Effect of hindlimb suspension on the soleus muscle: Blood flow, fatigue, and single fiber function
Abstract
This study examined the effect of hindlimb suspension (HS) on blood flow distribution and the relationship between soleus muscle blood flow and contractile activity in the rat and, second, the time course of change in the contractile properties of single rat soleus fibers elicited by HS. Blood flow was measured using radiolabeled microspheres in either control and 15 d HS conscious rats or in anesthetized rats whose soleus was stimulated (100 Hz, 120/min) in situ. Following 1, 2, or 3 wk HS, single soleus fibers were isolated and placed between a motor arm and force transducer for analysis of contractile parameters. During HS blood flow to the soleus was significantly lower compared to normal standing. However, during exercise there were no group differences in soleus muscle blood flow. The soleus from HS animals showed greater fatigability than the control, however, soleus blood flow was similar between groups during contractile activity. The diameter and absolute force production of single soleus fibers progressively declined through 3 wk HS. Fiber force per cross-sectional area (CSA) (P$\sb{\rm o}$) declined following HS, but to a lesser extent than the decrease in fiber stiffness/CSA. Fiber V$\sb{\rm max}$ and ATPase activities significantly increased during wk 1 and 3 of HS. The percentage of type IIa fibers progressively increased through 3 wk HS, however, following each duration of HS fibers expressing only slow myosin showed significant increases in V$\sb{\rm max}$ and ATPase. Peak fiber power output progressively decreased through 2 wk HS and then leveled off. In summary, peak soleus blood flow was not altered with HS and thus cannot explain the increased fatigability. The decline in fiber P$\sb{\rm o}$ with HS can be explained by a reduced number of myofibrillar cross-bridges. In fact, the number of fiber cross-bridges were reduced to a greater extent than the fall in P$\sb{\rm o}$, suggesting force per cross-bridge was increased. The HS-induced increase in fiber V$\sb{\rm max}$ is likely caused by the elevated rate of fiber ATP hydrolysis. The plateauing of peak fiber power output, despite a continued decline in absolute force, was the result of an altered force-velocity relationship.
This paper has been withdrawn.