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An in vivo Rodent Model of Contraction-induced Injury and Non-invasive Monitoring of Recovery
Published on: May 11, 2011
Temporal profile of rat skeletal muscle capillary haemodynamics during recovery from contractions
Leonardo F Ferreira1, Danielle J Padilla, Timothy I Musch
1Clarenburg Research Laboratory, Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506-5602, USA. poole@vet.ksu.edu.
Abstract:
In skeletal muscle capillaries, red blood cell (RBC) flux (F(RBC)), velocity (V(RBC)) and haematocrit (Hct(CAP)) are key determinants of microvascular O2 exchange. However, the mechanisms leading to the changes in F(RBC), V(RBC) and Hct(CAP) during muscle contractions and recovery thereafter are not fully understood. To address this issue we used intravital microscopy to investigate the temporal profile of the rat spinotrapezius muscle (n = 5) capillary haemodynamics during recovery from 3 min of twitch muscle contractions (1 Hz, 4-6 V). Specifically, we hypothesized that (1) during early recovery F(RBC) and V(RBC) would decrease rapidly and F(RBC) would display a biphasic response (consistent with a muscle pump effect on capillary haemodynamics), and (2) there would be a dynamic relationship between changes (Delta) in V(RBC) and Hct(CAP). The values at rest (R) and end-recovery (ER) were significantly lower (P < 0.05) than at end-contraction (EC) for F(RBC) (in cells s(-1), R = 30.1 +/- 7.8, EC = 46.2 +/- 7.3 and ER = 26.0 +/- 6.1), V(RBC) (in microm s(-1), R = 368 +/- 83, EC = 497 +/- 62 and ER = 334 +/- 59) and Hct(CAP) (R = 0.193 +/- 0.016, EC = 0.214 +/- 0.023 and ER = 0.185 +/- 0.019). The first data point where a significant decrease in F(RBC), Hct(CAP) and V(RBC) occurred was at 5, 5 and 20 s post-contraction, respectively. The decrease in F(RBC) approximated a monoexponential response (half-time of approximately 26 s). The relationship between DeltaV(RBC) and DeltaHct(CAP) was not significant (P > 0.05). Based on the early decrease in F(RBC) (within 5 s), overall dynamic profile of F(RBC) and the approximately 20 s 'delay' to the decrease in V(RBC) we conclude that the muscle pump does not appear to contribute substantially to the steady-state capillary haemodynamics in the contracting rat spinotrapezius muscle. Moreover, our findings suggest that alterations in V(RBC) do not obligate proportional changes in Hct(CAP) within individual capillaries following muscle contractions.
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