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Dissociation of hypoxia-induced calcium gain and rise in resting tension in isolated rat hearts.

When isolated hearts are perfused with substrate-free hypoxic buffer for prolonged periods of time, resting tension and tissue Ca increase. These two events may be interrelated. Isolated rat hearts were used to establish whether the hypoxia-induced increase in tissue Ca can be dissociated from the rise in resting tension. Tension generation was inhibited at the start of hypoxic perfusion by adding 2,3-butanedione monoxime (BDM, 30 mM). In other experiments the Ca2+ in the hypoxic buffer was reduced from 1.3 to 0.1 mM. After 30-120 min of hypoxia, ventricular muscle was assayed for ATP, creatine phosphate, Ca, and Na, and the perfusion defect was established. Resting tension was recorded before and throughout the hypoxic perfusion. Sixty minutes of perfusion with 1.3 mM Ca2+ glucose-free hypoxic buffer caused the tissue Ca to increase (P less than 0.01). Resting tension increased by 7.9 +/- 0.6 g (P less than 0.01). Sixty minutes of perfusion with 0.1 mM Ca2+ glucose-free hypoxic buffer failed to cause an increase in tissue Ca, but resting tension increased (P less than 0.01). During perfusion with glucose-free hypoxic buffer containing 2.6 mM Ca2+ and 30 mM BDM, resting tension remained low for up to 120 min, but after 60 min Ca accumulation occurred. After 120 min of BDM-hypoxic perfusion, tissue Ca reached 11.8 +/- 0.9 mumol/g dry wt. With or without BDM, hypoxia caused an early increase in tissue Na ahead of any increase in tissue Ca.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Relationships between resting tension and mechanical properties of papillary muscle.

The influence on mechanical properties of changes in resting tension over a range from 0.5 to 4.5 g was investigated in 12 isolated cat papillary muscles. At each resting tension, the muscles contracted isometrically with the exception of an externally applied sinusoidal stretch of 0.5% Lmax (deltaL) and 20 Hz. Stiffness (deltaT/deltaL) was determined from deltaL and the peak amplitudes (deltaT) of the individual cycles from the sinusoidal component of tension. Assuming that the muscle and experimental apparatus behaved as a linear second-order mechanical system, it was possible to divide stiffness into its elastic and viscous components. During rest, total stiffness and its components were linearly related to tension. During contraction, stiffness and its elastic component were linearly related to tension. Furthermore, increasing resting tension increased the intercept and decreased the slope of this linear stiffness-tension relationship. The relationship between viscous stiffness and tension during contraction is more complex in that it is a direct relationship at low resting tensions, but an inverse one at high resting tensions.

Animals↗

New "rest period" protocol for inducing tolerance to high O2 exposure in adult rats.

We report a new protocol for inducing marked tolerance to prolonged exposure to hyperoxia in adult rats that entails the use of a single "rest period" between exposures to a usually lethal concentration of O2. Exposure of adult rats to greater than 95% O2 for 48 h followed by a rest in air, or a rest even in 50-75% O2, consistently resulted in 100% survival with evidence of only slight pulmonary edema during continuation of exposure to greater than 95% O2 for 3-7 more days (7-day survival for rats rested in room air for 24 h = 23/23; for rats rested in 50-75% O2 for 24 h = 27/27; for continuously O2-exposed control rats = 0/11). Induction of tolerance to hyperoxia was associated with significant increases in the lungs' antioxidant enzyme activities during the reexposure to greater than 95% O2 following the rest period. The molecular means by which the events in this protocol lead to increased lung antioxidant enzyme activity is only partially known, but because of the marked tolerance produced, the elucidation of the mechanisms must be important to our understanding of tolerance to hyperoxia.

Animals↗

Effect of selective hepatic vagotomy on plasma FFA levels in resting and exercising rats.

Metabolic effects of a selective hepatic vagotomy (HV) were investigated in nonfasted (N) and 24-h fasted (F) rats, at rest and immediately after a 50-min exercise period (26 m/min, 0% grade). In nonfasted rats, no significant differences between HV and sham-operated (SHM) groups were found in blood substrates [free fatty acids (FFA) or glucose], insulin, and muscle glycogen levels, either at rest or after exercise. In F rats, liver glycogen was almost completely depleted at rest. This depletion was associated with a significantly (P less than 0.05) lower plasma FFA concentration at rest in HV compared with SHM rats (mean +/- SE, 0.57 +/- 0.04 vs. 0.83 +/- 0.1 mmol/l). No differences in FFA levels were observed between the same two groups after the exercise period. Exercise, however, resulted in a 2.5 times greater glycogen breakdown in the soleus muscle of HV compared with SHM rats. Hepatic vagotomy in the F condition was also associated with lower resting and exercising insulin concentrations. It is concluded that HV, when followed by a 24-h fast, may influence metabolic substrate regulation at rest and to a certain extent during exercise. These data support the concept of the existence of hepatic glucoreceptors responsive to a decrease in liver glycogen content.

Animals↗

Acclimation to humid heat lowers resting core temperature.

The purpose of this study was to test the hypothesis that a reduction in resting rectal temperature (Tre) is partially responsible for the attenuation in the rise of core temperature during the heat exposure following acclimation to humid heat. Nine male volunteers completed 7 days of acclimation, performing 2 h of exercise per day in a hot, humid environment (35 degrees C, 75% relative humidity). Mean (+/- SD) ending Tre significantly (P < 0.05) decreased from 38.9 +/- 0.5 degrees C on day 1 to 38.3 +/- 0.4 degrees C on day 7. Likewise, mean (+/- SD) resting Tre significantly (P < 0.05) decreased from 37 +/- 0.3 to 36.7 +/- 0.4 degrees C. In fact, all nine men showed a decrease in resting Tre from day 1 to day 7, ranging from -0.1 to -0.5 degrees C. In addition, resting Tre and ending Tre were significantly correlated (r = 0.68). However, the mean increases in Tre (ending Tre minus resting Tre) and heat storage that occurred on each of the 7 acclimation days were not significantly different. These results support the hypothesis that a reduction in resting Tre is partially responsible for the attenuation in ending Tre during heat exposure following short-term acclimation to humid heat.

Acclimatization↗

Interrelationship of FFA and glycerol turnovers in resting and exercising dogs.

Dogs with indwelling arterial and venous catheters ran on a treadmill on a 10% or on a 15% slope at 100 m/min. Glycerol turnover ([2-3H]-glycerol) and FFA turnover ([1-14C]palmitate) were measured simultaneously. Both turnovers were greatly increased by exercise. Similar increases were produced in resting dogs by norepinephrine infusions (0.5 mug/kg-min). At rest, as well as during exercise, there was a straight-line correlation between the ratio of disappearance of each substrate and their respective plasma concentrations. Over a wide range there was a straight-line correlation between the rate of production of FFA (RaFFA) and that of glycerol (RaGLY) at rest as well as during exercise. At any given RaFFA, RaGLY was higher in the running than in the resting dog. At rest the ratio of RaFFA/RaGLY was found to give the theoretical value of 3.0 only when RaFFA was 10-15 mumol/kg-min, below this the ratio was lower and above this it was higher. During exercise the ratio was lower than at rest and at heavier load lower than at lighter work. The results suggest that in vivo a combination of partial and complete lipolysis as well as reesterification occurs. The glucose equivalent of the glycerol turnover (if 100% converted) represents (under the given experimental conditions) 14-18% of the hepatic glucose output on the 15% slope and 20-25% of it on the 10% slope.

Adipose Tissue↗

Resting tension characteristics in differentiating intact rat fast- and slow-twitch muscle fibers.

The postnatal changes in resting muscle tension were investigated at 20 degrees C by using small muscle fiber bundles isolated from either the extensor digitorum longus or the soleus of both neonatal (7-21 days old) and adult rats. The results show that the tension-extension characteristics of the bundles depended on the age of the rats. For example, both the extensor digitorum longus and soleus bundles of rats older than 14 days showed characteristic differences that were absent in bundles from younger rats. Furthermore, the tension-extension relation of the adult slow muscle fiber bundles were similar to those of the two neonatal muscles and were shifted to longer sarcomere lengths relative to those of the adult fast-fiber bundles. Thus, at the extended sarcomere length of 2.9 microm, the adult fast muscle fiber bundles developed higher resting tensions (5.6 +/- 0.5 kN/m2) than either the two neonatal ( approximately 3 kN/m2) or the adult slow (3.1 +/- 0.4 kN/m2) muscle fiber bundles. At all ages examined, the resting tension responses to a ramp stretch were qualitatively similar and consisted of three components: a viscous, a viscoelastic, and an elastic tension. However, in rats older than 14 days, all three tension components showed clear fast- and slow-fiber type differences that were absent in younger rats. Bundles from 7-day-old rats also developed significantly lower resting tensions than the corresponding adult ones. Additionally, the resting tension characteristics of the adult muscles were not affected by chemical skinning. From these results, we conclude that in rats resting muscle tension, like active tension, differentiates within the first 3 wk after birth.

Aging↗

Effect of septal myotomy and myectomy on left ventricular systolic function at rest and during exercise in patients with IHSS.

Patients with idiopathic hypertrophic subaortic stenosis (IHSS) have supernormal left ventricular systolic function at rest. Septal myotomy/myectomy reduces outflow obstruction and symptoms. However, it has been proposed that operation causes myocardial damage, with consequent reduction in left ventricular function and potentially deleterious long-term consequences, despite relief of symptoms. To evaluate the effect of myotomy and mylectomy on left ventricular function, we employed noninvasive radionuclide cineangiography at rest and during maximal exercise in21 consecutive patients with IHSS, before and 6 months after operation. In 30 normal subjects, the ejection fraction (EF) was 57 +/- 2% at rest and 71 +/- 2% during exercise. Before operation in patients with IHSS, the EF was supernormal at rest (76 +/- 2%, p less than 0.001), and normal during exercise (71 +/- 3%, NS). All patients improved from NYHA functional class III-IV preoperatively to class I-II postoperatively; the maximal provocable gradient invariably diminished (average, 100 +/- , mm Hg preop, 33 +/- 9 mm Hg postop, p less than 0.001). Postoperatively, the EF at rest was 67 +/- 2%, still supernormal, but less than that noted preoperatively (p less than 0.001). During exercise, the EF was 66 +/- 4%, only mildly diminished (p less than 0.01) from that preoperatively. We conclude that muscle resection during myotomy and myectomy usually does not cause any important impairment of global left ventricular function at rest or during exercise stress.

Adolescent↗

Relation between coronary "steal" and contractile function at rest in collateral-dependent myocardium of humans with ischemic heart disease.

BACKGROUND: We tested the hypothesis that rest asynergy in collateral-dependent myocardium correlates with coronary steal. METHODS AND RESULTS: PET with [13N]ammonia measured myocardial blood flow and flow reserve in 15 patients with symptomatic chronic ischemic heart disease. Coronary angiography assessed stenosis severity and collateral blood supply. Echocardiography or contrast ventriculography evaluated regional wall motion. Collateral-dependent segments with normal flow at rest and supplied by coronary vessels having </=50% diameter stenosis were studied. Steal was defined as a decline in myocardial blood flow with adenosine >/=0.15 mL. min-1. g-1 versus rest. Blood flow at rest in asynergic, collateral-dependent segments with steal (1.15+/-0.35 mL. min-1. g-1) exceeded (P<0.0001) that of asynergic segments without steal (0.81+/-0.24) and those with normal contraction (0.77+/-0.18). Although the flow reserve ratio of segments with normal contraction (1.8+/-0.8) exceeded that of asynergic ones with (0.6+/-0.1) or without (1.3+/-0.4) steal, overlap was great. Correlation between basal contraction and flow reserve ratio in collateral-dependent myocardium was significant but weak (r=0.45, P<0.001). However, segments demonstrating "steal" with adenosine manifested asynergy in 22 of 23 collateral-dependent segments versus 24 of 39 nonsteal segments (chi2=7.10, P<0.01). CONCLUSIONS: Although myocardial flow reserve in collateral-dependent segments with normal contraction exceeded that of asynergic segments, overlap was great. However, in patients with angina or congestive heart failure, left ventricular segments demonstrating steal with adenosine almost always exhibit asynergy at rest. Thus, coronary steal may play an important role in the pathogenesis of chronic contractile impairment at rest, whereas simple reduction of flow reserve may be less important in selected patients.

Aged↗

Hibernating myocardium retains metabolic and contractile reserve despite regional reductions in flow, function, and oxygen consumption at rest.

Hibernating myocardium, characterized by reductions in flow and function at rest, has limited contractile reserve in response to increases in external workload. We hypothesized that this attenuation of function reflects an adaptive downregulation that prevents the development of metabolic evidence of ischemia during stress. To test this hypothesis, pigs were chronically instrumented with a proximal left anterior descending artery stenosis for 3 months, resulting in severe anteroapical hypokinesis with reduced resting perfusion (0.78+/-0.05 versus 0.94+/-0.07 mL x min(-1)x g(-1) in remote, P<0.01; and 0.99+/-0.08 in controls, P<0.05). Open-chest studies confirmed resting dysfunction compared with normal controls (segment shortening 9.2+/-2.2% versus 23.5+/-1.1%, P<0.05). Resting myocardial oxygen consumption was reduced (63+/-3 versus 77+/-6 microL x g(-1) x min(-1) in controls, P<0.05), yet lactate consumption was normal. Although subendocardial perfusion failed to increase during graded, intravenous epinephrine infusion (n=8), peak segment shortening (to 17.3+/-3.1%, P<0.05) and oxygen consumption (to 90+/-6 microL x g(-1) x min(-1), P<0.01) increased from the depressed resting levels. There was no lactate production in hibernating myocardium, and lactate uptake increased during stress (0.7+/-0.1 to 1.2+/-0.1 micromol x g(-1) x min(-1), P<0.05). The absence of metabolic evidence of ischemia was also confirmed during atrial pacing to a rate of 120 bpm (n=8). Thus, despite reductions in function and oxygen consumption at rest, hibernating myocardium retains the ability to increase metabolism without the development of acute ischemia. This supports the hypothesis that the downregulation of oxygen consumption and function in hibernating myocardium is an adaptive response that prevents a supply-demand imbalance during submaximal increases in cardiac workload when coronary flow reserve is limited.

Adaptation, Physiological↗

Contribution of prostaglandins to muscle blood flow in anesthetized dogs at rest, during exercise, and following inflow occlusion.

The role of locally formed cyclo-oxygenase products (endoperoxide intermediates, prostaglandins, or prostacyclins) in resistance to blood flow was studied in the hindlimbs of anesthetized dogs during rest, during exercise, and following release of inflow occlusion. Meclofenamic acid, indomethacin, or sodium meclofenamate reduced mean resting blood flows of 86, 113, and 118 ml/min to 54, 82, and 67 ml/min, respectively. Inhibitors of prostaglandin synthesis reduced the vasodilator response to arachidonic acid by 81%. In addition, prostaglandin synthesis inhibitors attenuated the hyperemic responses following inflow occlusions in the resting hindlimb. The attenuation was most marked following a 1-second occlusion (74%) and progressively less following a 10-second (44%) and a 300-second (24%) occlusion. However, the portion of the total postocclusive hyperemic response attributable to prostaglandins was constant and independent of occlusion duration. Inhibition of prostaglandin synthesis did not affect the hyperemia of exercise, but reduced significantly the postocclusion hyperemia that followed the release of a 1-second (63%) and a 2-second (43%) period of inflow occlusion in the exercising hindlimb; attenuation was minor following a 10-second occlusion (10%). In three of four exercising hindlimbs, the portion of the postocclusion hyperemia attributable to prostaglandins was inversely related to the duration of the occlusion. These data indicate that locally synthesized cyclo-oxygenase products, possibly prostaglandins, are important in the maintenance of blood flow in resting but not exercising muscle, contribute significantly to postocclusive hyperemia in resting and exercising hindlimbs, and mediate the hyperemia that follows occlusions of 5 seconds or less in resting and 2 seconds or less in exercising hindlimbs.

Animals↗

Bay K 8644 increases resting Ca2+ spark frequency in ferret ventricular myocytes independent of Ca influx: contrast with caffeine and ryanodine effects.

Bay K 8644, an L-type Ca2+ channel agonist, was shown previously to increase resting sarcoplasmic reticulum (SR) Ca2+ loss and convert post-rest potentiation to decay in dog and ferret ventricular muscle. Here, the effects of Bay K 8644 on local SR Ca2+ release events (Ca2+ sparks) were measured in isolated ferret ventricular myocytes, using laser scanning confocal microscopy and the fluorescent Ca2+ indicator fluo-3. The spark frequency under control conditions was fairly constant during 20 s of rest after interruption of electrical stimulation. Bay K 8644 (100 nmol/L) increased the spark frequency by 466+/-90% of control at constant SR Ca2+ load but did not change the spatial and temporal characteristics of individual sparks. The increase in spark frequency was maintained throughout the period of rest. The increase in Ca2+ spark frequency induced by Bay K 8644 was not affected by superfusion with Ca2+-free solution (with 10 mmol/L EGTA) but was suppressed by the addition of 10 micromol/L nifedipine (which by itself did not alter resting Ca2+ spark frequency). This suggests that the effect of Bay K 8644 on Ca2+ sparks is mediated by the sarcolemmal dihydropyridine receptor but is also independent of Ca2+ influx. Low concentrations of caffeine (0.5 mmol/L) increased both the average frequency and duration of sparks. Ryanodine (50 nmol/L) increased the spark frequency and also induced long-lasting Ca2+ signals. This may indicate long-lasting openings of SR Ca2+ release channels and a lack of local SR Ca2+ depletion. In lipid bilayers, Bay K 8644 had no effect on either single-channel current amplitude or open probability of the cardiac ryanodine receptor. It is concluded that Bay K 8644 activates SR Ca2+ release at rest, independent of Ca2+ influx and perhaps through a functional linkage between the sarcolemmal dihydropyridine receptor and the SR ryanodine receptor. In contrast, caffeine and ryanodine modulate Ca2+ sparks by a direct action on the SR Ca2+ release channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Validation of 2 approaches to predicting resting metabolic rate in critically ill patients.

BACKGROUND: Indirect calorimetry is the criterion method for determining resting metabolic rate for nutrition support in critically ill patients. However, calculation equations are more commonly used. In the current study we tested the validity of 2 such calculation systems. METHODS: Indirect calorimetry was performed with an open-circuit device in mechanically ventilated surgical, trauma, and medical patients at rest. Feedings were not stopped for the measurements. Two predictive equations by Ireton-Jones and 3 versions of a multivariate equation developed at our institution (referred to as Penn State equations) were then used to estimate resting metabolic rate. These estimates were compared on a percentage basis with the measured value of resting metabolic rate. Estimated resting metabolic rate within 10% of measured was considered accurate, whereas estimations >15% different from measured were considered large errors. RESULTS: Forty-seven subjects were measured. A larger percentage of subjects were estimated accurately by the Penn State equations (72% in the best equation) than by the Ireton-Jones equations (60% in the best equation; not significant). The incidence of errors >15% of measured was significantly lower in the Penn State equation (11% of subjects) compared with the Ireton-Jones equation (32% of subjects) (p < .05). CONCLUSIONS: The Penn State equation for resting metabolic rate in mechanically ventilated intensive care patients receiving nutrition support appears to be a valid clinical tool for determining energy goals in the absence of or as a supplement to indirect calorimetry. The Ireton-Jones equation performed less well, especially in that a higher number of large errors occurred.

Adolescent↗

Synergy among receptors on resting NK cells for the activation of natural cytotoxicity and cytokine secretion.

Freshly isolated, resting natural killer (NK) cells are generally less lytic against target cells than in vitro interleukin 2 (IL-2)-activated NK cells. To investigate the basis for this difference, the contribution of several receptors to activation of human NK cells was examined. Target-cell lysis by IL-2-activated NK cells in a redirected, antibody-dependent cytotoxicity assay was triggered by a number of receptors. In contrast, cytotoxicity by resting NK cells was induced only by CD16, and not by NKp46, NKG2D, 2B4 (CD244), DNAM-1 (CD226), or CD2. Calcium flux in resting NK cells was induced with antibodies to CD16 and, to a weaker extent, antibodies to NKp46 and 2B4. Although NKp46 did not enhance CD16-mediated calcium flux, it synergized with all other receptors. 2B4 synergized with 3 other receptors, NKG2D and DNAM-1 each synergized with 2 other receptors, and CD2 synergized with NKp46 only. Resting NK cells were induced to secrete tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma), and to kill target cells by engagement of specific, pair-wise combinations of receptors. Therefore, natural cytotoxicity by resting NK cells is induced only by mutual costimulation of nonactivating receptors. These results reveal distinct and specific patterns of synergy among receptors on resting NK cells.

Antigens, CD↗

Circulating growth factor studies in growth plate versus resting cartilage in vitro: tissue responsiveness.

We attempted to develop a system in which cartilage growth-plate responses could be examined in vitro. In vivo, rat osteochondral growth-plate width was decreased by hypophysectomy and restored toward normal by GH. Subsequently, segments of resting costal cartilage and osteochondral growth plate from hypophysectomized rats were incubated in vitro with [35S]sulfate and [3H]thymidine. Within ribs, growth plate generally had basal uptake greater than resting cartilage and a greater increase in activity on addition of normal rat serum. Across ribs 3-9, there was little change in growth plate or resting cartilage sulfate uptake, and only a modest increase in thymidine uptake caudally. Increasing concentrations of normal rat serum provided parallel stimulation for both growth plate and resting cartilage, with significant responses to as little as 1 microliter (sulfate uptake) or 5 microliters (thymidine uptake). Stimulation for both growth plate and resting cartilage by hypophysectomized rat serum was significantly less than by normal rat serum; activity was restored by GH in vivo, establishing growth plate responsiveness to GH- and pituitary-dependent factors. Growth plate and resting cartilage were generally unaffected by exposure in vitro to supraphysiological concentrations of GH, cortisol, testosterone, estradiol, or T3. Use of osteochondral junction tissue appears to yield an assay system that is sensitive and sufficiently reproducible to allow study of growth factor action at the growth plate in vitro.

Animals↗

The role of the resting zone in growth plate chondrogenesis.

In mammals, growth of long bones occurs at the growth plate, a cartilage structure that contains three principal layers: the resting, proliferative, and hypertrophic zones. The function of the resting zone is not well understood. We removed the proliferative and hypertrophic zones from the rabbit distal ulnar growth plate in vivo, leaving only the resting zone. Within 1 wk, a complete proliferative and hypertrophic zone often regenerated. Next, we manipulated growth plates in vivo to place resting zone cartilage ectopically alongside the proliferative columns. Ectopic resting zone cartilage induced a 90-degree shift in the orientation of nearby proliferative zone chondrocytes and seemed to inhibit their hypertrophic differentiation. Our findings suggest that resting zone cartilage makes important contributions to endochondral bone formation at the growth plate: 1) it contains stem-like cells that give rise to clones of proliferative chondrocytes; 2) it produces a growth plate-orienting factor, a morphogen, that directs the alignment of the proliferative clones into columns parallel to the long axis of the bone; and 3) it may also produce a morphogen that inhibits terminal differentiation of nearby proliferative zone chondrocytes and thus may be partially responsible for the organization of the growth plate into distinct zones of proliferation and hypertrophy.

Animals↗

Polysomal organization in growing and resting cultures and its relation to protein synthesis in Tetrahymena.

Cytosol from Tetrahymena cells growing at different rates was isolated and separated by centrifugation into polysomal and non-polysomal fractions. The RNAs of either fraction were separated chromatographically into poly(A)+ RNA and poly(A)-RNA. It was found that in resting cultures the total RNA per cell is only about half of that of rapidly growing cultures. All fractions of RNA were reduced proportionally. Thus, the percentage of polysomally bound total RNA (70% of cytosol RNA) and polysomally bound poly(A)+ RNA (72% of cytosol poly(A)+ RNA) is the same in growing and resting cultures. Differences, however, were found in the polysomal structure. Polysomes from resting cultures contained significantly fewer ribosomes. The amounts of RNA bound to polysomes were related to the rate of protein synthesis under different growth conditions. The decrease in cellular RNA corresponded well with the reduction in amino acid incorporation in resting cells. The rate of protein accumulation in resting cells, on the other hand, was considerably less, suggesting that polypeptides in resting cultures are less stable.

Amino Acids↗

Resting heart rate changes after endurance training in older adults: a meta-analysis.

PURPOSE: Question remains regarding endurance training and changes in resting heart rate (HR) among older individuals. The objective of this meta-analysis was to determine the effects of controlled aerobic training on resting HR among sedentary older adults. METHODS: Studies were identified by a systematic computer database search, hand article search, and cross-reference. The inclusion criteria were (i) controlled clinical trials, (ii) endurance exercise as the only intervention, (iii) a nonexercise control group, (iv) within-group mean ages of subjects > or = 60 yr, (v) a measure of changes in resting HR, (vi) studies published in English journals. RESULTS: Outcome was derived from 13 studies with a total of 651 individuals in 14 control (N = 241) and 16 exercise groups (N = 410). The pooled standardized effect size by a fixed-effect model showed an upper moderate effect of -0.58 +/- 0.08 (mean +/- SEM, 95% CI = -0.74 to -0.42). This homogeneity effect was statistically significant (P = 0.001). The magnitude of net change averaged -6 bpm (-2 to -12 bpm), representing an 8.4% reduction. Greater and statistically significant decrease of resting HR among the elderly was found in the studies with training length more than 30 wk. CONCLUSIONS: This meta-analytic investigation supports the efficacy of endurance exercise training in decreasing HR at rest in older adults. This training induced adaptation may have protective benefits for cardiovascular aging. A longer exercise training length, probably more than 30 wk, may be needed for older individuals to be more effective in terms of resting HR reduction.

Electrocardiography↗