scholarly journals Short term exercise‐induced protection of cardiovascular function and health: Why and how fast does the heart benefit from exercise?

2021 ◽  
Author(s):  
Dick H. J. Thijssen ◽  
Laween Uthman ◽  
Yasina Somani ◽  
Niels Royen
2020 ◽  
pp. 147451512094458
Author(s):  
Zhongyou Li ◽  
Wentao Jiang ◽  
Yu Chen ◽  
Guanshi Wang ◽  
Fei Yan ◽  
...  

Objective: The role of sauna bathing in cardiovascular function treatment has been increasingly explored, but insufficient attention has been paid to its efficacy. We performed a meta-analysis to provide more evidence for the efficacy of sauna treatment in cardiovascular nursing. Methods: Sixteen peer-reviewed journal articles were screened to summarize the efficacy of the sauna on cardiovascular function. Both acute (0–30 min after the sauna) and short-term (2–4 weeks following the sauna treatment) efficacies were investigated. Results: For pooled acute efficacy, body temperature and heart rate significantly ( p<0.001) grew by 0.94℃ and 17.86 beats/min, respectively; reductions of 5.55 mmHg ( p<0.001) and 6.50 mmHg ( p<0.001) were also observed in systolic blood pressure and diastole blood pressure, respectively. For combined short-term efficacy, left ventricular ejection fraction (LVEF), 6-min walk distance, and flow-mediated dilation ( p<0.001) increased by 3.27%, 48.11 m, and 1.71%, respectively; greater amelioration in LVEF was observed in participants with lower LVEF. The proportion of patients with New York Heart Association class III and IV decreased by 10.9% and 12.2%, respectively. Systolic blood pressure, diastolic blood pressure, brain natriuretic peptide concentration, left ventricular end-diastolic dimension, cardiothoracic ratio, and left atrial dimension reduced by 5.26 mmHg ( p<0.001), 4.14 mmHg ( p<0.001), 116.66 pg/mL ( p<0.001), 2.79 mm ( p<0.001), 2.628% ( p<0.05), and 1.88 mm ( p<0.05), respectively, while the concentration of norepinephrine in the plasma remained unchanged. Conclusion: Sauna treatment was found to play a positive role in improving cardiovascular function and physical activity levels, especially in patients with low cardiovascular function. These findings reveal that thermal intervention may be a promising means for cardiovascular nursing.


2006 ◽  
Vol 101 (3) ◽  
pp. 809-816 ◽  
Author(s):  
Alastair J. Thomson ◽  
Gordon B. Drummond ◽  
W. Stephen Waring ◽  
David J. Webb ◽  
Simon R. J. Maxwell

Both hypoxia and hyperoxia have major effects on cardiovascular function. However, both states affect ventilation and many previous studies have not controlled CO2 tension. We investigated whether hemodynamic effects previously attributed to modified O2 tension were still apparent under isocapnic conditions. In eight healthy men, we studied blood pressure (BP), heart rate (HR), cardiac index (CI), systemic vascular resistance index (SVRI) and arterial stiffness (augmentation index, AI) during 1 h of hyperoxia (mean end-tidal O2 79.6 ± 2.0%) or hypoxia (pulse oximeter oxygen saturation 82.6 ± 0.3%). Hyperoxia increased SVRI (18.9 ± 1.9%; P < 0.001) and reduced HR (−10.3 ± 1.0%; P < 0.001), CI (−10.3 ± 1.7%; P < 0.001), and stroke index (SI) (−7.3 ± 1.3%; P < 0.001) but had no effect on AI, whereas hypoxia reduced SVRI (−15.2 ± 1.2%; P < 0.001) and AI (−10.7 ± 1.1%; P < 0.001) and increased HR (18.2 ± 1.2%; P < 0.001), CI (20.2 ± 1.8%; P < 0.001), and pulse pressure (13.2 ± 2.3%; P = 0.02). The effects of hyperoxia on CI and SVRI, but not the other hemodynamic effects, persisted for up to 1 h after restoration of air breathing. Although increased oxidative stress has been proposed as a cause of the cardiovascular response to altered oxygenation, we found no significant changes in venous antioxidant or 8-iso-prostaglandin F2α levels. We conclude that both hyperoxia and hypoxia, when present during isocapnia, cause similar changes in cardiovascular function to those described with poikilocapnic conditions.


2012 ◽  
Vol 22 (10) ◽  
pp. 907-913 ◽  
Author(s):  
M. Garelnabi ◽  
E. Veledar ◽  
J. White-Welkley ◽  
N. Santanam ◽  
J. Abramson ◽  
...  

2018 ◽  
Vol 33 (12) ◽  
pp. 1515-1524 ◽  
Author(s):  
Setor K. Kunutsor ◽  
Arja Häkkinen ◽  
Francesco Zaccardi ◽  
Tanjaniina Laukkanen ◽  
Earric Lee ◽  
...  

Author(s):  
José Rizzo ◽  
Edil Rodrigues Filho ◽  
Adriana Gonçalves ◽  
Laienne Albuquerque ◽  
Eduardo Albuquerque ◽  
...  

BACKGROUND: Exercise-induced respiratory symptoms are frequently reported by asthmatics and exercise-induced bronchospasm (EIB) is a frequent cause that requires objective testing for diagnosis. Eucapnic voluntary hyperventilation (EVH) is recommended as an exercise surrogate stimulus for this purpose, but its short-term reproducibility is not yet established in young asthmatics. OBJECTIVE: To evaluate the short-term test-retest agreement and reproducibility of FEV1 changes after EVH in young asthmatics. METHODS: Asthmatics aged between 10 and 20 years underwent EVH for EIB diagnosis on two occasions 2-4 days apart at a specialized university clinic. FEV1 was measured 5, 15 and 30 minutes after EVH with a target ventilation rate 21 times baseline FEV1. EIB was diagnosed as a decrease >10% in FEV1 from baseline. RESULTS: Twenty-six of 62 recruited individuals tested positive for EIB on both visits (positive group) and 17 on one visit only (divergent group); and 19 tested negative on both visits (negative group). The overall agreement was 72.5% (95%CI 61.6%, 83.6%) and positive and negative agreement was 41.9% and 30.6% respectively. Despite overall low bias in FEV1 response between test days (0.87%), the limits of agreement were wide (+20.72%). There were no differences in pre-challenge FEV1 or achieved ventilation rate, between visits either between groups (p=0.097 and p=0.461) or within groups, (p=0.828 and p=0.780). No test was interrupted by symptoms and there were no safety issues. CONCLUSIONS: More than one EVH test should be performed in young asthmatics with a negative test to exclude EIB and minimize misdiagnosis and mistreatment.


1998 ◽  
Vol 8 (2) ◽  
pp. 175-295 ◽  
Author(s):  
Craig A. Horswill

As a result of exercise-induced sweating, athletes and trained individuals can lose up to 3 L of fluid per hour. Fluid replacement is required to maintain hydration and allow the athlete to continue to perform. Inadequate fluid intake will adversely affect temperature regulation, cardiovascular function, and muscle metabolism. To maximize fluid intake and effectively replace fluid, athletes must employ behavioral strategies. Athletes can also select beverages with characteristics that complement their behavioral efforts. Palatability, rapid absorption, retention of the fluid, and ergogenicity are the major attributes to consider for enhancing hydration during training and physical activity.


2010 ◽  
Vol 299 (5) ◽  
pp. H1515-H1524 ◽  
Author(s):  
Andreas N. Kavazis ◽  
Ashley J. Smuder ◽  
Kisuk Min ◽  
Nihal Tümer ◽  
Scott K. Powers

Doxorubicin (Dox) is an antitumor agent used in cancer treatment, but its clinical use is limited due to cardiotoxicity. Although exercise training can defend against Dox-mediated cardiac damage, the means for this cardioprotection remain unknown. To investigate the mechanism(s) responsible for exercise training-induced cardioprotection against Dox-mediated cardiotoxicity, we tested a two-pronged hypothesis: 1) exercise training protects against Dox-induced cardiotoxicity by preventing Dox-mediated mitochondrial damage/dysfunction and increased oxidative stress and 2) exercise training-induced cardiac expression of the inducible isoform of the 70-kDa heat shock protein 72 (HSP72) is essential to achieve exercise training-induced cardioprotection against Dox toxicity. Animals were randomly assigned to sedentary or exercise groups and paired with either placebo or Dox treatment (i.e., 20 mg/kg body wt ip Dox hydrochloride 24 h before euthanasia). Dox administration resulted in cardiac mitochondrial dysfunction, activation of proteases, and apoptosis. Exercise training increased cardiac antioxidant enzymes and HSP72 protein abundance and protected cardiac myocytes against Dox-induced mitochondrial damage, protease activation, and apoptosis. To determine whether exercise-induced expression of HSP72 in the heart is required for this cardioprotection, we utilized an innovative experimental strategy that successfully prevented exercise-induced increases in myocardial HSP72 levels. However, prevention of exercise-induced increases in myocardial HSP72 did not eliminate the exercise-induced cardioprotective phenotype that is resistant to Dox-mediated injury. Our results indicate that exercise training protects against the detrimental side effects of Dox in cardiac myocytes, in part, by protecting mitochondria against Dox-mediated damage. However, this exercise-induced cardioprotection is independent of myocardial HSP72 levels. Finally, our data are consistent with the concept that increases in cardiac mitochondrial antioxidant enzymes may contribute to exercise-induced cardioprotection.


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