Changes in contractile properties of skinned single rat soleus and diaphragm fibres after chronic hypoxia

Abstract

Hypoxia may be one of the factors underlying muscle dysfunction during ageing and chronic lung and heart failure. Here we tested the hypothesis that chronic hypoxia per se affects contractile properties of single fibres of the soleus and diaphragm muscle. To do this, the force-velocity relationship, rate of force redevelopment and calcium sensitivity of single skinned fibres from normoxic rats and rats exposed to 4 weeks of hypobaric hypoxia (410 mmHg) were investigated. The reduction in maximal force (P(0)) after hypoxia (p=0.031) was more pronounced in type IIa than type I fibres and was mainly attributable to a reduction in fibre cross-sectional area (p=0.044). In type IIa fibres this was aggravated by a reduction in specific tension (p=0.001). The maximal velocity of shortening (V (max)) and shape of the force velocity relation (a/P(0)), however, did not differ between normoxic and hypoxic muscle fibres and the reduction in maximal power of hypoxic fibres (p=0.012) was mainly due to a reduction in P(0). In conclusion, chronic hypoxia causes muscle fibre dysfunction which is not only due to a loss of muscle mass, but also to a diminished force generating capacity of the remaining contractile material. These effects are similar in the soleus and diaphragm muscle, but more pronounced in type IIa than I fibres.

Lymph flow pattern in pleural diaphragmatic lymphatics during intrinsic and extrinsic isotonic contraction

“…Hence, our ex vivo approach has broadened the spectrum of mechanical stimuli that can be applied to the diaphragmatic lymphatic vasculature while simultaneously recording several functional parameters otherwise not collectable in the in vivo, in situ preparation (17). In fact, the mean muscle fiber shortening (ϳ24% of precontractile length) attained with whole-field electrical stimulation, similar to that observed when contractions is elicited by KCl injections in the interstitial space among muscle fibers (23), is in good agreement with that expected in the diaphragm during spontaneous inspirations (4,7,42).…”

“…In the present experiments contraction was evoked in almost zero load conditions in the unconstrained diaphragm. In this condition the contraction velocity approaches V max and the force expressed by the muscle ought to be lower than the expected isometric force and fell on the flat portion of the diaphragmatic skeletal muscle force/velocity curve (7,34,39,42), where small changes in shortening speed may give rise to larger changes in force, which is generated. Therefore, one may reasonably expect the expressed force, and therefore the impact on lymph flow velocity, to be higher in the in situ-in vivo condition, when diaphragmatic fibers are held at a length closer to their resting one by the thoracic and crural physiological anatomical connection.…”

Muscle contractile properties as an explanation of the higher mean power output in marmosets than humans during jumping

“…Solutions were as described previously (Larsson and Moss, 1993;Degens and Larsson, 2007;Degens et al, 2010 …”

“…Before analysis, samples were denatured at 100°C for 2 min. MHCs were separated using SDS-PAGE as previously described (Larsson and Moss, 1993;Degens and Larsson, 2007;Degens et al, 2010). Briefly, samples were separated for 27 h at 275 V on a 7% polyacrylamide gel containing 35% glycerol.…”

Diaphragm Muscle Adaptation to Sustained Hypoxia: Lessons from Animal Models with Relevance to High Altitude and Chronic Respiratory Diseases

“…), it too poses a significant challenge for the maintenance of respiratory homeostasis in response to pathophysiological stressors (e.g., cancer cachexia, mechanical ventilation-induced atrophy, and respiratory diseases such as chronic obstructive pulmonary disease (COPD) etc.). One such physiological stressor, a condition of inadequate O 2 delivery to cells and tissues such that metabolic demands are not appropriately met (or impaired utilization of O 2 by cells), namely hypoxia, is a facet of several chronic respiratory diseases, which promotes muscle weakness and deterioration (Shiota et al, 2004; Degens et al, 2010; McMorrow et al, 2011; Lewis et al, 2016). Acute bouts of hypoxia typically provide, in conjunction with a mechanical stimulus, a signal to drive exercise-induced adaptations in skeletal muscles (Desplanches et al, 1993; Hoppeler and Vogt, 2001; Mason et al, 2007; Rasbach et al, 2010; Lindholm and Rundqvist, 2016).…”