Role of glycogen availability on SR Ca2+ kinetics in human skeletal muscle
Niels Ortenblad1,5, Joachim Nielsen2, Bengt Saltin3 and Hans Christer Holmberg4
Published online before print December 6, 2010, doi:10.1113/jphysiol.2010.195982
The Journal of Physiology
Little is known about the precise mechanism that relates skeletal muscle glycogen to muscle fatigue. The aim of the present study was to examine the effect of glycogen on sarcoplasmic reticulum (SR) function in the arm and leg muscles of elite cross-country skiers (n=10, V ̇O2 max 72±2 ml . kg-1 min-1) before, immediately after, and 4h and 22h after a fatiguing 1h ski race. During the first 4hrs recovery, skiers received either water or carbohydrate (CHO) and thereafter all received CHO enriched food. Immediately after the race, arm glycogen was reduced to 31±4% and SR Ca2+ release rate decreased to 85±2% of initial levels. Glycogen noticeably recovered after 4h recovery with CHO (59±5% initial) and the SR Ca2+ release rate returned to pre-exercise levels. However, in the absence of CHO during the first 4h recovery, glycogen and the SR Ca2+ release rate remained unchanged (29±2% and 77±8%, respectively), with both parameters becoming normal after the remaining 18h recovery with CHO. Leg muscle glycogen decreased to a lesser extent (71±10% initial), with no effects on the SR Ca2+ release rate. Interestingly, transmission electron microscopy (TEM) analysis revealed that the specific pool of intramyofibrillar glycogen, representing 10-15% total glycogen, was highly significantly correlated with the SR Ca2+ release rate. These observations strongly indicate that low glycogen and especially intramyofibrillar glycogen, as suggested by TEM, modulate the SR Ca2+ release rate in highly trained subjects. Thus, low glycogen during exercise may contribute to fatigue by causing a decreased SR Ca2+ release rate.
Skeletal muscle fatigue precedes the slow component of oxygen uptake kinetics during exercise in humans
Daniel T Cannon1, Ailish C White2, Melina F Andriano2, Fred W Kolkhorst2 and Harry B Rossiter1,3
Published online before print December 6, 2010, doi:10.1113/jphysiol.2010.197723
The Journal of Physiology
During constant work rate (CWR) exercise above the lactate threshold (LT), the exponential kinetics of oxygen uptake (VO2) are supplemented by a VO2 slow component (VO2sc) which reduces work efficiency. This has been hypothesised to result from “fatigue and recruitment”: where muscle fatigue during supra-LT exercise elicits recruitment of additional, but poorly-efficient, fibres to maintain power production. To test this hypothesis we characterised changes in the power-velocity relationship during sub- and supra-LT cycle ergometry in concert with VO2 kinetics. Eight healthy participants completed a randomized series of 18 experiments consisting of: 1) a CWR phase of 3 or 8 min followed immediately by; 2) a 5 s maximal isokinetic effort to characterize peak power at 60, 90 and 120 rpm. CWR bouts were: 20W (CON); 80%LT (MOD); 20%Δ (H); 60%Δ (VH); where Δ is the difference between the work rate at LT and VO2max. The VO2sc was 238 ± 128, and 686 ± 194 mL.min-1 during H and VH, with no discernible VO2sc during MOD. Peak power in CON was 1025 ± 400, 1219 ± 167, and 1298 ± 233 W, at 60, 90, and 120 rpm respectively, and was not different after MOD (p > 0.05). Velocity-specific peak power was significantly reduced (p < 0.05) by 3 min of H (-103 ± 46 W) and VH (-216 ± 60 W), with no further change by 8 min. The VO2sc was correlated with the reduction in peak power (R2 = 0.49; p < 0.05). These results suggest that muscle fatigue is requisite for the VO2sc. However, the maintenance of velocity-specific peak power between 3 and 8 min suggests that progressive muscle recruitment is not obligatory. Rather, a reduction in mechanical efficiency in fatigued fibres is implicated.
Plasma pH does not influence the cerebral metabolic ratio during maximal whole body exercise
Stefanos Volianitis1,4, Peter Rasmussen2, Thomas Seifert3, Henning Bay Nielsen2 and Niels H Secher2
Published online before print November 22, 2010, doi:10.1113/jphysiol.2010.195636
The Journal of Physiology
Exercise lowers the cerebral metabolic ratio of O2 to carbohydrate (glucose + ½ lactate) and metabolic acidosis appears to promote the cerebral lactate uptake. However, the influence of pH on cerebral lactate uptake and, in turn, on the cerebral metabolic ratio during exercise is not known. Sodium bicarbonate (Bic, 1 M; 350-500 ml) or an equal volume of normal saline (Sal) was infused intravenously at a constant rate during a "2,000-m" maximal ergometer row in six male oarsmen (23 ± 2 yrs; mean ± SD). During the Sal trial, pH decreased from 7.41 ± 0.01 at rest to 7.02 ± 0.02 but only to 7.36 ± 0.02 (P < 0.05) during the Bic trial. Arterial lactate increased to 21.4 ± 0.8 and 32.7 ± 2.3 mM during the Sal and Bic trials, respectively (P < 0.05). Also, the arterial-jugular venous lactate difference increased from -0.03 ± 0.01 mM at rest to 3.2 ± 0.9 mM (P < 0.05) and 3.4 ± 1.4 mM (P < 0.05) following the Sal and Bic trials, respectively. Accordingly, the cerebral metabolic ratio decreased equally during the Sal and Bic trials: from 5.8 ± 0.6 at rest to 1.7 ± 0.1 and 1.8 ± 0.2, respectively. The enlarged blood-buffering capacity after infusion of Bic eliminated metabolic acidosis during maximal exercise but that did not affect the cerebral lactate uptake and, therefore, the decrease in the cerebral metabolic ratio.