Effects of exercise training on contractile function in myocardial trabeculae after ischemia-reperfusion

2005 ◽  
Vol 99 (1) ◽  
pp. 230-236 ◽  
Author(s):  
Hyosook Hwang ◽  
Peter J. Reiser ◽  
George E. Billman
Keyword(s):  
Exercise Training ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Isometric Force ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Aerobic Exercise Training ◽  
Protective Effects ◽  
Shortening Velocity ◽  
Cross Sectional

Potential protective effects of aerobic exercise training on the myocardium, before an ischemic event, are not completely understood. The purpose of the study was to investigate the effects of exercise training on contractile function after ischemia-reperfusion (Langendorff preparation with 15-min global ischemia/30-min reperfusion). Trabeculae were isolated from the left ventricles of both sedentary control and 10- to 12-wk treadmill exercise-trained rats. The maximal normalized isometric force (force/cross-sectional area; Po/CSA) and shortening velocity ( Vo) in isolated, skinned ventricular trabeculae were measured using the slack test. Ischemia-reperfusion induced significant contractile dysfunction in hearts from both sedentary and trained animals; left ventricular developed pressure (LVDP) and maximal rates of pressure development and relaxation (±dP/d tmax) decreased, whereas end-diastolic pressure (EDP) increased. However, this dysfunction (as expressed as percent change from the last 5 min before ischemia) was attenuated in trained myocardium [LVDP: sedentary −60.8 ± 6.4% (32.0 ± 5.5 mmHg) vs. trained −15.6 ± 8.6% (64.9 ± 6.6 mmHg); +dP/d tmax: sedentary −54.1 ± 4.7% (1,058.7 ± 124.2 mmHg/s) vs. trained −16.7 ± 8.4% (1,931.9 ± 188.3 mmHg/s); −dP/d tmax: sedentary −44.4 ± 2.5% (−829.3 ± 52.0 mmHg/s) vs. trained −17.9 ± 7.2% (−1,341.3 ± 142.8 mmHg/s); EDP: sedentary 539.5 ± 147.6%; (41.3 ± 6.0 mmHg) vs. trained 71.6 ± 30.6%; 11.4 ± 1.2 mmHg]. There was an average 26% increase in Po/CSA in trained trabeculae compared with sedentary controls, and this increase was not affected by ischemia-reperfusion. Ischemia-reperfusion reduced V0 by 39% in both control and trained trabeculae. The relative amount of the β-isoform of myosin heavy chain (MHC-β) was twofold greater in trained trabeculae as well as in the ventricular free walls. Despite a possible increase in the economy in the trained heart, presumed from a greater amount of MHC-β, ischemia-reperfusion reduced Vo, to a similar extent in both control and trained animals. Nevertheless, the trained myocardium appears to have a greater maximum force-generating ability that may, at least partially, compensate for reduced contractile function induced by a brief period of ischemia.

Role of endogenous testosterone in myocardial proinflammatory and proapoptotic signaling after acute ischemia-reperfusion

2005 ◽  
Vol 288 (1) ◽  
pp. H221-H226 ◽  
Author(s):  
Meijing Wang ◽  
Ben M. Tsai ◽  
Ajay Kher ◽  
Lauren B. Baker ◽  
G. Mathenge Wairiuko ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Functional Recovery ◽  
Caspase 3 ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Acute Ischemia ◽  
Caspase 1 ◽  
Tnf Α

Myocardial ischemia is the leading cause of death in both men and women; however, very little information exists regarding the effect of testosterone on the response of myocardium to acute ischemic injury. We hypothesized that testosterone may exert deleterious effects on myocardial inflammatory cytokine production, p38 MAPK activation, apoptotic signaling, and myocardial functional recovery after acute ischemia-reperfusion (I/R). To study this, isolated, perfused rat hearts (Langendorff) from adult males, castrated males, and males treated with a testosterone receptor blocker (flutamide) were subjected to 25 min of ischemia followed by 40 min of reperfusion. Myocardial contractile function (left ventricular developed pressure, left ventricular end-diastolic pressure, positive and negative first derivative of pressure) was continuously recorded. After reperfusion, hearts were analyzed for expression of tissue TNF-α, IL-1β, and IL-6 (ELISA) and activation of p38 MAPK, caspase-1, caspase-3, caspase-11, and Bcl-2 (Western blot). All indices of postischemic myocardial functional recovery were significantly higher in castrated males or flutamide-treated males compared with untreated males. After I/R, castrated male and flutamide-treated male hearts had decreased TNF-α, IL-1β, and IL-6; decreased activated p38 MAPK; decreased caspase-1, caspase-3, and caspase-11; and increased Bcl-2 expression compared with untreated males. These results show that blocking the testosterone receptor (flutamide) or depleting testosterone (castration) in normal males improves myocardial function after I/R. These effects may be attributed to the proinflammatory and/or the proapoptotic properties of endogenous testosterone. Further understanding may allow therapeutic manipulation of sex hormone signaling mechanisms in the treatment of acute I/R.

scholarly journals P1: CHOLINERGIC RECEPTOR FUNCTION IN CARDIAC ISCHEMIC PRECONDITIONING

2016 ◽  
Vol 64 (3) ◽  
pp. 817.2-817
Author(s):  
CW Mullan ◽  
SA Mavropolous ◽  
K Ojamaa
Keyword(s):  
Ischemic Preconditioning ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Structural Complexity ◽  
Cholinergic Receptor ◽  
Left Ventricular ◽  
Sprague Dawley ◽  
Inner Mitochondrial Membrane ◽  
Cardiac Contractile Function

Purpose of StudyCardiac acetylcholine (ACh) signaling is protective, but the role of ACh in ischemic preconditioning (IPC) remains largely unknown. We studied the effect of selective alpha-7 nicotinic ACh receptor (a7nAChR) antagonism by methyllycaconitine (MLA) on the functional benefits of IPC and the effects of this on mitochondrial complexity and inner mitochondrial membrane potential (ψM).Methods UsedMale Sprague Dawley rats (n=17, 322±17 g) were heparinized and anesthetized with 80 mg/kg pentobarbital IP, and their hearts excised and perfused at constant pressure with a non-circulating Langendorff apparatus. Left ventricular (LV) pressure (LVDP) and heart rate (HR) were continually measured with a fluid filled latex balloon attached to a pressure transducer. Treatment groups were: ischemia-reperfusion (IR)(n=6): 20 min. perfusion, 30 min. of global ischemia, 45 min. of reperfusion; IPC (n=5): 10 min. perfusion, 3 min. ischemia with 2 min. reperfusion repeated 3 times prior to IR protocol, IPC+MLA (n=6): 6 min. perfusion, 4 min. of infusion of MLA at 233 nM, IPC with MLA during reperfusion periods, then IR. Mitochondria were isolated from the LV free wall, stained for ψM and for size, and examined by Flow Cytometry with a BD LSRFortessa. Controls (C) (n=4) were freshly excised hearts from similar animals with identical anesthesia.Summary of ResultsIPC increased LV work product (LVDP times HR) as a percent of pre-ischemia (%P) during reperfusion compared to IR control, and this effect was attenuated by MLA pretreatment (IR=24.1±4.5%P, IPC=49.8±2.8%P, IPC+MLA=33.8±3.5%P, p<0.01). IPC reduced end diastolic pressure from IR levels, and this was partially prevented by MLA treatment (IR=78.8±7.7 mm Hg, IPC=18.8±6.6 mm Hg, IPC+MLA=46.3±8.6 mm Hg, p<0.05). IPC maintained mitochondrial structural complexity compared to IR (C=65±6% of total mitochondria, IPC=61±5%, IR=32±4%, p<0.01). MLA reduced the effect of IPC on ψM in intact mitochondria to IR levels (IR=67±10% of intact population, IPC=88±3%, IPC+MLA=71±4%, p<0.01).ConclusionsSignaling through the a7nAChR is necessary for the effect of IPC on maintaining ψM and cardiac contractile function after IR injury.

Abstract 374: Targeted Deletion of A 2B Adenosine Receptors Attenuates the Protective Effects of Myocardial Postconditioning

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Xinglin Tan ◽  
Stephen L Tilley ◽  
Thomas Krahn ◽  
Bunyen Teng ◽  
S. J Mustafa ◽  
...  
Keyword(s):  
Adenosine Receptor ◽  
Troponin I ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Heart Weight ◽  
Receptor Subtypes ◽  
Protective Effects ◽  
Targeted Deletion ◽  
Beneficial Effects

Endogenous adenosine is an important ligand trigger for the cardioprotective effects of postconditioning (PostCon). To assess the hypothesis that A 2B adenosine receptor (A 2B AR) activation contributes to PostCon-induced protection, global ischemia-reperfusion was performed with and without PostCon or the selective A 2B agonist, BAY 60 – 6583 (BAY), in isolated wild-type (WT) and A 2B AR knockout (A 2B KO) mouse hearts. In WT hearts, PostCon improved post-ischemic recovery of left ventricular developed pressure (LVDP) to 63.3±1.6 % of pre-ischemic baseline vs. 49.9±1.6 % in non-PostCon controls (CTL), lowered end diastolic pressure (EDP) to 15.8±1.5 mmHg vs. 27.9±1.6 mmHg in CTL, and reduced coronary efflux of cardiac troponin I (cTnI) to 2507±359 ng/g heart weight vs. 4693±343 ng/g in CTL (n=12 both groups, p <0.05 each comparison). Treatment with BAY in the first two min of reperfusion mimicked beneficial effects of PostCon in WT hearts (LVDP: 64.7±2.0 % baseline, EDP: 16.2±2.0 mmHg, cTnI: 3311±366; n=13, not significant compared to respective PostCon values). Real-time PCR confirmed absence of A 2B AR in A 2B KO hearts and demonstrated no changes in expression of other adenosine receptor subtypes compared with WT hearts. In A 2B KO hearts, neither PostCon nor BAY improved recovery of LVDP (50.8±1.6 % baseline for CTL vs. 54.5±1.7 % with PostCon vs. 53.0±1.4 with BAY; n=6 each group), and neither affected EDP or release of cTnI. During reperfusion, both PostCon and BAY increased survival kinase signaling through Akt and ERK1/2 phosphorylation in WT but not A 2B KO hearts. In non-ischemic WT hearts, Akt and ERK1/2 phosphorylation was increased by both BAY treatment and application of the PostCon stimulus. These data demonstrate that the protective effects of PostCon are attenuated by targeted deletion of A 2B AR and are mimicked by selective A 2B AR activation, suggesting A 2B AR activation is an important trigger leading to PostCon-induced myocardial protection.

The cardioprotective effect of dual metallopeptidase inhibition: respective roles of endogenous kinins and natriuretic peptides

2005 ◽  
Vol 83 (2) ◽  
pp. 166-173 ◽  
Author(s):  
Marie-Josée Dumoulin ◽  
Albert Adam ◽  
John Burnett ◽  
Denise Heublein ◽  
Nobuharu Yamaguchi ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Natriuretic Peptides ◽  
Ace Inhibitor ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Cardioprotective Effect ◽  
Protective Effects ◽  
Hoe 140

The objective of the present study was to assess the cardioprotective effect of dual NEP–ACE inhibition in relation to endogenous cardiac bradykinin (BK), its active metabolite des-Arg9-BK, endogenous brain natriuretic peptides (BNP), and cGMP. Rats were treated with the dual metallopeptidase inhibitor, omapatrilat, or the ACE inhibitor, ramipril, for 7 d (1 mg·kg–1·d–1). Hearts were then isolated and subjected to a zero-flow ischemia and reperfusion (except controls), in the absence or presence of either a B2-receptor antagonist (Hoe-140), a B1-receptor antagonist (Lys-Leu8-des-Arg9-BK), or the GC-A/GC-B-receptor antagonist (HS-142-1). Chronic omapatrilat and ramipril increased the amount of endogenous BK collected upon reperfusion, but only ramipril increased that of des-Arg9-BK. Only omapatrilat increased both peak BNP and peak cGMP upon reperfusion, those increases being blocked by Hoe-140. Chronic omapatrilat (but not ramipril) decreased the total noradrenaline and lactate dehydrogenase release during the reperfusion period. Importantly, only omapatrilat improved the functional recovery of the ischemic reperfused heart, with a reduced left ventricular end-diastolic pressure, and improved developed left ventricular pressure. All cardio protective effects of omapatrilat were blocked by Hoe-140 and by HS-142-1, but not by the B1-receptor antagonist. In conclusion, a chronic treatment with a dual metallopeptidase inhibitor demonstrated a cardioprotective action not observed with an ACE inhibitor in a context of severe ischemia in rat isolated hearts, which was mediated by both endogenous BK and BNP.Key words: ACE inhibitors, omapatrilat, bradykinin, natriuretic peptide, ischemia, reperfusion.

Reperfusion at reduced flow rates enhances postischemic contractile recovery of perfused heart

1995 ◽  
Vol 268 (6) ◽  
pp. H2384-H2395 ◽  
Author(s):  
S. Takeo ◽  
J. X. Liu ◽  
K. Tanonaka ◽  
Y. Nasa ◽  
K. Yabe ◽  
...  
Keyword(s):  
Flow Rate ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Cardiac Contractile Function ◽  
Triphenyltetrazolium Chloride ◽  
Perfused Heart ◽  
Flow Rates ◽  
Reduced Flow

The effects of reperfusion at reduced flow rates on postischemic cardiac contractile function were examined in perfused rat hearts. Isolated hearts were subjected to 35-min ischemia followed by reperfusion at the preischemic flow rate (9.0 ml.g-1.min-1; ordinary flow rate) or at reduced flow rates (0.9-8.1 ml.g-1.min-1). Reperfusion at ordinary flow rate did not generate any left ventricular developed pressure (LVDP), whereas reperfusion at reduced flow rates (0.9-7.2 ml.g-1.min-1) elicited 13-57% of initial contractile force at reperfusion's end; optimal recovery occurred at 3.6 ml.g-1.min-1 (reduced flow rate). Reduced flow rate reperfusion attenuated ischemia-reperfusion-induced increase in left ventricular end-diastolic pressure (LVEDP) and perfusion pressure (PP), alteration in tissue Na+, K+, Ca2+, and Mg2+, release of creatine kinase and ATP metabolites, and development of triphenyltetrazolium chloride-unstained areas. Enhanced postischemic LVDP recovery was inversely related to higher coronary PP at the initial stage (4 min) of reperfusion (r = -0.763). The benefit of reduced flow rate reperfusion could not be attributed to rate of calcium delivery to the heart, formation of oxygen free radicals in myocardium, endothelium-dependent coronary artery dilation, or LVDEP reduction. Enhancement of postischemic LVDP recovery was associated with attenuation of ischemia-reperfusion-induced increases in myocardial sodium and calcium; failure of postischemic LVDP recovery was accompanied by an increase. Reduction in sodium and calcium overload may underlie the beneficial effects of reduced flow rate reperfusion in ischemic-reperfused heart.

scholarly journals Lack of the effect of superoxide dismutase and catalase on Na+,K+-ATPase activity in stunned rabbit hearts

2008 ◽  
pp. S61-S66
Author(s):  
P Kaplán ◽  
M Matejovičová ◽  
P Herijgers ◽  
W Flameng
Keyword(s):  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Atpase Activity ◽  
Cardiac Dysfunction ◽  
Myocardial Stunning ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Significant Loss ◽  
Protective Effects

Reactive oxygen species (ROS) have been implicated in the mechanism of postischemic contractile dysfunction, known as myocardial stunning. In this study, we examined protective effects of antioxidant enzymes, superoxide dismutase (SOD) and catalase, against ischemia/reperfusion-induced cardiac dysfunction and inhibition of Na+,K+-ATPase activity. Isolated Langendorff-perfused rabbit hearts were subjected to 15 min of global normothermic ischemia followed by 10 min reperfusion. The hearts treated with SOD plus catalase did not show significant recovery of left ventricular (LV) end-diastolic pressure compared with untreated ischemic reperfused hearts. Treatment with antioxidants had no protective effects on developed LV pressure or its maximal positive and negative first derivatives (+/-LVdP/dt). Myocardial stunning was accompanied by significant loss in sarcolemmal Na+,K+-ATPase activity and thiol group content. Inhibition of enzyme activity and oxidation of SH groups were not prevented by antioxidant enzymes. These results suggest that administration of SOD and catalase in perfusate do not protect significantly against cardiac dysfunction in stunned rabbit myocardium.

Activation of NF-κB is a critical element in the antiapoptotic effect of anesthetic preconditioning

2009 ◽  
Vol 296 (5) ◽  
pp. H1296-H1304 ◽  
Author(s):  
Xiyuan Lu ◽  
Hong Liu ◽  
Lianguo Wang ◽  
Saul Schaefer
Keyword(s):  
Cytochrome C ◽  
Caspase 3 ◽  
Diastolic Pressure ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Reversible Inhibitor ◽  
Critical Element ◽  
Protective Effects ◽  
Anesthetic Preconditioning

Anesthetic preconditioning (APC), defined as brief exposure to inhalational anesthetics before cardiac ischemia-reperfusion (I/R), limits injury in both animal models and in humans. APC can result in the production of reactive oxygen species (ROS), and prior work has shown that APC can modify activation of NF-κB during I/R, with consequent reduction in the expression of inflammatory mediators. However, the role of NF-κB activation before I/R is unknown. Therefore, these experiments tested the hypothesis that APC-induced ROS results in activation of NF-κB before I/R, with consequent increased expression of antiapoptotic proteins such as Bcl-2 and decreased apoptosis. Experiments utilized an established perfused heart rat model of sevoflurane APC and I/R. The role of NF-κB was defined by a novel method of transient inhibition of the regulatory kinase IKK using the reversible inhibitor SC-514. In addition to functional measures of left ventricular developed and end-diastolic pressure, phosphorylation of IκBα and activation of NF-κB were measured along with cytosolic protein content of Bcl-2, release of cytochrome c, and degradation of caspase-3. APC resulted in ROS-dependent phosphorylation of IκBα and activation of NF-κB before I/R. APC also increased the expression of Bcl-2 before I/R. In addition to functional protection following I/R, APC resulted in lower release of cytochrome c and caspase-3 degradation. These protective effects of APC were abolished by transient inhibition of IκBα phosphorylation and NF-κB activation by SC-514 followed by washout. ROS-dependent activation of NF-κB by APC before I/R is a critical element in the protective effect of APC. APC reduces apoptosis and functional impairment by increasing Bcl-2 expression before I/R. Interventions that increase NF-κB activation before I/R should protect hearts from I/R injury.

scholarly journals Protective Effects of Flavonoid Pomiferin on Heart Ischemia-Reperfusion

2007 ◽  
Vol 76 (3) ◽  
pp. 363-370
Author(s):  
J. Nečas ◽  
L. Bartošíková ◽  
T. Florian ◽  
J. Klusáková ◽  
V. Suchý ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Diastolic Pressure ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Left Ventricular ◽  
Lipid Peroxidation Product ◽  
Total Antioxidant Activity ◽  
Protective Effects ◽  
Rat Hearts ◽  
Total Antioxidant

The objective of the present 15-day study was to evaluate the cardioprotective potential of flavonoid pomiferin isolated from the infructences of Maclura pomifera, Moraceae, against ischemia-reperfusion induced injury in rat hearts as a model of antioxidant-based composite therapy. Studies were performed with isolated, modifi ed Langendorff-perfused rat hearts and ischemia of heart was initiated by stopping the coronary flow for 30 min, followed by 60 min of reperfusion (14 ml min-1). Wistar rats were divided into three groups. The treated group received pomiferin (5 mg/kg/day in 0.5% Avicel); the placebo group received only 0.5% Avicel; the intact group was left without any applications. Biochemical indicators of oxidative damage, lipid peroxidation product malondialdehyde, antioxidant enzymes (superoxide dismutase, glutathione peroxidase, total antioxidant activity in serum and myocardium has been evaluated. We also examined the effect of pomiferin on cardiac function (left ventricular end-diastolic pressure, left ventricular pressure, peak positive +dP/dt (rate of pressure development) after ischemia and reperfusion. Our results demonstrate that pomiferin attenuates the myocardial dysfunction provoked by ischemiareperfusion. This was confirmed by the increase in both the antioxidant enzyme values and the total antioxidant activity. The cardio-protection provided by pomiferin treatment results from the suppression of oxidative stress and correlates with the improved ventricular function.

Abstract 75: Ischemic Heart Failure is Exacerbated in CD39-null Mice

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Tatiana Novitskaya ◽  
Debra G Wheeler ◽  
Zhaobin Xu ◽  
Elena Chepurko ◽  
Bo Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Diastolic Pressure ◽  
Contractile Function ◽  
Ischemia Reperfusion ◽  
Smooth Muscles ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Coronary Artery Ligation ◽  
Genetic Ablation

Background: CD39 (ectonucleoside triphosphate diphosphohydrolase) is a nucleotidase expressed on endothelial cells, vascular smooth muscles cells, and leukocytes. CD39 plays a key role in vascular homeostasis, hydrolyzing extracellular ATP and ADP. CD39 has been shown to be important in models of ischemic preconditioning and cardiac ischemia reperfusion. However, the effect of CD39 activity on functional recovery of heart after myocardial infarction (MI) has not been evaluated. Hypothesis: Genetic ablation of CD39 expression exacerbates post-myocardial infarction cardiac function and fibrosis. Methods: Wild-type (WT) and CD39-null mice were subjected to coronary artery ligation. Cardiac function and protein evaluation of fibrotic markers was performed at day 28 post-MI. Results: Evaluation at Day 28 post-MI revealed that while mice of both genotypes had similarly reduced ejection fraction and equally compromised contractile function (dP/dtmax), there was a more pronounced negative effect on lusitropy (dP/dtmin) and increased left ventricular end-diastolic pressure in CD39-null mice. Therefore, cd39 gene ablation associates with the development of worsening cardiac performance. Histological analysis revealed increased collagen deposition and abundance of alpha-smooth muscle actin (αSMA) positive interstitial cells in the CD39-null hearts compared to WT hearts. To quantify these findings immunoblot analysis for collagen and αSMA was performed. We found that collagen and αSMA were increased at Day 28 post-MI, in CD39-null hearts compared to WT hearts. Conclusion: CD39 ablation has detrimental effects on post-MI recovery, resulting in diminished cardiac performance and increased fibrosis.

scholarly journals Examining Bone, Muscle and Fat in Middle-Aged Long-Term Endurance Runners: A Cross-Sectional Study

2020 ◽  
Vol 9 (2) ◽  
pp. 522
Author(s):  
Ulrike H. Mitchell ◽  
Bruce Bailey ◽  
Patrick J. Owen
Keyword(s):  
Exercise Training ◽  
Aerobic Exercise ◽  
Fat Mass ◽  
Lean Mass ◽  
Aerobic Exercise Training ◽  
Middle Aged ◽  
Cross Sectional ◽  
Endurance Runners ◽  
Total Body

Aerobic exercise training has many known cardiovascular benefits that may promote healthy aging. It is not known if long-term aerobic exercise training is also associated with structural benefits (e.g., lower fat mass, higher areal bone mineral density (BMD) and greater muscle mass). We evaluated these parameters in middle-aged long-term endurance runners compared to sex-, age-, height-, and weight-matched non-running controls. Total and regional lean and fat mass and areal BMD were assessed by dual-energy X-ray absorptiometry. Sagittal magnetic resonance images captured the cross-sectional area and thickness of the lumbar multifidus. Runners (n = 10; all male) had a mean (standard deviation; SD) age of 49 (4) years, height of 178.9 (4.9) cm, weight of 67.8 (5.8) kg, body mass index (BMI) of 21.4 (1.4) kg/m2 and had been running 82.6 (27.9) km/week for 23 (13) years. Controls (n = 9) had a mean (SD) age of 51 (5) years, height of 176.0 (5.1) cm, weight of 72.8 (7.1) kg, and BMI of 23.7 (2.1) kg/m2. BMI was greater in controls (p = 0.010). When compared to controls on average, runners had a 10 percentage-point greater total body lean mass than controls (p = 0.001) and 14% greater trunk lean mass (p = 0.010), as well as less total body (8.6 kg; p < 0.001), arm (58%; p = 0.002), leg (52%; p < 0.001), trunk (73%; p < 0.001), android (91%; p < 0.001), and gynoid fat mass (64%; p < 0.001). No differences were observed between groups for BMD outcomes or multifidus size. These results underscore the benefits of endurance running to body composition that carry over to middle-age.

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