Muscle hypertrophy in cancer patients and survivors via strength training. A meta-analysis and meta-regression.

BACKGROUND: Muscle wasting has a negative effect on treatment toxicity and cancer prognosis. Resistance training appears to be a promising approach to counteract the loss of muscle mass. METHODS: Pubmed, Cochrane Library, SportDiscus and CINAHL. Randomized controlled resistance training trials with cancer survivros where eligible if lean body mass (LBM) or muscle mass were assessed. RESULTS: A total of 34 trials were included into the primary analysis. Compared to the control individuals, the intervention groups show a superiority in LBM of 0.85 kg (95 % CI = 0.26-1.43, p = .004). Isolated, the participants in the intervention groups show an increase in LBM of 0.51 kg (95 % CI = -0.05-1.06, p = .072); the control groups displayed a decrease of -0.59 kg (95 % CI= -1.04 to 0.06, p = .078). Supervision displayed an mediating role. CONCLUSIONS: Resistance training can counteract the loss of muscle mass in cancer patients. Especially in a supervised setting.

A systematic review of home-based dietary interventions during radiation therapy for cancer.

PURPOSE: Our objectives are to assess (1) the acceptability and feasibility of dietary interventions for patients undergoing radiation therapy (RT), and (2) the impact of dietary interventions on patient reported outcomes, toxicities, and survival. METHODS: A PICOS/PRISMA/MOOSE selection protocol was used to include articles that evaluate adding dietary interventions to patients receiving RT. Acceptability was defined as (# accepting/# approached); feasibility was (# completing/# approached). Patient-reported outcomes were reported based on questionnaires used in each study and survival was measured from the date of diagnosis until death in each study. Level of evidence was assessed with Center for Evidence-Based Medicine (CEBM) criteria. RESULTS: Sixteen articles were included; among these, 2027 patients were approached regarding the intervention, and 1661 accepted (81.9%); of these, 1543 (92.9%) completed the prescribed diet + RT course. The most common cancers included were gynecological, head and neck, and gastrointestinal. For patients with pelvic cancers, a high fiber diet may improve diarrhea (CEBM level 1b). Enteral nutrition formula, including formulas with proteins such as L-arginine, lipids such as eicosapentaenoic acids, glucids, and ribonucleotides, may help prevent of malnutrition in head and neck cancer patients undergoing RT (level 2b). Vitamin C and ß-carotene may reduce of xerostomia in head and neck cancer patients; however, the studies evaluating these vitamins included vitamin E, which increases all-cause mortality (level 2b). No dietary intervention for cancer patients receiving RT has been shown to improve survival. CONCLUSION: There are limited data to support safe and efficacious use of dietary interventions during RT.

Cancer- and Chemotherapy-Induced Musculoskeletal Degradation.

Mobility in advanced cancer patients is a major health care concern and is often lost in advanced metastatic cancers. Erosion of mobility is a major component in determining quality of life but also starts a process of loss of muscle and bone mass that further devastates patients. In addition, treatment options become limited in these advanced cancer patients. Loss of bone and muscle occurs concomitantly. Advanced cancers that are metastatic to bone often lead to bone loss (osteolytic lesions) but may also lead to abnormal deposition of new bone (osteoblastic lesions). However, in both cases there is a disruption to normal bone remodeling and radiologic evidence of bone loss. Many antitumor therapies can also lead to loss of bone in cancer survivors. Bone loss releases cytokines (TGFß) stored in the mineralized matrix that can act on skeletal muscle and lead to weakness. Likewise, loss of skeletal muscle mass leads to reduced bone mass and quality via mechanical and endocrine signals. Collectively these interactions are termed bone-muscle cross-talk, which has garnered much attention recently as a prime target for musculoskeletal health. Pharmacological approaches as well as nutrition and exercise can improve muscle and bone but have fallen short in the context of advanced cancers and cachexia. This review highlights our current knowledge of these interventions and discusses the difficulties in treating severe musculoskeletal deficits with the emphasis on improving not only bone mass and muscle size but also functional outcomes. © 2019 The Authors. JBMR Plus published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

Bone resorption and bone metastasis risk.

Breast cancer tumors have a tendency to metastasize to the bone. After development of a bone metastasis, the median survival time is 40 months. Currently, little is known about the modifiable risk factors for developing bone metastases in women diagnosed with breast cancer. One possible modifiable risk factor is increased bone resorption. Increased bone resorption is caused by an imbalance between osteoblasts and osteoclasts favoring osteoclast-driven bone resorption. Osteoclast activity results in the release of growth factors from the bony matrix that are requirement for successful breast cancer tumor cell proliferation within the bone. Mice studies have shown that mice that have been genetically engineered to have higher bone mineral density, and thus lower bone resorption, have a decreased incidence of bone metastases. Alternatively, mice genetically engineered to have lower bone mineral density or increased bone resorption have a higher incidence of bone metastases. In human studies, antiosteoporotic drugs have been shown to decrease osteoclast activity and prevent bone metastases. These studies suggest that increased osteoclast activity, which results in low bone mineral density, may be a modifiable risk factor for developing bone metastases in women with breast cancer. Women undergoing chemotherapy for breast cancer develop low bone mineral density in response to the direct effects of chemotherapeutic drugs on bone cells-including osteoclasts, osteoblasts, and osteocytes-and through the decrease in circulating estrogen as a result of chemotherapy-induced ovarian dysfunction. Therefore, it is important for future studies to determine the risk of developing bone metastases associated with increasing bone resorption as measured by low or decreasing bone mineral density in women diagnosed with breast cancer, as well as to determine the best intervention(s) to promote a balance between osteoclasts and osteoblasts to favor osteoblast activity during chemotherapy treatment.

Exercise and chemotherapy-induced amenorrhea.

Chemotherapy-induced amenorrhea (CIA) is the temporary or permanent loss of menses experienced by premenopausal women undergoing chemotherapy treatment for cancer. Two possible mechanisms through which chemotherapy induces CIA have been identified: systemic endothelial dysfunction, resulting in decreased blood flow to the ovaries, and increased oxidative stress within the ovaries, both of which are proposed to lead to apoptosis of follicles. Endothelial dysfunction in ovarian arteries in women undergoing or who have undergone chemotherapy treatment is characterized by prothrombotic changes and thickening of the vascular wall. These changes result in occlusion of the blood vessels. Oxidative stress is increased and antioxidants decreased in the ovaries secondary to chemotherapy drugs, specifically cyclophosphamide. It is hypothesized that low to moderate intensity aerobic exercise during chemotherapy may prevent these changes and lessen the risk for developing CIA in premenopausal women. Low to moderate intensity aerobic exercise has been shown to improve endothelial function and blood flow in patients with cardiovascular disease-a disease state characterized by endothelial dysfunction and for which patients who have undergone chemotherapy are at increased risk. In mice, moderate intensity aerobic exercise has been shown to decrease the amount of oxidative stress within the ovaries, and in humans, chronic aerobic exercise has been shown to increase antioxidant production systemically. This hypothesis should be tested in both a mouse model, using sedentary and exercising mice treated with chemotherapy drugs that commonly result in CIA, as well as a human model to determine the effects of low to moderate intensity aerobic exercise on ovarian function in premenopausal women undergoing chemotherapy.