Ageing leads to a progressive loss of muscle function (MF) and quality (MQ: muscle strength (MS)/lean muscle mass (LM)). Power training and protein (PROT) supplementation have been proposed as efficient interventions to improve MF and MQ. Discrepancies between results appear to be mainly related to the type and/or dose of proteins used. The present study aimed at determining whether or not mixed power training (MPT) combined with fast-digested PROT (F-PROT) leads to greater improvements in MF and MQ in elderly men than MPT combined with slow-digested PROT (S-PROT) or MPT alone. Sixty elderly men (age 69 (sd 7) years; BMI 18-30 kg/m2) were randomised into three groups: (1) placebo + MPT (PLA; n 19); (2) F-PROT + MPT (n 21) and (3) S-PROT + MPT (n 20) completed the intervention. LM, handgrip and knee extensor MS and MQ, functional capacity, serum metabolic markers, skeletal muscle characteristics, dietary intake and total energy expenditure were measured. The interventions consisted in 12 weeks of MPT (3 times/week; 1 h/session) combined with a supplement (30 g:10 g per meal) of F-PROT (whey) or S-PROT (casein) or a placebo. No difference was observed among groups for age, BMI, number of steps and dietary intake pre- and post-intervention. All groups improved significantly their LM, lower limb MS/MQ, functional capacity, muscle characteristics and serum parameters following the MPT. Importantly, no difference between groups was observed following the MPT. Altogether, adding 30 g PROT/d to MPT, regardless of the type, does not provide additional benefits to MPT alone in older men ingesting an adequate (i.e. above RDA) amount of protein per d.

Introduction: Normal aging is often associated with a decline of muscle mass (MM), strength (MS) and quality (MQ: MS/MM), leading to functional incapacities. This aging-related deterioration of muscles may involve a decreased protein intake. Mixed power training has been recently shown to induce positive effects on MM, MS and MQ. However, to our knowledge, no study has examined if muscle adaptations following mixed power training could be influenced by the daily amount of protein ingested in elderly men. Methods: Twenty-one men completed the intervention and were divided into 2 groups based on their usual protein intake: PROT 1.1-(< 1.1 g.kg(-1).d(-1) [n = 10; 73 +/- 3 years]) and PROT 1.2+ (> 1.2 g.kg(-1).d(-1)[n = 11; 73 +/- 3 years]). Body composition (DXA: lean and fat masses), MS (1-maximal repetition on leg-press and handgrip strength), MQ (MS/body mass and MS/lower limb lean mass), functional capacities (Short Physical Performance Battery/Senior Fitness Test), dietary intake (3-day food record) and energy expenditure (accelerometer; 7 days) were measured. Mixed power training intervention consisted in power and functional exercises (12 weeks; 3 times/week; 1 h/session). Results: Lower limb MS increase in the PROT 1.2+ group was greater from that of the PROT 1.1-group when normalized to lower limbs lean mass (p = 0.036). In addition, a trend for greater gain in lower limb MS normalized to body mass (p = 0.053) was observed in the PROT 1.2+. Conclusion: To optimize mixed power training effects on muscle function, healthy older men should ingest daily at least 1.2 g.kg(-1).d(-1) of protein. These beneficial effects of a higher usual protein intake were observed especially for MQ, which is one of the best predictors of functional capacities in older adults.

Sarcopenia is an important component of frailty and its diagnosis could lead to specific intervention to improve functional capacity in older adults. There are several clinical oriented criteria definitions of sarcopenia available in literature for case finding based on low gait speed and handgrip strength. These criteria may be too sensitive, mandating unnecessary body composition measures. Total protein intake is important for muscle mass maintenance but we will present evidence from the Quebec Longitudinal Study on Nutrition and Successful Aging (NuAge) Study that distribution across meals may also prevent losses. Although muscle is considered the principal site of glucose uptake and its loss to contribute to the development of insulin resistance, these assumptions have not always been verified. The method used to present muscle mass index correcting absolute mass by either height squared or weight could account for the discrepancies in establishing the relationship with insulin resistance. Data from the NuAge Study will illustrate this concept and arguments will be brought forth to propose the most appropriate method. Furthermore, several hormonal and inflammatory factors associated with insulin resistance are also responsible for loss of muscle mass, therefore creating a false relationship between insulin resistance and low muscle mass. Using data from the NuAge Study, we will show how the application of logistic regression analysis of these factors along with muscle mass index will disentangle this spurious association.

In addition to total intake, protein distribution across meals may affect sarcopenia. An even distribution further increased muscle protein synthesis compared to a skewed intake, in young adults. We studied whether this short-term result translates into long-term preservation of lean mass (LM) and muscle strength in healthy older adults of the NuAge study (827 men, 914 women). Outcomes were measured at baseline and 2-3-year follow-up. Protein intake was calculated from 6x24-h food recalls. Results: In men and women, LM declined by 2.5% and 2.0%, muscle strength by 20.0% and 18.2%, and mobility score by 6.5% and 7.8 % (P<0.05). Rates of decline were not independently affected by the quantity and distribution of protein intake. Yet, participants with more evenly distributed protein intake had higher LM and muscle strength throughout follow-up, even after controlling for confounders (P<0.05). This could translate in delaying reaching a sarcopenic threshold, affecting functionality.

BACKGROUND:Prostate cancer (pca) is the most common non-skin cancer among men in Canada and other Western countries. Increased prevalence and higher cost of newer treatments have led to a significant rise in the economic burden of pca. The objectives of the present study were to systematically review the literature on direct costs for the initial management of pca, and to examine the methodologic considerations across studies.METHODS:Bibliographic databases were systematically searched for peer-reviewed articles in English. Studies were reviewed for methodologic considerations and mean direct cost of active surveillance or watchful waiting (as/ww) and initial treatments. Direct cost was standardized to 2011 Canadian dollars.RESULTS:After a review of abstracts and full-text papers, seventeen articles met the eligibility criteria and were included in the review. Studies were published during 1992-2010. The studies reported on health care systems in the United States, France, the United Kingdom, German, Italy, and Spain. Our review identified a lack of methodologic consensus, leading to variation in direct costs between studies. Nevertheless, results indicate a significant direct cost of pca treatments.CONCLUSIONS:The existing literature lacks methodologically rigorous studies on the direct costs of pca treatments specific to publicly funded health care systems. Additional studies are required to appreciate the direct costs of newer treatments and the impact of their adoption on the growing economic burden of pca management.

Hyperaminoacidaemia attenuates glucose disposal during hyperinsulinaemic clamps in healthy lean individuals, an effect thought to be mediated by negative feedback on insulin signalling, downstream of the mammalian target of rapamycin (mTOR) signalling pathway. This has been interpreted as amino acids causing insulin resistance in healthy people, and contributing to it in type 2 diabetes. However, the effect of hyperaminoacidaemia on glucose disposal in type 2 diabetic individuals remains to be determined.

Although protein is usually ignored when considering insulin resistance, we have shown resistance of protein concurrent with glucose metabolism in men with type 2 diabetes during a hyperinsulinaemic clamp at euglycaemia and fasting aminoacidaemia. We hypothesised that this resistance is even worse during conditions that simulate the postprandial state, when anabolism should be maximal.

To assess the accuracy of trans-rectal ultrasound (TRUS) in the estimation of prostate volume (PV) by comparing prostate gland measurements from diagnostic TRUS with the actual dimensions and weight of prostate specimens after radical prostatectomy. Data from 150 prostate cancer patients who underwent radical prostatectomy were analyzed. Dimensions, volumes and weights from fresh specimens were systemically recorded. PVs based on TRUS and specimen measurements were calculated using two different formulas: ellipsoid (length x height x width x [π/6]) and bullet-shaped (length x height x width x [π/4.8]). Estimative of PV by digital rectal examination (DRE) was also recorded in all cases. Clinical-pathological features (clinical stage, PSA, Gleason score, margins and extracapsular extension) were also analyzed. We considered errors superior to 10% in any measurements as being significant. The mean volumes and standard deviations based on surgical specimen weight, DRE, TRUS-ellipsoid formula and TRUS-bullet formula were 49.3 cc (±16.5), 38.7 cc (±11.1), 39.1 cc (±15.9) and 48.9 cc (±19.9), respectively. Considering for all analyses, the tolerable error as 10% above or below, DRE under- and overestimated the PV in 66.7% and 12.0%, respectively. TRUS, using the traditional ellipsoid formula, under- and overestimated the PV in 71.3% and 6.7%, respectively and TRUS, using the bullet shaped formula, under- and overestimate the PV in 38.7% and 30.0%, respectively. The overall rate of "precise" measurements was 21.3%, 22.0% and 31.3% for DRE, TRUS (ellipsoid) and TRUS (bullet). No statistical significant correlation was found between TRUS measurements errors and clinical-pathological features. Prostate measurements obtained using TRUS are often inaccurate. However, the bullet-shaped formula demonstrated better volume measurement accuracy. Caution is necessary when using PV estimated by TRUS as main criteria to select prostate cancer patients for brachytherapy implant.

Aim Type 2 diabetes is characterized by hyperglycaemia, delayed gastric emptying and a blunted response of gut hormones during feeding that may modulate satiety. We hypothesized that it is associated with more hunger when treated by medication. Methods We studied nine type 2 diabetic men (A1C: 6.7 +/- 0.3%, waist circumference: 104 +/- 4 cm) after an overnight fast, during 5 h in response to a 2.88 MJ breakfast, twice, in a crossover design, with or without antihyperglycaemic agents. Satiety ratings, thermic effect of meal, gastric emptying, plasma concentrations of gut peptides, leptin, insulin and substrates and intake from a subsequent buffet were determined. Results With medication, fasting and postprandial plasma glucose levels were lower but area under the curve (AUC) did not vary vs. without medication. Gastric emptying was shortened, branched chain amino acids (BCAA) AUC and thermic effect were lower, and postprandial glucagon-like peptide-1 (GLP-1) and peptide tyrosine tyrosine (PYY3-36) were maintained at higher levels beyond 4 h. Correlations were significant between duration of diabetes and fasting ghrelin (r = 0.779, p = 0.013) and peak insulin (r = -0.769, p = 0.016), 5-h postmeal ghrelin and peak glucose (r = 0.822, p = 0.007), 5-h glucose and GLP-1 (r = -0.788, p = 0.012), and 5-h hunger scores and energy intake at buffet (r = 0.828, p = 0.006). Without medication, fullness scores correlated with BCAA levels. Visual analogue scale scores, ghrelin and leptin levels did not differ between studies. Conclusions The decrease in factors associated with postprandial satiety with treatment is counterbalanced by higher GLP-1 and PYY3-36. Medication may normalize the link between perception of hunger and subsequent food intake.

Aim: Type 2 diabetes is characterized by hyperglycaemia, delayed gastric emptying and a blunted response of gut hormones during feeding that may modulate satiety. We hypothesized that it is associated with more hunger when treated by medication.Methods: We studied nine type 2 diabetic men (A1C: 6.7 ± 0.3%, waist circumference: 104 ± 4 cm) after an overnight fast, during 5 h in response to a 2.88 MJ breakfast, twice, in a crossover design, with or without antihyperglycaemic agents. Satiety ratings, thermic effect of meal, gastric emptying, plasma concentrations of gut peptides, leptin, insulin and substrates and intake from a subsequent buffet were determined.Results: With medication, fasting and postprandial plasma glucose levels were lower but area under the curve (AUC) did not vary vs. without medication. Gastric emptying was shortened, branched chain amino acids (BCAA) AUC and thermic effect were lower, and postprandial glucagon‐like peptide‐1 (GLP‐1) and peptide tyrosine tyrosine (PYY3–36) were maintained at higher levels beyond 4 h. Correlations were significant between duration of diabetes and fasting ghrelin (r = 0.779, p = 0.013) and peak insulin (r = −0.769, p = 0.016), 5‐h postmeal ghrelin and peak glucose (r = 0.822, p = 0.007), 5‐h glucose and GLP‐1 (r = −0.788, p = 0.012), and 5‐h hunger scores and energy intake at buffet (r = 0.828, p = 0.006). Without medication, fullness scores correlated with BCAA levels. Visual analogue scale scores, ghrelin and leptin levels did not differ between studies.Conclusions: The decrease in factors associated with postprandial satiety with treatment is counterbalanced by higher GLP‐1 and PYY3–36. Medication may normalize the link between perception of hunger and subsequent food intake.

We have shown a greater increase in protein anabolism, associated with lower glucose infusion and utilization rates, in a fed steady-state clamp (Hyper-3: insulin 798±74 pM, glycemia 7.9±0.0 mM, branched-chain amino acids [BCAA] 740±10 μM, n=9). These differences occurred when compared with a Hyper-1 clamp (insulin 450±22 pM, glycemia 5.5±0.0 mM, and BCAA 359±8 μM, n=10). Since endogenous insulin contributed to the higher than Hyper-1 postprandial hyperinsulinemia in Hyper-3 (C-peptide increased 5 fold), we performed a Hyper-3PC (pancreatic clamp) with octreotide and exogenous insulin, glucagon and growth hormone infusions. This suppressed C-peptide 46%, achieved insulinemia of 524 pM, with identical hyperglycemia and BCAA (n=9). Comparisons were made among these protocols in the three groups of men of similar age (26±1 yr), BMI (22±1 kg/m2) and fat-free mass (FFM, 60±1 kg). Protein turnover (in pmol/kgFFM^min) was estimated by primed-continuous infusion of 13C-leucine and that of glucose (in mg/kg•min) by 3H-glucose. Amino acid infusion rates were identical in Hyper-3PC (130±4) and Hyper-3 (142±9), and greater than in Hyper-1 (49±2 mg/min, P<0.01). Suppression of leucine endogenous Ra (protein breakdown) was −0.86±0.05, -0.64±0.11 and −0.43±0.06 respectively (Hyper-3PC > Hyper-1, P<0.001). Stimulation of nonoxidative Rd (synthesis) was 0.40±0.05, 0.78±0.06 and 0.39±0.07 (Hyper-3PC and Hyper-1 < Hyper-3, P<0.05). Increase in net balance (anabolism) was 1.26±0.06, 1.42±0.09 and 0.82±0.03 (both P<0.001 vs. Hyper-1). Leucine oxidation was markedly increased to 1.5±0.1 and 1.6±0.1 vs. 0.6±0.03, (P<0.001). Glucose infusion rate was 5.4±0.3, 7.1±0.6 and 8.3±6 (Hyper-3PC P<0.05 vs. both). Endogenous production was inhibited similarly, but utilization increased to only 5.6±0.3, vs. 7.0±0.5 and 8.0±5 (P<0.05), such that M (Rd/insulin) was 0.82±0.07 and 0.65±0.10, vs. 1.25±0.10 (mg/mm•pM, p<0.01). Therefore, with the postprandial hyperinsulinemia of Hyper-3PC, similar marked stimulation of anabolism occurred as with Hyper-3 clamps, though by somewhat different effects on synthesis vs. breakdown, perhaps related to different portal insulinemia. Postprandial hyperaminoacidemia to levels that exceed the maximum capacity for incorporation into protein synthesis results in their oxidation, that could be responsible for a physiological (not necessarily an insulin resistance-mediated) attenuation of the increased glucose uptake. As these findings were found in healthy, young, insulin-sensitive subjects, they may represent normal physiological mechanisms to maintain glucose and amino acid homeostasis, when provided in excess of immediate needs.

Increased circulating methylarginines (MA) have been linked to the metabolic syndrome to explain endothelial dysfunction and cardiovascular disease risk. Proteins that contain MA are regulatory and release them during catabolism. We hypothesised that increased protein turnover in insulin-resistant states contributes to an increase in circulating MA.