Exercise training alters length dependence of contractile properties in rat myocardium

2003 ◽  
Vol 94 (3) ◽  
pp. 1137-1144 ◽  
Author(s):  
Gary M. Diffee ◽  
Daniel F. Nagle
Keyword(s):  
Exercise Training ◽  
Cardiac Myocytes ◽  
Sarcomere Length ◽  
Myocardial Function ◽  
Citrate Synthase ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Cellular Mechanisms ◽  
Length Dependence ◽  
Maximal Tension

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. Exercise training increases the sensitivity of rat cardiac myocytes to activation by Ca2+, and this Ca2+ sensitivity has been shown to be highly dependent on sarcomere length. We tested the hypothesis that exercise training increases this length dependence in cardiac myocytes. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise-trained (T) groups. The T rats underwent 11 wk of progressive treadmill exercise. Heart weight increased by 14% in T compared with C rats, and plantaris muscle citrate synthase activity showed a 39% increase with training. Steady-state tension was determined in permeabilized myocytes by using solutions of various Ca2+concentration (pCa), and tension-pCa curves were generated at two different sarcomere lengths for each myocyte (1.9 and 2.3 μm). We found an increased sarcomere length dependence of both maximal tension and pCa50 (the Ca2+ concentration giving 50% of maximal tension) in T compared with C myocytes. The ΔpCa50 between the long and short sarcomere length was 0.084 ± 0.023 (mean ± SD) in myocytes from C hearts compared with 0.132 ± 0.014 in myocytes from T hearts ( n = 50 myocytes per group). The Δmaximal tension was 5.11 ± 1.42 kN/m2 in C myocytes and 9.01 ± 1.28 in T myocytes. We conclude that exercise training increases the length dependence of maximal and submaximal tension in cardiac myocytes, and this change may underlie, at least in part, training-induced enhancement of myocardial function.

Exercise training increases the Ca2+sensitivity of tension in rat cardiac myocytes

2001 ◽  
Vol 91 (1) ◽  
pp. 309-315 ◽  
Author(s):  
Gary M. Diffee ◽  
Eric A. Seversen ◽  
Marci M. Titus
Keyword(s):  
Steady State ◽  
Exercise Training ◽  
Cardiac Myocytes ◽  
Citrate Synthase ◽  
Contractile Function ◽  
Weight Ratio ◽  
Force Transducer ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Cellular Mechanisms

The heart is known to respond to a program of chronic exercise in ways that enhance cardiac function. However, the cellular mechanisms involved in training-induced improvements in the contractile function of the myocardium are not known. In this study we tested the hypothesis that increased contractility of the myocardium associated with exercise training is due, in part, to increases in the Ca2+ sensitivity of steady-state tension. Female Sprague-Dawley rats were randomly divided into sedentary control (C) and exercise-trained (T) groups. The T rats underwent 11 wk of progressive treadmill exercise (1 h/day, 5 days/wk, 26 m/min, 20% grade). Evidence of training effect included a 5.9% increase in heart mass, increases in heart weight-to-body weight ratio, and a 60% increase in skeletal muscle citrate synthase activity in T rats compared with C rats. After the training program, cardiac myocytes were isolated from T and C hearts. Myocytes were chemically skinned (i.e., the sarcolemma was removed) and attached to a force transducer, and steady-state tension was determined in solutions of various Ca2+ concentrations ([Ca2+]). Myocytes isolated from the hearts of T rats showed a significantly ( P < 0.01) increased sensitivity of tension to [Ca2+]. The [Ca2+] giving 50% of maximal tension (pCa50) was 5.90 ± 0.033 and 5.82 ± 0.023 (SD) in T and C myocytes, respectively ( n = 70 myocytes/group). This result suggests that exercise training affects the myofibrillar proteins, such that Ca2+ sensitivity is increased, and that this may be the mechanism that underlies, at least in part, the effect of training to increase myocardial contractility.

Regional differences in effects of exercise training on contractile and biochemical properties of rat cardiac myocytes

2003 ◽  
Vol 95 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Gary M. Diffee ◽  
Daniel F. Nagle
Keyword(s):  
Exercise Training ◽  
Cardiac Myocytes ◽  
Endurance Exercise ◽  
Biochemical Properties ◽  
Ventricular Wall ◽  
Sprague Dawley ◽  
Cellular Mechanisms ◽  
Endurance Exercise Training ◽  
Improved Function ◽  
Rat Cardiac Myocytes

Myocardial function is enhanced by endurance exercise training, but the cellular mechanisms underlying this improved function remain unclear. A number of studies have shown that the characteristics of cardiac myocytes vary across the width of the ventricular wall. We have previously shown that endurance exercise training alters the Ca2+ sensitivity of tension as well as contractile protein isoform expression in rat cardiac myocytes. We tested the hypothesis that these effects of training are not uniform across the ventricular wall but are more pronounced in the subendocardial (Endo) region of the myocardium. Female Sprague-Dawley rats were divided into sedentary control (C) and exercise trained (T) groups. T rats underwent 11 wk of progressive treadmill exercise. Myocytes were isolated from the Endo region of the myocardium and from the subepicardial (Epi) region of both T and C hearts. We found an increase in the Ca2+ sensitivity of tension in T cells compared with C cells, but this difference was larger in the Endo cells than in the Epi cells. In addition, we found a training-induced increase in atrial myosin light chain 1 (aMLC1) expression that was larger in the Endo compared with Epi samples. We conclude that effects of exercise training on myocyte contractile and biochemical properties are greater in myocytes from the Endo region of the myocardium than those from the Epi region. In addition, these results provide evidence that the increase in aMLC1 expression may be responsible for some of the training-induced increase in myocyte Ca2+ sensitivity of tension.

Exercise training and its effects with renal hypertensive rats

1985 ◽  
Vol 59 (5) ◽  
pp. 1410-1415 ◽  
Author(s):  
K. D. Marcus ◽  
C. M. Tipton
Keyword(s):  
Blood Pressure ◽  
Exercise Training ◽  
Capillary Density ◽  
Heart Weight ◽  
Sprague Dawley ◽  
Vo2 Max ◽  
Arterial Blood ◽  
Sprague Dawley Rats ◽  
Resting Blood Pressure ◽  
Renal Hypertensive Rats

The influence of endurance training on functional capacity [maximal O2 consumption (VO2 max)], caudal arterial blood pressure, and myocardial capillary density were investigated in normotensive rats and rats made hypertensive using the two-kidney one-clip approach (Goldblatt's hypertension). Male Sprague-Dawley rats were assigned to sham (N: 120–140 mmHg), moderately hypertensive (MH = 0.30-mm clips, 150–170 mmHg), or severely hypertensive (SH = 0.25-mm clips, 190–230 mmHg) groups. Rats designated to be runners (T) were exercised on a motor-driven treadmill equal to 50–70% of their VO2 max values for 8–12 wk. Compared with their nontrained (NT) controls, training was associated with significantly higher VO2 max values (12–15%) and muscle cytochrome-c oxidase activities (33–78%). Resting systolic blood pressure was not significantly changed in the N-and MH-T subgroups; however, it was 20–30 mmHg higher in the SH-T subgroup. Mean absolute heart weight for only the N-T group was significantly heavier than their NT controls. However, the mean predicted heart weights (heart wt = 0.639 X body wt of N-NT + 0.001 g) of the two SH groups were significantly higher than expected. The SH-T group had a lower (11%) subepicardial capillary density mean than its NT control and significantly fewer capillaries in the subendocardial region than the other five subgroups. It was concluded that moderate exercise training appeared to be detrimental to rats with severe hypertension because it increased resting blood pressure and decreased myocardial capillary density, even though it improved their functioning capacity.

scholarly journals Differential expression of stress proteins in rat myocardium after free wheel or treadmill run training

1999 ◽  
Vol 86 (5) ◽  
pp. 1696-1701 ◽  
Author(s):  
Earl G. Noble ◽  
Albert Moraska ◽  
Robert S. Mazzeo ◽  
David A. Roth ◽  
M. Charlotte Olsson ◽  
...  
Keyword(s):  
Exercise Training ◽  
Stress Proteins ◽  
Citrate Synthase ◽  
Treadmill Exercise ◽  
Stress Protein ◽  
Critical Factor ◽  
Voluntary Exercise ◽  
Similar Response ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

High-intensity treadmill exercise increases the expression of a cardioprotective, inducible 72-kDa stress protein (SP72) in cardiac muscle. This investigation examined whether voluntary free wheel exercise training would be sufficient to confer a similar response. Male Sprague-Dawley rats were randomly assigned to either treadmill (TM-Tr) or free wheel (FW-Tr) training groups. By the end of the 8-wk training period, TM-Tr animals ran 1 h/day, 5 days/wk up a 10% grade, covering a distance of 8,282 m/wk. FW-Tr rats ran, on average, 5,300 m/wk, with one-third of the animals covering distances similar to those for the TM-Tr group. At the time of death, hearts of trained and caged sedentary control (Sed) animals were divided into left (LV) and right (RV) ventricles. Citrate synthase activity and the relative immunoblot contents of SP72, SP73 (the constitutive isoform of the SP70 family), and a 75-kDa mitochondrial chaperone (SP75) were subsequently determined. LV and RV did not differ on any measure, and SP73, SP75, and citrate synthase were not affected by training. Cardiac SP72 levels were elevated over fourfold in both ventricles of TM-Tr compared with RV of FW-Sed rats. Despite the animals having run a similar total distance, cardiac SP72 content in FW-Tr rats was not different from that in Sed animals. These data indicate that voluntary exercise training is insufficient to elicit an elevation of SP72 in rat heart and suggest that exercise intensity may be a critical factor in evoking the cardioprotective SP72 response.

scholarly journals The Cellular Basis for Enhanced Volume-modulated Cardiac Output in Fish Hearts

2006 ◽  
Vol 128 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Holly A. Shiels ◽  
Sarah C. Calaghan ◽  
Ed White
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Cardiac Myocytes ◽  
Sarcomere Length ◽  
Fish Cell ◽  
Cellular Mechanisms ◽  
Fish Heart ◽  
Resting Tension ◽  
The Way

During vertebrate evolution there has been a shift in the way in which the heart varies cardiac output (the product of heart rate and stroke volume). While mammals, birds, and amphibians increase cardiac output through large increases in heart rate and only modest increases (∼30%) in stroke volume, fish and some reptiles use modest increases in heart rate and very large increases in stroke volume (up to 300%). The cellular mechanisms underlying these fundamentally different approaches to cardiac output modulation are unknown. We hypothesized that the divergence between volume modulation and frequency modulation lies in the response of different vertebrate myocardium to stretch. We tested this by progressively stretching individual cardiac myocytes from the fish heart while measuring sarcomere length (SL), developed tension, and intracellular Ca2+ ([Ca2+]i) transients. We show that in fish cardiac myocytes, active tension increases at SLs greater than those previously demonstrated for intact mammalian myocytes, representing a twofold increase in the functional ascending limb of the length–tension relationship. The mechanism of action is a length-dependent increase in myofilament Ca2+ sensitivity, rather than changes in the [Ca2+]i transient or actin filament length in the fish cell. The capacity for greater sarcomere extension in fish myocardium may be linked to the low resting tension that is developed during stretch. These adaptations allow the fish heart to volume modulate and thus underpin the fundamental difference between the way fish and higher vertebrates vary cardiac output.

scholarly journals Effects of exercise training on dendritic morphology in the cardiorespiratory and locomotor centers of the mature rat brain

2010 ◽  
Vol 108 (6) ◽  
pp. 1582-1590 ◽  
Author(s):  
Amanda J. Nelson ◽  
Janice M. Juraska ◽  
Brian G. Ragan ◽  
Gary A. Iwamoto
Keyword(s):  
Exercise Training ◽  
Rat Brain ◽  
Dendritic Morphology ◽  
Ventrolateral Medulla ◽  
Heart Weight ◽  
Activity Levels ◽  
Sprague Dawley ◽  
Hypothalamic Area ◽  
Early Postnatal Development ◽  
Dendritic Branching

It has been shown that dendritic branching in neural cardiorespiratory and locomotor centers can be attenuated with exercise training (ET) initiated immediately after weaning. The purpose of this study was to determine whether neuroplastic changes occur within cardiorespiratory and locomotor centers due to ET after maturation. Male Sprague-Dawley rats (21 days old, n = 28) were individually housed in standard cages. At 91 days of age, animals were divided into two groups: untrained (UN; n = 14) and trained (TR; n = 14). The TR group exercised spontaneously for 50 days on running wheels. ET indexes were obtained, including maximal O2 consumption, percent body fat, resting heart rate, and heart weight-to-body weight ratios. The brain was processed with a modified Golgi-Cox procedure. Impregnated neurons from the periaqueductal gray (PAG), posterior hypothalamic area (PH), nucleus of the tractus solitarius (NTS), cuneiform nucleus (CnF), rostral ventrolateral medulla, nucleus cuneatus, and cerebral cortex were examined. Neurons were traced and analyzed using the Sholl concentric ring analysis of dendritic branching. The mean total number of dendritic intersections with the concentric rings per neuron per animal were compared between UN and TR groups. There were significant differences between UN and TR groups in the PH, PAG, CnF, and NTS in the total number of intersections per animal. In some areas, the effect size was smaller when ET was initiated in mature animals, possibly related to their relatively reduced activity levels. In conclusion, the adult rat brain remains dynamic and adapts to chronic ET. However, some brain areas appear to be more affected if ET is initiated in early postnatal development.

Changes in insulin response to glucose after exercise training in partially pancreatectomized rats

1991 ◽  
Vol 70 (4) ◽  
pp. 1563-1568 ◽  
Author(s):  
P. A. Farrell ◽  
A. L. Caston ◽  
D. Rodd
Keyword(s):  
Exercise Training ◽  
Acute Exercise ◽  
Citrate Synthase ◽  
Blood Glucose Concentration ◽  
Insulin Response ◽  
Similar Response ◽  
Sprague Dawley ◽  
Partial Pancreatectomy ◽  
Fed State ◽  
Arterial Blood

The effects of exercise training on glucose-stimulated insulin secretion (GSIS) were studied in male Sprague-Dawley rats made mildly to severely diabetic by partial pancreatectomy. Exercise trained (10 wk treadmill; T) and untrained (Unt) rats were grouped according to posttraining fed-state hyperglycemia as follows: T less than 200 and Unt less than 200 (glucose concn less than 200 mg/dl), T 200-300 and Unt 200-300 (glucose concn 200-300 mg/dl), and T greater than 300 and Unt greater than 300 (glucose concn greater than 300 mg/dl). After exercise training, hyperglycemic glucose clamps were performed in awake rats by elevation of arterial blood glucose concentration 126 mg/dl above fasting basal levels for 90 min. Exercise training significantly increased muscle citrate synthase activity. Prevailing hyperglycemia was reduced during the 10-wk exercise training period in all T rats with fed-state glucose concentrations less than 300, and only 53% of Unt rats in these groups had reduced glycemia. GSIS was significantly higher in T less than 200 [2.4 +/- 0.7 (SD) ng/ml at 90 min] than in Unt less than 200 (1.5 +/- 0.3). A similar response was found for T 200-300 (1.1 +/- 0.3 ng/dl) vs. Unt 200-300 (0.7 +/- 0.1) but not T greater than 300 (0.36 +/- 0.2) vs Unt greater than 300 (0.44 +/- 0.05). Sham-operated control rats had insulin concentrations of 6.6 +/- 1.6 ng/ml at the 90th min of the clamp. Acute exercise reduced fed-state glycemia in rats with mild-to-moderate (less than 300 mg/dl) diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)

Porcine cardiac myocyte power output is increased after chronic exercise training

2006 ◽  
Vol 101 (1) ◽  
pp. 40-46 ◽  
Author(s):  
Aaron C. Hinken ◽  
F. Steven Korte ◽  
Kerry S. McDonald
Keyword(s):  
Exercise Training ◽  
Power Output ◽  
Cardiac Myocyte ◽  
Troponin I ◽  
Citrate Synthase ◽  
Contractile Function ◽  
Heart Weight ◽  
Peak Power Output ◽  
Chronic Exercise ◽  
Miniature Swine

Chronic exercise training increases the functional capacity of the heart, perhaps by increased myocyte contractile function, as has been observed in rodent exercise models. We examined whether cardiac myocyte function is enhanced after chronic exercise training in Yucatan miniature swine, whose heart characteristics are similar to humans. Animals were designated as either sedentary (Sed), i.e., cage confined, or exercise trained (Ex), i.e., underwent 16–20 wk of progressive treadmill training. Exercise training efficacy was shown with significantly increased heart weight-to-body weight ratios, skeletal muscle citrate synthase activity, and exercise tolerance. Force-velocity properties were measured by attaching skinned cardiac myocytes between a force transducer and position motor, and shortening velocities were measured over a range of loads during maximal Ca2+ activation. Myocytes ( n = 9) from nine Ex pigs had comparable force production but a ∼30% increase in peak power output compared with myocytes ( n = 8) from eight Sed. Interestingly, Ex myofibrillar samples also had higher baseline PKA-induced phosphorylation levels of cardiac troponin I, which may contribute to the increase in power. Overall, these results suggest that enhanced power-generating capacity of porcine cardiac myofibrils contributes to improved cardiac function after chronic exercise training.

Exercise-induced alterations in skeletal muscle myosin heavy chain phenotype: dose-response relationship

1999 ◽  
Vol 86 (3) ◽  
pp. 1002-1008 ◽  
Author(s):  
Haydar A. Demirel ◽  
Scott K. Powers ◽  
Hisashi Naito ◽  
Michael Hughes ◽  
Jeff S. Coombes
Keyword(s):  
Exercise Training ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Extensor Digitorum Longus ◽  
Citrate Synthase ◽  
Extensor Digitorum ◽  
Control Group ◽  
Sprague Dawley ◽  
Skeletal Muscle Myosin ◽  
Exercise Induced

This study investigated the effects of exercise training duration on the myosin heavy chain (MHC) isoform distribution in rat locomotor muscles. Female Sprague-Dawley rats (120 days old) were assigned to either a sedentary control group or to one of three endurance exercise training groups. Trained animals ran on a treadmill at ∼75% maximal O2 uptake for 10 wk (4–5 days/wk) at one of three different exercise durations (30, 60, or 90 min/day). Training resulted in increases ( P < 0.05) in citrate synthase activity in the soleus and extensor digitorum longus in both the 60 and 90 min/day duration groups and in the plantaris (Pla) in all three exercise groups. All durations of training resulted in a reduction ( P < 0.05) in the percentage of MHCIIb and an increase ( P < 0.05) in the percentage of MHCIIa in the Pla. The magnitude of change in the percentage of MHCIIb in the Pla increased as a function of the training duration. In the extensor digitorum longus, 90 min of daily exercise promoted a decrease ( P < 0.05) in percentage of MHCIIb and increases ( P < 0.05) in the percentages of MHCI, MHCIIa, and MHCIId/x. Finally, training durations ≥60 min resulted in an increase ( P < 0.05) in the percentage of MHCI and a concomitant decrease ( P < 0.05) in the percentage of MHCIIa in the soleus. These results demonstrate that increasing the training duration elevates the magnitude of the fast-to-slow shift in MHC phenotype in rat hindlimb muscles.

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