Cardioprotection Acquired Through Exercise: The Role of Ischemic Preconditioning

A great bulk of evidence supports the concept that regular exercise training can reduce the incidence of coronary events and increase survival chances after myocardial infarction. These exercise-induced beneficial effects on the myocardium are reached by means of the reduction of several risk factors relating to cardiovascular disease, such as high cholesterol, hypertension, obesity etc. Furthermore, it has been demonstrated that exercise can reproduce the “ischemic preconditioning” (IP), which refers to the capacity of short periods of ischemia to render the myocardium more resistant to subsequent ischemic insult and to limit infarct size during prolonged ischemia. However, IP is a complex phenomenon which, along with infarct size reduction, can also provide protection against arrhythmia and myocardial stunning due to ischemia-reperfusion. Several clues demonstrate that preconditioning may be directly induced by exercise, thus inducing a protective phenotype at the heart level without the necessity of causing ischemia. Exercise appears to act as a physiological stress that induces beneficial myocardial adaptive responses at cellular level. The purpose of the present paper is to review the latest data on the role played by exercise in triggering myocardial preconditioning.     

The effect of a three month,low-load- high-repetitions group-based exercise program versus pilates on physical fitness and body composition in inactive women

ObjectiveBoth low-load-high-repetitions (LLHR) and Pilates programs constitute popular forms of exercise, accompanied by health benefits for the participants involved. Notably, the effect of such programs on aerobic fitness is still controversial. The aim of this study was to examine the effects of both programs on physical fitness and body composition on previously inactive adult women.MethodsTwenty-six women (39.8 ± 9.1y) were assigned to a LLHR program, and sixteen women (39.1 ± 12.2y) were assigned to a Pilates program. Both programs were performed in a group setting, 3 times per week for 3 months. Aerobic fitness, flexibility, handgrip strength and lower extremities explosiveness were assessed by a battery of field testing. Total body fat and trunk fat levels were assessed by bioelectrical impedance analysis. Heart rate response during exercise was recorded once every month by using a telemetry system.ResultsAerobic fitness, lower extremities explosive power, left arm handgrip strength and body composition significantly improved in the LLHR group; while flexibility significantly improved only in the Pilates group, following the intervention period (p < 0.05). LLHR was superior to the Pilates program in improving aerobic fitness and body composition; whilst Pilates was superior in improving flexibility (p < 0.05).ConclusionLLHR group-based exercise programs may improve various aspects of physical fitness, including aerobic fitness, in inactive adult women. This medium-intensity form of exercise is generally well tolerated and might be used as an option for women who cannot perform training on higher intensities. In contrast, the Pilates program failed to improve physical fitness-related parameters except flexibility levels.     

Quantitative myotonia assessment with a commercially available dynamometer in myotonic dystrophy types 1 and 2

Introduction: The objective of this study was to develop a simple method for quantitative assessment of myotonia in patients with myotonic dystrophy type 1 (DM1) and DM2, to compare the myotonia severity, and to correlate this objective outcome with a subjective scale, the Myotonia Behaviour Scale (MBS). Methods: A commercially available dynamometer was used for all measurements. The relaxation time after voluntary contraction was measured in 20 patients with DM1, 25 patients with DM2, and 35 healthy controls. Results: The average relaxation time was 0.17 s in controls, 2.96 s in patients with DM1, and 0.4 s in patients with DM2. The correlation between relaxation time and MBS score was significant, 0.627 in patients with DM1 and 0.581 in patients with DM2. Discussion: Our method provides a valid and reliable quantitative measure of grip myotonia suitable as an outcome measure in clinical trials and as part of routine examinations to gather data on the natural history of myotonic disorders. Muscle Nerve 59:431–435, 2019     

Mechanisms of the warm-up phenomenon

The warm-up phenomenon, described in patients with coronaryartery disease, refers to the improved performance followinga first exercise test. The aim of this study was to investigatethe causes of the warm-up phenomenon. Fifteen patients with coronary artery disease and positive exercisetest were enrolled. Patients were off treatment throughout thestudy. They underwent two consecutive treadmill exercise testsaccording to the Bruce protocol, with a recovery period of 10min to re-establish baseline conditions. A third exercise testwas then performed 2 h later. Before the onset of ischaemia,the rate-pressure product for a similar degree of workload wassimilar during the first and second exercise test, while itwas lower during the third test (P<0·05). Time to1·5 mm ST-segment depression during the second and thirdexercise test was greater than during the first test (454 ±133 and 410 ± 161 vs 354 ± 127 s, P<0·01,respectively). Similarly, the time to anginal pain onset wasincreased during the second and third exercise tests, comparedto the first test (356 ± 208 and 310 ± 203 vs257 ± 204s, P<0·0l, respectively). In contrast,rate-pressure product at 1·5 mm ST-segment depressionduring the second test was higher than that during the firsttest (232±47 vs 210±39 beats. min^–1. mmHg.10², P<0·0l), while in the third test it was similarto that during the first (209 ± 43 beats. min^–1.mmHg. 10², P=ns). The warm-up phenomenon observed a few minutes after exerciseis characterized by an increase of both time to ischaemia andischaemic threshold; this adaptation to ischaemia may be dueto an improvement of myocardial perfusion or to preconditioning.Conversely, the warm-up phenomenon observed a few hours afterrepeated exercise is characterized by an increase of time toischaemia but not of ischaemic threshold and is caused by aslower increase of cardiac workload. Thus, the mechanisms ofthe warm-up phenomenon may be different, time dependent andrelated to previous training.     

Effects of K(ATP) channel blockade by glibenclamide on the warm-up phenomenon.

AIMS: The increased tolerance to myocardial ischaemia observed during the second of two sequential exercise tests, i.e. the warm-up phenomenon, has been proposed as a clinical model of ischaemic preconditioning. As ATP-sensitive K+ channels appear to be a mediator of ischaemic preconditioning in both experimental and clinical studies, the aim of this study was to investigate the role of K(ATP) channels in the warm-up phenomenon. METHODS AND RESULTS: Twenty-six patients with coronary artery disease were randomized to receive 10 mg oral glibenclamide, a selective ATP-sensitive K+ channel blocker, or placebo. Sixty minutes after glibenclamide or placebo administration, patients were given an infusion of 10% dextrose (8 ml x min(-1)) to correct glucose plasma levels or, respectively, an infusion of saline at the same infusion rate. Thirty minutes after the beginning of the infusions, both patient groups underwent two consecutive treadmill exercise tests, with a recovery period of 15 min to re-establish baseline conditions. Before exercise tests, blood glucose levels were similar in placebo and glibenclamide groups (96 +/- 10 vs 105 +/- 22 mg x 100 ml(-1), P=ns). After placebo administration, rate-pressure product at 1.5 mm ST-segment depression significantly increased during the second exercise test compared to the first (220 +/- 41 vs 186 +/- 29 beats x min(-1) x mmHg x 10(2), P<0.01), but it did not change after glibenclamide (191 +/- 34 vs 187 +/- 42 beats x min(-1) x mmHg x 10(2), P=ns), with a significant drug-test interaction (P=0.0091, at two-way ANOVA). CONCLUSIONS: Glibenclamide, at a dose previously shown to abolish ischaemic preconditioning during coronary angioplasty, prevents the increase of ischaemic threshold observed during the second of two sequential exercise tests. These findings confirm that ischaemic preconditioning plays a key role in the warm-up phenomenon and that in this setting is, at least partially, mediated by activation of ATP-sensitive K+ channels.     

Factors influencing assessment of maximal heart rate

The significance of warm-up time, time and number of runs, treadmill inclination and the degree of being rested for the assessment of maximal heart rate (HR_max were studied in 59 athletes. A protocol of 2 subsequent 3- to 4-min runs to exhaustion gave the highest average peak HR values. Being rested before the start of the test and the warm-up time were both decisive in reaching HR_max. Peak HR from field tests were significantly lower than values attained from lab tests. Mean peak HR from maximal oxygen uptake measurements were 5–6 beats · min⁻¹ lower than values from the specially designed HR_max test described above.