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Molecular adaptations to endurance exercise and skeletal muscle fibre plasticity
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Endurance exercise is typified by repeated rhythmic contractions of skeletal muscle. Because of the one-way valves in veins, the rhythmic contraction and relaxation of skeletal muscles, this produces a pumping action of the blood back towards the heart. As a greater volume of blood is returned to the heart, the end diastolic volume increases, causing a stretch on the cardiomyocytes. The stretch on the cardiomyocytes during diastole is referred to as the preload on the heart (just like with a slingshot, stretching further – adding more blood to the ventricle – resulting in greater force). The Frank-Starling Law of the heart states that as venous return (preload) increases, there is a proportional increase in stroke volume. Therefore, from the first rhythmic contractions of endurance exercise to the last, the heart sees a higher volume of blood during diastole and therefore the adaptation of the heart to endurance exercise is termed a volume overload.
In-Patient Rehabilitation of the Coronary Artery Bypass Surgery Patient and the Heart Transplantation Patient
Published in Mary C. Singleton, Eleanor F. Branch, Advances in Cardiac and Pulmonary Rehabilitation, 2018
In the normal population, during dynamic exercise heart rate increases immediately in a linear fashion and is mainly responsible for the increase in cardiac output seen early in exercise. Stroke volume, in the normal heart, stays about the same until more strenuous exercise occurs and then increases according to the Frank Starling law, causing an additional increase in cardiac output.24
Ventricular function
Published in Burt B. Hamrell, Cardiovascular Physiology, 2018
The volume of ventricular ejection, the stroke volume, is partly determined by the amount of preceding diastolic filling. The meaning of the relationship in Figure 10.1 is that the more a ventricle fills, the more it ejects. Ventricular filling stretches ventricular wall myocytes. With less filling, stroke volume is less and with increased filling, stroke volume increases. This is the Frank–Starling law of the heart. The law is another way of stating that the length of ventricular wall myocytes at the end of filling, the preload, is one major determinant of ventricular function. An increase in ventricular end-diastolic volume is accompanied by an increase in resting myocyte length and resting sarcomere length. Preload and the effect of resting myocyte length on cardiac muscle function is presented in the self-study module Clinical Heart Muscle Physiology, Part 2: Muscle Mechanics Made Easy.
Clinical pharmacology of cardiac cyclic AMP in human heart failure: too much or too little?
Published in Expert Review of Clinical Pharmacology, 2023
An equally central role is played by cAMP in cardiac relaxation (positive lusitropy). The importance of this sometimes gets diluted by the focus given on cAMP's actions toward positive inotropy. Nevertheless, cAMP is essential for cardiac relaxation, a process necessary for proper ventricular filling during diastole, which, in turn, is a critical determinant of cardiac function, i.e. of the force of the next contraction (based on the Frank–Starling law of normal cardiac operation) [25,26] (Figure 1). Additionally, proper diastolic function is important for cardiac muscle oxygenation and nourishment, as the coronary arteries can only deliver blood to the cardiac cells during diastole (compressed during systole/contraction) [252626, . PKA is again the main mediator of cAMP's effects in cardiac relaxation. PKA lowers the free intracellular [Ca2+] (removes Ca2+ from the cytosol) via SERCA2a activation in the SR membrane (by phosphorylating phospholamban) and Na+/K+-ATPase (NKA) activation in the plasma membrane (by phosphorylating phospholemman), which induces the Na+/Ca2+-exchanger (NCX) to remove Ca2+ out of the cardiomyocyte [17,19] (Figure 1). At the same time, PKA reduces the Ca2+ sensitivity of actomyosin filaments and increases their distensibility via phosphorylation of cardiac troponin I (cTnI), titin, and cardiac myosin-binding protein-C3 (MyBPC3) [27,28,29] (Figure 1).
Intact coronary and myocardial functions after 24 hours of non-ischemic heart preservation
Published in Scandinavian Cardiovascular Journal, 2020
Guangqi Qin, Björn Wohlfart, Long Zuo, Jingfeng Hu, Trygve Sjöberg, Stig Steen
The same type of organ bath as described above was used. Preformed loops of thread were tied at either side of the trabecula and these were used to mount the preparation in the organ bath between two metal holders, one connected to a force transducer (Figure 1). After mounting, there was a run-in period of 30–45 min with electric stimulation to obtain an equilibration in force development. The signals from stimulation and force were continuously stored on computer (AD instruments Ltd, Oxford, United Kingdom). The optimum muscle length for force production was established in each preparation by stretching the muscle in small steps and monitoring the force (Frank-Starling law). At optimal muscle tension the size of the trabecula was measured using the stereo microscope (Zeiss) at 10 × magnification. The size did not differ between the groups. The preparations had a mean length of 3.8 ± 1.2 (SD) mm and a diameter of 0.59 ± 0.17 (SD) mm. The diameters were used to measure force production in units of mN/mm2. Stimulation took place by means of a pair of electrodes placed under the muscle. The stimulus pulse was 5 ms in duration and with amplitude of 150% of the threshold value. Measurements were made at 60/min. A typical force recording is shown in Figure 1.
Left atrial phasic volumes and functions changes in asymptomatic patients with sarcoidosis: evaluation by three-dimensional echocardiography
Published in Acta Cardiologica, 2022
It is known that LA phasic function has three main mechanical components: reservoir function in systole when blood fills the left atrium, conduit function in early diastole corresponding to passive LV filling, and an active contractile function in late diastole [14]. In our study regarding LA phasic functional parameters derived from 3D-echocardiography, while AAEF and TAEF were found to be significantly different and reduced in asymptomatic sarcoidosis patients, PAEF was similar between the two groups. In accordance with our findings, Tigen et al. [47] found that 2D speckle tracking echocardiography derived LA reservoir functions were significantly lower in sarcoidosis patients than controls, whereas LA conduit function was similar between the two groups. In addition, in a recent study, it was demonstrated that speckle tracking echocardiography derived strain data suggested that LA conduit function was preserved in systemic sclerosis patients with preserved LV diastolic functions [46]. On the other hand, our findings are in contrast to the previous reports suggesting that, the LA pump function increases, whereas the conduit function decreases in the presence of mild LV diastolic dysfunction, and then LA pump function significantly decreases when LV diastolic dysfunction progresses to moderate according to Frank-Starling law [15,48–50]. Our findings may lead to the hypothesis that the impaired AAEF and TAEF reflect left atrial dysfunction as a result of direct atrial involvement of sarcoidosis. In addition, the fact that the LA is formed by thinner walls that are affected earlier than the LV wall, may have contributed to the development of early LA dysfunction.