Perceived risk for falls and decision-making in riding raised ramps in mountain biking: a pilot study.

Mountain biking (MTB) is a challenging activity where riders face constant decisions on whether to attempt technical paths or features (e.g., wooden ramps and jumps) that pose risk for falls and injuries. Risk homeostasis theory posits that riders pursue an optimal non-zero level of risk that balances the rewards of attempting challenging features with the need to avoid unreasonable risk for injury. Little is known on how riders judge risk, and the level of risk that riders deem unacceptable. We conducted experiments with experienced MTB riders (n = 17) to examine how their willingness to ride raised wooden ramps depended on their perceived probability for falling (Pf) and their perceived probability for injury in the event of a fall (Pi) while riding the ramp. In one experiment, participants viewed ramps of varying widths and heights and described their willingness to ride each ramp, along with Pf and Pi. We found that Pf and Pi were independent predictors of willingness to attempt ramps. Moreover, the product Pf*Pi (the perceived risk for injury in attempting the ramp) was a stronger predictor than Pf or Pi alone. In a second experiment, participants viewed ramps of different widths, and reported the maximum (threshold) height where they would ride each ramp, along with Pf and Pi. We found that Pf*Pi at the threshold height, averaging 13%, did not vary with ramp width. We conclude that decisions on riding ramps are based on the product Pf*Pi. On average, riders refused to ride ramps when Pf*Pi exceeded 13%.

Are Interactions between Epicardial Adipose Tissue, Cardiac Fibroblasts and Cardiac Myocytes Instrumental in Atrial Fibrosis and Atrial Fibrillation?

Atrial fibrillation is very common among the elderly and/or obese. While myocardial fibrosis is associated with atrial fibrillation, the exact mechanisms within atrial myocytes and surrounding non-myocytes are not fully understood. This review considers the potential roles of myocardial fibroblasts and myofibroblasts in fibrosis and modulating myocyte electrophysiology through electrotonic interactions. Coupling with (myo)fibroblasts in vitro and in silico prolonged myocyte action potential duration and caused resting depolarization; an optogenetic study has verified in vivo that fibroblasts depolarized when coupled myocytes produced action potentials. This review also introduces another non-myocyte which may modulate both myocardial (myo)fibroblasts and myocytes: epicardial adipose tissue. Epicardial adipocytes are in intimate contact with myocytes and (myo)fibroblasts and may infiltrate the myocardium. Adipocytes secrete numerous adipokines which modulate (myo)fibroblast and myocyte physiology. These adipokines are protective in healthy hearts, preventing inflammation and fibrosis. However, adipokines secreted from adipocytes may switch to pro-inflammatory and pro-fibrotic, associated with reactive oxygen species generation. Pro-fibrotic adipokines stimulate myofibroblast differentiation, causing pronounced fibrosis in the epicardial adipose tissue and the myocardium. Adipose tissue also influences myocyte electrophysiology, via the adipokines and/or through electrotonic interactions. Deeper understanding of the interactions between myocytes and non-myocytes is important to understand and manage atrial fibrillation.

Ischemia Reperfusion Injury Produces, and Ischemic Preconditioning Prevents, Rat Cardiac Fibroblast Differentiation: Role of KATP Channels.

Ischemic preconditioning (IPC) and activation of ATP-sensitive potassium channels (KATP) protect cardiac myocytes from ischemia reperfusion (IR) injury. We investigated the influence of IR injury, IPC and KATP in isolated rat cardiac fibroblasts. Hearts were removed under isoflurane anesthesia. IR was simulated in vitro by application and removal of paraffin oil over pelleted cells. Ischemia (30, 60 and 120 min) followed by 60 min reperfusion resulted in significant differentiation of fibroblasts into myofibroblasts in culture (mean % fibroblasts ± SEM in IR vs. time control: 12 ± 1% vs. 63 ± 2%, 30 min ischemia; 15 ± 3% vs. 71 ± 4%, 60 min ischemia; 8 ± 1% vs. 55 ± 2%, 120 min ischemia). IPC (15 min ischemia, 30 min reperfusion) significantly attenuated IR-induced fibroblast differentiation (52 ± 3%) compared to 60 min IR. IPC was mimicked by opening KATP with pinacidil (50 µM; 43 ± 6%) and by selectively opening mitochondrial KATP (mKATP) with diazoxide (100 µM; 53 ± 3%). Furthermore, IPC was attenuated by inhibiting KATP with glibenclamide (10 µM; 23 ± 5%) and by selectively blocking mKATP with 5-hydroxydecanoate (100 µM; 22 ± 9%). These results suggest that (a) IR injury evoked cardiac fibroblast to myofibroblast differentiation, (b) IPC attenuated IR-induced fibroblast differentiation, (c) KATP were involved in IPC and (d) this protection involved selective activation of mKATP.