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Repeated treatment of rats with ethanol (1 g/kg, once daily for 15 days) enhanced the locomotor effect of morphine, 3 weeks post-treatment. This ethanol-induced long-term behavioural sensitization to morphine was associated with an increase in the electrically evoked release of [3H]dopamine (DA) and [14C]acetylcholine (ACh) from nucleus accumbens slices. A similar enhanced responsiveness of accumbal dopaminergic and cholinergic neurons to depolarization was apparent 3 weeks after repeated morphine, amphetamine or cocaine administration. Prior ethanol exposure also caused a long-term enhancement of electrically evoked release of [3H]DA and [14C]ACh from slices of the caudate-putamen. Unlike the locomotor effect of morphine, that of amphetamine was not enhanced in ethanol-pretreated rats. These data indicate that ethanol administration may cause long-term behavioural sensitization associated with adaptive changes in dopaminergic and cholinergic neurons of rat nucleus accumbens and caudate-putamen. Furthermore, an enhanced reactivity of nucleus accumbens dopaminergic nerve terminals and dopamine-sensitive cholinergic neurons appears to be a common long-term neuroadaptive effect of distinct types of addictive drugs. However, since repeated ethanol exposure did not cause a long-term increase in the locomotor effect of amphetamine, these neuroadaptations may not always be sufficient to cause long-lasting behavioural (cross-)sensitization.

In the present study, the reactivity of striatal dopamine and dopamine-sensitive neurons in super-fused striatal slices of ethanol-experienced rats was compared to that of ethanol-naive rats, 3 weeks after oral ethanol self-administration. During the acquisition phase (17 days), rats were offered increasing concentrations of ethanol (from 2 to 10%, 24 h per day) on an alternate-day schedule in a free choice with water. Following 2 weeks of unrestricted 10% ethanol consumption, the highest and lowest drinkers (representing about 25% of the upper and lower extremes of the total population) were selected. Preliminary experiments revealed that both groups of rats displayed a profound increase in ethanol consumption and preference 3 weeks after cessation of ethanol self-administration (deprivation effect). This deprivation effect was associated with an increase in electrically evoked release of [3H]dopamine from superfused nucleus accumbens slices, whereas the evoked [3H]dopamine release from caudate putamen slices remained unchanged. In slices of the caudate putamen, but not in nucleus accumbens slices, postsynaptic dopamine D1 receptor-stimulated cyclic AMP production was also enhanced. In addition, prior ethanol consumption enhanced the electrically evoked release of [14C]acetylcholine release in both striatal regions. Interestingly, the magnitude of these long-term neuroadaptations correlated with the amount of daily ethanol consumption, i.e. neuronal hyperresponsiveness in the striatum was more profound in the high than in the low ethanol drinkers. These data show for the first time that unrestricted free-choice ethanol consumption in rats is associated with a long-term increase in dopaminergic and cholinergic neurotransmission in the nucleus accumbens and caudate putamen. These (and other) neuroadaptations may underlie the enhanced motivation to self-administer ethanol and the maintenance of ethanol consumption long after deprivation.

The main result of this study is that biarticular leg muscles contribute significantly to the work done at joints, due to transfer of power during explosive leg extensions. In particular, a net power transfer was shown from hip to knee joint during jumping and sprinting. Seven elite athletes performed explosive one legged jump and spring push offs. Kinematics, ground reaction forces and electromyography (EMG) of leg muscles were recorded. The mechanical output of six individual muscle groups was estimated by using Hill-based muscle models. The EMG and kinematics served as input to these models. For jumping as well as for sprinting, the model estimated similar results for the relative work contribution done about a joint due to transfer of power by the biarticular muscles. Rectus femoris showed a power transfer from hip to knee joint, while in contrast hamstrings showed a power transfer from knee to hip joint. Regardless of these opposite directions of power transfer, a net transfer occurred from the hip to the knee joint. The relative work contribution of hamstrings done in hip extension was 7% in jumping and 11% in sprinting. For rectus femoris, the relative work contribution done in knee extension was 21% in jumping and 31% in sprinting. Power transferring actions by gastrocnemius from knee to ankle contributed 25% in jumping and 28% in sprinting to the work done in plantar flexion. These results support the hypothesis that the action of biarticular muscles contributes to a net transfer of power from proximal to distal joints during explosive leg extensions. This action of the biarticular muscles causes an efficient conversion of body segment rotations into the desired translation of the body centre of gravity.

People after stroke often have a lower aerobic capacity than their healthy peers. On top of that, the aerobic load of daily activities such as walking is frequently (much) higher in this group. Often, these issues are investigated separately, but the actual impact on daily functioning can only be perceived when they are combined. A lower capacity and higher load will result in a high relative aerobic load of daily activities, i.e., people need to act at a high level of their maximal capacity. A high relative aerobic load may be a central cause of limitations in daily activities and participation as people either fatigue easily during tasks with a high load, have to slow their pace, or avoid these tasks all together. In this chapter, we review the current knowledge on aerobic capacity and aerobic load of daily activities in people after stroke. Moreover, we estimate the relative load experienced by stroke survivors performing these activities in an attempt to better understand the role of aerobic capacity and load in activity limitations in people after stroke.

The effects of low doses of alcohol on neural synchronization in muscular activity were investigated in ten participants during quiet standing with eyes open or closed. We focused on changes in common input to bilateral motor unit pools as evident in surface electromyographic (EMG) recordings of lower leg extensor and flexor muscles. The extensor muscles exhibited bilateral synchronization in two distinct frequency bands (i.e., 0–5 and 10–15 Hz), whereas synchronization between flexor muscles was minimal. As expected, alcohol ingestion affected postural sway, yielding increased sway at higher blood-alcohol levels. Whereas vision affected bilateral synchronization only at 0–5 Hz, alcohol ingestion resulted in a progressive decrease of synchronization at 10–15 Hz between the EMG activities of the extensor muscles. The decrease in common bilateral input is most likely related to reduced reticulospinal activity with alcohol ingestion.