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Seven men performed one‐legged isometric knee extension at 5% MVC for I h. Total body oxygen uptake amounted to 451 (42–471) ml min ‐1 and oxygen uptake over the contracting leg to 200 (172–216) ml min ‐1 , with no changes occurring during the in contraction. Venous O 2 tension decreased from 29.4 mmHg at rest to 23.1 mmHg with contraction and CO 2 tension tended to increase from a resting value of 50.5 mmHg to 57.2 mmHg (ns.). No similar changes occurred in arterial O 2 and CO 2 tensions. There was a small but continuous glucose uptake at both rest and throughout the contraction, whereas a lactate release occurred only in the early phase (2 min) of contraction. Muscle glycogen content was 312 mmol kg ‐1 dry wt at rest, no significant changes had occurred following 30 min or 1 h of contraction. Arterial and venous Hct and Hb values indicated that a flux of water occurred from the vascular bed to the contracting muscle, in which H 2 O increased from 3.06 I kg ‐1 dry wt at rest to 3.30 1 kg ‐1 dry wt after 1 h at 5 % MVC. Simultaneously potassium (K), was released from the muscle throughout contraction with a mean venous‐arterial difference of 0.25 mmol I ‐1 . With a plasma flow of 335 ml min ‐1 kg ‐1 wet wt the K loss amounted to 5 mmol kg ‐1 wet wt or roughly 5% of the total muscle K content. Results from analysis of muscle K content were in line with this, since the mean K content of 460 mmol kg ‐1 dry wt at the end of contraction tended to be lower than the mean resting value of 471 mmol kg ‐1 dry wt (n.s.). These results indicate that during low‐level contractions, the muscle is able to maintain homeostasis with respect to energy turnover, but not with respect to intra‐/extracellular K concentration. This K imbalance may well play a role in muscle fatigue.
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Gisela Sjøgaard (1988) studied this question.
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