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Slowing and loss of muscle power are major factors limiting physical performance but little is known about the molecular mechanisms involved. The slowing might be a consequence of slow detachment of cross bridges and, if this were the case, then a reduction in the ATP cost of an isometric contraction would be expected as the muscle fatigued. The human anterior tibialis muscle was stimulated repeatedly under ischaemic conditions at 50 Hz for 1.6 s with a 50% duty cycle and muscle metabolites measured by 31P magnetic resonance spectroscopy. Over the course of 20 contractions the half-time of relaxation increased from 36.5 ± 0.09 ms (mean ±s.e.m.) to 113 ± 17 ms and isometric force was reduced to 63 ± 3% of the initial value. ATP turnover was determined from the change in high energy phosphates and lactate production, the latter estimated from the change of intracellular pH. ATP turnover over the first three contractions was 2.45 ± 0.09 mm s−1 and decreased to 1.8 ± 0.06 mm s−1 over the last five tetani. However, when this latter value was normalised for the decrease in isometric force, it became 2.56 ± 0.3 mm s−1, which is the same as the turnover of the fresh muscle. The data suggest that the rate of cross bridge detachment is unaffected by fatigue and are consistent the suggestion that it is the rate of attachment which is slowed rather than the rate of detachment. The present results focus attention on stages in the cross bridge cycle concerned with attachment and the transition from low to high force states that may be influenced by metabolic changes in the fatiguing muscle.

Human subjects can quickly adapt and maintain performance of arm reaching when experiencing novel physical environments such as robot-induced velocity-dependent force fields. Using anodal transcranial direct current stimulation (tDCS) this study showed that the primary motor cortex may play a role in motor adaptation of this sort. Subjects performed arm reaching movement trials in three phases: in a null force field (baseline), in a velocity-dependent force field (adaptation; 25 N s m−1) and once again in a null force field (de-adaptation). Active or sham tDCS was directed to the motor cortex representation of biceps brachii muscle during the adaptation phase of the motor learning protocol. During the adaptation phase, the global error in arm reaching (summed error from an ideal trajectory) was similar in both tDCS conditions. However, active tDCS induced a significantly greater global reaching (overshoot) error during the early stage of de-adaptation compared to the sham tDCS condition. The overshoot error may be representative of the development of a greater predictive movement to overcome the expected imposed force. An estimate of the predictive, initial movement trajectory (signed error in the first 150 ms of movement) was significantly augmented during the adaptation phase with active tDCS compared to sham tDCS. Furthermore, this increase was linearly related to the change of the overshoot summed error in the de-adaptation process. Together the results suggest that anodal tDCS augments the development of an internal model of the novel adapted movement and suggests that the primary motor cortex is involved in adaptation of reaching movements of healthy human subjects.

1. The metabolic costs and physiological consequences of shortening contractions of a human muscle working in situ have been compared with those of the muscle maintaining a continuous isometric contraction and when performing repeated brief isometric contractions. 2. After a total of 10 s stimulation, the shortening and intermittent brief isometric protocols had very similar effects, causing a 30% loss of force and a threefold increase in the half-time of relaxation. This was in contrast to the continuous isometric contraction protocol where there was less than 10% loss of force or slowing of relaxation. 3. The ATP cost over the first 5 s of the continuous isometric protocol was 27 mmol (l intracellular water)-1 while for the shortening and repeated brief isometric protocols the costs were 48 and 46 mmol (l intracellular water)-1, respectively. 4. The results show that shortening and repeated brief isometric contractions are considerably more energetically demanding, and hence more fatiguing, than sustained isometric contractions.

Short-term (6 weeks) voluntary wheel running exercise in young female rats that were in an active growth phase resulted in whole-heart hypertrophy and myocyte concentric hypertrophy, when compared to sedentary controls. The cross-sectional area of ventricular myocytes from trained rats was significantly greater than for those isolated from sedentary rats, with the greatest change in morphology seen in sub-endocardial cells. There was no statistically significant effect of training on cell shortening in the absence of external mechanical loading, in [Ca2+](i) transients, or in myofilament Ca2+ sensitivity (assessed during re-lengthening following tetanic stimulation). Under the external mechanical load of carbon fibres, absolute force developed in myocytes from trained rats was significantly greater than in those from sedentary rats. This suggests that increased myocyte cross-sectional area is a major contractile adaptation to exercise in this model. Training did not alter the passive mechanical properties of myocytes or the relative distribution of titin isomers, which was exclusively of the short, N2B form. However, training did increase the steepness of the active tension-sarcomere length relationship, suggesting an exercise-induced modulation of the Frank-Starling mechanism. This effect would be expected to enhance cardiac contractility. Training lengthened the action potential duration of sub-epicardial myocytes, reducing the transmural gradient in action potential duration. This observation may be important in understanding the cellular causes of T-wave abnormalities found in the electrocardiograms of some athletes. Our study shows that voluntary exercise modulates the morphological, mechanical and electrical properties of cardiac myocytes, and that this modulation is dependent upon the regional origin of the myocytes.

1. The effects of artificial swim training on maximal oxygen consumption and heart rate, as well as on the capillarity and oxidative capacity of locomotory muscles, have been studied in the tufted duck, Aythya fuligula. 2. The artificial training programme resulted in a 27% increase in maximal oxygen consumption, mainly as a result of an increase in muscle capillarity (20% increase in capillary/fibre ratio). In addition, activity of an oxidative enzyme, citrate synthase, increased (by 42%) and there was a significant transformation of fibre types in the lateral gastrocnemius muscle. 3. Altering the duration and nature of the training stimulus, for example flying and diving, can bring about different degrees of muscular adaptation, particularly in oxidative capacity.