Prolonged asystolia in a young athlete: a case of sinus arrest during REM sleep

A young asymptomatic male athlete came to our laboratory to be enrolled in a research protocol on physical fatigue. Routine clinical and cardiological evaluations including echocardiogram were in the normal range. Several consecutive cardiopulmonary tests showed a fairly good tolerance to exercise, with no symptoms even when the effort was abruptly arrested. On the other hand, Holter ECG recordings showed long nocturnal sinus pauses. As he was absolutely asymptomatic and free from any structural heart disease, he underwent a follow-up with repeated Holter monitorings for one year. During this period he decided on his own to stop practising sports; in spite of this sharp reduction in his overall physical activity, consecutive Holter monitorings showed that the sinus pauses were progressively increasing in duration (up to 9.2 seconds). With the hypothesis of a malignant vagotonia, he underwent a tilt test; however, we could not elicit any pauses or symptoms. The pauses grew longer over time; a endocavitary electrophysiologic test was performed, which showed no evidence of disease. To rule out the hypothesis of a sleep apnoea syndrome, he also underwent a polysomnography, including EEG, eye movement electromyography, arterial blood oxygen saturation and thoracic impedance: no alterations were detected with the exception of the sinus pauses, which appeared to be strictly linked to REM sleep, as suggested by the concurrent increase in rapid eye movements and desynchronized EEG. We hence made a diagnosis of sinus arrest during REM sleep (SAdRS), a very uncommon disease belonging to the parasomnias. Pauses were then quantified for one month by implanting a ECG loop recorder. As the patient became more and more upset and worried, and the pauses increased to nearly 12 seconds, we decided to implant a pacemaker, which is the only therapeutic option established in the literature for patients with SAdRS.     

Retraining of a competitive master athlete following traumatic injury: a case study

PURPOSE: The purpose of this study was to examine the physiological effects of detraining and retraining in a female master cyclist (age, 49.5 yr; wt, 54 kg) following a surgically-treated clavicular fracture complicated by brachial plexus impingement. METHODS: Variables associated with cycling performance, including VO2max, lactate threshold (LT), power output at a blood lactate concentration of 4 mM (LT(4 mM)), peak power output (PPO), muscular resistance to fatigue measured by a timed ride to exhaustion at 110% of peak power output (PPO110), and body composition (hydrostatic weight) were assessed 2 d before the injury when the subject was at the peak of her competitive season, and at days 0, 14, 28, 42, and 77 of the retraining period. Retraining gradually increased from 3 h x wk(-1) to 9-10 h x wk(-1) with an increase in intensity from approximately 70 to 95+% of HRmax. RESULTS: Detraining resulted in a 25.7% decrease in VO2max and a 16.7% and 18.9% decrease in LT and LT(4 mM), respectively, while peak power output and PPO110 declined 18.2% and 16.6%, respectively. Body fat percent increased 2.1 percentage points, while fat-free mass decreased nearly 2 kg. After 2 wk of retraining, all variables except the LT and LT(4 mM) had improved considerably; however, VO2max was still 14.8% lower and PPO and PPO110 were 12.7% and 5.7% lower than preinjury values. By the 11th week of retraining, all variables had essentially returned to their preinjury values. CONCLUSION: These data demonstrate a pattern of retraining in which aerobic power steadily improved over 6 wk, while measures of lactate threshold did not change until the fourth week of retraining when the intensity of training was markedly increased. Additional data are needed to determine whether this pattern of retraining would be consistent in other master athletes.     

Recurrent rhabdomyolysis in a collegiate athlete: a case report

PURPOSE: Hereditary metabolic disorders can cause rhabdomyolysis in athletes. Team physicians should be aware of the presentation, workup, and management of the most common of these disorders, carnitine palmitoyltransferase (CPT) II deficiency and muscle phosphorylase deficiency. METHODS: The case of a collegiate athlete with recurrent bouts of rhabdomyolysis is presented, and the diagnostic workup is discussed. RESULTS: The patient described in this case has CPT II deficiency. The diagnosis and management of CPT II deficiency and muscle phosphorylase deficiency (McArdle's disease) are discussed. CONCLUSION: Athletes with rhabdomyolysis, in the absence of an obvious cause such as drug toxicity, severe trauma, or excessive exercise, should be evaluated for the presence of a metabolic myopathy.     

Syncope and neurologic deficits in a track athlete: a case report

Exercise-related syncope may result from various underlying medical conditions, with vasovagal reactions being the most common cause in young athletes. However, psychological causes also need to be considered in the differential diagnosis of syncope. This case report presents an athlete who suffered a syncopal event with residual motor and sensory deficits. The athlete was diagnosed with a conversion disorder and was able to return to full competition following psychotherapy and physical therapy.     

Paget-Schroetter syndrome in a non athlete - a case report

A young male waiter presented with left shoulder pain, with ultrasound showing thrombosis of the left subclavian vein. After exclusion of hypercoagulability, a dynamic MRI upper limb venogram was performed, confirming Paget-Schroetter syndrome (PSS). Our case is unusual as Paget Schroetter syndrome are seldom reported in non athletes. This is also the first report to show dynamic MRI images of PSS.     

Hemodynamic changes during neural deactivation in human brain: a positron emission tomography study of crossed cerebellar diaschisis

The mechanism of crossed cerebellar diaschisis (CCD) is considered to be secondary hypoperfusion due to neural deactivation. To elucidate the hemodynamics during neural deactivation, the hemodynamics of CCD was investigated. The cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral oxygen extraction fraction (OEF), cerebral metabolic rate of oxygen (CMRO2), and vascular responses to hypercapnia and acetazolamide stress for CCD were measured in 20 patients with cerebrovascular disease by positron emission tomography with H2(15O), C15O, and 15O2. Vascular responses to hypercapnia and acetazolamide stress were almost the same between CCD side and unaffected side of the cerebellum, a finding that supports the idea that the mechanism of CCD is secondary hypoperfusion due to neural deactivation. The degree of decrease in CBF on the CCD side was almost the same as that in CBV, indicating that vascular blood velocity does not change during neural deactivation. The relation between CBF and CBV of the CCD and unaffected sides was CBV = 0.29 CBF0.56. On the CCD side, the degree of deerease in CMRO2 was less than that in CBF, resulting in a significantly increased OEF. The increased OEF along with the decreased CBV on the CCD side might indicate that neural deactivation primarily causes vasoconstriction rather than a reduction of oxygen metabolism.     

Thigh compartment syndrome in a football athlete: a case report and review of the literature.

Although contusions of the thigh are common in all sports, a compartment syndrome from closed blunt trauma without a femur fracture is rare. Thigh compartment syndrome is unusual due to increased compliance of the thigh to accommodate increased expansion from hematoma or third space fluid. Compartment syndrome of the thigh is characterized by unrelenting pain, swelling, and limited knee range of motion. A single case of a thigh compartment syndrome caused by a direct blow to the anterior aspect of the thigh from a football helmet during kickoff occurred. Immediate thigh fasciotomy was performed. Early diagnosis with appropriate emergency treatment can avoid serious and permanent complications.     

Exertional heat stroke during a cool weather marathon: a case study

A well-trained male runner in his late 30s collapsed 10 m before the finish line, nearly completing the 42.1-km marathon course in 3 h, 15 min. He was responsive to pain, agitated, diaphoretic, and unable to walk. The race start temperature was 6 degrees C (43 degrees F) with relative humidity of 99% and the 3-h temperature was 9.5 degrees C (49 degrees F) with a 62% relative humidity. Approximately 27 min after his collapse, his rectal temperature in the emergency department was 40.7 degrees C (105.3 degrees F), and his failing respiratory status required intubation. His initial Glasgow coma score was 6-7 of 15. His renal output was minimal until he was cooled and given a large fluid flush. His initial echocardiogram showed a "stunned" myocardium with an ejection fraction of 35%. He had a viral syndrome the week prior to the race and was paced by a "fresh" runner the last 16 km of the race. He left the hospital in 5 d and has now returned to running without problems, although several months passed before he felt well while exercising. Exertional heat stroke can occur in cool conditions, and rectal temperature should be checked in all collapsed runners who do not progress with rapid recovery of vital signs and cognitive function. Runners should be instructed not to compete when ill and should not use nonparticipant pacers during the runs.     

Enlargement of the right heart in the endurance athlete: a two-dimensional echocardiographic study

M-mode echocardiographic studies of endurance-trained athletes have provided conflicting data for right ventricular (RV) dimensions and no data for right atrial (RA) size. Since two-dimensional echocardiography provides a more accurate measurement of the RV and RA, it was employed together with M-mode echocardiography to evaluate 12 male endurance athletes and 12 sedentary controls matched for body size and age. All subjects were screened by history, physical examination, ECG, and maximal exercise testing. RV and RA areas were planimetered in the apical four-chamber view while displaying maximal chamber sizes. Athletes had significantly greater left ventricular (LV) wall thickness (P less than 0.01), LV area (P less than 0.001), and left atrial (LA) area (P less than 0.01). They also had greater RV area (P less than 0.01), RV wall thickness (P less than or equal to 0.05), and RA area (P less than or equal to 0.01). Maintained proportionality of the cardiac chamber dimensions in the athletes was shown by similar ratios of right-to-left ventricular areas, right-to-left atrial areas, and right-to-left ventricular wall thicknesses in both groups. The symmetry of the greater athlete's heart differs from most pathological conditions which have heterogeneous effects on specific cardiac chambers.     

Heterotopic ossification of the ulnar collateral ligament: a description of a case in a top level weightlifting athlete

The purpose of this paper is to describe a case of heterotopic ossification of the ulnar collateral ligament in a 29-year-old top level weightlifter. Plain radiography of the elbow determined the extent and location of heterotopic ossification. Ultrasound and MR imaging completed the instrumental set-up. This symptomatic case had the resolution of pain after 2 months of a supervised rehabilitation program. At one year follow-up the athlete is asymptomatic referring occasional minor pain only in the periods of vigorous training.