Since the sentinel description of exercise-triggered ventricular arrhythmias in 21 children, our recognition and understanding of catecholaminergic polymorphic ventricular tachycardia has improved substantially. A variety of treatments are now available, but reaching a diagnosis before cardiac arrest remains a challenge. Most cases are related to variants in the gene encoding for ryanodine receptor-2 (RyR2), which mediates calcium-induced calcium release. Up to half of cases remain genetically elusive. The condition is presently incurable, but one basic intervention, the universal administration of β-blockers, has improved survival. In the past, implantable cardioverter-defibrillators (ICDs) were frequently implanted, especially in those with a history of cardiac arrest. Treatment limitations include under-dosing and poor compliance with β-blockers, and potentially lethal ICD-related electrical storm. Newer therapies include flecainide and sympathetic ganglionectomy. Limited data have suggested that genotype may predict phenotype in catecholaminergic polymorphic ventricular tachycardia, including a higher risk of life-threatening cardiac events in subjects with variants in the C-terminus of ryanodine receptor-2 (RyR2). At present, international efforts are underway to better understand this condition through large prospective registries. The recent publication of gene therapy in an animal model of the recessive form of the disease highlights the importance of improving our understanding of the genetic underpinnings of the disease.

The cardiovascular benefits of habitual exercise are well documented. In the current era, more of the population is exceeding the recommendations for physical activity as the popularity of endurance events increases. Recent data have proposed a U-shaped relationship between exercise intensity and cardiovascular outcomes. Regular participation in endurance activities has been shown to result in structural and functional changes in the heart. This re-modelling may be the substrate for cardiac dysfunction or arrhythmias. The risk of sudden cardiac death may also be elevated; however, in most cases of sudden cardiac death, the cause can be linked to an underlying cardiac pathology where exercise acted as the trigger for a lethal arrhythmia. This article serves to review whether excessive exercise may result in harm in some athletes.

Contractile, histochemical and biochemical properties of the triceps surae were compared in 13 aerobically trained male subjects aged 63 to 76 years. Electrical stimulation of the triceps surae was used to determine muscle twitch, tetanic, and fatigue parameters. From these tests, twitch tension (Pt), time to peak tension (TPT), half relaxation time (RT), tetanic tensions at 10(Po10), 20(Po20), and 50(Po50) Hz and a fatigue index (FI) were calculated. Muscle samples from the belly of the lateral head of the gastrocnemius were obtained using the needle biopsy technique. A portion of each sample was tested histochemically for myosin ATPase (pH 4.30, 4.58 and 10.00) and NADH-tetrazolium reductase in order to classify fibre types (ST, FTa, FTb) and to determine fibre areas. The remainder of each sample was analysed for succinic dehydrogenase (SDH) and phosphofructokinase (PFK) enzyme activities. Significant correlations were found between fibre areas (both ST and FT) and Po10/Po50 and FI. No significant relationships were noted between Pt, 1/2RT and MVC and any histochemical parameter. SDH and PFK activities did not correlate significantly with any histochemical or physiological parameter. Regular endurance exercise apparently does not retard the decline in contractile properties seen with the aging process. Substrate related regulatory enzyme activities (PFK) and marker enzyme activities (SDH) from skeletal muscle of the elderly are much lower than activities found in younger subjects, despite regular aerobic exercise.