http://www.researchonline.mq.edu.au/vital/access/services/Feed ${session.getAttribute("locale")} 5 http://www.researchonline.mq.edu.au/vital/access/manager/Repository/mq:23756 Evidence that unilateral training increases contralateral strength is inconsistent, possibly because existing studies have design limitations such as lack of control groups, lack of randomization, and insufficient statistical power. This study sought to determine whether unilateral resistance training increases contralateral strength. Subjects (n = 115) were randomly assigned to a control group or one of the following four training groups that performed supervised elbow flexion contractions: 1) one set at high speed, 2) one set at low speed, 3) three sets at high speed, or 4) three sets at low speed. Training was 3 times/wk for 6 wk with a six- to eight-repetition maximum load. Control subjects attended sessions but did not exercise. Elbow flexor strength was measured with a one-repetition maximum arm curl before and after training. Training with one set at slow speed did not produce an increase in contralateral strength (mean effect of -1% or -0.07 kg; 95% confidence interval: -0.42-0.28 kg; P = 0.68). However, three sets increased strength of the untrained arm by a mean of 7% of initial strength (additional mean effect of 0.41 kg; 95% confidence interval: 0.06-0.75 kg; P = 0.022). There was a tendency for training with fast contractions to produce a greater increase in contralateral strength than slow training (additional mean effect of 5% or 0.31 kg; 95% confidence interval: -0.03-0.66 kg; P = 0.08), but there was no interaction between the number of sets and training speed. We conclude that three sets of unilateral resistance exercise produce small contralateral increases in strength. 2013-01-14T18:02:04.935Z ]]> http://www.researchonline.mq.edu.au/vital/access/manager/Repository/mq:19904 A progressive and sustained increase in inspiratory-related motor output ("long-term facilitation") and an augmented ventilatory response to hypoxia occur following acute intermittent hypoxia (AIH). To date, acute plasticity in respiratory motor outputs active in the postinspiratory and expiratory phases has not been studied. The recurrent laryngeal nerve (RLN) innervates laryngeal abductor muscles that widen the glottic aperture during inspiration. Other efferent fibers in the RLN innervate adductor muscles that partially narrow the glottic aperture during postinspiration. The aim of this study was to investigate whether or not AIH elicits a serotonin-mediated long-term facilitation of laryngeal abductor muscles, and if recruitment of adductor muscle activity occurs following AIH. Urethane anesthetized, paralyzed, unilaterally vagotomized, and artificially ventilated adult male Sprague-Dawley rats were subjected to 10 exposures of hypoxia (10% O 2 in N 2, 45 s, separated by 5 min, n = 7). At 60 min post-AIH, phrenic nerve activity and inspiratory RLN activity were elevated (39 ± 11 and 23 ± 6% above baseline, respectively). These responses were abolished by pretreatment with the serotonin-receptor antagonist, methysergide (n = 4). No increase occurred in time control animals (n = 7). Animals that did not exhibit postinspiratory RLN activity at baseline did not show recruitment of this activity post-AIH (n = 6). A repeat hypoxia 60 min after AIH produced a significantly greater peak response in both phrenic and RLN activity, accompanied by a prolonged recovery time that was also prevented by pretreatment with methysergide. We conclude that AIH induces neural plasticity in laryngeal motoneurons, via serotonin-mediated mechanisms similar to that observed in phrenic motoneurons: the so-called "Q-pathway". We also provide evidence that the augmented responsiveness to repeat hypoxia following AIH also involves a serotonergic mechanism. 2012-06-18T09:42:48.188Z ]]> http://www.researchonline.mq.edu.au/vital/access/manager/Repository/mq:12478 Epidemiological studies link habitual snoring and stroke, but mechanisms involved are poorly understood. One previously advanced hypothesis is that transmitted snoring vibration energy may promote carotid atheromatous plaque formation or rupture. To test whether vibration energy is present in carotid artery walls during snoring we developed an animal model in which we examined induced snoring (IS)-associated tissue energy levels. In six male, supine, anesthetized, spontaneously breathing New Zealand White rabbits, we surgically inserted pressure transducer-tipped catheters (Millar) to monitor tissue pressure at the carotid artery bifurcation (PCT) and within the carotid sinus lumen (PCS; artery ligated). Snoring was induced via external compression (sandbag) over the pharyngeal region. Data were analyzed using power spectral analysis for frequency bands above and below 50 Hz. For frequencies below 50 Hz, PCT energy was 2.2 (1.1–12.3) cmH₂O² [median (interquartile range)] during tidal breathing (TB) increasing to 39.0 (2.5–95.0) cmH₂O² during IS (P = 0.05, Wilcoxon's signed-rank test). For frequencies >50 Hz, PCT energy increased from 9.2 (8.3–10.4) x 10⁻⁴ cmH₂O² during TB to 172.0 (118.0–569.0) x 10⁻⁴ cmH₂O² during IS (P = 0.03). Concurrently, PCS energy was 13.4 (8.5–18.0) x 10⁻⁴ cmH₂O² during TB and 151.0 (78.2–278.8) x 10⁻⁴ cmH₂O² during IS (P < 0.03). The PCS energy was greater than PCT energy for the 100–275 Hz bandwidth. In conclusion, during IS there is increased energy around and within the carotid artery, including lower frequency amplification for PCS. These findings may have implications for carotid atherogenesis and/or plaque rupture. 2011-04-07T05:00:30.246Z ]]>