Combined Effects of Physical Activity and Diet on Cancer Patients: A Systematic Review and Meta-Analysis.

BACKGROUND: The purpose of our systematic review was to examine the effects of any physical activity/exercise intervention combined with any diet/nutrition intervention on any biological/biochemical index, quality of life (QoL), and depression in breast, lung, colon and rectum, prostate, stomach, and liver cancer patients and/or cancer survivors. METHODS: A systematic review and meta-analysis were undertaken, using PRISMA guidelines and the Cochrane Handbook. The systematic review protocol can be found in the PROSPERO database; registration number: CRD42023481429. RESULTS: We found moderate-quality evidence that a combined intervention of physical activity/exercise and nutrition/diet reduced body mass index, body weight, fat mass, insulin, homeostatic model assessment for insulin resistance, C-reactive protein, triglycerides, and depression, while it increased high-density lipoprotein, the physical component of QoL, and general functional assessment of cancer therapy. CONCLUSIONS: We conclude that a combined intervention of physical activity/exercise and diet/nutrition may decrease body weight, fat mass, insulin levels, and inflammation, and improve lipidemic profile, the physical component of QoL, and depression in cancer patients and survivors. These outcomes indicate a lower risk for carcinogenesis; however, their applicability depends on the heterogeneity of the population and interventions, as well as the potential medical treatment of cancer patients and survivors.

Recovery during Successive 120-min Football Games: Results from the 120-min Placebo/Carbohydrate Randomized Controlled Trial.

PURPOSE: This study aimed to examine the recovery kinetics (i.e., time-dependent changes) of performance-related variables between two 120-min male football games performed 3 d apart with and without carbohydrate supplementation. METHODS: Twenty male players (20 ± 1 yr; body fat, 14.9% ± 5.1%; maximal oxygen consumption, 59.4 ± 3.7 mL·kg -1 ·min -1 ) participated in two 120-min football games (G1, G2) according to a randomized, two-trial, repeated-measures, crossover, double-blind design. Participants received carbohydrate/placebo supplements during recovery between games. Field activity was monitored during the games. Performance testing and blood sampling were performed before and at 90 and 120 min of each game. Muscle biopsies were collected at baseline and at 90 and 120 min of G1 and pre-G2. RESULTS: Compared with G1, G2 was associated with reduced total distance (10,870 vs 10,685 m during 90 min and 3327 vs 3089 m during extra 30 min; P = 0.007-0.038), average (6.7 vs 6.2 km/h during extra 30-min game-play; P = 0.007) and maximal speed (32.2 vs 30.2 km/h during 90 min and 29.0 vs 27.9 km/h during extra 30 min; P < 0.05), accelerations/decelerations ( P < 0.05), and mean heart rate ( P < 0.05). Repeated sprint ability ( P < 0.001), jumping ( P < 0.05), and strength ( P < 0.001) performance were compromised before and during G2. Muscle glycogen was not restored at G2 baseline ( P = 0.005). Extended game-play reduced lymphocyte, erythrocyte counts, hematocrit, hemoglobin, reduced glutathione ( P < 0.05) and increased delayed onset of muscle soreness, creatine kinase activity, blood glycerol, ammonia, and protein carbonyls ( P < 0.05) before and during G2. Pax7 + ( P = 0.004) and MyoD + cells ( P = 0.019) increased at baseline G2. Carbohydrate supplementation restored performance and glycogen, reduced glycerol and delayed onset of muscle soreness responses, and increased leukocyte counts and Pax7 + and MyoD + cells. CONCLUSIONS: Results suggest that extended football games induce a prolonged recovery of performance, which may be facilitated by carbohydrate supplementation during a congested game fixture.

Recovery kinetics following sprint training: resisted versus unresisted sprints.

PURPOSE: To determine the recovery kinetics of performance and exercise-induced muscle damage following different sprint-training protocols. METHODS: In a crossover design, ten male and female athletes (20.6 ± 2.4 years) performed 2 × (3 × 20 m: 2 min rest) and 1× (3 × 30 m: 3 min rest) of: (a) unresisted sprints (UST), (b) resisted sprints with 10% of body mass (BM) load (RST10), (c) resisted sprints with 20% BM load (RST20), against a control trial (no-training). RESULTS: Blood lactate (mmol/L) increased post-training versus pre-training in all sprint-training trials (6.7 ± 2.4 vs 1.2 ± 0.2, 5.6 ± 2.4 vs 1.3 ± 0.3, 7.3 ± 2.7 vs 1.2 ± 0.3, in UST, RST10, RST20, respectively), as did creatine kinase (U/L) 24 h, 48 h and 72 h post-training (UST: 251 ± 173, 238 ± 154, 209 ± 115 vs 155 ± 9, RST10: 252 ± 134, 240 ± 83, 218 ± 103 vs 164 ± 106; RST20: 237 ± 133, 323 ± 303, 262 ± 184 vs 179 ± 106, respectively). DOMS of knee-extensors (KE) and knee-flexors (KF) increased post-training up to 72 h in all sprint-training trials versus pre-training (ranging from 1.6 ± 1.3 to 3.8 ± 2.8 vs 1.0 ± 0, respectively). Eccentric torque (N m) of the KE of the non-dominant limb, decreased 24 h post-training versus pre-training in all sprint-training trials (UST: 249 ± 49 vs 266 ± 54; RST10: 229 ± 52 vs 273 ± 72; RST20: 253 ± 6 vs 262 ± 56), as did that of the KF of the dominant limb (UST: 135 ± 29 vs 144 ± 26; RST10: 130 ± 29 vs 140 ± 25; RST20: 139 ± 33 vs 142 ± 26). 10-m sprint-time (s) increased 48 h post-training versus pre-training (1.81 ± 0.15 vs 1.77 ± 0.11), and 30-m sprint-time increased 24 h, 48 h, 72 h post-training versus pre-training (4.35 ± 0.36, 4.40 ± 0.44, 4.33 ± 0.41 vs 4.21 ± 0.34, respectively), only in RST20. CONCLUSIONS: Unresisted and resisted sprint-training induces prolonged reduction of muscle strength (24 h), and sprinting performance (72 h), associated with prolonged increase of DOMS and CK (72 h).

Recovery kinetics following eccentric exercise is volume-dependent.

The present study compared the effect of 75 vs 150 vs 300 intensity-matched eccentric contractions on muscle damage and performance recovery kinetics. Ten healthy males participated in a randomized, cross-over study consisted of 4 experimental trials (ECC75, ECC150, ECC300 and Control - no exercise) with a 4-week washout period in-between. Performance and muscle damage, inflammatory and oxidative stress markers were evaluated at baseline, post-exercise, 24, 48 and 192 hours following each exercise protocol. Concentric and eccentric peak torque decreased similarly in ECC150 and ECC300 during the first 48 h of recovery (p < 0.05) but remained unaffected in ECC75. Countermovement jump indices decreased post-exercise and at 24 h in ECC150 and ECC300, with ECC300 inducing a more pronounced reduction (p < 0.05). Creatine kinase increased until 48 h of recovery in all trials and remained elevated up to 192 h only in ECC300 (p < 0.05). Delayed onset of muscle soreness increased, and knee-joint range of motion decreased in a volume-dependent manner during the first 48 h (p < 0.05). Likewise, a volume-dependent decline of glutathione and a rise of protein carbonyls was observed during the first 48 h of recovery (p < 0.05). Collectively, our results indicate that muscle damage and performance recovery following eccentric exercise is volume dependent, at least in lower limbs.

Safety and immunogenicity of booster immunization with 7-valent pneumococcal conjugate vaccine in children with idiopathic nephrotic syndrome.

Safety and immunogenicity of a booster dose of 7-valent pneumococcal conjugate vaccine (PCV7) were evaluated in 29 patients with idiopathic nephrotic syndrome (INS), who had been primed 12 months earlier with one dose of PCV7. PCV7 was not associated with increased risk of INS relapse (RR=0.77, p=0.8) and serotype-specific antibodies increased in all subjects at 1 month (p<0.01). The quantitative characteristics of immune response and the effect of treatment with mycophenolate mofetil and/or cyclosporine A following booster PCV7 were similar with primary response. Additional PCV7 doses could be safely given in children with INS to increase circulating antibodies above the protective threshold.

Development and validation of a PCR-based assay for the selection of patients more likely to benefit from therapeutic treatment with alkylating drugs.

WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Previous studies have indicated that the levels of DNA damage induced in peripheral blood mononuclear cells by the alkylating drugs melphalan, cisplatin and carboplatin can serve as useful biomarkers predictive of the therapeutic response of cancer patients to these drugs. WHAT THIS STUDY ADDS: In the present study we developed a quantitative PCR-based assay, for the measurement of DNA damage. The advantages of this methodology are based on: its far greater sensitivity (about 250 times) than the traditional Southern blot-based method (the detection limit is ~10-20 lesions/10(6) nucleotides from the equivalent DNA of ~8000 cells); its simplicity and speed (results obtained within ~8h); its excellent reproducibility, with a coefficient of variance of 10-15% for different DNA preparations from similarly treated cells; its requirement for only minute amounts of material, and; the avoidance of radioisotope labeling. Moreover, emphasis was given to translate basic research findings into clinical practice through the validation of this assay for prediction of clinical outcome in multiple myeloma patients. AIM: In order to develop and validate a simple, sensitive and rapid method for the quantitation of alkylating drug-induced DNA damage. METHODS: HepG2 cells and blood samples were treated with alkylating drugs (melphalan, cisplatin, carboplatin). Gene-specific damage was examined using Southern blot and a multiplex long quantitative PCR (QPCR) carried out in a 7 kb fragment (part of the p53 gene) and a 0.5 kb fragment (part of the IFN-ß1 sequence; internal standard). RESULTS: The extent of PCR amplification of a p53 fragment was inversely proportional to the treatment concentrations of all anticancer drugs examined, indicating a dose-related inhibition by the DNA adducts formed. Parallel analysis of the same samples using both Southern blot and QPCR showed that the DNA adducts measured by QPCR corresponded to the interstrand cross-links in the case of melphalan, and to total drug-induced lesions in the case of the platinum drugs. The detection limit was ~10-20 lesions/10(6) nucleotides using DNA from ~8000 cells. The method is about 250 times more sensitive than the Southern blot-based method and the reproducibility is excellent, with an intraday coefficient of variance (CV) of 5-9% and an interday CV of 4-12%. Application of the QPCR assay to ex vivo melphalan-treated peripheral blood mononuclear cells from multiple myeloma patients, showed that the positive predictive value of this assay for clinical response to melphalan therapy was 92.9%. CONCLUSION: The PCR-based assay developed in this study can be used for the selection of cancer patients more likely to benefit from therapeutic treatment with alkylating drugs.

Safety, immunogenicity and kinetics of immune response to 7-valent pneumococcal conjugate vaccine in children with idiopathic nephrotic syndrome.

Safety, immunogenicity and kinetics of 7-valent pneumococcal-conjugate vaccine (PCV7) immune response were evaluated in 33 children with idiopathic nephrotic syndrome (INS) and 16 controls. PCV7 was not associated with increased risk of relapse (RR=0.80, p=0.61). Serotype (PS)-specific antibodies increased in all subjects at 1 month (p<0.01) with inferior immunogenicity for 3/7 PS in patients on immunomodulators (p<0.02). Most patients retained protective antibodies at 12-14 months although at lower levels for 4/7 PS (p<0.08). Different PS kinetics in INS suggests antibody monitoring and revaccination when necessary for protection from pneumococcal infections.