Exercise-induced adrenocorticotropic hormone response is cooperatively regulated by hypothalamic arginine vasopressin and corticotrophin-releasing hormone

2021 ◽  
Author(s):  
Kanako Takahashi ◽  
Takeru Shima ◽  
Mariko Soya ◽  
Jang Soo Yook ◽  
Hikaru Koizumi ◽  
...  

Introduction: Exercise becomes a stress when performed at an intensity above the lactate threshold (LT) because at that point the plasma adrenocorticotropic hormone (ACTH), a marker of stress response, increases. It is possible that the exercise-induced ACTH response is regulated at least by arginine vasopressin (AVP) and possibly by corticotropin-releasing hormone (CRH), but this remains unclear. To clarify the involvement of these factors, it is useful to intervene pharmacologically in the regulatory mechanisms, with a physiologically acceptable exercise model. Methods: We used a special stress model of treadmill running (aerobic exercise) for male Wistar rats, which mimic the human physiological response, where plasma ACTH levels increase at just above the LT for 30 min. Animals were administered the AVP V1b receptor antagonist SSR149415 (SSR) and/or the CRH type 1 receptor antagonist CP154526 (CP) intraperitoneally before the exercise, which allowed the monitoring of exercise-induced ACTH response. Immunocytochemical evaluation of activated AVP and CRH neurons with exercise was performed for the animals’ hypothalami. Results: A single injection of either antagonist, SSR or CP, resulted in inhibited ACTH levels after exercise stress. Moreover, the combined injection of SSR and CP strongly suppressed ACTH secretion during treadmill running to a greater extent than each alone. The running-exercise-induced activation of both AVP and CRH neurons in the hypothalamus was also confirmed. Conclusion: These results lead us to hypothesize that AVP and CRH are cooperatively involved in exercise-induced ACTH response just above the LT. This may also reflect the stress response with moderate-intensity exercise in humans.

2019 ◽  
Vol 30 (2) ◽  
pp. 525-533 ◽  
Author(s):  
J J Steventon ◽  
C Foster ◽  
H Furby ◽  
D Helme ◽  
R G Wise ◽  
...  

Abstract Long-term exercise interventions have been shown to be a potent trigger for both neurogenesis and vascular plasticity. However, little is known about the underlying temporal dynamics and specifically when exercise-induced vascular adaptations first occur, which is vital for therapeutic applications. In this study, we investigated whether a single session of moderate-intensity exercise was sufficient to induce changes in the cerebral vasculature. We employed arterial spin labeling magnetic resonance imaging to measure global and regional cerebral blood flow (CBF) before and after 20 min of cycling. The blood vessels’ ability to dilate, measured by cerebrovascular reactivity (CVR) to CO2 inhalation, was measured at baseline and 25-min postexercise. Our data showed that CBF was selectively increased by 10–12% in the hippocampus 15, 40, and 60 min after exercise cessation, whereas CVR to CO2 was unchanged in all regions. The absence of a corresponding change in hippocampal CVR suggests that the immediate and transient hippocampal adaptations observed after exercise are not driven by a mechanical vascular change and more likely represents an adaptive metabolic change, providing a framework for exploring the therapeutic potential of exercise-induced plasticity (neural, vascular, or both) in clinical and aged populations.


Animals ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 486
Author(s):  
Wendy Pearson ◽  
Julia Guazzelli Pezzali ◽  
Renan Antunes Donadelli ◽  
Ashley Wagner ◽  
Preston Buff

There is little information available to describe the inflammatory consequences of and recovery from moderate-intensity exercise bouts in hunting dogs. The purpose of the current study is to generate pilot data on the appearance and disappearance of biomarkers of inflammation and inflammation resolution following a typical one-hour exercise bout in basset hounds. Four hounds were set out to find a scent and freely adopted running or walking over wooded terrain for approximately one hour. Venous blood samples were obtained before the exercise and at 1, 2, 4, 6, and 10 h following cessation of exercise and were analyzed for biomarkers of inflammation (prostaglandin E2 (PGE2), nitric oxide (NO), interleukin 1β (IL-1β)) tumour necrosis factor-α (TNF-α)), and inflammation resolution (resolvin D1 (RvD1)). There was an increase in inflammation one hour after the exercise, shown by a significant increase in PGE2. Following this peak, PGE2 steadily declined at the same time as RvD1 increased, with RvD1 peaking at six hours. This pilot study provides evidence that dogs that undergo an hour of hunt exercise experience transient inflammation that peaks one hour after the end of exercise; inflammation resolution peaks six hours after the end of exercise. Future studies should seek to further understand the distinct and combined roles of PGE2 and RvD1 in dog adaptation to exercise stress.


1984 ◽  
Vol 247 (5) ◽  
pp. R880-R883 ◽  
Author(s):  
S. H. Constable ◽  
J. C. Young ◽  
M. Higuchi ◽  
J. O. Holloszy

This study was undertaken to determine whether glycogen resynthesis can occur in glycogen-depleted muscles in response to glucose feeding during prolonged exercise. Rats were exercised for 40 min with a treadmill running program designed to deplete muscle glycogen. One group was studied immediately after the glycogen-depletion exercise. A second group was given 1 g glucose by stomach tube and exercised for an additional 90 min at a running speed of 22 m/min on a treadmill set at an 8 degree incline; they were given additional 1-g glucose feedings after 30 and 60 min of running. The initial 40-min run resulted in liver glycogen depletion, large decreases in plasma glucose and insulin concentrations, and a marked lowering of muscle glycogen. The glucose feedings resulted in greater than twofold increases in the concentrations of glucose and insulin in plasma, and of glycogen in leg muscles, during the 90 min of running. No repletion of liver glycogen occurred. These results provide evidence that glycogen resynthesis can occur in glycogen-depleted muscle despite continued moderate intensity exercise if sufficient glucose is made available.


2015 ◽  
Vol 119 (7) ◽  
pp. 831-839 ◽  
Author(s):  
Pavarana Vutthasathien ◽  
Jonggonnee Wattanapermpool

Data from the trial known as Testosterone in Older Men with Mobility Limitations (TOM) has indicated an association between testosterone administration and a greater risk for adverse cardiovascular events. We therefore propose that regular exercise is a cardioprotective alternative that prevents detrimental changes in contractile activation when a deficiency in male sex hormones exists. Ten-week-old orchidectomized (ORX) rats were subjected to a 9-wk treadmill running program at moderate intensity starting 1 wk after surgery. Although exercise-induced cardiac hypertrophy was observed both in rats that underwent ORX and sham surgery, regular exercise enhanced cardiac myofilament Ca2+ sensitivity and myosin light-chain 2 phosphorylation only in rats that underwent a sham operation. Although the rats that had sham surgery and and given exercise exhibited no change in maximum developed tension, regular running prevented the suppression of maximum active tension in the hearts of ORX rats. Regular exercise also prevented a shift in myosin heavy chain (MHC) isoforms toward β-MHC, a reduction in sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) activity, and an increase in SERCA sensitivity in the hearts of ORX rats. Neither SERCA content nor its modulating component, phospholamban (PLB), was altered by exercise in either sham-operated or ORX rats. However, decreases in the phosphorylated Thr17 form of PLB and the phosphorylated Thr287 form of Ca2+/calmodulin-dependent kinase II in the hearts of ORX rats were abolished after regular exercise. These results thus support the use of regular running as a cardioprotective alternative to testosterone replacement in hypogonadal conditions.


2010 ◽  
Vol 103 (10) ◽  
pp. 1480-1484 ◽  
Author(s):  
Narelle M. Berry ◽  
Kade Davison ◽  
Alison M. Coates ◽  
Jonathan D. Buckley ◽  
Peter R. C. Howe

Impaired endothelial vasodilatation may contribute to the exaggerated blood pressure (BP) responses to exercise in individuals who are overweight/obese. The present study investigated whether consumption of cocoa flavanols, which improve endothelium-dependent flow-mediated dilatation (FMD), can modify BP responsiveness to exercise. Twenty-one volunteers (eight females and thirteen males, 54·9 (se2·2) years, BMI 31·6 (se0·8) kg/m2, systolic BP 134 (se2) mmHg, diastolic BP (DBP) 87 (se2) mmHg) were randomised to consume single servings of either a high-flavanol (HF, 701 mg) or a low-flavanol (LF, 22 mg) cocoa beverage in a double-blind, cross-over design with 3–7-d washout between treatments. Two hours after cocoa consumption, FMD was measured, followed by continuous beat-to-beat assessment (Finapres™) of BP before and during 10 min of cycling at 75 % of age-predicted maximum heart rate. Averaged data from two assessments on each type of beverage were compared by analysis of covariance using pre-exercise BP as the covariate. Pre-exercise BP was similar after taking LF and HF (153 (se3)/88 (se3)v. 153 (se4)/87 (se2) mmHg, respectively,P>0·05). However, the BP response to exercise (area under BP curve) was attenuated by HF compared with LF. BP increases were 68 % lower for DBP (P = 0·03) and 14 % lower for mean BP (P = 0·05). FMD measurements were higher after taking HF than after taking LF (6·1 (se0·6) %v. 3·4 (se0·5) %,P < 0·001). By facilitating vasodilation and attenuating exercise-induced increases in BP, cocoa flavanols may decrease cardiovascular risk and enhance the cardiovascular benefits of moderate intensity exercise in at-risk individuals.


2014 ◽  
Vol 34 (12) ◽  
pp. 1873-1876 ◽  
Author(s):  
Julien V Brugniaux ◽  
Christopher J Marley ◽  
Danielle A Hodson ◽  
Karl J New ◽  
Damian M Bailey

Elevated cardiorespiratory fitness improves resting cerebral perfusion, although to what extent this is further amplified during acute exposure to exercise stress and the corresponding implications for cerebral oxygenation remain unknown. To examine this, we recruited 12 moderately active and 12 sedentary healthy males. Middle cerebral artery blood velocity (MCAv) and prefrontal cortical oxyhemoglobin (cO2Hb) concentration were monitored continuously at rest and throughout an incremental cycling test to exhaustion. Despite a subtle elevation in the maximal oxygen uptake (active: 52 ± 9 ml/kg per minute versus sedentary: 33 ± 5 ml/kg per minute, P < 0.05), resting MCAv was not different between groups. However, more marked increases in both MCAv (+28 ± 13% versus +18 ± 6%, P < 0.05) and cO2Hb (+5 ±4% versus −2 ± 3%, P < 0.05) were observed in the active group during the transition from low- to moderate-intensity exercise. Collectively, these findings indicate that the long-term benefits associated with moderate increase in physical activity are not observed in the resting state and only become apparent when the cerebrovasculature is challenged by acute exertional stress. This has important clinical implications when assessing the true extent of cerebrovascular adaptation.


1988 ◽  
Vol 64 (4) ◽  
pp. 1333-1336 ◽  
Author(s):  
H. M. Alessio ◽  
A. H. Goldfarb

This study was designed to determine whether endurance training would influence the production of lipid peroxidation (LI-POX) by-products as indicated by malondialdehyde (MDA) at rest and after an acute exercise run. Additionally, the scavenger enzymes catalase (CAT) and superoxide dismutase (SOD) were examined to determine whether changes in LIPOX are associated with alterations in enzyme activity both at rest and after exercise. Male Sprague-Dawley rats (n = 32) were randomly assigned to either trained or sedentary groups and were killed either at rest or after 20 min of treadmill running. The training program increased oxidative capacity 64% in leg muscle. After exercise, the sedentary group demonstrated increased LIPOX levels in liver and white skeletal muscle, whereas the endurance-trained group did not show increases in LIPOX after exercise. CAT activity was higher in both red and white muscle after exercise in the trained animals. Total SOD activity was unaffected by either acute or chronic exercise. These data suggest that endurance training can result in a reduction in LIPOX levels as indicated by MDA during moderate-intensity exercise. It is possible that activation of the enzyme catalase and the increase in respiratory capacity were contributory factors responsible for regulating LIPOX after training during exercise.


2015 ◽  
Vol 4 (1) ◽  
pp. 118-125
Author(s):  
Jeffrey A. Woods ◽  
Brandt D. Pence

Exercise immunology is a relatively new discipline in the exercise sciences that seeks to understand how exercise affects the immune system and susceptibility to infectious and chronic diseases. This brief review will focus on three major observations that have driven the field to date including: (1) acute exercise-induced leukocytosis, (2) the observation that intense, prolonged exercise results in upper respiratory tract symptoms, and (3) the paradoxical effect of acute and chronic exercise on inflammation. This framework will be used to examine the mechanisms and implications behind these seminal observations. Data generally support the conclusion that moderate intensity exercise enhances immune function, whereas prolonged, intense exercise diminishes immune function.


2021 ◽  
Author(s):  
Xuchang Zhou ◽  
Hong Cao ◽  
Miao Wang ◽  
Jun Zou ◽  
wei wu

Abstract Background The purpose of this study was to explore whether moderate-intensity exercise can alleviate motion-induced post-traumatic osteoarthritis (PTOA) and the expression change of lncRNA H19 during this progression.Methods Twenty-week-old male C57BL/6 mice were randomly divided into five groups: model control group (CM group, n = 6), treadmill model group (M group, n = 6), rehabilitation control group (CK group, n = 6), treadmill model + rehabilitation training group (K group, n = 6) and treadmill model + rest group (J group, n = 6). Paraffin sections were used to observe the pathological changes in the mouse knee joint in each group. A micro-CT was used to scan the knee joint to obtain the morphological indexes of tibial plateau bone. Real-time PCR was used to detect the mRNA levels of inflammatory factors, synthetic and catabolic factors in cartilage. Results After high-intensity exercise for four weeks, the inflammation and catabolism of the mouse knee cartilage were enhanced, and the anabolism was weakened. Further study showed that these results were partially reversed after four-week moderate-intensity training. The results of hematoxylin-eosin staining confirmed this finding. Meanwhile, high-intensity exercise reduced the expression of lncRNA H19 in cartilage, while the expression of lncRNA H19 increased after four weeks of moderate-intensity exercise.Conclusion High-intensity treadmill running can cause injury to the knee cartilage in C57BL/6 mice which leads to PTOA and an decrease of lncRNA H19 expression in cartilage. Moderate-intensity exercise can relieve PTOA and partially reverse lncRNA H19 expression.


2007 ◽  
Vol 103 (1) ◽  
pp. 111-118 ◽  
Author(s):  
Alastair N. H. Hodges ◽  
A. William Sheel ◽  
John R. Mayo ◽  
Donald C. McKenzie

The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (V̇o2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 ± 7.4 and 100.7 ± 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 ± 9.5% V̇o2 max) and 55.5 ± 9.8 and 104.3 ± 9.1 min following 60 min cycling exercise in H (intensity = 65.4 ± 7.1% hypoxic V̇o2 max), where V̇o2 max = 65.0 ± 7.5 ml·kg−1·min−1 (N) and 54.1 ± 7.0 ml·kg−1·min−1 (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 ± 1.1%) as measured noninvasively during the V̇o2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 ± 0.019, 0.181 ± 0.019, and 0.173 ± 0.019 g/ml (N) and 0.178 ± 0.021, 0.174 ± 0.022, and 0.176 ± 0.019 g/ml (H), respectively. No significant differences ( P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.


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