Seasonal variation in muscle glycogen in beef steers

Dark-cutting in beef carcasses is a quality and economic problem for the grass-fed beef industry in Australia, with ~10% of carcasses graded as dark-cutting. Dark-cutting results from low muscle glycogen levels at the time of slaughter. An experiment was designed to examine the relationship between season and muscle glycogen levels for cattle at pasture. Sixty steers were allocated to 2 stocking rate treatments, low and high (1.5 and 2.5 steers/ha, respectively) with 3 replicates for each treatment and grazed in 6 separate paddocks. Monthly samples of the M. semimembranosus (SM) and M. semitendinosus (ST) were taken by biopsy from all cattle and analysed for glycogen and lactate content. Significant differences in muscle glycogen were found between seasons. Average muscle glycogen levels for autumn, winter, spring and summer were 1.24, 1.00, 1.15 and 0.82 mg/g SM and 0.85, 0.91, 1.05 and 0.76 mg/g ST, respectively. The seasonal effects on muscle glycogen were not influenced by stocking rate, but it is postulated that they were influenced by nutrition, with the peak in muscle glycogen level generally coinciding with the peak in pasture quantity and quality in spring.

More tetanic contractions are required for activating glucose transport maximally in trained muscle

Kawanaka, Kentaro, Izumi Tabata, and Mitsuru Higuchi. More tetanic contractions are required for activating glucose transport maximally in trained muscle. J. Appl. Physiol. 83(2): 429–433, 1997.—Exercise training increases contraction-stimulated maximal glucose transport and muscle glycogen level in skeletal muscle. However, there is a possibility that more muscle contractions are required to maximally activate glucose transport in trained than in untrained muscle, because increased glycogen level after training may inhibit glucose transport. Therefore, the purpose of this study was to investigate the relationship between the increase in glucose transport and the number of tetanic contractions in trained and untrained muscle. Male rats swam 2 h/day for 15 days. In untrained epitrochlearis muscle, resting glycogen was 26.6 μmol glucose/g muscle. Ten, 10-s-long tetani at a rate of 1 contraction/min decreased glycogen level to 15.4 μmol glucose/g muscle and maximally increased 2-deoxy-d-glucose (2-DG) transport. Training increased contraction-stimulated maximal 2-DG transport (+71%; P < 0.01), GLUT-4 protein content (+78%; P < 0.01), and resting glycogen level (to 39.3 μmol glucose/g muscle; P < 0.01) on the next day after the training ended, although this training effect might be due, at least in part, to last bout of exercise. In trained muscle, 20 tetani were necessary to maximally activate glucose transport. Twenty tetani decreased muscle glycogen to a lower level than 10 tetani (18.9 vs. 24.0 μmol glucose/g muscle; P < 0.01). Contraction-stimulated 2-DG transport was negatively correlated with postcontraction muscle glycogen level in trained ( r = −0.60; P < 0.01) and untrained muscle ( r = −0.57; P < 0.01).

Adenine nucleotide degradation in human skeletal muscle during prolonged exercise

Eight healthy men cycled at a work load corresponding to approximately 70% of maximal O2 uptake (VO2max) to fatigue (exercise I). Exercise to fatigue at the same work load was repeated after 75 min of rest (exercise II). Exercise duration averaged 65 and 21 min for exercise I and II, respectively. Muscle (quadriceps femoris) content of glycogen decreased from 492 +/- 27 to 92 +/- 20 (SE) mmol/kg dry wt and from 148 +/- 17 to 56 +/- 17 (SE) mmol/kg dry wt during exercise I and II, respectively. Muscle and blood lactate were only moderately increased during exercise. The total adenine nucleotide pool (TAN = ATP + ADP + AMP) decreased and inosine 5′-monophosphate (IMP) increased in the working muscle during both exercise I (P less than 0.001) and II (P less than 0.01). Muscle content of ammonia (NH3) increased four- and eight-fold during exercise I and II, respectively. The working legs released NH3, and plasma NH3 increased progressively during exercise. The release of NH3 at the end of exercise II was fivefold higher than that at the same time point in exercise I (P less than 0.001, exercise I vs. II). It is concluded that submaximal exercise to fatigue results in a breakdown of the TAN in the working muscle through deamination of AMP to IMP and NH3. The relatively low lactate levels demonstrate that acidosis is not a necessary prerequisite for activation of AMP deaminase. It is suggested that the higher average rate of AMP deamination during exercise II vs. exercise I is due to a relative impairment of ATP resynthesis caused by the low muscle glycogen level.

Muscle and Liver Glycogen of Mouse Strains Susceptible or Resistant to Nutritionally Induced Obesity

Muscle and liver glycogen levels of mice differing in their susceptibility to nutritionally induced obesity were studied in relation to inherited differences in metabolic and endocrine patterns. The I/Fn strain, resistant to nutritional obesity, is characterized by a muscle glycogen level four to six times higher than those of strains which can be made obese. The liver glycogen of the I strain mouse is significantly lower than those of the other strains. Muscle glycogen levels were found to reach a maximum at about 6 months of age in all but one of our strains.