The effect of hypoxia on shortening contractions in rat diaphragm muscle

Abstract

Hypoxia is known to reduce isometric contractile properties of isolated rat diaphragm bundles. Its effect on isotonic contractile properties (i.e. force-velocity relationship and power output) has not been studied. We hypothesized that hypoxia reduces velocity of shortening and consequently power output of the unfatigued muscle, and shortens endurance time during isotonic contractions. Force-velocity relationship, power output, and fatigue resistance of rat diaphragm muscle bundles were measured during hypoxia (PO2: 6.6 +/- 0.2 kPa) and compared with hyperoxia (PO2: 91.8 +/- 0.7 kPa). Force was clamped from 1 to 100% of maximal tetanic force (Po). Fatigue during isotonic contractions was induced by repeated stimulation every 2 s at a clamp level of 33% of Po. Hypoxia did not affect isometric force generation compared with hyperoxia, nor contraction or relaxation time. In contrast, maximum shortening velocity decreased significantly (hypoxia: 4.2 +/- 0.3, hyperoxia: 6.0 +/- 0.2 Lo/s, P < 0.05). The force-velocity curve shifted downwards (P < 0.05). Hypoxia lowered power output at each load compared with hyperoxia (P < 0.05). The isotonic endurance time was shorter during hypoxia compared with hyperoxia (80 +/- 2 vs. 130 +/- 3 s, P < 0.05). These data show that hypoxia depresses isotonic contractile properties and power output, and reduces endurance time during repeated isotonic contractions.

Cardiorespiratory failure in rat induced by severe inspiratory resistive loading

“…A decrease in diaphragmatic length due to an increase in end-expiratory lung volume is unlikely to be responsible because we observed no increases in end-expiratory Pes during loading. Hypoxia depresses in vitro diaphragmatic contractility (30), but this cannot account for our findings because in the present study, Pdi/͐Phr fell within 4 min while in the previous study (43) the rats experienced over 2 h of a similar degree of load-induced hypoxia without a change in contractility, suggesting that hypoxia is not responsible. Whether respiratory acidosis causes diaphragmatic fatigue is unresolved (26,40,41), but the generation of intracellular acidosis and inorganic phosphate as a result of increased contractile activity have been well recognized to impair force generation (for reviews, see Refs.…”

Acute hypoxia limits endurance but does not affect muscle contractile properties

“…It is also unlikely that the duration of exposure to hypoxia plays a role as a decline in force was already detected after 2 min of hypoxia, 6 whereas others found no change in MVC even after a 40-day simulated climb. 10 Whereas in vivo force-generating capacity of the muscle tissue itself seems to be maintained during hypoxia, in vitro studies generally show a decline in force-generating capacity 2,17,20,26 and a downward shift of the force-frequency relation. 18 We did not find such a depression of force or shift in the forcefrequency relation in the in vivo situation.…”

“…Yet, others 23 and we did not observe a change in contraction and half relaxation times in vivo. Also, in vitro, the contraction and relaxation times have been reported to be unaltered 17 or even reduced 18 during hypoxia. The similar rates of contraction and relaxation during normoxia and hypoxia in our in vivo study correspond with the unaltered force-frequency relation.…”

“…The PaO 2 was similar or even lower than that obtained in many in vitro studies. 2,17,26 To compensate for the reduced supply of O 2 to the tissues, the heart rate was elevated in order to increase cardiac output.…”

Effects of Hyperoxia Exposure on Free Radicals Accumulation in Relation to Ultrastructural Pathological Changes of Diaphragm

“…This decreases the content of CO 2 carried in the form of the carbamino load and consequently decreases CO 2 elimination at the lung capillaries leading to an increase in brain tissue PCO 2 that would stimulate respiration via the central chemoreceptors. Another mechanism that could participate in the hyperoxic enhancement of ventilation is the Haldane effect [16]. Normally, 30% of CO 2 eliminated in the lungs comes from the carbamino sources carried with the venous blood hemoglobin.…”