scholarly journals Structural remodeling of coronary resistance arteries: effects of age and exercise training

2014 ◽  
Vol 117 (6) ◽  
pp. 616-623 ◽  
Author(s):  
Mina A. Hanna ◽  
Curtis R. Taylor ◽  
Bei Chen ◽  
Hae-Sun La ◽  
Joshua J. Maraj ◽  
...  
Keyword(s):  
Exercise Training ◽  
Wall Thickness ◽  
Effective Elastic Modulus ◽  
Vascular Wall ◽  
Intraluminal Pressure ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Fischer 344 ◽  
Wall Stiffness ◽  
Old Rats

Age is known to induce remodeling and stiffening of large-conduit arteries; however, little is known of the effects of age on remodeling and mechanical properties of coronary resistance arteries. We employed a rat model of aging to investigate whether 1) age increases wall thickness and stiffness of coronary resistance arteries, and 2) exercise training reverses putative age-induced increases in wall thickness and stiffness of coronary resistance arteries. Young (4 mo) and old (21 mo) Fischer 344 rats remained sedentary or underwent 10 wk of treadmill exercise training. Coronary resistance arteries were isolated for determination of wall-to-lumen ratio, effective elastic modulus, and active and passive responses to changes in intraluminal pressure. Elastin and collagen content of the vascular wall were assessed histologically. Wall-to-lumen ratio increased with age, but this increase was reversed by exercise training. In contrast, age reduced stiffness, and exercise training increased stiffness in coronary resistance arteries from old rats. Myogenic responsiveness was reduced with age and restored by exercise training. Collagen-to-elastin ratio (C/E) of the wall did not change with age and was reduced with exercise training in arteries from old rats. Thus age induces hypertrophic remodeling of the vessel wall and reduces the stiffness and myogenic function of coronary resistance arteries. Exercise training reduces wall-to-lumen ratio, increases wall stiffness, and restores myogenic function in aged coronary resistance arteries. The restorative effect of exercise training on myogenic function of coronary resistance arteries may be due to both changes in vascular smooth muscle phenotype and expression of extracellular matrix proteins.

Exercise training enhances flow-induced vasodilation in skeletal muscle resistance arteries of aged rats: role of PGI2 and nitric oxide

2007 ◽  
Vol 292 (6) ◽  
pp. H3119-H3127 ◽  
Author(s):  
Scott A. Spier ◽  
Michael D. Delp ◽  
John N. Stallone ◽  
James M. Dominguez ◽  
Judy M. Muller-Delp
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Exercise Training ◽  
Gastrocnemius Muscle ◽  
Aged Rats ◽  
Resistance Arteries ◽  
Fischer 344 ◽  
Young Rats ◽  
Old Rats ◽  
Gastrocnemius Muscles

Flow-induced vasodilation is attenuated with old age in rat skeletal muscle arterioles. The purpose of this study was to determine whether diminished cyclooxygenase (COX) signaling contributes to the age-induced attenuation of flow-induced vasodilation in gastrocnemius muscle arterioles and to determine whether, and through which mechanism(s), exercise training restores this deficit in old rats. Fischer 344 rats (3 and 22 mo old) were assigned to a sedentary or exercise-trained group. First-order arterioles were isolated from the gastrocnemius muscles, cannulated, and pressurized to 70 cmH2O. Diameter changes were determined in response to graded increases in intraluminal flow in the presence and absence of nitric oxide synthase (NOS) inhibition [10−5 M NG-nitro-l-arginine methyl ester (l-NAME)], COX inhibition (10−5 M indomethacin), or combination NOS (10−5 Ml-NAME) plus COX (10−5 M indomethacin) inhibition. Aging reduced flow-induced vasodilation in gastrocnemius muscle arterioles. Exercise training restored responsiveness to flow in arterioles of aged rats and enhanced flow-induced vasodilation in arterioles from young rats. l-NAME inhibition of flow-induced vasodilation was greater in arterioles from old rats compared with those from young rats and was increased after exercise training in arterioles from both young and old rats. Although the indomethacin-sensitive portion of flow-induced dilation was not altered by age or training, both COX-1 mRNA expression and PGI2 production increased with training in arterioles from old rats. These data demonstrate that exercise training restores flow-induced vasodilation in gastrocnemius muscle arterioles from old rats and enhances flow-induced vasodilation in gastrocnemius muscle arterioles from young rats. In arterioles from both old and young rats, the exercise training-induced enhancement of flow-induced dilation occurs primarily through a NOS mechanism.

Exercise training alters myogenic responses in porcine coronary resistance arteries

1993 ◽  
Vol 75 (6) ◽  
pp. 2677-2682 ◽  
Author(s):  
J. M. Muller ◽  
P. R. Myers ◽  
M. H. Laughlin
Keyword(s):  
Exercise Training ◽  
Weight Ratio ◽  
Oxidative Capacity ◽  
Intraluminal Pressure ◽  
Heart Weight ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Miniature Swine ◽  
Myogenic Responses

The purpose of this study was to test the hypothesis that myogenic responsiveness in porcine coronary resistance arteries is attenuated by exercise training. Twenty-four female Yucatan miniature swine were randomly separated into two groups of 12 pigs: exercise trained (ET) and sedentary control (SED). The ET pigs were trained on a motor-driven treadmill for 16–22 wk while the SED pigs remained confined to their pens. After training, heart weight-to-body weight ratio, skeletal muscle oxidative capacity, and exercise tolerance were significantly increased in ET pigs compared with SED pigs. Coronary resistance arteries 75–150 microns diam were isolated for in vitro evaluation of myogenic responses to changes in intraluminal pressure in the absence of intraluminal flow. Coronary resistance arteries from ET and SED pigs developed spontaneous tone at 40 mmHg intraluminal pressure. Active changes in diameter measured in response to intraluminal pressures < 40 mmHg were similar in coronary resistance arteries from ET and SED pigs. When pressure was raised above 40 mmHg, myogenic constriction was greater in coronary resistance arteries from ET pigs, as indicated by significantly greater reductions in diameter. At 60 and 70 mmHg intraluminal pressure, constriction was 8 and 16% greater, respectively, in resistance arteries from ET pigs. After maximal relaxation with sodium nitroprusside (100 microM), passive diameter changes measured in response to changes in intraluminal pressure from 10 to 80 mmHg were not significantly different in coronary resistance arteries from ET and SED pigs. We conclude that, contrary to our hypothesis, exercise training in pigs enhances myogenic constrictor responses in coronary resistance arteries.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Vasoconstrictor responses of coronary resistance arteries in exercise-trained pigs

1998 ◽  
Vol 84 (3) ◽  
pp. 884-889 ◽  
Author(s):  
M. Harold Laughlin ◽  
Judy M. Muller
Keyword(s):  
Exercise Training ◽  
Saline Solution ◽  
Physiological Saline ◽  
Bay K 8644 ◽  
Intraluminal Pressure ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Cellular Mechanisms ◽  
Miniature Swine ◽  
Physiological Saline Solution

Coronary resistance arteries isolated from exercise-trained pigs have been shown to exhibit enhanced myogenic reactivity (J. M. Muller, P. R. Myers, and M. Harold Laughlin. J. Appl. Physiol.75: 2677–2682, 1993). The purpose of this study was to test the hypothesis that exercise training results in enhanced vasoconstrictor responses of these arteries to all vasoconstrictor stimuli [specifically acetylcholine (ACh), endothelin-1 (ET-1), KCl, and the Ca2+ channel-agonist Bay K 8644]. Female Yucatan miniature swine were trained (Trn) on a motor-driven treadmill ( n = 16) or remained sedentary (Sed, n = 15) for 16–20 wk. Arteries 50–120 μm in diameter were isolated and cannulated with micropipettes, and intraluminal pressure was set at 60 cmH2O throughout experiments. Vasoreactivity was evaluated by examining constrictor responses to increasing concentrations of ACh (10−9 to 10−4 M), ET-1 (10−10 to 10−8 M), KCl (bath replacement with isotonic physiological saline solution containing 30 or 80 mM), and Bay K 8644 (10−9 to 10−6 M). Constricted diameters are expressed relative to the passive diameter observed after 100 μM SNP. All four constrictors produced similar decreases in diameter in arteries from both groups [ACh: 0.52 ± 0.07 (Trn) and 0.54 ± 0,06 (Sed); ET-1: 0.66 ± 0.05 (Trn) and 0.70 ± 0.07 (Sed); KCl: 0.66 ± 0.05 (Trn) and 0.70 ± 0.07 (Sed); Bay K 8644: 0.86 ± 0.05 (Trn) and 0.76 ± 0.05 (Sed)]. Present results combined with previous observations indicate that exercise training does not alter vasoconstrictor responses of porcine coronary resistance arteries but specifically increases myogenic reactivity. Thus the underlying cellular mechanisms for myogenic tone are altered by training but not receptor-mediated mechanisms (ACh and ET-1) nor voltage-gated Ca2+ channels (KCl and Bay K 8644) in coronary resistance arteries.

Cold-induced thermogenesis in younger and older Fischer 344 rats following exercise training

1988 ◽  
Vol 254 (6) ◽  
pp. R908-R916 ◽  
Author(s):  
R. B. McDonald ◽  
B. A. Horwitz ◽  
J. S. Stern
Keyword(s):  
Exercise Training ◽  
Body Mass ◽  
Cold Exposure ◽  
O2 Consumption ◽  
Fischer 344 ◽  
Before And After ◽  
Old Rats ◽  
F344 Rats ◽  
Maintain Body Temperature ◽  
Brown Fat Mitochondria

The inability of old rats to maintain body temperature during cold exposure has been well documented. This study evaluated the effect of exercise on the rates of cold-induced O2 consumption and the contribution of nonshivering thermogenesis (NST) to these rates. Younger (12 mo) and older (24 mo) male Fischer 344 (F344) rats were divided into exercised and sedentary groups. Exercised rats were run on a motor-driven treadmill 60 min/day, at 19-24 m/min, 5 days/wk for 6 mo. At the conclusion of the 6-mo training period, O2 consumption of all four groups was measured at thermoneutrality (26 degrees C) and during 6 h of exposure to 6 degrees C. Rectal temperatures were recorded before and after cold exposure. NST was estimated from the ability of isolated brown fat mitochondria to bind guanosine 5'-diphosphate (GDP). Core temperature of older sedentary rats fell 5.1 +/- 0.4 degrees C after cold exposure (36.3 +/- 0.3 vs. 31.2 +/- 0.8 degrees C). Exercise training in older animals prevented this fall from occurring (36.4 +/- 0.2 vs. 35.3 +/- 0.3 degrees C). Core temperatures of cold-exposed younger exercised and sedentary rats did not differ from thermoneutral values. Exercise did not alter the rates of resting body mass-independent (ml.min-1.kg body mass-0.67) O2 consumption in younger or older rats. However, body mass-independent and lean body mass (LBM)-independent (ml.min-1.g LBM-0.67) cold-induced O2 consumptions of older exercised rats were significantly elevated relative to those of older sedentary animals. This effect of exercise was not seen in younger rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise training induces glycogen sparing during exercise by old rats

1988 ◽  
Vol 64 (1) ◽  
pp. 259-265 ◽  
Author(s):  
G. D. Cartee ◽  
R. P. Farrar
Keyword(s):  
Exercise Training ◽  
Liver Glycogen ◽  
Trained Group ◽  
Respiratory Capacity ◽  
Fischer 344 ◽  
Hindlimb Muscle ◽  
Old Rats ◽  
Glycogen Utilization ◽  
Glycogen Sparing ◽  
Training Protocol

Glycogen utilization during exercise appears to be related to muscle respiratory capacity. Since the decline in hindlimb muscle respiratory capacity that occurs in rats during old age is eliminated when young and old rats undergo an identical exercise training protocol, liver and gastrocnemius glycogen concentrations were determined in identically trained young and old Fischer 344 rats at rest and immediately after a 30-min run requiring approximately 75% of maximal O2 consumption. These values were also compared with untrained age-matched control animals. The animals, which were 10 or 24 mo old after 6 mo of training, were fasted for 24 h before they were killed. Resting gastrocnemius glycogen did not differ among the groups. After 30 min of running, gastrocnemius glycogen was lower in the untrained than the trained groups and was not different between the trained groups. Resting liver glycogen was lower in the old trained group than the untrained groups but not statistically different from the young trained group. The postrun liver glycogen did not differ among the groups. Estimated gastrocnemius and liver glycogen utilization during exercise was decreased in both trained groups compared with untrained age-matched controls. These results indicate that the training-induced glycogen sparing during exercise of the same relative intensity was not diminished with age in identically trained young and old rats.

scholarly journals Structural remodeling of coronary resistance arteries: effects of age and exercise training (1079.24)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Mina Hanna ◽  
Curtis Taylor ◽  
Bei Chen ◽  
Hae‐Sun La ◽  
Joshua Maraj ◽  
...  
Keyword(s):  
Exercise Training ◽  
Coronary Resistance ◽  
Resistance Arteries ◽  
Structural Remodeling

scholarly journals Exercise training reverses aging-induced impairment of myogenic constriction in skeletal muscle arterioles

2015 ◽  
Vol 118 (7) ◽  
pp. 904-911 ◽  
Author(s):  
Payal Ghosh ◽  
Fredy R. Mora Solis ◽  
James M. Dominguez ◽  
Scott A. Spier ◽  
Anthony J. Donato ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Channel Blocker ◽  
Fischer 344 Rats ◽  
Channel Blockade ◽  
Fischer 344 ◽  
Young Rats ◽  
Age Related ◽  
Old Rats ◽  
And Training

To investigate whether exercise training can reverse age-related impairment of myogenic vasoconstriction in skeletal muscle arterioles, young (4 mo) and old (22 mo) male Fischer 344 rats were randomly assigned to either sedentary or exercise-trained groups. The roles of the endothelium and Kv1 channels in age- and exercise training-induced adaptations of myogenic responses were assessed through evaluation of pressure-induced constriction in endothelium-intact and denuded soleus muscle arterioles in the presence and absence of the Kv1 channel blocker, correolide. Exercise training enhanced myogenic constriction in arterioles from both old and young rats. In arterioles from old rats, exercise training restored myogenic constriction to a level similar to that of arterioles from young sedentary rats. Removal of the endothelium did not alter myogenic constriction of arterioles from young sedentary rats, but reduced myogenic constriction in arterioles from young exercise-trained rats. In contrast, endothelial removal had no effect on myogenic constriction of arterioles from old exercise-trained rats, but increased myogenic vasoconstriction in old sedentary rats. The effect of Kv1 channel blockade was also dependent on age and training status. In arterioles from young sedentary rats, Kv1 blockade had little effect on myogenic constriction, whereas in old sedentary rats Kv1 blockade increased myogenic constriction. After exercise training, Kv1 channel blockade increased myogenic constriction in arterioles from both young and old rats. Thus exercise training restores myogenic constriction of arterioles from old rats and enhances myogenic constriction from young rats through adaptations of the endothelium and smooth muscle Kv1 channels.

Abstract 533: Vascular Smooth Muscle Na/Ca Exchanger-1 Modulates Myogenic Reactivity and Blood Pressure in Chronic Intermittent Hypoxia

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Ling Chen ◽  
Youhua Wang ◽  
Jingyu Wang ◽  
Jin Zhang
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Wall Thickness ◽  
Intermittent Hypoxia ◽  
Vascular Reactivity ◽  
Intraluminal Pressure ◽  
Chronic Intermittent Hypoxia ◽  
Resistance Arteries ◽  
Small Resistance

Chronic intermittent hypoxia (CIH) results in systemic hypertension and altered vascular reactivity in human and rodents. We hypothesize that vascular smooth muscle (VSM) Na/Ca exchanger type-1 (NCX1) is a potential molecular mechanism mediating CIH-induced changes in vascular reactivity and blood pressure (BP). Wild type (WT) and transgenic (TG) mice with VSM-specific NCX1 overexpression were exposed to either CIH (1 min 5% nadir O 2 , followed by 1 min 21% O 2 ; 8 hrs/day for 5 weeks), or normoxia (constant 21% O 2 ). CIH resulted in greater BP elevation in TG (102 ± 3 mm Hg vs. 92 ± 6 mm Hg in normoxia, P < 0.05, n = 6 and 3, measured by intra-carotid artery catheterization under 1.5% isoflurane) than in WT (88 ± 4 mm Hg vs. 83 ± 2 mm Hg in normoxia, NS, n = 3 and 5) mice. Mesenteric small resistance arteries were then isolated and pressurized for diameter and wall thickness measurement. Compared to normoxia controls, CIH-exposed WT arteries exhibited increased resting myogenic tone (21 ± 2% vs. 16 ± 2% of PD in normoxia, P < 0.05, n = 5 each group). Moreover, myogenic reactivity in WT arteries of CIH-exposed mice shifted downward at lower range of intraluminal pressure (20-80 mm Hg), and upward at higher pressure (100-140 mm Hg). The effects of CIH were significantly greater in TG arteries compared to those in WT arteries, suggesting that VSM NCX1 augmented the myogenic response to CIH. Vasoconstrictions induced by phenylephrine (0.003-100 μM), greater in TG arteries, or high (60 mM) external K + solution, were similar between control and CIH groups in the same genotype, suggesting that arterial contractility to agonist stimulation was not affected by CIH. Arterial wall thickness or passive diameters under various intraluminal pressures in Ca 2+ -free solution were not different between control and CIH groups in either genotype, suggesting a lack of arterial stiffness or remodeling. In summary, 1) CIH results in greater BP elevation in TG mice; 2) CIH leads to biphasic changes in myogenic reactivity in small resistance arteries; 3) Overexpression of VSM NCX1 exaggerates BP elevation in CIH, likely by modulating myogenic reactivity, suggesting that VSM NCX1 is a potential mechanism mediating CIH-induced hypertension.

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