Higher risk of Achilles tendon ruptures at competition than training sites in female collegiate gymnasts.

BACKGROUND: Reportedly, 17.2% of collegiate female gymnasts experience Achilles tendon ruptures (ATRs). Cumulative microtraumas resulting in chronic tendinopathy/tendinitis may contribute to this high injury risk. We hypothesized that the risk of ATRs in female collegiate gymnasts increases with years of competitive gymnastics, that non-steroidal anti-inflammatory drug (NSAID) use is associated with less ATRs, and that the risk is larger during competition than training. METHODS: Female gymnasts from 78 USA collegiate teams completed a survey assessing the prevalence of ATRs, NSAID use, age at which competitive gymnastics started and age at which ATR occurred, and whether ATRs occurred during training or competition. RESULTS: Twenty-one of 103 gymnasts (20.4%, 95% CI: 13.6% to 29.4%) experienced ATRs. Eighteen of 21 ruptures (85.7%, 95% CI: 61.3% to 95.8%) occurred after more than ten years of competitive gymnastics (mean: 14.0±2.6 years, 95% CI: 12.8 to 15.2 years). ATRs occurred 0.08±0.01 (95% CI: 0.06 to 0.11) times per 1000 hours at training versus 1.85±0.11 (95% CI: 1.60 to 2.10) times per 1000 hours at competition (P<0.05). Prevalence of NSAID use was 27.6% (95% CI: 18.6% to 39.0%) in gymnasts without ATR but only 5.5% (95% CI: 0.6% to 35.5%, P=0.09) in gymnasts with ATR. Multiple regression analysis demonstrated a negative association between NSAID use and incidence of ATRs (P<0.05). CONCLUSIONS: Female collegiate gymnasts are at high risk for ATRs, especially after more than ten years of competitive gymnastics and during competition.

A framework for the interpretation of heart rate variability applied to transcutaneous auricular vagus nerve stimulation and osteopathic manipulation.

Reports on autonomic responses to transcutaneous auricular vagus nerve stimulation (taVNS) and osteopathic manipulative techniques have been equivocal, partly due to inconsistent interpretation of heart rate variability (HRV). We developed a mechanistic framework for the interpretation of HRV based on a model of sinus node automaticity that considers autonomic effects on Phase 3 repolarization and Phase 4 depolarization of the sinoatrial action potential. The model was applied to HRV parameters calculated from ECG recordings (healthy adult humans, both genders) before (30 min), during (15 min), and after (30 min) a time control intervention (rest, n = 23), taVNS (10 Hz, 300 µs, 1-2 mA, cymba concha, left ear, n = 12), or occipitoatlantal decompression (OA-D, n = 14). The experimental protocol was repeated on 3 consecutive days. The model simulation revealed that low frequency (LF) HRV best predicts sympathetic tone when calculated from heart rate time series, while high frequency (HF) HRV best predicts parasympathetic tone when calculated from heart period time series. Applying our model to the HRV responses to taVNS and OA-D, revealed that taVNS increases cardiac parasympathetic tone, while OA-D elicits a mild decrease in cardiac sympathetic tone.

Physiology mechanisms of heart rate variability

The purpose of this article is to review the physiologic 01 mechanisms causing heart rate variability. In addition, the n rationale for using low (LF) and high frequency (HF) components of heart rate variability to study cardiac sympa- tho-vagal balance is discussed based on these physiologic mechanisms. Heart rate variability is almost exclusively IJ mediated by the autonomic nervous system, as indicated r by the finding that heart rate is virtually constant in patients I following heart transplantation. Sympathetic actions on : the sinus nade are mediated by the intracellular second I messenger cAMPo Thus, sympathetic-mediated heart rate fluctuations require likewise fluctuations in intracellular cAMP concentration, which is dependent on the activities of adenylyl cyclase and phosphodiesterase. In contrast, parasympathetic modulation of sinus node function does not depend on intracellular second messengers and can...