Summary Of Mechanisms By Which Exercise Is Beneficial in Alleviating Kidney Disease
Feb 07, 2023
There is growing evidence that exercise improves chronic inflammation, cardiovascular health, muscle, and bone in adults with chronic kidney disease (CKD), kidney failure, or kidney transplant patients. However, few physicians have focused on the underlying mechanisms behind these benefits. Some scholars believe that understanding the mechanism by which exercise affects patients with kidney disease will benefit the formulation of exercise prescriptions and improve the safety and efficacy of exercise prescriptions. In addition, these mechanisms may identify new therapeutic targets and opportunities for future research.
Click on bioflavonoids tablets for kidney disease
On January 17, 2023, Nature review of Nephrology published a review by scholars from many countries, which elaborated on the mechanism by which exercise is beneficial to kidney disease, and showed that exercise is not only an adjuvant therapy for kidney disabuse, but its mechanism may also Assist in the development of new drugs.
Chronic inflammation
Accumulation of uremic toxins can lead to immune dysfunction manifested by immunosuppression, decreased reactivity to antigens (including vaccination), and chronic inflammation. Immune dysfunction is closely associated with decreased renal function and increases the risk of cardiovascular disease (CVD) and infection in CKD patients. Notably, CVD and infection are the two leading causes of death in patients with kidney disease. Therefore, controlling chronic inflammation is beneficial to the ultimate prognosis of CKD patients.
Currently, studies have found that regular exercise can help reduce inflammatory markers in non-dialysis CKD patients. For example, in one study, it was found that in CKD patients stimulated with the superantigen staphylococcal enterotoxin B, brisk walking for 30 minutes five times a week for 6 months could reduce the levels of CD4 and CD8, while those who did not receive exercise intervention CD4 and CD8 levels did not change significantly. In addition, IL-6 decreased and IL-10 increased in the brisk walking group, but there was no change in the ratio of IL-6 to IL-10 in the patients who did not exercise.
Clinical data also support regular exercise in dialysis patients. A study of 38 hemodialysis patients showed that after 6 months of follow-up, patients who exercised regularly (n = 22) had significantly more pro-inflammatory cells and an inflammatory state compared with patients who exercised irregularly (n = 1Improvementsment, such as TNF, I,L-1β and IL-6. It is worth noting that the T cell levels of patients in the irregular exercise group decreased significantly compared with baseline, while the T cell levels of patients in the regular exercise group increased significantly. This suggests that exercise reduces the inflammatory state without compromising the immune system.
It is worth noting that some studies have found that if patients with kidney disease only insist on exercising for 2 months, their inflammation-related biological indicators will not change significantly. This suggests that exercise intervention may take at least 3 months to achieve anti-inflammatory effects. In terms of exercise intensity, moderate and high-intensity intermittent exercise is safe for kidney transplant patients, but the specific exercise intensity needs to be determined according to the patient's conditions (such as age, comorbidities, exercise history, etc.). Individualized exercise prescriptions include: Helps you exercise safely and effectively.
Overall, regular exercise improves levels of inflammatory markers in CKD patients, dialysis patients, and kidney transplant patients in several studies. Exercise improved anti-inflammatory leukocyte profiles in non-dialysis CKD patients but not in dialysis and kidney transplant patients. This may be related to the increased activity of the NRF2 pathway caused by dialysis.
Cardiovascular health
In CKD patients, the risk of CVD is much higher than the risk of renal failure, which is the main cause of death in CKD patients. VO2 max is an important independent predictor for assessing cardiovascular health and risk of all-cause mortality. In a meta-analysis of 6 studies involving a total of 512 non-dialysis CKD patients, it was found that patients with CKD stages 3b-5 had significantly lower maximal oxygen uptake than patients with CKD stages 2-3a. This study shows that the progression of CKD disease can lead to cardiovascular damage a and decline in the physical fitness of patients.
However, CKD patients who exercised regularly had higher levels of maximal oxygen uptake compared with CKD patients who were sedentary or who exercised irregularly. In addition, multiple studies worldwide have found increased nitric oxide release and bioavailability in CKD patients who exercise regularly. This will improve vasodilation, arteriosclerosiand s, lower systolic and diastolic blood pressure, and benefit the cardiovascular health of CKD patients.
Studies have shown tintradialyticysis exercise will help improve hypertension, left ventricular mass, and hyperphosphatemia in dialysis patients. However, the reduction of blood phosphorus may be related to the increase of blood flow rate by exercise, which can help increase the total amount of dialysis, thereby removing more phosphate. The CYCLE-HD study showed that 6 months of regular exercise was associated with decreased LV mass and was associated with beneficial LV remodeling. Patients in the regular exercise group had reduced myocardial inflammation and fibrosis compared with those in the irregular exercise group. The above two factors are important causes of arrhythmia and sudden cardiac death. In short, exercise is a non-drug intervention for the prevention of arrhythmias and sudden cardiac death in CKD patients.
However, the CYCLE-HD study also found that if the exercise intensity of patients is too low (lower than that of cardiac rehabilitation patients), ideal benefits cannot be obtained. However, patients with low-intensity exercise may still gain certain benefits through mechanisms such as mRNA release, but more research is needed on the specific benefits.
In general, a certain intensity of regular exercise is beneficial to improve the release and bioavailability of nitric oxide, hypertension, left ventricular mass, hyperphosphatemia, arrhyt,hmia and sudden cardiac death in patients with CKD.
Dyslipidemia and insulin resistance
Dyslipidemia and insulin resistance are hallmarks of CKD. Most CKD patients have high levels of triglycerides, low-density lipoprotein cholesterol (LDL-C), and low levels of high-density lipoprotein cholesterol (HDL-C). This is due to impaired lipoprotein metabolism. In early CKD patients, high triglyceride and LDL-C levels were associated with increased mortality risk, whereas in advanced CKD patients, lower serum cholesterol was associated with higher mortality. This paradox may be related to systemic inflammation and oxidative stress.
Insulin resistance is an early feature of CKD and affects nearly all patients with renal failure. Several studies have shown that insulin resistance is an independent risk marker for CVD in CKD patients. However, some studies did not get the same results.
Early studies have shown that moderate-intensity (40%–50% of maximal oxygen uptake) exercise for prolonperiodstime can be tolerated in hemodialysis patients without adverse cardiovascular and metabolic responses. At the same time, long-term regular exercise for 6 months can improve patients' dyslipidemia and insulin resistance. However, the conclusions of some studies do not support this view. Therefore, more studies are needed to elucidate the effect of exercise on dyslipidemia and insulin resistance in CKD patients.
Sarcopenia
Loss of muscle strength, mass, and function is known as sarcopenia and is common in patients with CKD. Sarcopenia can occur in patients with early CKD, which is related to the increased rate of proteolysis in CKD patients. An increased rate of proteolysis inhibits skeletal muscle growth and accelerates muscle atrophy. As CKD progresses, metabolic acidosis, uremic toxin accumulation, insulin resistance, inflammation, dysregulation of mRNA expression, and decreased physical activity increase, which together accelerate muscle atrophy. However, available data suggest that exercise can delay muscle wasting and even increase muscle mass in CKD patients. However, the relevant mechanism remains to be fully elucidated.
Existing data indicate that CKD patients have increased expression of inflammatory cytokines, E3-linked enzyme messenger RNA (mRNA), and increased antioxidant capacity after a single bout of exercise. However, a single bout of exercise can also cause impaired satellite cell activation (satellite cells involved in muscle fiber repair) and metabolic resistance. The long-term effects of exercise on CKD patients include decreased myostatin-related mRNA expression, decreased inflammatory response, improved muscle anabolic response, increased IGF-1 mRNA expression, and increased muscle mass. Effects on muscle mitochondria. However, this still shows that whether it is a single exercise or long-term exercise, there are certain benefits to the muscles of CKD patients, but relatively speaking, long-term regular exercise is more helpful to CKD patients.
Bone health
In addition to the filtering function, a healthy kidney also shoulders the function of hormone regulation. After renal function deterioration, the regulation and metabolism of vitamin D, parathyroid hormone (PTH), fibroblast growth factor (FG,F23) and Klotho protein are disturbed, resulting in problems with the transformation, volume, gr,owth or strength of bones and may cause vascular and other soft tissue abnormalities in calcification. The above disorder is known as Chronic Kidney Disease-Mineral and Bone Disorders (CKD-MBD).
Although physical activity is beneficial for reducing the risk of osteoporosis and fractures, not all exercise is beneficial for CKD-MBD. Currently, some research shows that impact-load training (such as skipping rope and jumping) and progressive resistance training (muscle training) can stimulate boand ne, restore growth and bone turnover.
Osteogenesis is a complex process associated with multiple pathways, of which Wnt-β-Catenin is the most prominent one. The activation of this pathway is caused by the transmission of Wnt ligands to β-Catenin through low-density lipoprotein receptors. After Wnt combines with β-Catenin, it will induce gene transcription and promote osteoblast differentiation and bone cell formation. This pathway is negatively regulated by other endogenous secretion inhibitors whose secretion is associated with mechanical loading. In short, more impact load training will down-regulate the secretion of endogenous secretion inhibitors and promote the formation of osteocytes; less impact load training will promote the secretion of endogenous secretion inhibitors and inhibit the formation of osteocytes.
As renal function declines, the Wnt-β-Catenin pathway is downregulated, while sclerostin levels are elevated. Downregulation of sclerostin promotes bone formation. A study of 193 hemodialysis patients showed that dynamic resistance training (3 times a week) before each dialysis session for 6 months reduced sclerostin levels and increased bone density. Another preliminary study of 13 hemodialysis patients found that after 8 weeks of dialysis resistance training, patients had no change in sclerostin levels but increased bone basic phosphate levels, suggesting increased activity of osteoblasts. Another study showed that 6 months of aerobic exercise did not improve the levels of bone metabolism markers in overweight/obese CKD patients.
In conclusion, exercise can promote bone health and reduce the impact of CKD-MBD in CKD patients. However, not all types of exercise contribute to bone formation, or improve CKD-MBD, and further research and clinical practice should pay attention to the impact of exercise types on CKD patients.
for more information:ali.ma@wecistanche.com
