TL;DR: It is suggested that physical exercise induces adaptive hypertrophy in cardiac myocytes with improved contractile function after intensity controlled aerobic endurance training in the rat, and higher myofilament Ca2+ sensitivity is the dominant effect responsible for enhanced myocyte contractility in TR.
Abstract: Objective: Regular exercise enhances cardiac function and modulates myocyte growth in healthy individuals. The purpose of the present study was to assess contractile function and expression of selected genes associated with intracellular Ca2+ regulation after intensity controlled aerobic endurance training in the rat. Methods: Female Sprague–Dawley rats were randomly assigned to sedentary control (SED) or treadmill running (TR) 2 h per day, 5 days per week for 2, 4 or 13 weeks. Rats ran 8-min intervals at 85–90% of V O2max separated by 2 min at 50–60%. Myocyte length, intracellular Ca2+ (Fura-2), and intracellular pH (BCECF) were measured in dissociated cells in response to electrical stimulation at a range of stimulation rates. Results: The increase in V O2max plateaued after 6–8 weeks, 60% above SED. After 13 weeks, left and right ventricular weights were 39 and 36% higher than in SED. Left ventricular myocytes were 13% longer, whereas width remained unchanged. After 4 weeks training, myocyte contractility was approximately 20% higher in TR. Peak systolic intracellular Ca2+ and time for the decay from systole were 20–35 and 12–17% lower, respectively. These results suggest that increased myofilament Ca2+ sensitivity is the dominant effect responsible for enhanced myocyte contractility in TR. Intracellular pH progressively decreased as stimulation frequency was increased in the SED group. This decrease was markedly attenuated in TR and the intracellular pH was significantly higher in the TR group at a stimulation rate of 5–10 Hz. This effect may contribute to the increased contractility observed at the higher stimulation frequencies in TR. A higher intrinsic myofilament Ca2+ sensitivity was observed in permeabilised myocytes from the TR group under conditions of constant pH and [Ca2+]. Western blot analysis indicated 21 and 46% higher myocardial SERCA-2 and phospholamban, but unaltered Na+/Ca2+-exchanger levels. Competitive RT-PCR revealed that TR significantly increased Na+/H+-exchanger mRNA. Conclusion: Intensity controlled interval training increases cardiomyocyte contractility. Higher myofilament Ca2+-sensitivity, and enhanced Ca2+-handling and pH-regulation are putative mechanisms. Our results suggest that physical exercise induces adaptive hypertrophy in cardiac myocytes with improved contractile function.
TL;DR: The smartphone-based intervention to monitor and decrease SED in overweight/obese individuals, and compared 3 approaches to prompting physical activity (PA) breaks and delivering feedback on SED significantly reduced SED, suggests that Prompting frequent short activity breaks may be the most effective way to decreasing SED and increase PA in obese individuals.
Abstract: Purpose
Excessive sedentary time (SED) has been linked to obesity and other adverse health outcomes. However, few sedentary-reducing interventions exist and none have utilized smartphones to automate behavioral strategies to decrease SED. We tested a smartphone-based intervention to monitor and decrease SED in overweight/obese individuals, and compared 3 approaches to prompting physical activity (PA) breaks and delivering feedback on SED.
Design and Methods
Participants [N = 30; Age = 47.5(13.5) years; 83% female; Body Mass Index (BMI) = 36.2(7.5) kg/m2] wore the SenseWear Mini Armband (SWA) to objectively measure SED for 7 days at baseline. Participants were then presented with 3 smartphone-based PA break conditions in counterbalanced order: (1) 3-min break after 30 SED min; (2) 6-min break after 60 SED min; and (3) 12-min break after 120 SED min. Participants followed each condition for 7 days and wore the SWA throughout.
Results
All PA break conditions yielded significant decreases in SED and increases in light (LPA) and moderate-to-vigorous PA (MVPA) (p<0.005). Average % SED at baseline (72.2%) decreased by 5.9%, 5.6%, and 3.3% [i.e. by mean (95% CI) −47.2(−66.3, −28.2), −44.5(−65.2, −23.8), and −26.2(−40.7, −11.6) min/d] in the 3-, 6-, and 12-min conditions, respectively. Conversely, % LPA increased from 22.8% to 26.7%, 26.7%, and 24.7% [i.e. by 31.0(15.8, 46.2), 31.0(13.6, 48.4), and 15.3(3.9, 26.8) min/d], and % MVPA increased from 5.0% to 7.0%, 6.7%, and 6.3% (i.e. by 16.2(8.5, 24.0), 13.5(6.3, 20.6), and 10.8(4.2, 17.5) min/d] in the 3-, 6-, and 12-min conditions, respectively. Planned pairwise comparisons revealed the 3-min condition was superior to the 12-min condition in decreasing SED and increasing LPA (p<0.05).
Conclusion
The smartphone-based intervention significantly reduced SED. Prompting frequent short activity breaks may be the most effective way to decrease SED and increase PA in overweight/obese individuals. Future investigations should determine whether these SED reductions can be maintained long-term.
Trial Registration
ClinicalTrials.gov NCT01688804
TL;DR: The rise in resting blood pressure with hydrocortisone is associated with an increased cardiac output (presumably due to increased blood volume) and the increased responsiveness of the peripheral vasculature to reflex pressor stimuli appears to be due to changes in end-organ responsiveness since similar changes occurred with local administration of norepinephrine.
Abstract: Oral hydrocortisone increases blood pressure and enhances pressor responsiveness in normal human subjects. We studied the effects of 1 week of oral hydrocortisone (200 mg/day) on blood pressure, cardiac output, total peripheral resistance, forearm vascular resistance, and norepinephrine spillover to plasma in eight healthy male volunteers. Although diastolic blood pressure remained unchanged, systolic blood pressure increased from 119 to 135 mm Hg (SED +/- 3.4, p less than 0.01), associated with an increased cardiac output (5.85-7.73 l/min, SED +/- 0.46, p less than 0.01). Total peripheral vascular resistance fell from 15.1 to 12.2 mm Hg/l/min (SED +/- 1.03, p less than 0.05). Resting forearm vascular resistance remained unchanged, but the reflex response to the cold pressor test was accentuated, the rise in resistance increasing from 10.5 mm Hg/ml/100 ml/min (R units) before treatment to 32.6 R units after treatment (SED +/- 6.4, p less than 0.025). The rise in forearm vascular resistance accompanying intra-arterial norepinephrine (25, 50, and 100 ng/min) was also significantly greater after hydrocortisone, increasing from an average of 14.9 +/- 2.4 R units before treatment to 35.1 +/- 5.5 R units after hydrocortisone (SED +/- 6.0, p less than 0.05). A shift to the left in the dose-response relation and fall in threshold suggested increased sensitivity to norepinephrine after treatment. Measurement of resting norepinephrine spillover rate to plasma and norepinephrine uptake indicated that overall resting sympathetic nervous system activity was not increased. The rise in resting blood pressure with hydrocortisone is associated with an increased cardiac output (presumably due to increased blood volume).(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: Ten Holstein heifers were fed a selenium-deficient diet 3 months before calving and throughout their first lactation, and cows were challenge-exposed to Escherichia coli by administering 15 to 40 colony-forming units into 1 mammary gland.
Abstract: Ten Holstein heifers were fed a selenium-deficient (SeD) diet (0.04 mg of Se/kg on a total ration dry-matter basis) 3 months before calving and throughout their first lactation. A selenium-supplemented (SeS) diet (2 mg of Se/head/d) was fed to a group of 10 heifers. In about the 14th week of lactation, the cows were challenge-exposed to Escherichia coli by administering 15 to 40 colony-forming units (CFU) into 1 mammary gland. Selenium concentration (microgram/ml) in blood around the time of challenge exposure was 0.033 +/- 0.002 (mean +/- SEM) in SeD and 0.132 +/- 0.006 in SeS cows. Infections were established in all challenge-exposed quarters. The frequency of quarter atrophy and agalactia, and reduction in whole-udder milk yield in the first 4 days after challenge exposure, were greater (P less than 0.05) in the SeD cows. Log10 peak bacterial concentrations in milk were higher (P less than 0.05) in SeD (7.63 +/- 0.34 CFU/ml) than in SeS cows (5.57 +/- 0.66 CFU/ml). Mean log bacterial concentration was significantly higher (P less than 0.05) from 12 to 20 hours after challenge exposure in SeD than in SeS cows. Duration of infection was significantly greater (P less than 0.05) in SeD (162.0 +/- 12.0) than in SeS cows (114.4 +/- 18.0 hours). Milk somatic cell counts increased significantly more slowly (P less than 0.05) in SeD than in SeS cows from 8 to 16 hours after challenge exposure. Ratios of milk somatic cells to bacteria in milk were significantly lower (P less than 0.05) in SeD than in SeS cows at 12 and 16 hours after challenge exposure.
TL;DR: Results indicate that previous physical activity potentiates HSP72 expression after a wide range of stressors, and may contribute to the increased stress resistance previously reported in physically active organisms.
Abstract: The mechanism(s) for how physically active organisms are resistant to many damaging effects of acute stressor exposure is unknown Cellular induction of heat-shock proteins (eg, HSP72) is one successful strategy used by the cell to survive the damaging effects of stress It is possible, therefore, that the stress-buffering effect of physical activity may be due to an improved HSP72 response to stress Thus the purpose of the current study was to determine whether prior voluntary freewheel running facilitates the stress-induced induction of HSP72 in central (brain), peripheral, and immune tissues Adult male Fischer 344 rats were housed with either a mobile running wheel (Active) or a locked, immobile wheel [sedentary (Sed)] for 8 wk before stressor exposure Rats were exposed to either inescapable tail-shock stress (IS; 100 16-mA tail shocks, 5-s duration, 60-s intertrial interval), exhaustive exercise stress (EXS; treadmill running to exhaustion), or no stress (controls) Blood, brain, and peripheral tissues were collected 2 h after stressor termination The kinetics of HSP72 induction after IS was determined in cultured mesenteric lymph node cells Activation of the stress response was verified by measuring serum corticosterone (RIA) Tissue and cellular HSP72 content were measured using HSP72 ELISA in cell lysates Both Active and Sed rats had elevated levels of serum corticosterone after stress In contrast, Active but not Sed rats exposed to IS and/or EXS had elevated HSP72 in dorsal vagal complex, frontal cortex, hippocampus, pituitary, adrenal, liver, spleen, mesenteric lymph nodes, and heart In addition, Active rats exposed to IS demonstrated a faster induction of lymphocyte HSP72 compared with Sed rats Thus Active rats responded to stress with both greater and faster HSP72 responses compared with Sed rats These results indicate that previous physical activity potentiates HSP72 expression after a wide range of stressors Facilitated induction of HSP72 may contribute to the increased stress resistance previously reported in physically active organisms