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Focal dystonia can result in a variety of technical problems in the performing musician, most often affecting control of finger movement, and embouchure. Less common is the effect of focal dystonia on the vibrato of string players. The professional cellist in our study presented with difficulty controlling her vibrato, which fluctuated both in speed and amplitude, causing an inconsistency of sound. This study investigated whether instrumental retraining could alleviate her condition. We report the novel finding that instrumental retraining can significantly improve the symptoms of a dystonic vibrato in a cellist.

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Focal dystonia (FD) is a devastating neurological condition which causes involuntary muscle contractions and often results in the loss of a musician's playing ability. Our study investigated whether retraining via video conferencing could be helpful in the treatment of a professional pianist with a 5-year history of FD. Although full recovery was not seen, improvement was observed at slow tempi, and his hand was visibly less cramped as training sessions progressed. We conclude that video conferencing could be an acceptable medium to assist pianism retraining in pianists with FD when location prevents on-site retraining. However, in this study it did not seem as effective as previously reported, similar, one-on-one retraining in the same location.

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CONTEXT: Although the primary cause of exercise-associated hyponatremia (EAH) is relative overconsumption of fluids beyond the kidneys' ability to excrete excess fluid, the mechanisms limiting maximum renal excretory ability during exercise remain to be elucidated. OBJECTIVE: The objective of the study was to: 1) perform a comprehensive evaluation of the endocrine secretion of pituitary, natriuretic and adrenal steroid hormones, and cytokines immediately before and after running an ultramarathon; and 2) evaluate the relationship between osmotic and nonosmotic stimuli to arginine vasopressin (AVP) secretion within the overall context of assessing the hormonal regulation of fluid balance during prolonged endurance exercise. DESIGN: This was an observational study. SETTING: The study setting was a 56-km ultramarathon. PARTICIPANTS: Eighty-two runners participated in the study. INTERVENTIONS: There were no interventions. MAIN OUTCOME MEASURES: Plasma sodium concentration [Na(+)] and plasma volume [(AVP)(p)] were measured. RESULTS: Fluid homeostasis during exercise (356 +/- 4 min) was maintained with ad libitum fluid intakes. [Na(+)] was maintained from before the race (139.3 +/- 0.3 mmol/liter) to after the race (138.1 +/- 0.4 mmol/liter) with a significant decrease in plasma volume (-8.5 +/- 0.1%, P < 0.01). Increases in the plasma (AVP)(p) (3.9-fold), oxytocin (1.9-fold), brain natriuretic peptide (4.5-fold), and IL-6 (12.5-fold) were highly significant (P < 0.0001). Changes in brain natriuretic peptide, oxytocin, and corticosterone were associated with 47% of the variance noted in (AVP)(p) and 13% of the variance in plasma [Na(+)] in pathway analyses. CONCLUSIONS: (AVP)(p) was markedly elevated after the ultramarathon despite unchanged plasma [Na(+)](.) Therefore, an inability to maximally suppress (AVP)(P) during exercise as a result of nonosmotic stimulation of AVP secretion may contribute to the pathogenesis of exercise-associated hyponatremia if voluntary fluid intake were to exceed fluid output.

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PURPOSE: Exertional hyponatremia ((Na) < 135 mmol x L(-1)) is a potentially serious condition associated with endurance sports. It has been postulated that nonsteroidal antiinflammatory drug (NSAID) use may be a risk factor. This observational cohort study aimed to determine whether NSAID use is a risk factor for exertional hyponatremia and altered renal function during endurance exercise. METHODS: A total of 330 athletes in the 2004 New Zealand Ironman triathlon (3.8-km swim, 180-km cycle, and 42.2-km run) were weighed before and after the race. A blood sample was drawn for measurement of plasma sodium (Na), potassium (K), urea (urea), and creatinine (creatinine) concentrations postrace. RESULTS: The incidence of NSAID use was 30%, whereas the overall incidence of hyponatremia was 1.8%. NSAID use was related to the incidence of hyponatremia (P = 0.0002). The NSAID group had lower plasma Na (P = 0.02) and higher plasma K (P = 0.002), urea (P = 0.05), and creatinine (P = 0.01). Lower Na was also significantly related to female gender, lower prerace body weight, younger age and a smaller weight loss during the race. Race times were not associated with plasma Na; however, faster triathletes lost more weight. Estimated fluid intake was not different in the NSAID group, but heavier triathletes reported greater fluid intakes. CONCLUSIONS: NSAIDs are commonly used by athletes competing in endurance events and are a risk factor for hyponatremia and altered renal function. Notwithstanding high rates of NSAID use, the incidence of hyponatremia was low. We attribute this to changes in fluid replacement guidelines and drink station availability that reduce the risk of overdrinking, the principal cause of this condition.

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OBJECTIVE: To study hematological and biochemical parameters prospectively in runners completing a standard 42.2-km marathon run. To determine the incidence of hyponatremia in runners, and whether consumption of nonsteroidal anti-inflammatory medications (NSAIDs) was associated with alterations in serum biochemical parameters. DESIGN: Observational cohort study. SETTING: City of Christchurch (New Zealand) Marathon, June 2002. PARTICIPANTS: One hundred fifty-five of the 296 athletes entered in the 2002 City of Christchurch Marathon were enrolled in the study. MAIN OUTCOME MEASURES: Athletes were weighed at race registration and immediately after the race. Blood was drawn postrace for measurement of serum sodium, potassium, creatinine, and urea concentrations and for hematological analysis (hemoglobin concentration, hematocrit, leukocyte distribution). RESULTS: Complete data sets including prerace and postrace weights, and postrace hematological and biochemical analyses were collected on 134 marathon finishers. Postrace serum sodium concentrations were directly related to changes in body weight (P < 0.0001). There were no cases of biochemical or symptomatic hyponatremia. Thirteen percent of runners had taken an NSAID in the 24 hours prior to the race. Mean values for serum creatinine (P = 0.03) and serum potassium (P = 0.007) concentrations were significantly higher in runners who had taken an NSAID. No athlete who had taken an NSAID had a postrace serum creatinine concentration less than 0.09 mmol/L. Ninety-eight percent of runners had a postrace leukocytosis (mean white cell count, 18.97 b/L), of which the major component was a raised neutrophil count (mean neutrophil count, 15.69 b/L). CONCLUSIONS: This study found no cases of hyponatremia in runners completing a standard distance marathon. This finding relates to a marathon run under ideal conditions (minimal climatic stress) and in which there were fewer aid stations (every 5 km) than is common in North American marathons (every 1.6 km). Also, aggressive hydration practices were not promoted. Consumption of NSAIDs in the 24 hours prior to distance running was associated with altered renal function.

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Exercise-associated collapse (EAC) is the most common reason that athletes are treated in the medical tent following an endurance event. The pathophysiology of EAC is postural hypotension that results when the loss of muscle pumping action caused by the cessation of exercise is combined with cutaneous vasodilation. EAC usually occurs after an athlete crosses the finish line. If an athlete collapses during a race, then another serious medical cause is more likely. A brief assessment of the collapsed athlete should be carried out to obtain a working diagnosis. Prompt treatment of EAC includes elevating the legs and pelvis of the athlete.

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OBJECTIVE: The objective of this study was to determine whether sodium supplementation 1) influences changes in body weight, serum sodium [Na], and plasma volume (PV), and 2) prevents hyponatremia in Ironman triathletes. SETTING: The study was carried out at the South African Ironman triathlon. PARTICIPANTS: Thirty-eight athletes competing in the triathlon were given salt tablets to ingest during the race. Data collected from these athletes [salt intake group (SI)] were compared with data from athletes not given salt [no salt group (NS)]. INTERVENTIONS: Salt tablets were given to the SI group to provide approximately 700 mg/h of sodium. MAIN OUTCOME MEASUREMENTS: Serum sodium, hemoglobin, and hematocrit were measured at race registration and after the race. Weights were measured before and after the race. Members of SI were retrospectively matched to subjects in NS for 1) weight change and 2) pre-race [Na]. RESULTS: The SI group developed a 3.3-kg weight loss (p < 0.0001) and significantly increased their [Na] (delta[Na] 1.52 mmol/L; p = 0.005). When matched for weight change during the race, SI increased their [Na] compared with NS (mean 1.52 versus 0.04 mmol/L), but this did not reach statistical significance (p = 0.08). When matched for pre-race [Na], SI had a significantly smaller percent body weight loss than NS (-4.3% versus -5.1%; p = 0.04). There was no significant difference in the increase of [Na] in both groups (1.57 versus 0.84 mmol/L). PV increased equally in both groups. None of the subjects finished the race with [Na] < 135 mmol/L. CONCLUSIONS: Sodium ingestion was associated with a decrease in the extent of weight loss during the race. There was no evidence that sodium ingestion significantly influenced changes in [Na] or PV more than fluid replacement alone in the Ironman triathletes in this study. Sodium supplementation was not necessary to prevent the development of hyponatremia in these athletes who lost weight, indicating that they had only partially replaced their fluid and other losses during the Ironman triathlon.

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Energy balance of 10 male and 8 female triathletes participating in an Ironman event (3.8-km swim, 180-km cycle, 42.2-km run) was investigated. Energy intake (EI) was monitored at 7 designated points by dietary recall of food and fluid consumption. Energy expenditure (EE) during cycling and running was calculated using heart rate-VO, regression equations and during swimming by the multiple regression equation: Y = 3.65v+ 0.02W- 2.545 where Yis VO,in L x min(-1), v is the velocity in m s(-1), Wis the body weight in kilograms. Total EE (10,036 +/- 931 and 8,570 +/- 1,014 kcal) was significantly greater than total EI (3,940 +/- 868 and 3,115 +/- 914 kcal, p <.001) for males and females, respectively, although energy balance was not different between genders. Finishing time was inversely related to carbohydrate (CHO) intake (g x kg(-1) x h(-1)) during the marathon run for males (r = -.75,p <.05), and not females, suggesting that increasing CHO ingestion during the run may have been a useful strategy for improving Ironman performance in male triathletes.

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