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Does pre-operational exercise affect recovery from surgery? Statistical Analysis

Does pre-operational exercise affect recovery from surgery? Statistical Analysis


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https://www.medicaljournals.se/jrm/content/html/10.2340/16501977-2210

I understand the difference between statistical significance and effect size, but I am having trouble interpreting the data on Table III in the article linked above. I am evaluating the WOMAC scores. My first question is can effect size confidence intervals cross zero and still be valid? My second question is about the negative and positive values of the Hedges'g. The first study scores the WOMAC in a way where the higher the score, the better the outcome. The second two studies score the WOMAC in a way where the lower the score, the better the outcome. Does this mean that in the first study a positive Hedges'g indicate larger effect for the treatment group and a negative Hedges' g for the other two studies indicate larger effect for the treatment group?


Regarding your first question, the effect size is not invalid if the confidence interval (CI) crosses 0. The effect size is a point estimate. When the CI -a range estimate of the coverage probability- includes 0, the probability that the range of the effect size can include 0 cannot be rejected at the $1-alpha$ level of confidence.

Regarding your second question, from the definition of Hedge's g:

$$g = frac{ar{x_1} - ar{x_2}}{sd_{pooled}}$$

we can see that if $ar{x_2}$ is larger than $ar{x_1}$ then $g$ will be negative. So, the sign only determines which of the estimates is larger and that will depend on which estimate is considered as the reference.


Life in Motion

Many people know that regular exercise can aid in weight loss, improve your mood, and boost energy. But did you know that exercise has both short and long term effects on the cardiovascular system? The cardiovascular system delivers nutrients and oxygen to all cells in the body, and consists of the heart and the blood vessels.

In honor of American Heart Month, Dr. Frederick Basilico, Physician in Chief for Medicine at NEBH explains the benefits of exercise on the cardiovascular system, and what you can do to gain the benefits.

In order to gain short and long term benefits on your cardiovascular system, you will need to exercise regularly. It is advised that you perform light exercise such as walking for at least 30 minutes 5 days a week. Alternatively, you can perform moderate exercise such as running or bicycling for at least 30 minutes 3 days a week.

Short Term Effects of Exercise on the Cardiovascular System

Many short-term effects take place during physical activity, including:

  • Faster heart contractions. This leads to an increased heart rate and increased circulation, which gets oxygenated blood to your muscles quicker.
  • More forceful heart contractions with each heartbeat, which leads to a greater amount of blood being pumped throughout the body.

Long Term Effects of Exercise on the Cardiovascular System

A fairly well conditioned athlete can see long term cardiovascular effects from exercising in as little as two weeks. People who are just beginning to exercise will see effects in up to four weeks. These effects include:

  • The heart and lungs become more efficient as your cardiovascular training increases.
  • Decreased resting heart rate, which means your heart doesn’t have to beat as often to circulate blood.
  • Improved ability to draw in deeper and longer breaths, and take fewer breaths.
  • Reduced risk of heart disease.

If you have any health concerns, consult your doctor before beginning a new exercise routine.

Read More


Introduction

Rehabilitation after cardiac surgery improves physical and psychological outcomes. A recent Cochrane review reported improved quality of life, reduced hospital readmissions and mortality [1]. Core components of cardiac rehabilitation include patient assessment, exercise training, diet counseling, risk factor control, patient education and psychosocial management with exercise training [2, 3]. In addition, promoting early training exercise, such as daily walking, may reduce muscle atrophy and recovery time [4, 5].

Hospital discharge is getting earlier and earlier after cardiac surgery [6]. Patient follow-up is a concern as major complications mainly occur within the first month. Decreased physical activity is an independent predictor for a complicated postoperative recovery in patients aged 65 years or older undergoing elective cardiac surgery [7].

The use of connected bracelets and smartwatches is increasing in medicine following significant improvements into both hardware and software components [8]. They seem to be well tolerated by the patients. A portable wearable wristband-type hand orthotic was rated overall satisfactory by stroke survivors [9].

This study was designed to measure the physical activity of patients after cardiac surgery using a connected bracelet and further, to see if this activity may be predicted by the perioperative status and/or may predict the occurrence of complications.


Methods

This observational feasibility study was conducted in a 25-bed University Teaching Hospital ICU in the United Kingdom. Ethical approval was granted by South Central – Hampshire National Research and Ethics Service. Reference: 14/SC/1398.

Patient recruitment

All patients admitted to the ICU with a medical diagnosis and requiring intubation and ventilation for at least 48 hours join an Early Mobility Program (EMP). This programme provides a progressive mobility pathway starting with daily passive upper/lower limb exercise sessions by means of an ergometer in addition to their routine physiotherapy. Inclusion criteria for enrolment into the study included: patient being on the EMP pathway of which the criteria were cardiovascular stability (stable vasopressor dose for two hours) stable heart rate (< 140 bpm) and rhythm and the presence of a jugular central venous pressure (CVP) line and arterial line. Exclusion criteria included any prior rapidly deteriorating neuromuscular disease, any upper limb problem precluding cycle ergometry, pyrexia (temp > 38 °C), raised intracranial pressure, patients with poor prognostic outcomes and lack of agreement from clinician or NOK/LR not understanding English. 149 patients accepted onto the EMP were screened for study eligibility.

All included patients had monitoring in place that included: electrocardiogram (ECG) set, saturation probe, CVP line and an arterial line. Patients were sedated according to the ICU sedation protocol using a combination of fentanyl, midazolam and/or propofol aiming for a RASS score between − 1 and + 1. Vasopressors were used to maintain a mean arterial blood pressure of > 75 mmHg. Sedative infusion rates and ventilation settings were not changed during the protocol.

Patients were ventilated using pressure or volume control modes or support mode using an Engstrom Carestation™ ventilator. Flow volumes were directly measured by a ventilator D-lite™ sensor, which measures pressure difference between two ports and calculates gas/air flow (GE Healthcare, Chicago, Illinois).

Early mobility interventions

Patients were positioned in bed, in a semi recumbent position with their arms in the limb supports of the cycle ergometer (MOTOmed letto2 – Reck, Reckstr 1–5, Betzenweiler 88,422, Germany). Sixty minutes of data was collected. The first 10 minutes were with patients upper limbs positioned in the limb supports and at rest followed by 30 minutes passive upper limb cycling at a frequency of 20 revolutions per minute, and finally 20 minutes with the patients upper limbs left in the limb supports during which the patient was at rest undisturbed. Safety criteria used for patient initiation and continued use of the ergometer was based on the traffic light system recommended from Hodgson et al. [14] .

Measurements

Continuous heart rate (HR), blood pressure (BP), heart rhythm and saturations were measured throughout the 60-minute study period for each patient. Continuous cardiac output (CO) L/min, HR (bpm), BP (mmHg), and stroke volume (SV) m/L were monitored by the LiDCO™. The LiDCO™ was calibrated as per manufacturer guidance, prior to patient enrolment. Minute by minute values of inspiratory and expiratory O2 and CO2, respiratory rate (RR) breaths/min, minute volume (MV) mL and tidal volume (VT) mL were measured by the ventilator's E-COVX module. Values for all continuous data were averaged over the five minutes leading up to each 10-minute interval within the 60-minute study period. If any data was missing within those last five minutes the average was calculated by the number of available data within that time frame.

Paired central mixed venous blood and arterial blood gas samples were taken at 10 minutes prior to ergometry starting, and then at 0, 10, 20 and 30 minutes, during ergometry and again 10 and 20 minutes after ergometry finished.

Oxygen delivery (DO2) was calculated using the equation: DO2 = CaO2 x CO where CaO2 (arterial oxygen content) = (1.34 x Hb x SaO2 x 0.01) + (0.023 x PaO2). The value 1.34 is known as Hufners constant and 0.023 is the volume of O2 dissolved per 100 ml plasma per kPa.

CO2 production (VCO2) was calculated from values of inspired concentrations of CO2 (FiCO2) and expired concentrations of CO2 (FeCO2) by the E-COVX module via the ventilator using the Bohr equation: VCO2 kPa = FiCO2 – FeCO2. Oxygen uptake (VO2) was calculated by two methods.

Method one: The reverse Fick method uses the measure of CO from the LiDCO™ with paired central mixed venous and arterial blood gas samples: VO2 mL/min = CO x (CaO2 - CvO2) x10 [15].

Method two: Indirect calorimetry calculated VO2 using the E-COVX metabolic module via the ventilator from the value of fraction of inspired O2 (FiO2), expiratory minute volume (MV), expired concentrations of O2 (FeO2) and CO2 (FeCO2) using the equation: VO2 ml/min = MV (FiO2 –FeO2 – FiO2 (FeCO2))/1-FiO2. [16]

Statistical analysis

This is a feasibility study the results of which may be used to power a larger study if appropriate. The study population number was guided by previous work in our unit [17]. All statistical analyses were performed using the SPSS 11 for Mac OS X (version 11.0.2). Demographics were presented for each patient. Continuous data was presented graphically as the mean for the five minutes leading up to each blood gas sampling, unless otherwise stated, except for the first blood sample. For repeated measures an analysis of variance was carried out using the Friedman test to determine any changes occurring in the physiological parameters from baseline to the six different time points. Correlation between the methods was assessed using a Pearson’s correlation. The significance difference was set at p < 0.05. Percentage changes in physiological parameters are expressed as interquartile range (IQR) and range.


Go out for some vigorous exercise. A bike ride, jog or using an elliptical machine at the gym will suffice. Get your heart rate up to about 60 to 80 percent of your maximum heart rate, which you can estimate by subtracting your age from 220.

Once you've reached that level, stop and immediately take your pulse using your index and middle finger on the carotid artery in your neck or the radial artery on the inside of your wrist. Using a stopwatch, count the number of beats in 20 seconds, then multiply by three. Make note of that number.

Remain still, either seated or standing, and take your pulse again 60 seconds later. You don't need this number to determine heart rate recovery, but it is important to know for purposes of assessing markers of physical fitness.

At 2 minutes, take your pulse again. Subtract this number from your peak heart rate during exercise to find your recovery heart rate.


Discussion

Our studies have relevance for patients who are suffering from muscle ischemia due to PAD, which affects a large number of patients and carries a significant threat of amputation in those who are not candidates for bypass or endovascular treatment (Marston et al. 2006). There are few effective medical treatments and so additional and alternative pharmacological attempts to improve perfusion and/or the response to ischemia may help attenuate the risk of limb loss in PAD patients. CQ and its derivative hydroxychloroquine (HCQ) have been suggested as potential treatments for PAD patients, and our previous studies showed similar potential protective effects in our mouse models. However, the exact mechanisms of action associated with many CQ and HCQ effects is not clear.

Recently, CQ and HCQ have been proposed as a potential protective treatment against the novel coronavirus, SARS-CoV-2, which causes COVID-19 disease (Shi et al. 2019). Since PAD affects a population primarily older than 65 years (Selvin and Erlinger 2004), this is also the population at high risk for infectious complications of SARS-CoV-2. PAD along with associated cardiovascular disease present significant risks for infected patients including contributing to the highest risk of death. Cytokine storm secondary to infectious activation of pathways including inflammasome and caspase-1/11 were shown to contribute to infectious complications of a similar coronavirus causing severe acute respiratory syndrome (SARS) in 2002–2003 (Shi et al. 2019). In this current study, as well as in our previous study, we show that CQ actually increases caspase-1 expression in muscle and this has both positive and detrimental effects. Our data suggest the need for caution using CQ and HCQ for COVID-19 patients without more fully understanding the pathways these drugs affect, particularly in end organ tissues such as liver and muscle.

Activation of both caspase-1 and caspase-11 can result in inflammatory cell death (pyroptosis) via cleavage of gasdermin D in monocytes and macrophages, which induces release of inflammatory cytokines (e.g. IL1β) and danger signals (Kayagaki et al. 2015) (Van Opdenbosch et al. 2014). However, in non-immune cells such as hepatocytes caspase-1/11 activation is protective in ischemic injury and promotes cell survival pathways such as autophagy (Sun et al. 2017b). Our data here suggest myocytes and hepatocytes share autophagy as an alternative function for caspase-1/11, with neither cell type being a major producer of caspase-1/11-mediated cytokines, IL1β and IL18, and both having excellent regenerative capacities.

Autophagy is likely to play multiple roles in recovery from muscle injury (Mammucari et al. 2008). Many studies suggest that autophagy is likely protective in skeletal muscle, preventing atrophy, and maintaining muscle mass (Masiero and Sandri n.d.). In inducible knockout mice lacking muscle-specific autophagy associated gene Atg7, muscle tissue was not protected from denervation-induced atrophy (Masiero and Sandri n.d.). CQ is known to inhibit autophagy by preventing autophagosome fusion with lysosomes, and it also effects lysosomal pH (Gallagher et al. 2017). Knowing the likely protective effect of autophagy on muscle, we were initially surprised by our previous finding that CQ resulted in less fat replacement in muscle tissue, suggesting protection rather than increased injury (Xu et al. 2018). Fat replacement and fibrosis may result from inflammation, and since CQ is known to be anti-inflammatory (Park et al. 2019) we hypothesized that CQ would reduce inflammatory markers, including those associated with inflammasome signaling, such as caspase-1. Instead, we found that CQ increased caspase-1 expression, cleavage and activity in C2C12 mouse myoblasts without increasing cell death (Xu et al. 2018). We therefore wondered whether caspase-1, which we knew can also induce autophagy and cellular protection (Cao et al. 2019) was influenced or influencing CQ effects in muscle related to autophagy, understanding that the effects would likely be both linked and complex. As caspase-1KO mice were not available to us, we used caspase1/11KO mice understanding the limitations of also knocking out caspase-11. We originally hypothesized that CQ-mediated increased caspase-1 in skeletal muscle would be protective, and that these protective effects of CQ would therefore be absent in caspase1/11KO mice. Our results demonstrated a more complex picture, with mixed effects of CQ on ischemic skeletal muscle, some of which were dependent on caspase-1/11 signaling, and some of which were independent.

In our previous report, we found that CQ disrupted autophagic flux resulting in accumulation of LC3IIB expression indicative of autophagosome formation, as well as decreased autophagic consumption of p62/SQTM (Xu et al. 2018). In our current study, CQ predictably resulted in an increase in autophagosomes in muscle, and also increased caspase-1 expression, including in between myofibers where capillaries and arterioles are found (Henning et al. 2019). In contrast to our hypothesis of protective effects of CQ in ischemic skeletal muscle, CQ reduced perfusion recovery after 21 days in WT mice but not caspase-1/11KO mice. Perfusion recovery in the murine model of hindlimb ischemia is dependent on arteriogenesis and angiogenesis (Carmeliet 2000 Buschmann and Schaper 2000) suggesting CQ effects on perfusion were caspase-1/11-dependent. Others have shown that inhibition of caspase-1 is associated with improved perfusion in a mouse hind-limb ischemia model, strengthening the idea that a CQ-induced increase in caspase-1 might ultimately be detrimental to perfusion (Lopez-Pastrana et al. 2015). We did not assess endothelial caspase-1 levels, and it is possible that these are important in the reperfusion effects of CQ. Further studies will be needed to elucidate the cell type responsible.

In other ways, however, our hypothesis of CQ protection was supported by our data. CQ reduced fat replacement and fibrosis in ischemic skeletal muscle in WT mice, with CQ effects dependent on caspase1/11 signaling in ischemic muscle at least in regards to histologic recovery. Additionally, CQ resulted in smaller myocytes in WT mice but not caspase1/11KO mice compared with PBS controls, which were potentially reflected in the fusion ability of MuSC (Ganassi et al. 2018), which was notably diminished in both CQ and caspase1/11KO mice. Decreased myofiber size may also reflect myofiber typing differences, and our data suggested a significant role for caspase-1/11 in determining fiber type after ischemic injury. Specifically, loss of caspase-1/11 signaling resulted in the near absence of slow twitch fibers, which was partially reversed by the addition of CQ. This is the first report describing skeletal muscle fiber-typing dependency on the presence of caspase1/11 signaling and is an intriguing finding that will lead to future studies.

Our fiber-typing suggested that caspase-1/11KO mice lacked slow twitch fibers except in the presence of CQ, and these data were supported peak force measurements after tetanic stimulation (von Roth et al. 2013). CQ resulted in significantly lower peak force during tetanic stimulation in caspase-1/11KO mice, but not in WT mice. Preservation of slow twitch fibers is optimal for sustained exercise like maintenance of posture, and walking (Askew et al. 2005) and these are the main fibers affected in muscular dystrophies (Lloyd et al. 2019 Ciciliot et al. 2013). More study is required to understand if there are therapeutic benefits of preserving one fibertype over the other in ischemic disease, but our data clearly show potential effects of autophagy on fibertype and downstream functionality.

Different myofiber types have different metabolic profiles, and as caspase-1 has been shown to degrade glycolytic enzymes (Shao et al. 2007), this may have played a role in the differences seen in our model. Our studies were performed on tibialis anterior which is predominantly fast-twitch and glycolytic. Indeed, most of the regenerating fibers in WT stained positively for fast-twitch specific myosin heavy chain. However, addition of CQ in the caspase-1/11KO mice was associated with increased in slow twitch fibers over the baseline in the KO mice, which may indicate protective effects of caspase-1/11 for preserving slow twitch fibers. Differences in fiber-typing between WT and KO mice, matched metabolic status of MuSC in our model. Both CQ and absence of caspase-1/11 reduced parameters associated with mitochondrial respiration, which suggests damaged or malfunctioning mitochondria unable to be removed by mitochondrial autophagy.

Our study has some important limitations. The murine hind-limb ischemia model is not a perfect model of PAD which is a chronic disease that takes many years to develop. There are some elements that may be similar physiologically, in that mice undergoing FAL develop a robust collateral network, and may thus experience intermittent episodes of ischemia/reperfusion similar to patients. We have optimized ways to harvest muscle satellite cells from patients with PAD and are evaluating the effects of CQ/caspase-1 signaling on those cells for a more relevant dataset. Additionally, we performed the FAL on relatively younger, and exclusively male mice which is not an adequate reflection of the population of people who suffer from PAD. This was done because we have noted gender-based variability in responses to FAL in mice in past experiments. These differences would be very interesting to pursue in the future, particularly because potential gender-specific effects of CQ in ischemic muscle is clinically relevant patients with PAD are not only older and but also include both genders. These variables will be areas of future study in our laboratory.


Anderson, L. et al. Exercise-based cardiac rehabilitation for coronary heart disease. Cochrane Database of Systematic Reviews. Issue 1, 1–209 (2016).

Yusuf, S., Reddy, S., Ounpuu, S. & Anand, S. Global burden of cardiovascular diseases: Part I: general considerations, the epidemiologic transition, risk factors, and impact of urbanization. Circulation. 104, 2746–53 (2001).

Smith, S. C. Jr. et al. A report of the american college of cardiology/american heart association task force on practice guidelines. J Am Coll Cardiol. 37, 2215–39 (2001).

Pan, Y. L., Tan, Y., Li, B. & Li, X. D. Efficacy of high-dose rosuvastatin preloading in patients undergoing percutaneous coronary intervention: a meta-analysis of fourteen randomized controlled trials. Lipids Health Dis. 14, 97 (2015).

Herrmann, J. Peri-procedural myocardial injury: 2005 update. Eur Heart J. 26, 2493–519 (2005).

Zhang, Y., Ma, X. J. & Shi, D. Z. Effect of Trimetazidine in Patients Undergoing Percutaneous Coronary Intervention: A Meta-Analysis. Plos One. 10, e0137775 (2015).

Zhou, X. & Chen, J. C. Is treatment with trimetazidine beneficial in patients with chronic heart failure? Plos One. 9, e94660 (2014).

Gao, D., Ning, N., Niu, X., Hao, G. & Meng, Z. Trimetazidine: a meta-analysis of randomised controlled trials in heart failure. Heart. 97, 278–86 (2011).

Lavie, C. J. et al. Exercise and the Cardiovascular System: Clinical Science and Cardiovascular Outcomes. Circ Res. 117, 207–19 (2015).

Buttar, H. S., Li, T. & Ravi, N. Prevention of cardiovascular diseases: Role of exercise, dietary interventions, obesity and smoking cessation. Exp Clin Cardiol. 10, 229–49 (2005).

Balady, G. J. et al. Referral, enrollment, and delivery of cardiac rehabilitation/secondary prevention programs at clinical centers and beyond: a presidential advisory from the American Heart Association. Circulation. 124, 2951–60 (2011).

Smith, S. C. Jr. et al. AHA/ACCF secondary prevention and risk reduction therapy for patients with coronary and other atherosclerotic vascular disease: 2011 update: a guideline from the American Heart Association and American College of Cardiology Foundation. J Am Coll Cardiol. 58, 2432–46 (2011).

Perk, J. et al. European guidelines on cardiovascular disease prevention in clinical practice. Int J Behav Med. 19, 403–88 (2012).

Uchiyama, M., Jin, X., Yin, E., Shimokawa, T. & Niimi, M. Treadmill exercise induces murine cardiac allograft survival and generates regulatory T cell. Transpl Int. 28, 352–62 (2015).

DeWeerdt, S. Activity is the best medicine. Nature. 475, S16–7 (2011).

He, C. et al. Exercise-induced BCL2-regulated autophagy is required for muscle glucose homeostasis. Nature. 481, 511–5 (2012).

Belardinelli, R., Georgiou, D., Cianci, G. & Purcaro, A. Randomized, controlled trial of long-term moderate exercise training in chronic heart failure: effects on functional capacity, quality of life, and clinical outcome. Circulation. 99, 1173–82 (1999).

Fletcher, G. F. et al. Exercise standards for testing and training: a scientific statement from the American Heart Association. Circulation. 128, 873–934 (2013).

Yamamoto, S., Hotta, K., Ota, E., Mori, R. & Matsunaga, A. Effects of resistance training on muscle strength, exercise capacity, and mobility in middle-aged and elderly patients with coronary artery disease: A meta-analysis. J Cardiol. 68, 125–34 (2016).

Cohen, J. Statistical power analysis for the behavioral sciences. 2nd edn, Chapter 8 the analysis of variance and covariance, 273–274 (Lawrence Erlbaum Associates, 1988).

Higgins, P. J. et al. Cochrane Handbook for Systematic Reviews of Interventions (ver5.1.0) Available from: http://handbook.cochrane.org/front_page.htm. (Accessed: 1th January 2016) (2011).

Higgins, P. J. et al. Cochrane Handbook for Systematic Reviews of Interventions (ver5.1.0). Available from: http://handbook.cochrane.org/front_page.htm. (Accessed: 1th January 2016) (2008).

Wu, X. H., Su, Y. Y., Zhang, C. X. & Mao, X. Q. Effect of Rehabilitation Therapy on Cardiovascular Events and Quality of Life in Patients with Coronary Heart Disease undergoing PCI. China’s health care nutrition. 9, 92–93 (2013).

Hofman-bang, C. et al. Two-year results of a controlled study of residential rehabilitation for patients treated with percutaneous transluminal coronary angioplasty. Eur Heart J. 20, 1465–74 (1999).

Liu, Z. H. Real-time exercise therapy on the prognosis of patients with coronary heart disease percutaneous coronary intervention postoperative clinical evaluation. Chin J Gerontol. 20, 5765–5766 (2015).

Belardinelli, R. et al. Exercise training intervention after coronary angioplasty: the ETICA trial. J Am Coll Cardiol. 37, 1891–900 (2001).

Mei, J. et al. Effects of Early Exercise Prescription on Myocardial Infarction Patients’ Rehabilitation and Restenosis after Stent Implantation plus Percutaneous Transluminal Coronary Angioplasty. Nurs J Chin PLA. 26, 11–13 (2009).

Cui, F. et al. Effects of rehabilitation training on exercise tolerance of patients with coronary heart disease after percutaneous coronary intervention. Chin J Phys Med Rehabil. 28, 177–179 (2006).

Higgins, P. J., Thompson, S. G., Deeks, J. J. & Altman, D. G. Measuring inconsistency in meta-analyses. BMJ. 327, 557–60 (2003).

Isaksen, K., Morken, I. M., Munk, P. S. & Larsen, A. I. Exercise training and cardiac rehabilitation in patients with implantable cardioverter defibrillators: a review of current literature focusing on safety, effects of exercise training, and the psychological impact of programme participation. Eur J Prev Cardiol. 19, 804–812 (2012).

Gupta, R., Sanderson, B. K. & Bittner, V. Outcomes at one-year follow-up of women and men with coronary artery disease discharged from cardiac rehabilitation: what benefits are maintained? J Cardiopulm Rehabil Prev. 27, 11–8 (2007).

Jahnke, R., Larkey, L., Rogers, C., Etnier, J. & Lin, F. A comprehensive review of health benefits of qigong and tai chi. Am J Health Promot. 24, e1–e25 (2010).

Sesso, H. D., Paffenbarger, R. S. Jr. & Lee, I. M. Physical activity and coronary heart disease in men: The Harvard Alumni Health Study. Circulation. 102, 975–80 (2000).

Ades, P. A. & Coello, C. E. Effects of exercise and cardiac rehabilitation on cardiovascular outcomes. Med Clin North Am. 84, 251–65 (2000).

Stewart, K. J., Badenhop, D., Brubaker, P. H., Keteyian, S. J. & King, M. Cardiac rehabilitation following percutaneous revascularization, heart transplant, heart valve surgery, and for chronic heart failure. Chest. 123, 2104–11 (2003).

Hansson, G. K., Robertson, A. K. & Soderberg-Naucler, C. Inflammation and atherosclerosis. Annu Rev Pathol. 1, 297–329 (2006).


  • At least 150 minutes of moderate aerobic exercise like brisk walking or 75 minutes of rigorous exercise like running (or an equivalent mix of both) every week. It&rsquos fine to break up exercise into smaller sessions as long as each one lasts at least 10 minutes.
  • Strength-training that works all major muscle groups&mdashlegs, hips, back, abdomen, chest, shoulders, and arms&mdashat least two days a week. Strength training may involve lifting weights, using resistance bands, or exercises like push-ups and sit-ups, in which your body weight furnishes the resistance.

The guidelines for aerobic exercise are considered safe for most pregnant women. The CDC makes no recommendation for strength training. It&rsquos a good idea to review your exercise plan with your doctor.


What Affects Your Recovery Time

The recovery period after exercise is considered the time from the end of your workout until your subsequent return to a recovered state, according to an April 2017 review in the ​Journal of Applied Physiology​.

One way to monitor recovery time after exercise is to use a heart rate monitor. According to the journal review, this monitor allows you to observe the heart rate variability that can occur after your heart rate is elevated during exercise and while it drops to a pre-exercise state during recovery.

In addition to your heart rate after a bout of exercise, the review authors suggest using other recovery markers as well, such as fatigue, irritability and an inability to attain higher heart rates during future training. As to how long this takes, the authors point out that recovery for the cardiovascular system can take minutes to hours.

Jodi Rund, a certified trainer for Fit Body Boot Camp in West Palm Beach, Florida, says several factors affect your recovery time, such as genetic predispositions, age, stress, current health (are you fighting an infection?) and your overall physical condition. However, the biggest factors, she says, are sleep, nutrition, exercise frequency and exercise intensity.


The power of the placebo effect

Your mind can be a powerful healing tool when given the chance. The idea that your brain can convince your body a fake treatment is the real thing — the so-called placebo effect — and thus stimulate healing has been around for millennia. Now science has found that under the right circumstances, a placebo can be just as effective as traditional treatments.

"The placebo effect is more than positive thinking — believing a treatment or procedure will work. It's about creating a stronger connection between the brain and body and how they work together," says Professor Ted Kaptchuk of Harvard-affiliated Beth Israel Deaconess Medical Center, whose research focuses on the placebo effect.

Placebos won't lower your cholesterol or shrink a tumor. Instead, placebos work on symptoms modulated by the brain, like the perception of pain. "Placebos may make you feel better, but they will not cure you," says Kaptchuk. "They have been shown to be most effective for conditions like pain management, stress-related insomnia, and cancer treatment side effects like fatigue and nausea."

Does the placebo effect mean failure or success?

For years, a placebo effect was considered a sign of failure. A placebo is used in clinical trials to test the effectiveness of treatments and is most often used in drug studies. For instance, people in one group get the tested drug, while the others receive a fake drug, or placebo, that they think is the real thing. This way, the researchers can measure if the drug works by comparing how both groups react. If they both have the same reaction — improvement or not — the drug is deemed not to work.

More recently, however, experts have concluded that reacting to a placebo is not proof that a certain treatment doesn't work, but rather that another, non-pharmacological mechanism may be present.

How placebos work is still not quite understood, but it involves a complex neurobiological reaction that includes everything from increases in feel-good neurotransmitters, like endorphins and dopamine, to greater activity in certain brain regions linked to moods, emotional reactions, and self-awareness. All of it can have therapeutic benefit. "The placebo effect is a way for your brain to tell the body what it needs to feel better," says Kaptchuk.

But placebos are not all about releasing brainpower. You also need the ritual of treatment. "When you look at these studies that compare drugs with placebos, there is the entire environmental and ritual factor at work," says Kaptchuk. "You have to go to a clinic at certain times and be examined by medical professionals in white coats. You receive all kinds of exotic pills and undergo strange procedures. All this can have a profound impact on how the body perceives symptoms because you feel you are getting attention and care."

Give yourself a placebo

Placebos often work because people don't know they are getting one. But what happens if you know you are getting a placebo?

A 2014 study led by Kaptchuk and published in Science Translational Medicine explored this by testing how people reacted to migraine pain medication. One group took a migraine drug labeled with the drug's name, another took a placebo labeled "placebo," and a third group took nothing. The researchers discovered that the placebo was 50% as effective as the real drug to reduce pain after a migraine attack.

The researchers speculated that a driving force beyond this reaction was the simple act of taking a pill. "People associate the ritual of taking medicine as a positive healing effect," says Kaptchuk. "Even if they know it's not medicine, the action itself can stimulate the brain into thinking the body is being healed."

How can you give yourself a placebo besides taking a fake pill? Practicing self-help methods is one way. "Engaging in the ritual of healthy living — eating right, exercising, yoga, quality social time, meditating — probably provides some of the key ingredients of a placebo effect," says Kaptchuk.

While these activities are positive interventions in their own right, the level of attention you give can enhance their benefits. "The attention and emotional support you give yourself is often not something you can easily measure, but it can help you feel more comfortable in the world, and that can go a long way when it comes to healing."

The placebo sweet spot


Image: © PhonlamaiPhoto/Thinkstock

A study published online Oct. 27, 2016, by PLOS Biology may have identified what goes on in the brain during a placebo effect. Researchers used functional magnetic resonance imaging to scan the brains of people with chronic pain from knee osteoarthritis. Then everyone was given a placebo and had another brain scan. The researchers noticed that those who felt pain relief had greater activity in the middle frontal gyrus brain region, which makes up about one-third of the frontal lobe.


Watch the video: Διαδικτυακό Συνέδριο ΕΛΙΟΣ-ΕΕΜΜΟ: Φθινοπωρινές Ημέρες Οστεοπόρωσης: Ανάλυση Περιστατικού 7 (September 2022).


Comments:

  1. Virr

    I seem to have read it carefully, but did not understand

  2. Finnobarr

    Sorry for interfering, I would like to suggest another solution



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