Key result
Myoglobin knockout in mice reduces cardiac contractility by ~16% and impairs exercise endurance versus wild-type.
Why the study?
Does myoglobin deficiency impair cardiac function and exercise endurance in mice?
Does myoglobin deficiency impair cardiac function and exercise endurance in mice?
Absolute Event Rate: 3883% vs 4618%
p-value: p=<0.005
Myoglobin deficiency in mice leads to impaired cardiac function and reduced exercise endurance, highlighting its role in oxygen supply and nitric oxide scavenging.
Hypothesis-generating in mice; leaves open myoglobin's relevance to human cardiac dysfunction or exercise capacity.
Recent studies of myoglobin (Mb) knockout (myo-/-) mice have extended our understanding of Mb's diverse functions and have demonstrated a complex array of compensatory mechanisms. The present study was aimed at detailed analysis of cardiac function and exercise endurance in myo-/- mice and at providing evidence for Mb's functional relevance. Myo-/- isolated working hearts display decreased contractility (dP/dtmax 3883+/-351 vs. 4618+/-268 mmHg/sec, myo-/- vs. WT, P<0.005). Due to a shift in sympathetic/parasympathetic tone, heart rate is reduced in conscious myo mice-/- (615+/-33 vs. 645+/-27 bpm, myo-/- vs. WT, P<0.001). Oxygen consumption (VO2) under resting conditions (3082+/-413 vs. 4452+/-552 ml x kg(-1) x h(-1), myo-/- vs. WT, P<0.001) and exercise endurance, as determined by spiroergometry, are decreased (466+/-113 vs. 585+/-153 m, myo-/- vs. WT, P<0.01). Conscious myo-/- mice evaluated by echocardiography display lowered cardiac output (0.64+/-0.06 vs. 0.75+/-0.09 ml x min(-1) x g(-1), myo-/- vs. WT, P<0.001), impaired systolic shortening (60+/-3.5 vs. 65+/-4%, myo-/- vs. WT, P<0.001) and fail to respond to beta1-stimulation. Strikingly, the latter cardiac effects of Mb deficiency can be partially attenuated by NOS inhibition. Loss of Mb results in a distinct phenotype, even under resting conditions, and the importance of oxygen supply and nitric oxide scavenging by Mb is clearly demonstrated at the conscious animal level.
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Merx et al. (2005) studied Myoglobin deficiency. Myoglobin knockout (myo-/-) vs. Wild-type (WT) mice was evaluated on Cardiac contractility (dP/dtmax in mmHg/sec) (p=<0.005). Myoglobin knockout mice exhibited significantly decreased cardiac contractility (3883 vs. 4618 mmHg/sec, P<0.005) and reduced exercise endurance compared to wild-type mice.
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