Do verbal coaching cues and analogies affect motor skill performance in youth populations?

PURPOSE: The way coaching cues are worded can impact on the quality with which a subsequent motor skill is executed. However, there have been few investigations on the effect of coaching cues on basic motor skill performance in youths. METHOD: Across several international locations, a series of experiments were undertaken to determine the effect of external coaching cues (EC), internal coaching cues (IC), analogies with a directional component (ADC) and neutral control cues on sprint time (20 m) and vertical jump height in youth performers. These data were combined using internal meta-analytical techniques to pool results across each test location. This approach was amalgamated with a repeated-measures analysis to determine if there were any differences between the ECs, ICs and ADCs within the different experiments. RESULTS: 173 participants took part. There were no differences between the neutral control and experimental cues in any of the internal meta-analyses except where the control was superior to the IC for vertical jump (d = -0.30, [-0.54, -0.05], p = 0.02). Just three of eleven repeated-measures analyses showed significant differences between the cues at each experimental location. Where significant differences were noted, the control cue was most effective with some limited evidence supporting the use of ADCs (d = 0.32 to 0.62). CONCLUSION: These results suggest the type of cue or analogy provided to a youth performer has little subsequent effect on sprint or jump performance. Accordingly, coaches might take a more specific approach that is suited to the level or preferences of a particular individual.

A two-phase cohort study of the sleep phenotype within primary Sjögren's syndrome and its clinical correlates.

OBJECTIVES: To characterise the sleep profile of patients with primary Sjögren's syndrome (pSS) and its relationship between hyper-somnolence and other clinical parameters. METHODS: In phase one of the study, we utilised cross-sectional data on daytime hyper-somnolence from the United Kingdom Primary Sjögren's Syndrome Registry (UKPSSR) cohort (n=857, female=92.7%). Phase two relied on clinical data from a cohort of patients (n=30) with PSS, utilising symptom assessment questionnaires and sleep diaries. RESULTS: Within the UKPSSR, daytime hyper-somnolence was prevalent (ESS, 8.2±5.1) amongst pSS patients with a positive correlation between daytime hyper-somnolence and fatigue (Spearman's rs = 0.42, p<0.0001). Amongst the clinical cohort, 100% of patients had problematic sleep. Participants with pSS awoke frequently (NWAK, 2.2±1.3), had difficulty in returning back to sleep (WASO, 59.9±50.2 min vs. normal of <30min) and a reduced sleep efficiency (SE, 65.7±18.5% vs. >85%). Fatigue (FIS, 82.4 ±33.5) and orthostatic symptoms (OGS, 6.7 ±3.7) remained high in these patients. CONCLUSIONS: Sleep disturbances are a problem in pSS, comprising difficulty in maintaining sleep, frequent awakenings throughout the night and difficulties in returning back to sleep. As such, the total time in bed without sleep is much greater and sleep efficiency greatly reduced. These patients in addition have a high symptomatic burden possibly contributing to and/or contributed by poor and disordered sleep.

Maturation-related adaptations in running speed in response to sprint training in youth soccer players.

OBJECTIVES: This study investigated the effects of a previously recommended dose of sprint training (ST) in young male soccer players of differing maturity status. DESIGN: Quasi-experimental design. METHODS: Male soccer players from two professional academies were divided into Pre-PHV (Training: n=12; Control: n=13) and Mid-PHV (Training: n=7; Control=10) groups. The training groups completed 16 sprints of 20m with 90s recovery, once per week for 8weeks. RESULTS: Between-group effect sizes (ES) were substantially larger in Pre-PHV (10m [1.54, CI: 0.74-2.23]; 20m [1.49, CI: 0.75-2.23]; 5-10-5 [0.92, CI: 0.23-1.61]) than in Mid-PHV (10m [-0.00, CI: -0.81 to 0.81]; 20m [-0.12, CI: -0.93 to 0.69]; 5-10-5 [-0.41, CI: -1.22 to 0.41]). Within-group effects demonstrated a similar, though less accentuated, trend which revealed ST to be effective in both Pre-PHV (10m [0.44, CI: -0.24 to 1.12]; 20m [0.45, CI: -0.23 to 1.13]; 5-10-5 [0.69, CI: 0.00-1.38]) and Mid-PHV (10m [0.51, CI: -0.38 to 1.40]; 20m [0.33, CI: -0.56 to 1.21]; 5-10-5 [0.43, CI: -0.46 to 1.32]). CONCLUSIONS: ST, in the amount of 16 sprints over 20m with a 90s rest, may be more effective in Pre-PHV youths than in Mid-PHV youths.

Reduced thoracic fluid content in early-stage primary biliary cirrhosis that associates with impaired cardiac inotropy.

Primary biliary cirrhosis (PBC) is a chronic liver disease characterized by cholestasis. Recent MRI studies have confirmed the presence of cardiac abnormalities in noncirrhotic PBC patients. However, cardiorespiratory consequences of these abnormalities have not been explored. Thoracic fluid content (TFC) is a noninvasive bioelectrical impedance measure of the electrical conductivity of the chest cavity. We explored TFC and its relationship with cardiac contractility parameters in early-stage PBC patients, compared with chronic liver disease and community controls. TFC was measured in early-stage PBC (noncirrhotic; n = 78), nonalcoholic fatty liver disease (n = 23), and primary sclerosing cholangitis (n = 18) and in a community control population (n = 78). Myocardial contractility was measured as index of contractility, acceleration index, cardiac index, stroke index, left ventricular ejection time, and left ventricular work index. We also measured total arterial compliance and the Heather Index (HI; cardiac inotropy). The PBC group had significantly lower TFC compared with controls and the chronic liver disease groups (P < 0.0001). There was an association between increasing TFC and markers of cardiac function (cardiac index, stroke index, end-diastolic index, index of contractility, and acceleration index), together with indicators of cardiac inotropy and total arterial compliance. Multivariate analysis confirmed that the only parameter that independently associated with TFC was the marker of cardiac inotropy HI (P = 0.037; ß 0.5). This study has confirmed that TFC is reduced in those with PBC, that this is specific to PBC, and that it associates independently with markers of cardiac inotropy.

Is chronic fatigue syndrome in older patients a different disease? -- a clinical cohort study.

BACKGROUND: Chronic fatigue syndrome (CFS) is a disabling disorder characterised by persistent fatigue with a typical age of diagnosis of 35-50 years. CFS does present in those aged over 50 but whether this is a different disease in older age groups has not been considered. Therefore, we performed a clinical cohort study to examine and differentiate the clinical and autonomic features in CFS patients aged over 50. DESIGN: A total of 179 Fukuda diagnosed CFS patients were recruited, and 25 older CFS patients (50 + years) were matched case by case for gender and length of history to 25 younger CFS patients (16-29 years). A range of symptomatic-based questionnaires were used in addition to heart rate variability and baroreceptor sensitivity to assess autonomic function. RESULTS: Chronic fatigue syndrome can present for the first time in an older population. Older CFS patients demonstrate increased fatigue (Fatigue impact scale; 85 ± 33 vs. 107 ± 27, P = 0·02) (Chalder fatigue scale; 9 ± 3 vs. 11 ± 1, P = 0·002) and caseness for depression (Hospital Anxiety and Depression scale; 7 ± 3 vs. 10 ± 4; P = 0·005). There is a greater autonomic dysfunction in older CFS patients, with reduced parasympathetic function (HFnu; 49·1 ± 18 vs. 36·2 ± 18, P = 0·01, RR30 : 15; ± , P = 0·02) and increased sympathetic function (LFnu; 51·5 ± 17 vs. 63·8 ± 18, P = 0·01). Baroreflex sensitivity was substantially reduced (BRS; 19·7 ± 12 vs. 9·9 ± 5, P = 0·0004), and left ventricular ejection time prolonged (LVET; 274·6 ± 16 vs. 285·8 ± 9, P = 0·004). CONCLUSIONS: Older CFS patients demonstrate a disease phenotype very different from younger patients. The combination of differing underlying pathogenic mechanisms and the physiological aspects of ageing result in a greater disease impact in older CFS patients.