Combination of hyperoxia and a right-shifted HbO2 dissociation curve delays VÌo2 kinetics during maximal contractions in isolated muscle.
J Appl Physiol (1985)
; 135(2): 456-466, 2023 08 01.
Article
em En
| MEDLINE
| ID: mdl-37391886
ABSTRACT
Acute enhancement of peripheral O2 diffusion may accelerate skeletal muscle O2 uptake (VÌo2) kinetics and lessen fatigue during transitions from rest to maximal contractions. Surgically isolated canine gastrocnemius muscles in situ (n = 6) were studied during transitions from rest to 4 min of electrically stimulated isometric tetanic contractions at VÌo2peak, in two conditions normoxia (CTRL) and hyperoxia ([Formula see text] = 1.00) + administration of a drug (RSR-13), which right shifts the Hb-O2 dissociation curve (Hyperoxia + RSR-13). Before and during contractions, muscles were pump-perfused with blood at constant elevated flow ([Formula see text]) and infused with the vasodilator adenosine. Arterial ([Formula see text]) and muscle venous ([Formula see text]) O2 concentrations were determined at rest and at 5- to 7-s intervals during contractions; VÌo2 was calculated as [Formula see text]·([Formula see text] - [Formula see text]). Po2 at 50% of Hb saturation (standard P50) and mean microvascular Po2 ([Formula see text]) were calculated by the Hill equation and a numerical integration technique. P50 [42 ± 7 (means ± SD) mmHg vs. 33 ± 2 mmHg, P = 0.02] and [Formula see text] (218 ± 73 mmHg vs. 49 ± 4 mmHg, P = 0.003) were higher in Hyperoxia + RSR-13. Muscle force and fatigue were not different in the two conditions. VÌo2 kinetics (monoexponential fitting) were unexpectedly slower in Hyperoxia + RSR-13, due to a longer time delay (TD) [9.9 ± 1.7 s vs. 4.4 ± 2.2 s (P = 0.001)], whereas the time constant (τ) was not different [13.7 ± 4.3 s vs. 12.3 ± 1.9 s (P = 0.37)]; the mean response time (TD + τ) was longer in Hyperoxia + RSR-13 [23.6 ± 3.5 s vs. 16.7 ± 3.2 s (P = 0.003)]. Increased O2 availability deriving, in Hyperoxia + RSR-13, from higher [Formula see text] and from presumably greater intramuscular O2 stores did not accelerate the primary component of the VÌo2 kinetics, and delayed the metabolic activation of oxidative phosphorylation.NEW & NOTEWORTHY In isolated perfused skeletal muscle, during transitions from rest to VÌo2peak, hyperoxia and a right-shifted oxyhemoglobin dissociation curve increased O2 availability by increasing microvascular Po2 and by presumably increasing intramuscular O2 stores. The interventions did not accelerate the primary component of the VÌo2 kinetics (as calculated from blood O2 unloading) and delayed the metabolic activation of oxidative phosphorylation. VÌo2 kinetics appear to be mainly controlled by intramuscular factors related to the use of high-energy "buffers."
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Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Hiperóxia
Limite:
Animals
Idioma:
En
Revista:
J Appl Physiol (1985)
Assunto da revista:
FISIOLOGIA
Ano de publicação:
2023
Tipo de documento:
Article
País de afiliação:
Itália