Combination of estrogen replacement and exercise protects against HDL oxidation in post-menopausal women.

The incidence of atherosclerosis and cardiovascular disease (CVD) in women increases following menopause and has been associated with a reduction in circulating estrogen. Increased CVD risk is also perpetuated by sedentary lifestyle. Growing evidence indicates that oxidation of lipoproteins leads to a powerful immune response, disruption of normal lipoprotein function, and deposition of atherosclerotic plaques. For example, once high-density lipoproteins (HDL) are oxidized, they lose the ability to a) participate in reverse transport of cholesterol to the liver, and b) protect low-density lipoproteins (LDL) against oxidation. The purpose of this study was to determine the effects of combining estrogen replacement and exercise upon lipid peroxidation of the HDL fraction (HDL-ox). Blood samples were drawn from 34 post-menopausal women from four groups: women who were not receiving estrogen replacement and who were sedentary (NSD) (n = 9); women who were not receiving estrogen replacement and who were participating in regular exercise (NEX) (n = 8); women who were receiving estrogen replacement and who were sedentary (ESD) (n = 8); and women who were receiving estrogen replacement and who were participating in regular exercise (EEX) (n = 9). Total-HDL cholesterol was significantly higher (p<0.05) in EEX when compared with NEX, NSD, and ESD. HDL-ox was assessed via malondialdehyde (MDA). Mean (+/- SEM) values for HDL MDA expressed in nM are as follows: NSD = 903.3 +/- 118.4; NEX = 1226.7 +/- 247.7; ESD = 876.7 +/- 116.3; EEX = 537.4 +/- 74.8. EEX lipid peroxidation was significantly (p = 0.02) lower than NEX. Lipid peroxidation tended to be lower in EEX than in NSD and ESD (p = 0.07). These data indicate that the combination of estrogen replacement and regular exercise in post-menopausal women may be most effective in reducing oxidation of HDL in vivo.

Relationship between NADP-specific isocitrate dehydrogenase and glutathione peroxidase in aging rat skeletal muscle.

The glutathione peroxidase (GPX) system detoxifies hydroperoxides in cells and uses NADPH to regenerate reduced glutathione. Enzymatic sources of NADPH in skeletal muscle include NADP-specific isocitrate dehydrogenase (ICDP), glucose-6-phosphate dehydrogenase (G6PD), and malic enzyme (ME). Our purpose was to explore the relationship in skeletal muscle between GPX and ICDP along with other NADPH-generating enzymes as a function of progressive age and muscle fiber-type. Soleus (SOL), red gastrocnemius (RG), and white gastrocnemius (WG) muscles were extracted from Fischer-344 rats of three different ages: 4 months old (Y); 18 months old (M); and 24 months old (O). Assays were conducted to determine activities of GPX, ICDP, G6PD, and ME along with levels of lipid hydroperoxides. GPX activities were significantly greater in RG and WG of old rats than in younger. ICDP activities were higher in the WG of old and middle aged rats when compared to young adults. GPX and ICDP activities exhibited similar differences among the muscles tested (SOL>RG>WG). In contrast, G6PD and ME activities were not significantly different across muscles. G6PD activities increased in RG with age, but were well over an order of magnitude lower than ICDP in all muscles. ME activities were universally lower than ICDP in all muscles, and decreased with old age in the WG and RG. Lipid hydroperoxides were significantly higher with aging in RG. Significant correlations were found between GPX and ICDP in all muscles. Stepwise regression resulted in a model (R(2)=0.82) that included ICDP and ME in predicting GPX. In summary, these data are consistent with the hypotheses that ICDP is higher in more oxidative fibers, inducible with aging, and most closely associated with the glutathione peroxidase system in skeletal muscle.

Interaction of nitric oxide and reactive oxygen species on rat diaphragm contractility.

Growing evidence indicates that reactive oxygen species (ROS) as well as nitric oxide (NO) have a profound influence on contractile function of skeletal muscle possibly through modulation of excitation-contraction coupling. We hypothesized that if NO and xanthine oxidase (XO) interact at key sites in excitation-contraction coupling, the effects of XO with nitric oxide synthase (NOS) inhibitors and NO donors on contractile function of the unfatigued diaphragm would not be additive. Diaphragm fibre bundles were extracted from 4-month Fischer-344 rats and placed in Krebs solution bubbled with 95% O2, 5% CO2. Baseline twitch tension, tension at 20 Hz (low-frequency), and maximal tetanic tension (Po) at 120 Hz were then measured (PRE). In Experiment 1 diaphragm fibre bundles were exposed to Krebs with 200 microM hypoxanthine as a control (CON); 0.02 U mL-1 XO + 200 microM hypoxanthine; 1 mM of the NOS inhibitor N-nitro-L-arginine (L-NNA) or L-NNA + XO. Five minutes were allowed for equilibration, and a second set of contractile measures was taken (POST). In Experiment 2 we exposed diaphragm fibre bundles to one of the following four solutions: CON, XO, 100 microM of the NO donor sodium nitroprusside (SNP) and XO + SNP, and evaluated contractile function as described above. In Experiment 3 we tested to determine if peroxynitrite production from the reaction of superoxide anion and NO affected the above results for SNP using 30 microM ebselen as a peroxynitrite quencher. Xanthine oxidase resulted in a significant potentiation of diaphragm twitch tension and tension at 20 Hz (+29%) without affecting Po. L-NNA also significantly increased 20 Hz tension but did not alter Po. However, the combination of XO + L-NNA did not further increase low-frequency contractility. Sodium nitroprusside alone did not affect diaphragm contractility, but did attenuate XO-induced potentiation in the XO + SNP group. Ebselen did not alter the impact of SNP on XO in the diaphragm. These data support the hypothesis that XO and NO interact or compete at similar sites of action that modulate contractility of the unfatigued diaphragm.

Airflow limitation and control of end-expiratory lung volume during exercise.

To test the hypothesis that the presence of airflow limitation (AFL) influences the control of end-expiratory lung volume (EELV) during exercise, 11 subjects with normal lung function, performed submaximal exercise (SM) on a cycle ergometer, with and without AFL. AFL was achieved during exercise by increasing the density of the air via a hyperbaric chamber, compressed to a depth of 3 atm (3 ATA; with AFL). Five subjects achieved AFL during SM exercise at 3 ATA while the remaining six subjects did not achieve AFL. SM exercise was performed with the same apparatus in the hyperbaric chamber at sea level pressure with none of the subjects achieving AFL (SL; no-AFL). EELV (% of TLC, BTPS), was significantly larger during exercise at 3 ATA than during exercise at SL for the AFL group (SL = 44 +/- 6%; 3 ATA-AFL = 51 +/- 9%, P < 0.05; but, was not for the no-AFL group (SL = 46 +/- 6%; 3 ATA-no AFL = 46 +/- 7%). End inspiratory lung volume was significantly elevated during exercise at 3 ATA compared with SL in the AFL group (SL = 80 +/- 6%; 3 ATA-AFL = 86 +/- 6%; P = 0.01) but not in the no-AFL group (SL = 82 +/- 4%; 3 ATA-no AFL = 84 +/- 4%). Tidal volume and ventilation were not different for any condition. These data suggest that the occurrence of AFL influences the control of EELV.

Ageing alters aortic antioxidant enzyme activities in Fischer-344 rats.

Oxidative stress imposed by reactive oxygen species is now believed to contribute to hypertension, atherosclerosis and ageing of the vasculature all involving a loss of relaxation. The antioxidant enzymes glutathione peroxidase, superoxide dismutase and catalase play a crucial role in defending against the ravages of oxidative stress. Our purpose was to characterize age-related changes in glutathione peroxidase, superoxide dismutase and catalase in the rat aorta. Aortas were extracted from seven young (4 months), seven middle aged (18 months) and seven old (24 months) animals. Analysis of variance was used with Fisher-LSD post hoc to determine mean differences among glutathione peroxidase, superoxide dismutase and catalase. Aortic glutathione peroxidase activities rose steadily with age expressed in micromol mg protein-1 min-1 +/- SEM (young: 141 +/- 22; middle aged: 198 +/- 18; old: 229 +/- 26) reaching significance between young and old. Superoxide dismutase activities significantly decreased in middle aged when compared with young (young: 22 +/- 2 vs. middle aged: 15 +/- 2 U mg protein-1) before trending upward again in old age (19 +/- 2). Catalase activities dropped significantly between young and old when expressed in mU mg protein-1 (young: 230 +/- 30; middle aged: 173 +/- 18; old: 144 +/- 23). Ratios for the various enzymes indicate a shrinking contribution of catalase with ageing, with an enhanced role for glutathione peroxidase in the antioxidant defence. These data in aortas of ageing rats show a complex alteration of the antioxidant profile.

A chest wall restrictor to study effects on pulmonary function and exercise. 2. The energetics of restrictive breathing.

Chest wall restriction, whether caused by disease or mechanical constraints such as protective outerwear, can cause decrements in pulmonary function and exercise capacity. However, the study of the oxygen cost associated with mechanical chest restriction has so far been purely qualitative. The previous paper in this series described a device to impose external chest wall restriction, its effects on forced spirometric volumes, and its test-retest reliability. The purpose of this experiment was to measure the oxygen cost associated with varied levels of external chest wall restriction. Oxygen uptake and electromyogram (EMG) of the external intercostals were recorded during chest restriction in 10 healthy males. Subjects rested for 9 min before undergoing volitional isocapnic hyperpnea for 6 min. Subjects breathed at minute ventilations (V.I) of 30, 60, and 90 liters/min with chest wall loads of 0, 25, 50 and 75 mm Hg applied. Frequency of breathing was set at 15, 30, and 45 breaths per minute with a constant tidal volume (VT) of 2 liters. Oxygen uptake was measured continuously at rest and throughout the hyperventilation bouts, while controlling V.I and VT. Integrated EMG (IEMG) from the 3rd intercostal space was recorded during each minute of rest and hyperventilation. Two-way ANOVA with repeated measures revealed that chest wall loading and hyperpnea significantly increased V.O2 values (p < 0.01). External intercostal IEMG levels were significantly increased (p < 0.05) at higher restrictive load (50 and 75 mm Hg) and at the highest minute ventilation (90 liters/min). These data suggest that there is a significant and quantifiable increase in the oxygen cost associated with external chest wall restriction which is directly related to the level of chest wall restriction.

Effect of reactive oxygen species on K+ contractures in the rat diaphragm.

Reactive oxygen species (ROS) are postulated to alter low-frequency contractility of the unfatigued and fatigued diaphragm. It has been proposed that ROS affect contractility through changes in membrane excitability and excitation-contraction coupling. If this hypothesis is true, then ROS should alter depolarization-dependent K+ contractures. Xanthine oxidase (0.01 U/ml) + hypoxanthine (1 mM) were used as a source of superoxide anion eliciting oxidative stress on diaphragm fiber bundles in vitro. Diaphragm fiber bundles from 4-mo-old Fischer 344 rats were extracted and immediately placed in Krebs solution bubbled with 95% O2-5% CO2. After 10 min of equilibration, a K+ contracture (Pre; 135 mM KCl) was induced. Fiber bundles were assigned to the following treatment groups: normal Krebs-Ringer (KR; Con) and the xanthine oxidase system (XO) in KR solution. After 15 min of treatment exposure, a second (Post) K+ contracture was elicited. Mean time-to-peak tension for contractures was significantly decreased in Post vs. Pre (16.0 +/- 0.7 vs. 19.8 +/- 1.0 s) with XO; no change was noted with Con. Furthermore, peak contracture tension was significantly higher (31.5%) in the XO group Post compared with Pre; again, no significant change was found with KR. The relaxation phase was also altered with XO but not with KR. Additional experiments were conducted with application of 1 mM hypoxanthine, with results similar to the Con group. We conclude that the application of ROS altered the dynamics of K+ contractures in the rat diaphragm, indicating changes in voltage-dependent excitation-contraction coupling.

Oxidative stress, antioxidant status, and the contracting diaphragm.

Reactive oxygen species, including free radicals, are produced through a number of biochemical reactions, often as a consequence of aerobic metabolism. A system of antioxidant enzymes and scavenger substrates provides protection of membrane lipids, proteins, and DNA. An imbalance between production of reactive oxygen species and antioxidant protection results in "oxidative stress." Oxidative stress is believed to contribute to numerous pathological conditions including atherosclerosis, obstructive lung disease, aging, and fatigue of skeletal muscles including the diaphragm. Strenuous exercise, inflammation, infection, obstructive lung diseases, etc. increase exposure of the diaphragm to reactive oxygen species. Emerging data indicate that reactive oxygen species alter diaphragm contractions primarily in response to low-frequency stimulation. The response of the diaphragm is profoundly influenced by the degree of oxidative stress, fatigue state, glutathione status, and age. Exercise training results in an upregulation of antioxidant enzyme activities in the diaphragm and thus could provide additional protection against oxidative stress.

Correlation of injury occurrence data with estimated maximal aerobic capacity and body composition in a high-frequency manual materials handling task.

This article evaluates the correlation between injury occurrence, step test estimated maximal aerobic capacity (VO2max), and body composition in a high-frequency manual materials handling task. The study used 212 highly trained male manual material handlers working for a major materials handling company. Three locations across the United States (western, midwestern, and southeastern) were chosen based on similarity of size and function. An estimated maximal aerobic capacity was obtained for each participant using a submaximal bench step protocol. Also, a percentage body fat estimation was randomly obtained for approximately 25% of the participants. The correlation between injury occurrences, absolute VO2max, relative VO2max, and percentage body fat were analyzed. Also, the relationship between both VO2max estimations and percentage body fat was analyzed. Finally, the correlation between location VO2max and percentage body fat was studied. Results indicated no significant difference between absolute VO2max, injury, or percentage body fat. Relative VO2max suggested a significant relationship with injury occurrences and body composition. Body composition also indicated a significant correlation with injury occurrences. Finally, location played a significant factor in injury occurrence, step test estimated VO2max, and estimated body composition. This investigation demonstrates significant evidence of the predictability of employee injury occurrence and the fitness estimation methods used. In a high-frequency manual materials handling task, high occurrences of injury were significantly correlated with low estimated relative maximal aerobic capacity and high estimated percentage body fat.

Effect of oxidative stress and acidosis on diaphragm contractile function.

Acidosis during exercise has long been associated with skeletal muscle fatigue. Recent evidence also has linked reactive oxygen species (ROS) with fatigue in skeletal muscle, including the diaphragm. We hypothesized that acidosis (designed to mimic blood pH during maximal exercise) would worsen ROS-induced depression of diaphragm contractility. The xanthine oxidase (XO) reaction in solution (0.01 U/ml) allows direct assessment of the effects of oxidant stress by ROS. Costal diaphragm fiber bundles from 24 Sprague-Dawley rats (200-250 g) were divided into four treatment groups: 1) pH 7.4, no XO (H); 2) pH 7.4 + XO (HXO); 3) pH 7.0, no XO (L); and 4) pH 7.0 + XO (LXO). Baseline twitch mechanics and force-frequency relationships (Pre) were determined in control Krebs solution (pH 7.4, no XO) before treatment. Treatment solutions were introduced, and the diaphragm underwent 2 min of contractions at 25 Hz (250 ms) at a rate of 1/s. After 10 min of recovery, the control solution was reintroduced into the bath and postcontractile function (Post) was measured. Significant reductions in twitch tension and low-frequency tetanic tension were greater in HXO and LXO compared with H, without an effect on maximal tetanic tension. One-half relaxation time was prolonged only by the combination of acidosis and oxidative stress. Addition of superoxide dismutase (50 U/ml) worsened and catalase (1,800 U/ml) attenuated XO-induced depression of diaphragm contractility. We concluded that XO induced a reduction of low-frequency tension in the fatigued diaphragm, which was mediated directly or indirectly through hydrogen peroxide and was exacerbated to a modest extent with acidosis.

Effect of oxidant challenge on contractile function of the aging rat diaphragm.

Although controversial, growing evidence indicates that reactive oxygen species (ROS) alter contractions of skeletal muscle, including the diaphragm. However, the impact of ROS on contractility of the aging diaphragm is unknown. The xanthine oxidase (0.01 U/ml) system was used as an ROS generator, imposing an oxidant challenge. Contractile function [twitch tension; twitch time to peak tension; twitch one-half relaxation time; tension at 10 and 20 Hz; maximal tetanic tension (Po) at 100 Hz] of costal diaphragm fiber bundles from young (4 mo) and old (25 mo) Fischer 344 rats was examined in vitro before and after treatment with control Krebs solution [young control (YC) and old control (OC)], or with xanthine oxidase (XO; 0.01 U/ml) plus hypoxanthine (0.29 mg/ml) substrate [young XO treated (YXO) and old XO treated (OXO)]. Contractile function of fiber bundles was reassessed after oxidant challenge in an unfatigued state (Post-u) or 10 min after a fatiguing stimulation protocol (Post-f). Oxidant challenge in the unfatigued fiber bundles increased twitch tension and tension at 10 and 20 Hz in YXO, but not OXO, without increasing Po. Conversely, XO significantly depressed fatigued diaphragm twitch and low-frequency tension in both OXO and YXO, compared with controls. Po was depressed Post-f in OXO but not YXO. Oxidant challenge also increased twitch one-half relaxation time of the fatigued diaphragm in both age groups. Furthermore, fiber bundles from old rats suffered greater fatigue during the stimulation protocol. We conclude that the response to oxidant challenge and increased contractile demand is impaired in the aging diaphragm.

Lactic acidosis and diaphragmatic function in vitro.

Diaphragm fatigue occurs during heavy exercise. Acidosis leads to skeletal muscle fatigue, yet the diaphragm is not a net producer of either lactic acid or hydrogen ions. We tested the hypothesis that hydrogen ion and lactic acid concentrations similar to those seen in arterial blood at maximal exercise decrease contractility of the in vitro isolated rat diaphragm. Diaphragm strips were exposed to a control solution for 15 min and then to one of the following treatment solutions: control (C, pH = 7.4) or 10 mM lactic acid buffered to pH 7.4 (L74), pH 7.2 (L72), pH 7.1 (L71), or pH 6.8 (L68). After 15 min, the force-frequency relationship of the strip was measured. The strips were then stressed with 75 contractions at 25 Hz (250-ms train duration) at the rate of one per second and the force-frequency curve was measured after 15 min of recovery. The L74, L72, and L71 strips responded similarly to the C strips at all times and frequencies. Decrements in force associated with acidosis were only seen in L68. Within L68, we found decreases in force at stimulation frequencies < 100 Hz. These data suggest that physiologic levels of exogenous hydrogen ions are not a primary cause of in vitro diaphragm fatigue.

Effects of inspired O2 and CO2 on ventilatory responses to LBNP-release and acute head-down tilt.

Increases in blood flow and CO2 return to the heart and lungs at the onset of exercise have been proposed to initiate reflexive feedback which increases ventilation (VE), via mechanoreceptors in the heart and/or intrapulmonary CO2 flow receptors. Both lower body negative pressure (-40 mm Hg) release (LBNP-release) and acute head-down (-30 degrees) tilt (TILT) provide physiological models to focus upon the effects of increased venous return and CO2 flow on VE, without the confounding influence of limb afferents or the descending efferents associated with central command. We examined the ventilatory responses to LBNP-release and TILT while inhaling one of four gas mixtures: a) room air (R); b) 95% O2 (O); c) 95% O2, 1.25% CO2 (LC); and d) 95% O2, 2.25% CO2 (HC). Breath-by-breath measurements for VE end-tidal CO2 (PETCO2), tidal volume (VT), and breathing frequency (fB) were taken. VE and VT for HC were significantly higher (p < 0.05) than those for R, O, and LC throughout the test session, while fB and PETCO2 were not significantly different among the gas treatments. VE increased (p < 0.05) above resting baseline with LBNP-release and TILT for R, O, LC, and HC primarily through an elevation of fB. Further, the maximal change in VE following LBNP-release or TILT were not different among inhaled gas mixtures. However, area under the VE curve following LBNP-release and TILT was higher for HC compared to the other gas mixtures. We conclude that these results are inconsistent with the theory that carotid bodies are essential in driving VE with these models.(ABSTRACT TRUNCATED AT 250 WORDS)

Gender differences in diaphragmatic metabolic properties of the adult Sprague-Dawley rat.

Adult male Sprague-Dawley rats (> or = 180 days old) develop an obesity-exacerbated insulin resistance in contrast with female animals of the same strain. Given the fact the maintenance of muscle mass requires an adequate supply of insulin and active insulin receptors, we postulated that gender differences might exist in both protein content and metabolic properties of skeletal and cardiac muscle in adult Sprague-Dawley rats. Therefore, to test this hypothesis, we examined activities of bioenergetic enzymes and total protein content in the diaphragm, the heart and the plantaris muscle in 12-month-old male and female animals. Mean (+/- SD) body weights of male animals were significantly (P < 0.05) greater than female animals (598 +/- 8 vs. 362 +/- 19 g) and the diaphragm weight/body weight ratio was significantly lower in males compared to females (2.36 +/- 0.05 vs. 3.02 +/- 0.13 mg/g). The activities of isocitrate dehydrogenase (NADP-specific) and succinate dehydrogenase were significantly lower (P < 0.05) in male animals compared to females in both the crural and costal regions of the diaphragm, the heart, and the plantaris muscle. In contrast, no gender differences (P > 0.05) existed in lactate dehydrogenase activity in any of the muscles studied. Finally, muscle protein concentration was significantly higher in female animals when compared to males (P < 0.05) in all muscles studied except the heart. These data support the hypothesis that gender differences exist for adult Sprague-Dawley rats in general and specific protein content of the diaphragm, locomotor muscles, and the heart.

Metabolic and antioxidant enzyme activities in the diaphragm: effects of acute exercise.

Disruption of cellular constituents including inhibition or "downregulation" of metabolic enzyme activity has been associated with free radical stress in locomotor muscle with acute, strenuous exercise. However, the effects of acute, strenuous exercise on important metabolic and antioxidant enzyme activity levels in the diaphragm are unknown. Twenty 4-month-old and twenty 24-month-old female Fischer-344 rats were divided at random into young exercised (YE; n = 10)/old exercised (OE; n = 10); young control (YC; n = 10)/old control (OC; n = 10) groups. Animals in both young and old exercise groups ran on a treadmill (10% uphill grade) for 40 min at approximately 75% of age group VO2 max. Immediately following the treadmill run, both exercise and control groups were euthanized with sodium pentobarbital. Costal (COD) and crural diaphragm (CRD) were quickly removed and frozen in liquid nitrogen. Lipid peroxidation was significantly increased (P < 0.05) in COD of YE vs. YC rats. Activity of the antioxidant enzyme glutathione peroxidase (GPX) was unaltered in the diaphragm by acute exercise (P > 0.05) in both age groups. There was a significant increase in superoxide dismutase (SOD) activity with exercise (P < 0.05). Post-hocs revealed SOD activity was approximately 20% greater (P = 0.066) in YE CRD only. Activities of the metabolic enzymes phosphofructokinase (PFK), succinate dehydrogenase (SDH), and citrate synthase (CS) were not affected by acute exercise in YE or OE. Strenuous exercise resulted in a small trend towards a decrease in 3-hydroxyacyl-CoA dehydrogenase (HADH) activity in YE COD (P = 0.115) and YE CRD (P = 0.082). We conclude that the employed bout of exercise induces some free radical stress, while metabolic enzymes are protected, in the diaphragm.

Acute exercise and skeletal muscle antioxidant and metabolic enzymes: effects of fiber type and age.

Inhibition of metabolic enzyme activity has been associated with free radical stress in locomotor muscle with prolonged or intense exercise. However, it is not known whether such alterations with acute exercise in skeletal muscle are influenced by muscle fiber type or age. Twenty 4-mo-old and twenty 24-mo-old female Fischer-344 rats were divided at random into young exercised (YE; n = 10), old exercised (OE; n = 10), young control (YC; n = 10), and old control (OC; n = 10) groups. Animals in both YE and OE groups ran on a treadmill (10% uphill grade) for 40 min at approximately 75% of each age-group's maximal O2 consumption. Immediately after the treadmill run, white gastrocnemius (WG), red gastrocnemius (RG), and soleus (SOL) muscles were removed and quick-frozen in liquid nitrogen. Malondialdehyde was significantly increased (P < 0.05) in RG of YE vs. YC rats. Glutathione peroxidase activity was significantly elevated (P < 0.05) in the WG of YE rats. Analysis of variance revealed a significant over-all increase in superoxide dismutase activity with exercise. Activities of phosphofructokinase (PFK), citrate synthase, succinate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase were unchanged (P > 0.05) with acute exercise in the SOL. However, PFK activity was decreased in the WG by 60% in OE but only 33% in YE, and in the RG by 41% in OE but only 21% in YE. We conclude that maximal glycolytic flux in the gastrocnemius may be adversely affected by acute exercise, and this effect was more pronounced in the 24-mo-old group.

Oxygen cost of treadmill running in 24-month-old Fischer-344 rats.

The oxygen cost of treadmill running is well documented in young adult rats. However, to our knowledge there are no detailed reports concerning the oxygen cost of treadmill running in senescent rats. Young adult (4 months; N = 8) and senescent (24 months; N = 8) female Fischer-344 rats were tested for O2 cost of treadmill running. One-half of the animals tested in each age group had completed 10 wk of endurance training. Oxygen cost of treadmill running, using a flow-through system, was measured on a per minute basis from 7-10 min of each work bout and averaged. Separate work bouts were performed at 0%, 5%, and 10% grade at 15, 20, 25, and 30 m.min-1. Oxygen cost of treadmill running for trained rats for all speeds and grades were not significantly different (P = 0.77) from untrained animals; thus, data were pooled for oxygen cost of running. Results revealed significantly lower (P < 0.05) VO2 (expressed as ml.kg-1.min-1) for senescent rats vs young adult rats rest and at all comparable treadmill grades and speeds except for 5% grade, 25 m.min-1 and 10% grade, 20 m.min-1. In addition, resting VO2 was significantly lower (P < 0.05) in old rats when compared with young rats. Thus, we conclude that the oxygen cost of treadmill running is lower for 24-month-old rats than in 4-month-old rats except at higher work levels.

Inducibility of NADP-specific isocitrate dehydrogenase with endurance training in skeletal muscle.

NADP(+)-specific isocitrate dehydrogenase (ICDH-NADP: EC 1 x 1 x 1 x 42) is primarily a mitochondrial matrix enzyme in both mammalian skeletal muscle and heart and has markedly higher activity levels than the NAD(+)-specific isozyme. To date, it is unknown whether ICDH-NADP activity is inducible with in vivo exercise training in locomotor or respiratory skeletal muscle. Therefore, the purpose of this investigation was to quantify alterations in ICDH-NADP activity in respiratory muscles (costal and crural diaphragm) and locomotor muscles (medial gastrocnemius, plantaris and soleus) following 8 weeks of treadmill endurance training. Ten of the animals had been assigned randomly to an exercise group (TR) and had completed 8 weeks of progressive (5 days week-1: 45 min day-1) treadmill endurance training while the remaining 10 animals comprised a sedentary control (C). Mean ICDH-NADP activities in Tr were significantly higher (P < 0.05) when compared with C in the medial gastrocnemius (61.3%), plantaris (42.9%) soleus (21.4%). Mean costal diaphragm ICDH-NADP activity noted in trained animals when compared to the sedentary control group was not significantly higher (10.8% greater for TR; P = 0.14). No mean differences (P = 0.58) were noted in the crural diaphragm. The results indicate that ICDH-NADP is inducible with endurance training in locomotor skeletal muscle. A coefficient of determination of 0.624 (i.e. 62.4% of the variance could be explained) for ICDH-NADP was calculated, with the oxidative enzyme marker succinate dehydrogenase (P < 0.05) indicating a positive, moderate relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Social evaluation research: the evaluation of two police patrolling strategies.

In most social evaluation research it is difficult to achieve the degree of experimental rigor possible in an applied behavioral study. This study illustrates how the evaluation researcher can increase experimental rigor in the analysis of social interventions. In the first evaluation, a variation of the time-series design that offered maximum experimental control given the limitations of the situation, was employed to evaluate the effects of a specialized home-burglary police patrol. This design revealed that no effects could be attributed to the patrol. In the second evaluation, a multiple baseline-like design was possible in determining the effects of a police walking patrol. This design revealed that the patrol produced an increase in crime reporting but not in arrests. Social interventions often occur in a manner that allows varying degrees of experimental analysis. The evaluation researcher must attain optimal experimental analysis given the limitations of each social intervention.