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Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle.
Fiorenza, M, Gunnarsson, TP, Hostrup, M, Iaia, FM, Schena, F, Pilegaard, H, Bangsbo, J
The Journal of physiology. 2018;596(14):2823-2840
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Endurance exercise stimulates mitochondrial biogenesis in skeletal muscles, a crucial adaptive protective mechanism against various metabolic disorders. Mitochondrial biogenesis is a process that involves the expansion of mitochondrial volume and changes in mitochondrial composition. Continuous moderate‐intensity exercise (CM) may lead to mild but prolonged metabolic disturbances, and low‐volume intense intermittent exercise regimes such as repeated‐sprint (RE) and speed endurance (SE) exercises may lead to a distinct degree of metabolic stress. This randomised counter-balanced crossover trial included 12 healthy trained men to investigate the effect of RE and SE exercise and high‐volume CM on metabolic perturbations and its impact on the regulation of molecular response stimulating mitochondrial biogenesis in human skeletal muscle. Compared to CM, PGC‐1α mRNA (Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (PGC‐1α) mRNA) showed elevation in response to RS and SE exercises in well-trained subjects, and this was associated with high accumulation of muscle lactate, greater decline in muscle pH and elevated plasma adrenaline levels. Elevated metabolic perturbations lead to enhanced mitochondrial biogenesis-related mRNA responses. SE was associated with a greater increase in the PGC‐1α mRNA and severe metabolic stress. SE and CM elevated exercise-induced signalling and mRNA content of genes controlling mtDNA. Further robust research is required to elucidate the role of metabolic stress in initiating mitochondrial biogenesis in skeletal muscles in response to acute exercise, regulating genes modulating mtDNA transcription and mitochondrial remodelling dynamics. However, healthcare professionals can use the results of this study to understand that low-volume high-intensity exercise programmes can promote mitochondrial biogenesis in skeletal muscles in healthy trained men and have a similar effect to that of high-volume moderate-intensity exercise programmes.
Abstract
KEY POINTS Low-volume high-intensity exercise training promotes muscle mitochondrial adaptations that resemble those associated with high-volume moderate-intensity exercise training. These training-induced mitochondrial adaptations stem from the cumulative effects of transient transcriptional responses to each acute exercise bout. However, whether metabolic stress is a key mediator of the acute molecular responses to high-intensity exercise is still incompletely understood. Here we show that, by comparing different work-matched low-volume high-intensity exercise protocols, more marked metabolic perturbations were associated with enhanced mitochondrial biogenesis-related muscle mRNA responses. Furthermore, when compared with high-volume moderate-intensity exercise, only the low-volume high-intensity exercise eliciting severe metabolic stress compensated for reduced exercise volume in the induction of mitochondrial biogenic mRNA responses. The present results, besides improving our understanding of the mechanisms mediating exercise-induced mitochondrial biogenesis, may have implications for applied and clinical research that adopts exercise as a means to increase muscle mitochondrial content and function in healthy or diseased individuals. ABSTRACT The aim of the present study was to examine the impact of exercise-induced metabolic stress on regulation of the molecular responses promoting skeletal muscle mitochondrial biogenesis. Twelve endurance-trained men performed three cycling exercise protocols characterized by different metabolic profiles in a randomized, counter-balanced order. Specifically, two work-matched low-volume supramaximal-intensity intermittent regimes, consisting of repeated-sprint (RS) and speed endurance (SE) exercise, were employed and compared with a high-volume continuous moderate-intensity exercise (CM) protocol. Vastus lateralis muscle samples were obtained before, immediately after, and 3 h after exercise. SE produced the most marked metabolic perturbations as evidenced by the greatest changes in muscle lactate and pH, concomitantly with higher post-exercise plasma adrenaline levels in comparison with RS and CM. Exercise-induced phosphorylation of CaMKII and p38 MAPK was greater in SE than in RS and CM. The exercise-induced PGC-1α mRNA response was higher in SE and CM than in RS, with no difference between SE and CM. Muscle NRF-2, TFAM, MFN2, DRP1 and SOD2 mRNA content was elevated to the same extent by SE and CM, while RS had no effect on these mRNAs. The exercise-induced HSP72 mRNA response was larger in SE than in RS and CM. Thus, the present results suggest that, for a given exercise volume, the initial events associated with mitochondrial biogenesis are modulated by metabolic stress. In addition, high-intensity exercise seems to compensate for reduced exercise volume in the induction of mitochondrial biogenic molecular responses only when the intense exercise elicits marked metabolic perturbations.
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Adipose tissue inflammation in breast cancer survivors: effects of a 16-week combined aerobic and resistance exercise training intervention.
Dieli-Conwright, CM, Parmentier, JH, Sami, N, Lee, K, Spicer, D, Mack, WJ, Sattler, F, Mittelman, SD
Breast cancer research and treatment. 2018;168(1):147-157
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Obese breast cancer patients have double the mortality compared to non-obese patients. This is thought to be mediated by low grade inflammation of the adipose (fat) tissue. The main type of immune cells involved in the process are called adipose tissue macrophages (ATMs), of which there are two types: M1 and M2 ATMs, with the M2 ATMs having a mostly anti-inflammatory effect, whilst the M1 ATMs are more pro-inflammatory and are thought to promote cancer growth and recurrence. This 16-week randomised pilot study assessed whether exercise can positively influence adipose tissue inflammation in breast cancer survivors. Participants were randomised to either an exercise (EX) group, who had three supervised exercise sessions per week with a combination of aerobic and resistance exercise, or a control (CON) group. Outcome measures included body composition, blood biomarkers for systemic inflammation and adipose tissue biopsies which were analysed for tissue inflammatory markers, including M1 and M2 ATMs. The EX group had significant improvements in body weight and composition, as well as in metabolic blood parameters (including those for lipid and glucose metabolism) and inflammatory markers, whilst the CON group experienced a worsening of these parameters. The EX participants also had a decrease in the pro-inflammatory M1 ATMs and an increase in the anti-inflammatory M2 ATMs. The authors state that the results were not only statistically, but also clinically significant. The authors conclude that moderate-to-vigorous intensity resistance and aerobic exercise can improve adipose tissue inflammation in obese breast cancer survivors.
Abstract
PURPOSE Obesity is a leading modifiable contributor to breast cancer mortality due to its association with increased recurrence and decreased overall survival rate. Obesity stimulates cancer progression through chronic, low-grade inflammation in white adipose tissue, leading to accumulation of adipose tissue macrophages (ATMs), in particular, the pro-inflammatory M1 phenotype macrophage. Exercise has been shown to reduce M1 ATMs and increase the more anti-inflammatory M2 ATMs in obese adults. The purpose of this study was to determine whether a 16-week exercise intervention would positively alter ATM phenotype in obese postmenopausal breast cancer survivors. METHODS Twenty obese postmenopausal breast cancer survivors were randomized to a 16-week aerobic and resistance exercise (EX) intervention or delayed intervention control (CON). The EX group participated in 16 weeks of supervised exercise sessions 3 times/week. Participants provided fasting blood, dual-energy X-ray absorptiometry (DXA), and superficial subcutaneous abdominal adipose tissue biopsies at baseline and following the 16-week study period. RESULTS EX participants experienced significant improvements in body composition, cardiometabolic biomarkers, and systemic inflammation (all p < 0.03 vs. CON). Adipose tissue from EX participants showed a significant decrease in ATM M1 (p < 0.001), an increase in ATM M2 (p < 0.001), increased adipose tissue secretion of anti-inflammatory cytokines such as adiponectin, and decreased secretion of the pro-inflammatory cytokines IL-6 and TNF- α (all p < 0.055). CONCLUSIONS A 16-week aerobic and resistance exercise intervention attenuates adipose tissue inflammation in obese postmenopausal breast cancer survivors. Future large randomized trials are warranted to investigate the impact of exercise-induced reductions in adipose tissue inflammation and breast cancer recurrence.
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Presurgical weight loss affects tumour traits and circulating biomarkers in men with prostate cancer.
Demark-Wahnefried, W, Rais-Bahrami, S, Desmond, RA, Gordetsky, JB, Hunter, GR, Yang, ES, Azrad, M, Frugé, AD, Tsuruta, Y, Norian, LA, et al
British journal of cancer. 2017;117(9):1303-1313
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Obesity is a risk factor for 13 different cancers and a recent meta-analysis has shown increased weight to be associated with biochemical recurrence in men with prostate cancer. However, few studies have explored whether presurgical intentional weight loss results in improved prostate cancer outcomes. The aim of this trial was to explore the efficacy of weight loss among overweight and obese men with prostate cancer. Forty participants were randomised to either the presurgical weight loss intervention group or control arm, and changes in weight, body composition, quality of life, tumour biology and biomarkers were recorded. This study found that intentional weight loss caused mixed effects on tumour proliferation and gene expression. Based on these results, the authors recommend that more research is needed before effectively recommending presurgical weight loss among overweight men with prostate cancer.
Abstract
BACKGROUND Obesity is associated with aggressive prostate cancer. To explore whether weight loss favourably affects tumour biology and other outcomes, we undertook a presurgical trial among overweight and obese men with prostate cancer. METHODS This single-blinded, two-arm randomised controlled trial explored outcomes of a presurgical weight loss intervention (WLI) that promoted ∼1 kg per week loss via caloric restriction and increased physical activity (PA). Forty overweight/obese men with clinically confirmed prostate cancer were randomised to the WLI presurgery or to a control arm; changes in weight, body composition, quality-of-life, circulating biomarkers, gene expression, and immunohistochemical markers in tumour and benign prostatic tissue were evaluated. RESULTS The study period averaged 50 days. Mean (s.d.) change scores for the WLI vs control arms were as follows: weight: -4.7 (3.1) kg vs -2.2 (4.4) kg (P=0.0508); caloric intake: -500 (636) vs -159 (600) kcal per day (P=0.0034); PA: +0.9 (3.1) vs +1.7 (4.6) MET-hours per day (NS); vitality: +5.3 (7.l4) vs -1.8 (8.1) (P=0.0491); testosterone: +55.1 (86.0) vs -48.3 (203.7) ng dl-1 (P=0.0418); sex hormone-binding globulin: +14.0 (14.6) vs +1.8 (7.6) nmol l-1 (P=0.0023); and leptin: -2.16 (2.6) vs -0.03 (3.75) (P=0.0355). Follow-up Ki67 was significantly higher in WLI vs control arms; median (interquartile range): 5.0 (2.5,10.0) vs 0.0 (0.0,2.5) (P=0.0061) and several genes were upregulated, for example, CTSL, GSK3B, MED12, and LAMC2. CONCLUSIONS Intentional weight loss shows mixed effects on circulating biomarkers, tumour gene expression, and proliferative markers. More study is needed before recommending weight loss, in particular rapid weight loss, among men with prostate cancer.
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The Effects of 52 Weeks of Soccer or Resistance Training on Body Composition and Muscle Function in +65-Year-Old Healthy Males--A Randomized Controlled Trial.
Andersen, TR, Schmidt, JF, Pedersen, MT, Krustrup, P, Bangsbo, J
PloS one. 2016;11(2):e0148236
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Aging adversely impacts muscular structure and function, and sedentary subjects have an increased risk of developing lifestyle-related disease. Physical activity in aging subjects has repeatedly been shown to counteract these adverse effects, and in particular, the health benefits of recreational soccer have been investigated. The aim of this randomised trial was to examine the long-term effects of soccer training compared to resistance training on a range of musculo-skeletal structural and functional variables. Twenty-seven healthy elderly males aged 63-74 were randomly assigned to participate in either a soccer training group, a resistance training group or inactive control group for 52-weeks. Participants performed a one-hour training session twice per week for the first 16 weeks, and three times a week for the following 36 weeks. This study showed that 52 weeks of regular soccer training lead to decreases in BMI, improved skeletal muscle anti-oxidative potential, and favourably altered glucose control when compared with resistance training in elderly men.
Abstract
The effects of 52 weeks of soccer or resistance training were investigated in untrained elderly men. The subjects aged 68.1±2.1 yrs were randomised into a soccer (SG; n = 9), a resistance (RG; n = 9) and a control group (CG; n = 8). The subjects in SG and RG, respectively, trained 1.7±0.3 and 1.8±0.3 times weekly on average during the intervention period. Muscle function and body composition were determined before and after 16 and 52 weeks of the intervention period. In SG, BMI was reduced by 1.5% and 3.0% (p<0.05) after 16 and 52 weeks, respectively, unchanged in RG and 2% higher (p<0.05) in CG after 52 weeks of the intervention period. In SG, the response to a glucose tolerance test was 16% lower (p<0.05) after 16 wks, but not after 52 wks, compared to before the intervention period, and unchanged in RG and CG. In SG, superoxide dismutase-2 expression was 59% higher (p<0.05) after 52 wks compared to before the intervention period, and unchanged in RG and CG. In RG, upper body lean mass was 3 and 2% higher (p<0.05) after 16 and 52 wks, respectively, compared to before the intervention period, and unchanged in SG and CG. In RG, Akt-2 expression increased by 28% (p<0.01) and follistatin expression decreased by 38% (p<0.05) during the 52-wk intervention period, and was unchanged in SG and CG. Thus, long-term soccer training reduces BMI and improves anti-oxidative capacity, while long-term resistance training impacts muscle protein enzyme expression and increases lean body mass in elderly men. Trial Registration: ClinicalTrials.gov: NCT01530035.