Use of a smartphone electrocardiogram to diagnose arrhythmias during exercise in athletes: a case series.

Background: While athletes are generally very fit, intense exercise can increase the risk of atrial fibrillation. Moreover, other arrhythmias such as atrial flutter or supraventricular tachycardia can cause distressing, exercise-related symptoms. Given symptoms are infrequent and may occur during intense exertion, traditional monitoring devices are often impractical to use during exercise. Smartphone electrocardiograms (ECGs) such as the Alivecor Kardia device may be the portable and reliable tool required to help identify arrhythmias in this challenging population. This case series highlights the use of such devices in aiding the diagnosis of arrhythmias in the setting of exercise-related symptoms in athletes. Case summary: The six cases in this series included one elite non-endurance athlete, two elite cricketers, one amateur middle-distance runner, and two semi-elite ultra-endurance runners, with an age range of 16-48 years. An accurate diagnosis of an arrhythmia was obtained in five cases (atrial fibrillation/flutter and supraventricular tachycardias) using the smartphone ECG, which helped guide definitive treatment. No arrhythmia was identified in the final case despite using the device during multiple symptomatic events. Discussion: The smartphone ECG was able to accurately detect arrhythmias and provide a diagnosis in cases where traditional monitoring had not. The utility of detecting no arrhythmia during symptoms in one case was also highlighted, providing the athlete with the confidence to continue exercising. This reassurance and confidence across all cases is perhaps the most valuable aspect of this device, where clinicians and athletes can be more certain of reaching a diagnosis and undertaking appropriate management.

Life after COVID-19: The importance of a safe return to physical activity.

The Australasian College of Sport and Exercise Physicians has developed a guideline for primary care practitioners to assist with safe return of patients to physical activity after COVID-19.

Does moxonidine reduce Achilles tendon or musculoskeletal pain in women with polycystic ovarian syndrome? A secondary analysis of a randomised controlled trial.

BACKGROUND: Sympathetic activity and insulin resistance have recently been linked with chronic tendon and musculoskeletal pain. Polycystic ovarian syndrome is linked with insulin resistance and increased sympathetic drive and was therefore an appropriate condition to study the effects of modulating sympathetic activity on Achilles tendon and musculoskeletal symptoms. METHODS: A secondary analysis of a double-blinded, randomised controlled trial on women with polycystic ovarian syndrome was conducted. Participants received 12 weeks of moxonidine (n = 14) or placebo (n = 18). Musculoskeletal symptom and Victorian Institute of Sport Assessment - Achilles (VISA-A) questionnaires were distributed, and ultrasound tissue characterisation quantified tendon structure at 0 and 12 weeks. 2-way ANOVA was used for multiple comparisons. RESULTS: There was no difference in mean change in musculoskeletal symptoms (- 0.6 ± 1.7 vs - 0.4 ± 1.8, p = 0.69) or VISA-A (moxonidine - 0.2 ± 8.8 vs placebo + 4.2 ± 14.6, p = 0.24) attributable to the intervention. There was no difference in any measures of Achilles structure. Moxonidine did not reduce sympathetic drive when compared to placebo. CONCLUSIONS: This was the first study to investigate the effects of blocking sympathetic drive on musculoskeletal and Achilles tendon symptoms in a metabolically diverse population. While the study was limited by small sample size and lack of sympathetic modulation, moxonidine did not change tendon pain/structure or musculoskeletal symptoms. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01504321 . Registered 5 January 2012.

The sympathetic nervous system and tendinopathy: a systematic review.

BACKGROUND: Tendinopathy is a clinical diagnosis of localised tendon pain often confirmed by imaging findings. The pathophysiological cause of the pain is unknown and the sympathetic nervous system (SNS) may be implicated. OBJECTIVE: To review what is known regarding the role of the SNS in human tendinopathy. STUDY SELECTION: Published data describing sympathetic innervation or an index of sympathetic activity in human tendons were eligible for inclusion. DATA SOURCES: Bibliographical databases (AMED, Biological Abstracts, CINAHL Plus, EMBASE, MEDLINE, Scopus, SPORTDiscus and Web of Science) were searched for relevant articles. Reference lists from included articles were screened for additional articles. STUDY APPRAISAL: Studies were scored with a quality assessment tool to identify potential sources of bias. Each question had an explicit decision rule to guide assessment. RESULTS: Nine case-control and four cross-sectional studies examined sympathetic innervation of tendons. There was evidence suggesting a lack of difference in sympathetic innervation of tendon proper between tendinopathy biopsies and healthy controls. In contrast, the paratendinous tissue showed evidence of increased sympathetic innervation in painful tendons. The most notable increase in SNS markers was seen in abnormal tenocytes from painful tendons. Data from two studies were suitable for meta-analysis. These heterogeneous studies revealed no difference in sympathetic innervation between painful and pain-free tendons. No studies recorded SNS activity in vivo. CONCLUSION: Sympathetic innervation in painful tendons depends on tissue type. Abnormal tenocytes may have increased capacity for self-production of sympathetic neurotransmitters. Future insight may be gained by measuring global in vivo sympathetic drive in tendinopathy.