The heart is capable of responding to stressful situations by increasing muscle mass, which is broadly defined as cardiac hypertrophy. This phenomenon minimizes ventricular wall stress for the heart undergoing a greater than normal workload. At initial stages, cardiac hypertrophy is associated with normal or enhanced cardiac function and is considered to be adaptive or physiological; however, at later stages, if the stimulus is not removed, it is associated with contractile dysfunction and is termed as pathological cardiac hypertrophy. It is during physiological cardiac hypertrophy where the function of subcellular organelles, including the sarcolemma, sarcoplasmic reticulum, mitochondria, and myofibrils, may be upregulated, while pathological cardiac hypertrophy is associated with downregulation of these subcellular activities. The transition of physiological cardiac hypertrophy to pathological cardiac hypertrophy may be due to the reduction in blood supply to hypertrophied myocardium as a consequence of reduced capillary density. Oxidative stress, inflammatory processes, Ca²⁺-handling abnormalities, and apoptosis in cardiomyocytes are suggested to play a critical role in the depression of contractile function during the development of pathological hypertrophy.

Objective: To determine the feasibility of a cardiac prehabilitation (Prehab) program for patients waiting for elective coronary artery bypass graft (CABG). Design: A two-group parallel randomized controlled trial. Setting: Medical fitness facility. Subjects: Seventeen preoperative elective CABG surgery patients were randomized to standard care ( n = 9) or Prehab ( n = 8). Intervention: Standard care: three-hour preassessment appointment. Prehab: exercise and education classes for 60 minutes/day, twice weekly for at least four weeks. Main measures: Data were collected at baseline, one week preoperatively, and three months postoperatively. The primary outcome measure was walking distance using a 6-minute walk test. Secondary outcome variables included 5-meter gait speed, and cardiac rehabilitation attendance three months postoperatively. Results: Fifteen patients (standard care, n = 7; Prehab, n = 8) completed the study. No Prehab patients developed cardiac symptoms during study participation. Walking distance remained unchanged in the standard care group; whereas, the Prehab group increased their walking distance to mean ± SD 474 ±101 and 487 ±106 m at the preoperative and three month postoperative assessments ( p < 0.05). Gait speed was unchanged in the standard care group, but improved in the Prehab group by 27% and 33% preoperatively and three months postoperatively, respectively ( p < 0.05). Enrollment in cardiac rehabilitation three months postoperatively was higher for Prehab participants (100%) than standard care participants (43%; p < 0.05). Conclusion: These data provide evidence for the feasibility of a Prehab intervention to improve the health status of patients waiting for elective CABG surgery. A larger trial of 92 patients will be utilized to demonstrate the safety and efficacy of Prehab.

The sarco(endo)plasmic reticulum calcium ATPase (SERCA) is responsible for transporting calcium (Ca²⁺) from the cytosol into the lumen of the sarcoplasmic reticulum (SR) following muscular contraction. The Ca²⁺ sequestering activity of SERCA facilitates muscular relaxation in both cardiac and skeletal muscle. There are more than 10 distinct isoforms of SERCA expressed in different tissues. SERCA2a is the primary isoform expressed in cardiac tissue, whereas SERCA1a is the predominant isoform expressed in fast-twitch skeletal muscle. The Ca²⁺ sequestering activity of SERCA is regulated at the level of protein content and is further modified by the endogenous proteins phospholamban (PLN) and sarcolipin (SLN). Additionally, several novel mechanisms, including post-translational modifications and microRNAs (miRNAs) are emerging as integral regulators of Ca²⁺ transport activity. These regulatory mechanisms are clinically relevant, as dysregulated SERCA function has been implicated in the pathology of several disease states, including heart failure. Currently, several clinical trials are underway that utilize novel therapeutic approaches to restore SERCA2a activity in humans. The purpose of this review is to examine the regulatory mechanisms of the SERCA pump, with a particular emphasis on the influence of exercise in preventing the pathological conditions associated with impaired SERCA function.

There is little certainty as to the prevalence of frailty in Canadians in younger adulthood. This study examines and compares the prevalence of frailty in Canadians 18–79 years old using the Accumulation of Deficits and Fried models of frailty. The Canadian Health Measures Study data were used to estimate the prevalence of frailty in adults 18–79 years old. A 23-item Frailty Index using the Accumulation of Deficits Model (cycles 1–3; n = 10,995) was developed; frailty was defined as having the presence of 25% or more indices, including symptoms, chronic conditions, and laboratory variables. Fried frailty (cycles 1–2; n = 7,353) included the presence of ≥3 criteria: exhaustion, physical inactivity, poor mobility, unintentional weight loss, and poor grip strength. The prevalence of frailty was 8.6 and 6.6% with the Accumulation of Deficits and the Fried Model. Comparing the Fried vs. the Accumulation of Deficits Model, the prevalence of frailty was 5.3% vs. 1.8% in the 18–34 age group, 5.7% vs. 4.3% in the 35–49 age group, 6.9% vs. 11.6% in the 50–64 age group, and 7.8% vs. 20.2% in the 65+ age group. Some indices were higher in the younger age groups, including persistent cough, poor health compared to a year ago, and asthma for the accumulation of deficits model, and exhaustion, unintentional weight loss, and weak grip strength for the Fried model, compared to the older age groups. These data show that frailty is prevalent in younger adults, but varies depending on which frailty tool is used. Further research is needed to determine the health impact of frailty in younger adults.