Sarcopenia is the loss of muscle strength, mass, and function, which is often exacerbated by chronic comorbidities including cardiovascular diseases, chronic kidney disease, and cancer. Sarcopenia is associated with faster progression of cardiovascular diseases and higher risk of mortality, falls, and reduced quality of life, particularly among older adults. Although the pathophysiologic mechanisms are complex, the broad underlying cause of sarcopenia includes an imbalance between anabolic and catabolic muscle homeostasis with or without neuronal degeneration. The intrinsic molecular mechanisms of aging, chronic illness, malnutrition, and immobility are associated with the development of sarcopenia. Screening and testing for sarcopenia may be particularly important among those with chronic disease states. Early recognition of sarcopenia is important because it can provide an opportunity for interventions to reverse or delay the progression of muscle disorder, which may ultimately impact cardiovascular outcomes. Relying on body mass index is not useful for screening because many patients will have sarcopenic obesity, a particularly important phenotype among older cardiac patients. In this review, we aimed to: (1) provide a definition of sarcopenia within the context of muscle wasting disorders; (2) summarize the associations between sarcopenia and different cardiovascular diseases; (3) highlight an approach for a diagnostic evaluation; (4) discuss management strategies for sarcopenia; and (5) outline key gaps in knowledge with implications for the future of the field.

Introduction Resting heart rate (RHR) declines with exercise training. Possible mechanisms include: 1) increased parasympathetic tone, 2) decreased responsiveness to beta-adrenergic stimulation, 3) decreased intrinsic heart rate or 4) combination of these factors. Objective To determine whether an increase in resting parasympathetic tone or decrease in response to beta-adrenergic stimulation contribute to the decrease in RHR with training. Methods 51 screened healthy subjects aged 18–32 (n= 20, mean age 26, 11 female) or 65–80 (n= 31, mean age 69, 16 female) were tested before and after 6 months of supervised exercise training. Heart rate response to parasympathetic withdrawal was assessed using atropine and beta-adrenergic responsiveness during parasympathetic withdrawal using isoproterenol. Results Training increased VO2 max by 17 % (28.7 ± 7.7 to 33.6± 9.20 ml/kg/min, p<0.001). RHR decreased from 62.8 ± 6.6 to 57.6 ± 7.2 beats per minute (p<0.0001). The increase in heart rate in response to parasympathetic withdrawal was unchanged after training (+37.3 ± 12.8 pre vs. +36.4 ± 12.2 beats per min post, p=0.41). There was no change in the heart rate response to isoproterenol after parasympathetic blockade with training (+31.9±10.9 pre vs. +31.0±12.0 post beats per min, p=0.56). The findings were similar in all four subgroups. Conclusions We did not find evidence that increase in parasympathetic tone or a decrease in responsiveness to beta-adrenergic activity accounts for the reduction in resting heart rate with exercise training. We suggest that decline in heart rate with training is most likely due to decrease in the intrinsic heart rate.

Speckle tracking may be a sensitive tool for assessing RV dysfunction and predicting mortality in patients with PE in this pilot study.

No abstract

With age, presynaptic uptake as measured by PSnt declines, but there were no differences in β'max. Endurance training significantly increased VO2 max but did not cause any changes in the measures of cardiac sympathetic nervous system function. These findings suggest that significant changes do not occur or that current PET imaging methods may be inadequate to measure small serial differences in a highly reproducible manner.