Does a period of detraining cause a decrease in serum brain-derived neurotrophic factor?

Brain-derived neurotrophic factor (BDNF) is one of the neurotrophins promoting cognitive function and contributing to neurogenesis and neuroprotection. Available evidence suggests that exercise influences serum BDNF concentrations, but that the effect is transient. The purpose of this study is to determine whether a period of aerobic training, followed by a period of detraining, can influence basal serum BDNF levels in humans. Sixteen young, sedentary subjects were assigned to an experimental group (n = 9) and a control group (n = 7). The experimental group performed an aerobic training program during 8 weeks, followed by 8 weeks of detraining, during which subjects returned to their previous, sedentary activity level. The control group remained physically inactive during 16 weeks. In both groups, performance on short-term (Digit Span test) and mid-term memory (Recall of Images) was assessed. Aerobic training significantly increased the VO₂ peak in the experimental group, and these values returned to baseline after 8 weeks of detraining. Basal serum BDNF was not influenced by 8 weeks of aerobic training and detraining did not seem to have an effect on basal peripheral BDNF concentrations. Both training and detraining did not clearly influence short-term memory performance on the Digit Span test and no differences were present between the experimental and control group on the mid-term memory test. Future studies should focus on patient groups and elderly to further investigate the effect of training and detraining on neurotrophic factors and cognitive function, and on the effects of training and detraining on the BDNF response to acute exercise.     

Exercise does not increase cyclooxygenase-2 myocardial levels in young or senescent hearts

Increased myocardial cyclooxygenase-2 (COX-2) activity is essential for late phase ischemic preconditioning (IPC). Currently unknown is whether cardioprotection elicited by exercise also involves elevated myocardial COX-2 activity. This investigation tested whether aerobic exercise elevates myocardial COX-2 protein content or enzyme activity in young and senescent male Fisher 344 rats assigned to sedentary or cardioprotective endurance exercise treatments (3 consecutive days of treadmill exercise, 60 min/day @~70% VO₂max). Assay of cardiac COX-2 protein content, catalytic activity, and inducible nitric oxide synthase (iNOS) protein content reveal that exercise did not alter COX-2 activity (PGE₂, p = 0.866; PGF1α, p = 0.796) or protein levels (p = 0.397) within young or senescent hearts. In contrast, myocardial iNOS, an up-stream mediator of COX-2 expression, was over-expressed by an average of 37% in aged hearts (p = 0.005), though iNOS was not influenced by exercise. Findings reveal exercise does not elevate cardiac COX-2 activity and suggests that mechanisms responsible for cardioprotection differ between IPC and aerobic exercise.     

The concentrations of serum,plasma and platelet BDNF are all increased by treadmill VO2max performance in healthy college men

The most current human-based studies in which brain-derived neurotrophic factor (BDNF) levels in the peripheral blood system are analyzed use it as an indicator that represents BDNF levels in the CNS. However, whether circulating BDNF (serum and plasma) is positively or inversely associated with cardiorespiratory fitness levels (VO_2max) is still controversial, and no study has done to investigate exercise effects on the concentration of BDNF stored in circulating platelets which, in fact, store a large amount of circulating BDNF. Thus, the purpose of this study was to determine the relation between VO_2max and all circulating BDNF levels (serum, plasma and platelets) in college male students (N = 18; age, 19 ± 1 years; height, 173.22 ± 7.65 cm; weight, 78.25 ± 14.25 kg; body fat percent, 13.82 ± 5.68%). Dual X-ray energy absorptiometry whole body scan was used to measure their body composition. After the overnight fast, all participants were performed VO_2max test, and their blood was collected at rest and immediately after the exercise. Our data resulted in significant increases in platelet counts and serum, plasma and platelet BDNF levels immediately after the exercise (p < 0.01). VO_2max had a significant negative correlation with serum BDNF, plasma BDNF and platelet BDNF at rest (p < 0.05) but a significant positive correlation with serum, plasma BDNF, and platelet BDNF immediately after the exercise (p < 0.01). However, our data show no correlation between VO_2max and platelet count both at rest and immediately after the exercise. In conclusion, this is the first study showing that basal BDNF levels are inversely correlated with cardiorespiratory fitness levels but that the inverse correlations turn into positive correlations with all circulating BDNF levels immediately after the exercise. Moreover, it is the first time to provide evidence that platelet BDNF levels are also positively affected by the exercise. However, future studies will be needed to investigate what tissues provide BDNF into the circulating system and to elucidate the role of circulating BDNF.     

Effects of incremental exercise on cerebral oxygenation measured by near-infrared spectroscopy: A systematic review

We conducted a systematic review and meta-regression analysis to quantify effects of exercise on brain hemodynamics measured by near-infrared spectroscopy (NIRS). The results indicate that acute incremental exercise (categorized relative to aerobic capacity (VO₂peak) as low – <30% VO₂peak; moderate – ≥30% VO₂peak to <60% VO₂peak; hard – ≥60% VO₂peak to <VO₂peak; and very hard – ≥VO₂peak intensities) performed by 291 healthy people in 21 studies is accompanied by moderate-to-large increases (mean effect, dz ± 95% CI) in the prefrontal cortex of oxygenated hemoglobin (O₂Hb) or other measures of oxygen level (O₂Hbdiff) or saturation (SCO₂) (0.92 ± 0.67, 1.17), deoxygenated hemoglobin (dHb) (0.87 ± 0.56, 1.19), and blood volume estimated by total hemoglobin (tHb) (1.21 ± 0.84, 1.59). After peaking at hard intensities, cerebral oxygen levels dropped during very hard intensities. People who were aerobically trained attained higher levels of cortical oxygen, dHb, and tHb than untrained people during very hard intensities. Among untrained people, a marked drop in oxygen levels and a small increase in dHb at very hard intensities accompanied declines in tHb, implying reduced blood flow. In 6 studies of 222 patients with heart or lung conditions, oxygenation and dHb were lowered or unchanged during exercise compared to baseline. In conclusion, prefrontal oxygenation measured with NIRS in healthy people showed a quadratic response to incremental exercise, rising between moderate and hard intensities, then falling at very hard intensities. Training status influenced the responses. While methodological improvements in measures of brain oxygen are forthcoming, these results extend the evidence relevant to existing models of central limitations to maximal exercise.     

Mitochondrial function in physically active elders with sarcopenia

Physical activity is reported to protect against sarcopenia and preserve mitochondrial function. Healthy normal lean (NL: n = 15) and sarcopenic (SS: n = 9) participants were recruited based on body composition (DXA, Lunar DPX™), age, and physical activity. Gastrocnemius mitochondrial function was assessed by ³¹P MRS using steady-state exercise in a 4 T Bruker Biospin. Total work (429.3 ± 160.2 J vs. 851.0 ± 211.7 J, p < 0.001) and muscle volume (p = 0.006) were lower in SS, although these variables were not correlated (NL r = −0.31, p = 0.33, SS r = (0.03, p = 0.93). In the SS resting ATP/ADP was lower (p = 0.03) and ATP hydrolysis higher (p = 0.02) at rest. Free energy ATP hydrolysis was greater at the end of exercise (p = 0.02) and [ADP] relative to total work output was higher in SS (ANCOVA, p = 0.005). [PCr] recovery kinetics were not different between the groups. Adjusting these parameters for differences in total work output and muscle volume did not explain these findings. These data suggest that aerobic metabolism in physically active older adults with sarcopenia is mildly impaired at rest and during modest levels of exercise where acidosis was avoided. Muscle energetics is coordinated at multiple cellular levels and further studies are needed to determine the loci/locus of energy instability in sarcopenia.     

Cardio-respiratory fitness,habitual physical activity and serum brain derived neurotrophic factor (BDNF) in men and women

Short episodes of high intensity exercise transiently increase serum levels of BDNF in humans, but serum levels of BDNF at rest appear to be lower in more physically active humans with greater levels of energy expenditure. The relationship between serum BDNF concentration, cardio-respiratory fitness (Åstrand–Rhyming test estimated VO₂ max) and volume of long-term, regular exercise and sporting activity (Baecke Habitual Physical Activity Index) was investigated in 44 men and women between the age range of 18–57 years. In this group an inverse relationship between resting serum BDNF concentration and measures of both estimated VO₂ max (r = −0.352; P < 0.05) and long-term sporting activity (r = −0.428, P < 0.01) was found. These results indicate that increased levels of cardio-respiratory fitness and habitual exercise are associated with lower resting levels of serum BDNF in healthy humans. This is the first study to demonstrate an inverse relationship between a physiological estimate of cardio-respiratory fitness and serum BDNF.     

Effect of physical training on age-related reduction of GH secretion during exercise in normally cycling women

Objective

To evaluate whether prolonged physical activity (25 km/week running for 8 years) modifies GH decline.

Design

The GH response to maximal exercise on bicycle-ergometer was tested in younger (26–30 years) and older (42–46 years) healthy women. Each age group included 2 subgroups of 10 sedentary and 10 runners, which were compared. The workload was increased at 3 min intervals from time 0 until exhaustion. Subjects with a low maximal capacity (as established in a preliminary test) pedalled for 3–4 min against no workload at the beginning of the test, so that exercises lasted about 15 min in all individuals.

Results

At exhaustion, heart rate and systolic pressure were significantly higher in sedentary than in trained subjects, whereas VO₂max$V_{{\text{O}}_2\text{max}}$, blood glucose and plasma lactate levels were similar in all groups. Exercise induced similar GH responses in younger sedentary and exercise-trained subjects and in older exercise-trained subjects, with mean peak levels 7.5 times higher than baseline. In contrast, in older sedentary women peak GH level was only 4.4 times higher than baseline and was significantly lower than in the other groups.

Conclusion

These data suggest that in women prolonged physical training exerts protective effects against age-dependent decline in GH secretion.     

Effects of ageing and fitness on skin-microvessel vasodilator function in humans

The impact of cardiopulmonary fitness ([(V)\dot] \dot{V} O_2max) on the age-related decline in skin-microvessel vasodilator function has not been fully established and the inter-relationships among different measures of microvascular vasodilator function are unknown. We used laser Doppler flowmetry to assess relative changes in forearm skin blood flow to various stimuli in three groups of adults: young (n = 15; 27 ± 2 years), older sedentary (n = 14; 65 ± 6 years) and older fit (n = 15; 61 ± 5 years). Local-heating induced and post-occlusive hyperaemia responses were higher in the young and older fit groups compared to the older sedentary group (P < 0.05) and were moderately correlated with [(V)\dot] \dot{V} O_2max in the pooled cohort of older adults (r = 0.49–0.58; P < 0.05). Peak hyperaemia responses to acetylcholine and sodium nitroprusside were higher in young compared to older sedentary adults (P < 0.05) and were not associated with [(V)\dot] \dot{V} O_2max in older adults (P > 0.05). Associations among different measures of microvascular vasodilator function were generally moderate at best. In summary, the local heating and reactive hyperaemia data indicate that the age-related decline in skin-microvessel vasodilator function can be ameliorated through regular aerobic exercise training. As this is not supported by the iontophoresis data, we recommend that, when assessing microvascular function, the use of a single physiological or pharmacological stimulation coupled to laser Doppler flowmetry should be avoided. Finally, the moderate correlations between outcomes probably reflect the distinct mediators that are responsible for the vasodilator response to each test.     

Protein intake induced an increase in exercise stimulated fat oxidation during stable body weight

Background

Protein-rich weight-loss diets spare fat-free mass at the cost of fat mass. The objective was to examine if there is a change in stimulated fat oxidation related to protein intake during stable body weight.

Methods

Subjects' (BMI 22 ± 2 kg/m², age 25 ± 8 years) maximal fat oxidation (Fat_max) was assessed during a graded bicycle test, before and after a 3-month dietary-intervention of 2 MJ/day supplements exchanged with 2 MJ/d of habitual energy intake. The parallel design consisted of protein-rich supplements in the protein group and an isocaloric combination of carbohydrate and fat supplements in the control group. Daily protein intake was determined according to 24-h urine nitrogen. Body composition was measured according to a 4-compartment model by a combination of underwater-weighing technique, deuterium-dilution technique and whole-body dual-energy X-ray absorptiometry (DXA).

Results

Subjects were weight stable and did not change their physical activity. The protein group (n = 12) increased protein intake (11 ± 14 g, P < 0.05) and had significantly higher daily protein intake vs. control (n = 4) (80 ± 21 vs.59 ± 11 g, P < 0.05). Fat_max increased significantly in the protein group (0.08 ± 0.08 g/min, P < 0.01). Fat-free mass increased independent of change in body weight (P < 0.01), and fat mass and fat percentage decreased (P < 0.05). Change in Fat_max was a function of change in protein intake (r = 0.623, P < 0.05), and not of changes in body composition or VO₂max.

Conclusion

Increased stimulated fat oxidation was related to increased protein intake.     

Oxygenation and exercise performance-enhancing effects attributed to the breathe-right nasal dilator

Recently, many professional football players have elected to wear spring-loaded nasal dilators during competition. Many athletes believe that wearing the “Breathe-Right” nasal dilator will increase nasal gas conduction and oxygenation to their body, subsequently improving their performance. The purpose of this experiment was to investigate the advantages of wearing a nasal dilator while performing aerobic and anaerobic exercise, as opposed to not wearing a nasal dilator. It was hypothesized that the “Breathe-Right” nasal dilator, manufactured by CNS, Inc (Chanhassen, MN) would increase nasal gaseous conduction and increase oxygenation to the body. Nasal gaseous conduction and oxygenation are essential components for using aerobic power. We examined whether wearing a nasal dilator improves performance by using a ramped cycle ergometer stress test on athletes until they reached VO₂ maximum progressing from aerobic to anaerobic exercise. Baseline data were collected (ie, VO₂, VO₂/Kg, respiratory exchange ratio, anaerobic threshold time, and onset of VO₂ max) using a MedGraphics CardiO₂ System. The subjects included 16 college-aged male athletes. Dependent t-tests implemented on each physiological response; VO₂ max, peak VO₂ kg, onset of anaerobic threshold, onset of VO₂ max, respiratory exchange ratio at VO₂ max, and maximum WATT output, showed there was no difference in the athletes' performance when they wore the nasal dilators and when they did not wear the dilators.     

Influence of functional tryptophan hydroxylase 2 gene variation and sex on the startle response in children, young adults, and older adults

Serotonin, a key regulator of emotional behavior, is synthesized by tryptophan hydroxylase (TPH). Allelic variation of TPH2 gene expression influences serotonin synthesis in the brain and therefore may modulate emotional processing. Here, we investigated the influence of the −703 G/T polymorphism in the regulatory promoter region of the TPH2 gene on the startle response in three different age samples: children (N = 110), young adults (N = 209), and older adults (N = 95). Startle magnitudes to intense noise bursts were recorded during baseline and while participants viewed unpleasant, pleasant or neutral pictures. There was a significant TPH2 × sex interaction effect in young adults with male T allele carriers showing stronger overall startle responses compared to male G/G homozygotes while in young women this effect appeared to be reversed. The difference between TPH2 genotype groups also reached significance in the female subsample when including menstrual cycle phase. In contrast, there was no effect of TPH2 or a TPH2 × sex interaction effect in children or in older adults.     

Fitness alters fluid regulatory but not behavioural responses to hypohydrated exercise

Dehydration is typical during prolonged exercise. Because training stimulates numerous adaptations, some involving fluid regulation, it is conceivable that training involves adaptations to dehydration. This study tested the hypothesis that trained individuals have altered fluid regulatory, but not behavioural or perceptual responses to exercise when hypohydrated. Six trained (V.O_{2 peak}: 65 ± 8 mL kg^− 1 min^− 1) and six untrained (V.O_{2 peak}: 45 ± 4 mL kg⁻¹ min⁻¹) males cycled for 40 min at 70%V.O_{2 peak}, once whilst euhydrated (EUH) and once whilst hypohydrated by ~ 2% body mass (HYPO), before a 40-min performance trial with euhydration (in EUH) or ad libitum drinking (in HYPO), in temperate conditions (24.3 °C, 50% rh). Baseline hydration was achieved by complete or partial rehydration from exercise + heat stress on the previous evening. Body mass was reduced (− 1.8 ± 0.1%) and plasma osmolality was increased (5 ± 1 mosmol kg^− 1) similarly between fitness groups in HYPO compared to EUH (P < 0.05). During exercise, plasma [AVP] rose more in HYPO than EUH; the elevation was greater in the Untrained (4.1 ± 1.7 vs. 2.0 ± 0.8 pmol L^− 1, P < 0.01) than Trained (1.4 ± 0.6 vs. 1.1 ± 0.5 pmol L^− 1, P < 0.01; P = 0.02). Increases in plasma [AVP] relative to osmolality were higher in Untrained than Trained (0.47 ± 0.06 vs. 0.025 ± 0.05 pmol mosmol^− 1, P = 0.03). Fitness groups had equivalent thirst ratings during fixed exercise but Trained were thirstier than Untrained when self regulating in HYPO (4.0 ± 1.5 vs. 2.7 ± 1.2; P = 0.05); thus Trained tended to consume more fluid (1.20 ± 0.16 vs. 0.88 ± 0.16 L; P = 0.19), but maintained similar hypohydration consistent with their greater sweat rate during HYPO. In conclusion, aerobic fitness attenuates the neuroendocrine ([AVP]) response to hypohydrated exercise, but not perceptual (thirst) or behavioural (ad libitum drinking) responses.     

Exercise improves cardiovascular control in a model of dislipidemia and menopause

The present study investigated the effects of exercise training on arterial pressure, baroreflex sensitivity, cardiovascular autonomic control and metabolic parameters on female LDL-receptor knockout ovariectomized mice. Mice were divided into two groups: sedentary and trained. Trained group was submitted to an exercise training protocol. Blood cholesterol was measured. Arterial pressure (AP) signals were directly recorded in conscious mice. Baroreflex sensitivity was evaluated by tachycardic and bradycardic responses to AP changes. Cardiovascular autonomic modulation was measured in frequency (FFT) and time domains. Maximal exercise capacity was increased in trained as compared to sedentary group. Blood cholesterol was diminished in trained mice (191 ± 8 mg/dL) when compared to sedentary mice (250 ± 9 mg/dL, p < 0.05). Mean AP and HR were reduced in trained group (101 ± 3 mmHg and 535 ± 14 bpm, p < 0.05) when compared with sedentary group (125 ± 3 mmHg and 600 ± 12 bpm). Exercise training induced improvement in bradycardic reflex response in trained animals (−4.24 ± 0.62 bpm/mmHg) in relation to sedentary animals (−1.49 ± 0.15 bpm/mmHg, p < 0.01); tachycardic reflex responses were similar between studied groups. Exercise training increased the variance (34 ± 8 vs. 6.6 ± 1.5 ms² in sedentary, p < 0.005) and the high-frequency band (HF) of the pulse interval (IP) (53 ± 7% vs. 26 ± 6% in sedentary, p < 0.01). It is tempting to speculate that results of this experimental study might represent a rationale for this non-pharmacological intervention in the management of cardiovascular risk factors in dyslipidemic post-menopause women.     

The effects of an integrated health education and exercise program in community-dwelling older adults with hypertension: A randomized controlled trial

Objective

The aim of this study was to examine the effectiveness of HAHA (Healthy Aging and Happy Aging) program, which is an integrated health education and exercise program for community-dwelling older adults with hypertension. Methods: Older adults with hypertension from one senior center were randomly allocated to experimental (n = 18) or control group (n = 22). Experimental group received health education, individual counseling and tailored exercise program for 12 weeks. Results: The mean ages were 71 years (experimental group) and 69 (control group). After the intervention, systolic blood pressure of experimental group was significantly decreased than that of control group. Scores of exercise self-efficacy, general health, vitality, social functioning, and mental health in SF-36 were statistically higher than those of control group. Conclusion: The HAHA program was effective in control of systolic blood pressure and improving self-efficacy for exercise and health-related quality of life.     

Ergogenic effect of varied doses of coffee-caffeine on maximal aerobic power of young African subjects

Background

Caffeine one of the readily available stimulants consumed daily by more than 80% of the world''s population, making it the most widely consumed drug in history. The objective of this study was to determine the effects of different doses (5, 10 &15 mg.kg⁻¹) of caffeine per kilogram body weight on maximal aerobic power of normal young black African (Nigerian) male adults.

Method

Twenty apparently healthy young male adults volunteers, participated. A repeated measure four randomized crossover (counter balanced) double blind design was used in data collection. Subjects engaged in 20 meter shuttle run test (20 MST) one hour post caffeine (5, 10 & 15 mg.kg⁻¹) and placebo doses ingestion. Endurance performance index (VO₂ max, run time & number of exercise laps) were measured and recorded.

Result

Repeated measures ANOVA was used to assess the level of significant difference between caffeine doses and placebo dose in VO₂ max, run time and number of exercise laps. The result showed no significant effect of caffeine doses over placebo dose.

Conclusion

It was concluded that caffeine dose of up to 15mg/kg seems not to have any ergogenic effect on maximum aerobic power of young black African male adults.     

Early treadmill training promotes motor function after hemorrhagic stroke in rats

Rehabilitation after a stroke is very important because it has beneficial effects on brain function, including the promotion of plasticity. However, an optimal time window for rehabilitation interventions after hemorrhagic stroke has not been clearly defined. The aim of this study was to determine whether early exercise training initiated 24 h after an intracerebral hemorrhage (ICH) might enhance neurologic recovery more than exercise initiated 1 week after ICH without hematoma expansion and edema volume increase. We subjected adult male Sprague–Dawley rats to experimental ICH by the intrastriatal administration of bacterial collagenase. The rats were randomly divided into the following 2 groups: early training group (treadmill exercise started 24 h post-ICH; n = 18) and late training group (treadmill exercise started 1-week post-ICH; n = 18). Two weeks after surgery we performed neurologic tests (rota-rod, modified limb-placing, and adhesive-dot removal tests), and measured hematoma volumes and brain water content. In the late training group, compared with the pre-ICH performance on the rota-rod test (98.3 ± 69.4 s), the animals had significantly worse performance after the post-ICH rehabilitation (40.5 ± 52.6 s; p < 0.01, paired t-test). In the early training group however, the motor performance after the post-ICH rehabilitation (56.4 ± 73.5 s) was not significantly different from the baseline pre-ICH performance (79.8 ± 33.9 s; p = 0.24). There were no significant differences between the two groups with respect to the other neurologic tests. Early exercise did not increase hematoma size or brain water content. Early treadmill training could be performed safely, and enhanced motor recovery in a rat model of ICH. Further studies are required to translate the results into clinical significance.     

Leukocyte telomere length, breast cancer risk in the offspring: the relations with father's age at birth

Recent studies have reported that leukocyte telomere length (LTL) is longer in offspring of older fathers. Longer telomeres might increase cancer risk. We examined the relation of father's age at the birth of the offspring (FAB) with LTL in the offspring in 2177 participants of the Family Heart Study and the probability of developing breast cancer in 1405 women from the Framingham Heart Study (offspring cohort). For each year of increase in FAB (adjusted for mother's age at birth), LTLs in the daughters and sons were longer by 19.4 bp and 12.2 bp, respectively (p < 0.0001). Daughters of older fathers were less likely to stay free of breast cancer compared to daughters of younger fathers in empirical (p = 0.014) and Cox regression analyses (p = 0.0012) adjusted for relevant covariates. We conclude that older fathers endow their offspring with a longer LTL and their daughters with increased susceptibility to breast cancer. These independent observations cannot provide evidence for a causal relationship, mediated by telomere length, between FAB and increased breast cancer risk in daughters. However, with couples delaying having children in today's society, studies exploring the LTL association with increased breast cancer risk in daughters of older fathers might be timely and relevant.     

Effects of age and regular exercise on muscle strength and endurance

Summary Twenty male and 20 female non-professional tennis players were classified into two different age groups (n=10 per group): young active men (30.4±3.3 years), young active women (27.5±4.3 years), elderly active men (64.4±3.7 years), and elderly active women (65.3±4.5 years). These individuals were matched (n = 10 per group) according to sex, age, height and mass to sedentary individuals of the same socio-economical background: young sedentary men (29.2±3.4 years), young sedentary women (25.6±4.4 years), elderly sedentary men (65.2 ± 3.2 years) and elderly sedentary women (65.6±4.4 years). An isokinetic dynamometer was used to measure the strength of the knee extensors and flexors (two separate occasions) and the endurance of the extensors. Vastus lateralis electromyogram (EMG) was measured concomitantly. Significant sex, age and exercise effects (P<0.001) were observed for peak torque of both muscle groups. The effect of age on extensor strength was more pronounced at high speeds where men were also able to generate larger relative torques than women.No age or sex effects were noted for muscle endurance. However, muscles of active individuals demonstrated a greater resistance to fatigue than those of sedentary individuals. In conclusion, men were found to be stronger than women, age was associated with a decrease in muscle strength, but not of muscle endurance, and tennis players were stronger and had muscles that were more resistant to fatigue than their sedentary pairs in both age groups. Although the results of this study cannot be generalized to other types of sports activities, they do give credence to the health benefits of moderate exercise in the maintenance of muscle function with age.     

Cardiac remodeling and function following exercise and angiotensin II receptor antagonism

The purpose of this study was to test the impact of chronic exercise training combined with selective angiotensin II receptor (AT1) antagonism on systolic blood pressure (SBP) and the left-ventricular pressure–volume relationship in normotensive, non-infarcted rat hearts. Wistar rats (N = 19) were randomly assigned to either a sedentary control group (N = 8) or an exercise-trained group (N = 11). Losartan was administered to individually caged rats via the drinking water (10 mg/kg/d). Exercise training consisted of running on a motorized driven treadmill for 6 weeks at 30 m/min, 60 min/day, 5 days/week. Tail cuff SBP was measured weekly. Left ventricular performance was assessed in an ex vivo Langendorff isovolumic mode. One week of losartan treatment significantly reduced SBP in both groups by 13% relative to baseline (P < 0.05). SBP was lower in exercise-trained animals versus sedentary animals in the later weeks of the protocol (P < 0.05) Body weight was significantly lower in exercise-trained animals versus sedentary animals, but heart weight, heart to body weight ratio, atrial weight, and absolute left ventricular mass and length were similar between groups. The LV systolic pressure–volume relationship (PV) and systolic elastance were significantly greater in exercise-trained animals versus sedentary controls (P < 0.05). The left ventricular end-diastolic PV and diastolic stiffness were similar between exercise-trained and sedentary animals. These data suggest that chronic aerobic exercise training can improve the Starling response in the presence of AT1 receptor blockade without altering absolute cardiac size.     

Amyloid load in nondemented brains correlates with APOE e4

179 cognitively healthy adults enrolled in the Sun Health Brain Donation program between 7/91 and 12/07 were at least 60 years old and nondemented at the time of death (21 had developed mild cognitive impairment [MCI]). Amyloid plaque density, congophilic amyloid angiopathy (CAA), and neurofibrillary tangle (NFT) density scores were based on CERAD criteria and compared in apolipoprotein E (APOE) e4 carriers (n = 42) and noncarriers (NC) (n = 137). Mean age (83.4 ± .6), gender (45% women), interval between death and brain harvest (3.1 ± 2.4 h), and brain weight (1200 ± 119 g) did not differ between e4 carriers (n = 42) and NC. Total plaque density was higher in e4 carriers than NC (6.8 ± 4.9 vs. 4.3 ± 4.4, p = .002), and this was true in each of 5 subregions examined. Total CAA (p = .002) and all subregion CAA burden was also higher in e4 carriers. Total neuritic plaque density (1.2 ± 1.0 vs. 1.0 ± 1.0, p = .18) and total NFT density (3.9 ± 2.4 vs. 3.6 ± 2.3, p = .50) did not differ between e4 carriers and NC, nor in any subregion. Eliminating the 21 with MCI did not alter these results. Nondemented APOE e4 carriers over age 60 have a higher burden of total parenchymal and vascular amyloid neuropathology than NC, but no difference in neuritic plaque and NFT pathology.