To examine some possible sites of fatigue during short-lasting maximally intensive stretch-shortening cycle exercise, drop jumps on an inclined sledge apparatus were analyzed. Twelve healthy volunteers performed jumps until they were unable to maintain jumping height > 90% of their maximum. After the workout, the increases in the blood lactate concentration and serum creatine kinase activation were statistically significant (P < 0.001 and P < 0.05, respectively) but rather small in physiological terms. The major changes after the workout were as follows: the single twitch was characterized by smaller peak torque (P < 0.05) and shorter time to peak (P < 0.05) and half-relaxation time (P < 0.01). The double-twitch torque remained at the same level (P > 0.05), but with a steeper maximal slope of torque rise (P < 0.05); during 20- and 100-Hz stimulation the torque declined (both P < 0.01) and the maximal voluntary torque changed nonsignificantly but with a smaller maximal slope of torque rise (P < 0.01) and a higher activation level (P < 0.05), accompanied by an increased electromyogram amplitude. These findings indicate that the muscle response after the short-lasting consecutive maximum jumps on the sledge apparatus may involve two distinct mechanisms acting in opposite directions: 1) The contractile mechanism seems to be potentiated through a shorter Ca2+ transient and faster cross-bridge cycling, as implied by twitch changes. 2) High-frequency action potential propagation shows an impairment, which is suggested as the possible dominant reason for fatigue in exercise of this type.

Neural control of muscle contraction seems to be unique during muscle lengthening. The present study aimed to determine the specific sites of modulatory control for lengthening compared with isometric contractions. We used stimulation of the motor cortex and corticospinal tract to observe changes at the spinal and cortical levels. Motor-evoked potentials (MEPs) and cervicomedullary MEPs (CMEPs) were evoked in biceps brachii and brachioradialis during maximal and submaximal lengthening and isometric contractions at the same elbow angle. Sizes of CMEPs and MEPs were lower in lengthening contractions for both muscles (by approximately 28 and approximately 16%, respectively; P < 0.01), but MEP-to-CMEP ratios increased (by approximately 21%; P < 0.05). These results indicate reduced excitability at the spinal level but enhanced motor cortical excitability for lengthening compared with isometric muscle contractions.

The bilateral deficit phenomenon, characterized by a reduction in the amount of force from a single limb during maximal bilateral actions, has been shown in various movement tasks, contraction types and different populations. However, bilateral deficit appears to be an inconsistent phenomenon, with high variability in magnitude and existence, and seems to be plastic, as bilateral facilitation has also been shown to occur. Furthermore, many mechanisms underlying this phenomenon have been proposed over the years, but still remain largely unknown. The purpose of this review was to clarify and critically discuss some of the important issues relevant to bilateral deficit. The main findings of this review were: (1) bilateral deficit does not seem to be contraction-type dependent; however, it is more consistent in dynamic compared to isometric contractions; (2) postural stabilization requirements and/or ability to use counterbalances during unilateral actions seem to influence the expression of bilateral deficit to a great extent; strong evidence has been provided for higher-order neural inhibition as a possible mechanism, but requires further exploration using a lower limb model; biomechanical mechanisms, such as differences in shortening velocity between contraction modes and displacement of the force-velocity curve, seem to underlie bilateral deficit in ballistic and explosive contractions; (3) task familiarity has a large influence on bilateral deficit and thus adequate testing specificity is warranted in training/cross-sectional experiments; (4) the literature investigating the relationship between bilateral deficit and athletic performance and injury remains scarce; hence, further research in this area is required.

The aim of this study was to evaluate muscle fatigue in upper body muscles during 100-m all-out front crawl. Surface electromyogram (EMG) was collected from the pectoralis major, latissimus dorsi and triceps brachii muscles of 11 experienced swimmers. Blood lactate concentration level increased to 14.1 ± 2.9 mmol l(-1) 5 min after the swim. The velocity, stroke length and stroke rate calculated based on video analysis decreased by 15.0, 5.8 and 7.4%, respectively, during the swim. EMG amplitude of the triceps and the lower part of the latissimus muscles increased, whilst the mean power frequency (MNF) of all muscles significantly decreased by 20-25%. No significant differences in the relative MNF decrease were observed amongst the muscles; however, the differences in the rate of the MNF decrease between the lower part of the latissimus and the triceps brachii muscles were found (P < 0.05). The time of rest between the muscle activation of the two consecutive arm strokes at the end of swimming was extended (P < 0.05). It was concluded that 100-m all-out crawl induced significant fatigue with no evident differences amongst the analysed muscles.

The force-length relationship of the human muscle-tendon complex (MTC) of the triceps surae and the achilles tendon was investigated in various stretch load conditions. Six male subjects performed various vertical jumps with maximal effort: squat jumps (SJ), counter movement jumps (CMJ) and drop jumps (DJ) from a height of 24 cm, 40 cm and 56 cm. The force-length relationship was calculated from the signals of the components of the ground reaction forces and the kinematic data obtained from the high-speed film records. Surface electromyograms (EMG) of the soleus, gastrocnemius and tibialis anterior muscles were also recorded. The force-length diagrams showed individually high sensitivity to the imposed stretch load. In conditions with relatively low stretch load requirements there was a counter-clockwise direction observable, indicating that the energy absorbed during the eccentric, or lengthening phase was lower than the energy delivered during the concentric, or shortening phase. In high load conditions this relationship was reversed indicating a negative energy balance. The EMG-length diagrams of SJ and CMJ consisted of an initial isometric loading of the muscle, followed by a shortening phase with only slightly reduced EMG amplitudes. In DJ, however, the diagrams showed an initial lengthening of the MTC with fairly constant activation amplitudes. After 40 ms an isometric loading of the muscle, lasting for approximately 80 ms, was followed by a shortening phase. It was concluded that segmental stretch reflex activation represented the predominant activation process during the isometric loading phase, to meet the adequate stiffness properties of the MTC.

Resistance training may be associated with unfavorable cardiovascular responses (such as hemodynamic alterations, anginal symptoms or ventricular arrhythmias). In healthy adults, blood flow-restricted (BFR) resistance training improves muscle strength and hypertrophy improvements at lower loads with minimal systemic cardiovascular adverse responses. The aim of this study was to assess the safety and efficacy of BFR resistance training in patients with coronary artery disease (CAD) compared to usual care. Patients with stable CAD were randomized to either 8 weeks of supervised biweekly BFR resistance training (30–40% 1RM unilateral knee extension) or usual exercise routine. At baseline and after 8 weeks, patients underwent 1-RM knee extension tests, ultrasonographic appraisal of vastus lateralis (VL) muscle diameter and of systemic (brachial artery) flow-mediated dilation, and determination of markers of inflammation (CD40 ligand and tumor necrosis factor alfa), and fasting glucose and insulin levels for homeostatic model assessment (HOMA). A total of 24 patients [12 per group, mean age 60 ± 2 years, 6 (25%) women] were included. No training-related adverse events were recorded. At baseline groups significantly differ in age (mean difference: 8.7 years, p < 0.001), systolic blood pressure (mean difference: 12.17 mmHg, p = 0.024) and in metabolic control [insulin ( p = 0.014) and HOMA IR ( p = 0.014)]. BFR-resistance training significantly increased muscle strength (1-RM, +8.96 kg, p < 0.001), and decreased systolic blood pressure (-6.77 mmHg; p = 0.030), whereas VL diameter (+0.09 cm, p = 0.096), brachial artery flow-mediated vasodilation (+1.55%; p = 0.079) and insulin sensitivity (HOMA IR change of 1.15, p = 0.079) did not improve significantly. Blood flow restricted resistance training is safe and associated with significant improvements in muscle strength, and may be therefore provided as an additional exercise option to aerobic exercise to improve skeletal muscle functioning in patients with CAD. Clinical Trial Registration: www.ClinicalTrials.gov , identifier: NCT03087292.

To assess the extent of the level of muscle activation during maximal voluntary effort, a method of superimposed trains of electrical impulses delivered at 100 Hz was employed. During a maximal voluntary contraction (MVC) in isometric knee extension, a submaximal superimposed electrical stimulation (ES) of differing train durations was induced to the quadriceps muscle, when maximal voluntary torque was achieved. For all train durations the force increased during ES. During 100 ms and longer trains, the additional torque reached a plateau. The same principle of submaximal electrical stimulation superimposed over MVC was used in explosive isometric knee extensions, comparing the rate of force growth in trials with and without ES. In all subjects ES had an augmenting effect during the increase in force and up to the maximal force. It was concluded that the subjects were not able voluntarily to activate fully their quadriceps muscle. This was true both for maximal force and for the increase in force. It seems that the existence of an activation deficit is a fact, the question is how to quantify it in a reliable and valid way.

It was concluded that after submaximal stretch-shortening exercise, the low-frequency fatigue occurred, very likely caused by lower Ca2+ release per single action potential.