assessed in healthy, trained male athletes. On separate days, eight participants completed three constant-workload trials on a bicycle ergometer at fixed workloads (314 +/- 13 W). The first trial was performed while the subjects breathed a hypoxic gas mixture [inspired O2 fraction (Fi(O2)) = 0.15, Hb saturation = 81.6%, Ca(O2) = 18.2 ml O2/dl blood; Hypo] until exhaustion (4.5 +/- 0.4 min). The remaining two trials were randomized and time matched with Hypo. The second and third trials were performed while the subjects breathed a normoxic (Fi(O2) = 0.21, Hb saturation = 95.0%, Ca(O2) = 21.3 ml O2/dl blood; Norm) and a hyperoxic (Fi(O2) = 1.0, Hb saturation = 100%, Ca(O2) = 23.8 ml O2/dl blood; Hyper) gas mixture, respectively. Quadriceps muscle fatigue was assessed via magnetic femoral nerve stimulation (1-100 Hz) before and 2.5 min after exercise. Myoelectrical activity of the vastus lateralis was obtained from surface electrodes throughout exercise. Immediately after exercise, the mean force response across 1-100 Hz decreased from preexercise values (P < 0.01) by -26 +/- 2, -17 +/- 2, and -13 +/- 2% for Hypo, Norm, and Hyper, respectively; each of the decrements differed significantly (P < 0.05). Integrated electromyogram increased significantly throughout exercise (P < 0.01) by 23 +/- 3, 10 +/- 1, and 6 +/- 1% for Hypo, Norm, and Hyper, respectively; each of the increments differed significantly (P < 0.05). Mean power frequency fell more (P < 0.05) during Hypo (-15 +/- 2%); the difference between Norm (-7 +/- 1%) and Hyper (-6 +/- 1%) was not significant (P = 0.32). We conclude that deltaCa(O2) during strenuous systemic exercise at equal workloads and durations affects the rate of locomotor muscle fatigue development.

Cerebral perturbations during exercise in hypoxia

“…When comparing iEMG during cycling at the same absolute workload in normoxia and hypoxia, greater iEMG increases for the same exercise duration have been reported in hypoxia (12,13,106), similar to the results during leg extensions. Therefore, during submaximal whole body exercise in acute hypoxia, the CNS is able to increase motor drive above levels observed in normoxia to sustain the workload to compensate for increased levels of contractile fatigue (87).…”

“…Spinal opioid receptor muscle afferents may influence cerebral adaptations to exercise by facilitating intracortical inhibition (45). Consequently, under moderate hypoxic conditions, muscle fatigue may represent a key factor responsible for impaired central drive in hypoxia through enhanced muscle inhibitory afferent signals because of an accelerated development of locomotor muscle fatigue (12,54). This statement is supported by the parallel hypoxia-induced (FI O 2 ϭ 0.15) reductions in integrated EMG (iEMG) and power output during a 5-km cycling time trial, while peripheral muscle fatigue at exhaustion does not differ (7).…”

“…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. Reduced muscle O 2 delivery and exercise performance may result from impairments in pulmonary gas exchange [e.g., alveolarcapillary O 2 diffusion limitation (109)], reductions in maximal cardiac output and blood flow to locomotor muscles (17), and respiratory muscle fatigue (23) (for a review see Ref.…”

The interactive effect of cooling and hypoxia on forearm fatigue development

“…However, increases in muscle fatigue during prolonged exercise in hypoxia have been observed during both whole-body (Amann & Calbet 2007) and repeated contractions of isolated muscle groups (Fulco 1994;Katayama et al 2007;Perrey & Rupp 2009;Millet et al 2008;Christian et al 2014a). The rise in muscle fatigue during hypoxia can be largely attributed to a shift of the relative exercise intensity, higher muscle fibre recruitment, and thereby increased intramuscular metabolic disturbance (Edwards 1981;Fulco et al 1996;Amann et al 2006a;2006b;2007a;2007b;Fulco et al 1994, Katayama et al 2007Christian et al 2014a). Specifically, the increase in inorganic phosphate, reactive oxygen species and hydrogen ion production and their interference with the contractile proteins and sarcoplasmic Ca 2+ release mechanisms are thought to be a major factor behind the increase in muscle fatigue development Hogan et al 1999;Amann & Calbet 2007;Perrey & Rupp 2008).…”

“…Studies that have examined combined hypoxiccold stress have focused largely on thermogenesis, skin blood flow and thermal sensitivity (Robinson & Haymes 1991;Johnston et al 1996;Gautier et al 1987, Wood 1991Cipriano & Goldman 1975;Simmons et al 2010;, leaving fatigue development and human performance relatively unexamined (Tipton 2012). Given the potential for hypoxic-cold to severely compromise oxygen delivery to the active muscle -through simultaneous reductions in oxygen transport (muscle blood flow) and arterial oxygen content (hypoxemia) (Yanagisawa et al, 2007;Gregson et al, 2011;Amann & Calbet 2007) -as well as greatly increase metabolite production -through simultaneous rises in agonist-antagonist co-activation in the cold and type II recruitment in hypoxia (Edwards 1981;Fulco et al 1996;Oksa et al, 2002;Amann et al 2006a;2006b;2007a;2007b;Fulco et al 1994, Katayama et al 2007Christian et al 2014a) -we sought to investigate the independent and combined (interactive) effects of hypoxia and cold on forearm fatigue.…”