Abstract

This study investigated the relationship between hypoxia and the rate of fatigue development in contracting rat hindlimb muscles composed primarily of different fibre types. Hindlimb muscles of 11 rats were exposed, and the soleus (SOL) and gastrocnemius/plantaris (GP) were each isolated with circulation intact and attached to individual force transducers. Rats were then equilibrated with either normoxic (N; arterial partial pressure of O(2) 87.7 +/- 1.5 mmHg) or hypoxic conditions (H; arterial partial pressure of O(2) 30.0 +/- 2.4 mmHg) using an inspired O(2) fraction of 0.21 and 0.10, respectively. The stimulation protocol consisted of 2 min each at 0.125, 0.25, 0.33 and 0.5 tetanic contractions s(-1) sequentially for both conditions. Following the 8 min stimulation period, relative developed muscle tension (% of maximal) was nearly identical for both H and N in SOL (54.2 +/- 3.5 versus 54.3 +/- 4.2%), but was significantly (P < 0.05) lower in H than N (10.8 +/- 0.9 versus 43.0 +/- 8.9%) in GP, indicating a greater amount of fatigue during hypoxia only in the GP. Soleus phosphocreatine (PCr) content fell to similar levels (24.1 +/- 1.6 versus 21.1 +/- 4.9 mmol (kg dry weight (dw))(-1)) during both H and N, but in the white portion of the gastrocnemius (WG), PCr was significantly lower following H than N (14.3 +/- 1.5 versus 34.0 +/- 6.0 mmol (kg dw)(-1)). Similarly, muscle lactate increased in both fibre types at fatigue, but only in WG was the increase significantly greater with H (SOL 7.1 +/- 2.0 versus 5.3 +/- 1.1 mmol (kg dw)(-1); WG 13.7 +/- 4.5 versus 5.3 +/- 2.2 mmol (kg dw)(-1)). Increases in calculated muscle [H(+)], free ADP and free AMP were similar between N and H in SOL but were significantly greater during H compared with N in WG. These data demonstrate that hypoxia induces greater fatigue and disruption of cellular homeostasis in rat hindlimb muscle composed primarily of fibres with low oxidative capacity compared with those of a more oxidative type.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.