Exercise training-induced effects on the abdominal subcutaneous adipose tissue phenotype in humans with obesity.

Rodent studies have indicated that physical exercise may improve adipose tissue function. We investigated the effects of a 12-wk supervised, progressive exercise training program on adipocyte morphology and abdominal subcutaneous adipose tissue function in metabolically well-phenotyped subjects with obesity. Men with obesity ( n = 21) participated in a 12-wk supervised, progressive, combined exercise training program consisting of aerobic exercise (30 min at 70% of maximal power output 2 times/wk) and resistance exercise (3 × 10 repetitions at 60% of 1 repeated maximum 1 time/wk), with adjustment of exercise intensity every 4 wk. At baseline and after intervention, abdominal subcutaneous adipose tissue biopsies were collected to determine 1) adipocyte morphology, 2) gene expression of markers for lipolysis, inflammation, browning, adipokines, and mitochondrial biogenesis/function, 3) protein expression of mitochondrial oxidative phosphorylation (OXPHOS) complexes, and 4) ex vivo basal and ß2-adrenergic stimulated lipolysis. The exercise training program, which increased maximal aerobic capacity ( P < 0.001) and muscle strength ( P < 0.001), slightly reduced adipose tissue mass (~0.7 kg, P = 0.021) but did not affect abdominal subcutaneous adipocyte size ( P = 0.744), adipose tissue gene expression of markers for mitochondrial biogenesis and function, browning, lipolysis, inflammation and adipokines, total OXPHOS protein content ( P = 0.789), or ß2-adrenergic sensitivity of lipolysis ( P = 0.555). A 12-wk supervised, progressive exercise training program did not alter abdominal subcutaneous adipocyte morphology and adipose tissue gene/protein expression of markers related to adipose tissue function or ß2-adrenergic sensitivity of lipolysis in male subjects with obesity. NEW & NOTEWORTHY Studies that investigated the effects of exercise training on adipose tissue function in well-phenotyped humans are scarce. We demonstrate that 12 wk of supervised exercise training improved physical fitness and peripheral insulin sensitivity but did not alter abdominal subcutaneous adipocyte morphology, adipose tissue gene and protein expression of markers related to adipose tissue function, or ß2-adrenergic receptor-mediated lipolysis in men with obesity. A prolonged and/or more intense training program may be required to improve human adipose tissue function.

Effect of increased protein intake on renal acid load and renal hemodynamic responses.

Increased protein intake versus maltodextrin intake for 4 weeks lowers blood pressure. Concerns exist that high-protein diets reduce renal function. Effects of acute and 4-week protein intake versus maltodextrin intake on renal acid load, glomerular filtration rate and related parameters were compared in this study. Seventy-nine overweight individuals with untreated elevated blood pressure and normal kidney function were randomized to consume a mix of protein isolates (60 g/day) or maltodextrin (60 g/day) for 4 weeks in energy balance. Twenty-four-hour urinary potential renal acid load (uPRAL) was compared between groups. A subgroup (maltodextrin N = 27, protein mix N = 25) participated in extra test days investigating fasting levels and postprandial effects of meals supplemented with a moderate protein- or maltodextrin-load on glomerular filtration rate, effective renal plasma flow, plasma renin, aldosterone, pH, and bicarbonate. uPRAL was significantly higher in the protein group after 4 weeks (P ≤ 0.001). Postprandial filtration fraction decreased further after the protein-supplemented breakfast than after the maltodextrin-supplemented breakfast after 4 weeks of supplementation (P ≤ 0.001). Fasting and postprandial levels of glomerular filtration rate, effective renal plasma flow, renin, aldosterone, angiotensin-converting enzyme, pH and bicarbonate did not differ between groups. In conclusion, 4 weeks on an increased protein diet (25% of energy intake) increased renal acid load, but did not affect renal function. Postprandial changes, except for filtration fraction, also did not differ between groups. These data suggest that a moderate increase in protein intake by consumption of a protein mix for 4 weeks causes no (undesirable) effects on kidney function in overweight and obese individuals with normal kidney function.

Dietary proteins improve endothelial function under fasting conditions but not in the postprandial state, with no effects on markers of low-grade inflammation.

Endothelial dysfunction (ED) and low-grade inflammation (LGI) have a role in the development of CVD. The two studies reported here explored the effects of dietary proteins and carbohydrates on markers of ED and LGI in overweight/obese individuals with untreated elevated blood pressure. In the first study, fifty-two participants consumed a protein mix or maltodextrin (3×20 g/d) for 4 weeks. Fasting levels and 12 h postprandial responses of markers of ED (soluble intercellular adhesion molecule 1 (sICAM), soluble vascular cell adhesion molecule 1 (sVCAM), soluble endothelial selectin and von Willebrand factor) and markers of LGI (serum amyloid A, C-reactive protein and sICAM) were evaluated before and after intervention. Biomarkers were also combined into mean Z-scores of ED and LGI. The second study compared 4 h postprandial responses of ED and LGI markers in forty-eight participants after ingestion of 0·6 g/kg pea protein, milk protein and egg-white protein. In addition, postprandial responses after maltodextrin intake were compared with a protein mix and sucrose. The first study showed significantly lower fasting ED Z-scores and sICAM after 4 weeks on the high-protein diet (P≤0·02). The postprandial studies found no clear differences of ED and LGI between test meals. However, postprandial sVCAM decreased more after the protein mix compared with maltodextrin in both studies (P≤0·04). In conclusion, dietary protein is beneficial for fasting ED, but not for fasting LGI, after 4 weeks of supplementation. On the basis of Z-scores, postprandial ED and LGI were not differentially affected by protein sources or carbohydrates.

Differential effects of proteins and carbohydrates on postprandial blood pressure-related responses.

Diet composition may affect blood pressure (BP), but the mechanisms are unclear. The aim of the present study was to compare postprandial BP-related responses to the ingestion of pea protein, milk protein and egg-white protein. In addition, postprandial BP-related responses to the ingestion of maltodextrin were compared with those to the ingestion of sucrose and a protein mix. We hypothesised that lower postprandial total peripheral resistance (TPR) and BP levels would be accompanied by higher plasma concentrations of nitric oxide, insulin, glucagon-like peptide 1 (GLP-1) and glucagon. On separate occasions, six meals were tested in a randomised order in forty-eight overweight or obese adults with untreated elevated BP. Postprandial responses of TPR, BP and plasma concentrations of insulin, glucagon, GLP-1 and nitrite, nitroso compounds (RXNO) and S-nitrosothiols (NO(x)) were measured for 4 h. No differences were observed in TPR responses. Postprandial BP levels were higher after the ingestion of the egg-white-protein meal than after that of meals containing the other two proteins (P≤ 0·01). The ingestion of the pea-protein meal induced the highest NO(x) response (P≤ 0·006). Insulin and glucagon concentrations were lowest after the ingestion of the egg-white-protein meal (P≤ 0·009). Postprandial BP levels were lower after the ingestion of the maltodextrin meal than after that of the protein mix and sucrose meals (P≤ 0·004), while postprandial insulin concentrations were higher after the ingestion of the maltodextrin meal than after that of the sucrose and protein mix meals after 1-2 h (P≤ 0·0001). Postprandial NO(x), GLP-1 and glucagon concentrations were lower after the ingestion of the maltodextrin meal than after that of the protein mix meal (P≤ 0·008). In conclusion, different protein and carbohydrate sources induce different postprandial BP-related responses, which may be important for BP management. Lower postprandial BP levels are not necessarily accompanied by higher NO(x), insulin, glucagon or GLP-1 responses.

Blood pressure decreases more after high-carbohydrate meals than after high-protein meals in overweight adults with elevated blood pressure, but there is no difference after 4 weeks of consuming a carbohydrate-rich or protein-rich diet.

The replacement of dietary carbohydrates with proteins can lower blood pressure (BP), but the mechanisms remain unclear. This randomized, double-blind, parallel-group study aimed to compare 12-h postprandial sympathetic and hemodynamic responses after high-protein (HP) meals and high-carbohydrate (HC) meals. Fifty-two men and women with untreated elevated BP were tested on d 1 and after 4 wk of supplementation [3 × 20 g protein (HP) or maltodextrin (HC) per day]. No between-group differences were found in postprandial plasma norepinephrine on d 1 and at wk 4. On d 1, postprandial mean arterial pressure (MAP) decreased more in the HC group than in the HP group (P = 0.002). This difference was not present at 4 wk, because the postprandial decline in MAP tended to become larger in the HP group after 4 wk of supplementation (P = 0.07). On both test days, postprandial total peripheral resistance tended to decrease more in the HC group (P < 0.08). After 4 wk of supplementation, cardiac output tended to increase more in the HC group (P = 0.08). In conclusion, ingestion of an HP diet induced a smaller decrease in BP on d 1 than did ingestion of an HC diet. This difference disappeared after 4 wk due to a more pronounced decrease in BP in the HP group after 4 wk than on d 1. These findings cannot explain the BP-lowering effect ascribed to dietary proteins.

The role of dietary protein in blood pressure regulation.

PURPOSE OF REVIEW: Despite a considerable amount of research, the blood pressure (BP) lowering effect of dietary proteins is still not fully established. This review discusses the most recent findings on BP lowering of dietary proteins and protein sources, the possible mechanisms and the safety of increasing protein intake. RECENT FINDINGS: Recent short-term, strictly controlled, randomized clinical trials show a BP lowering effect of increased protein intake. Longer-term trials, however, show inconsistent results. Because all recent trials exchanged carbohydrates, and not fats, for proteins, the question remains whether potential beneficial effects of high protein diets are due to increased protein intake or decreased carbohydrate intake. No clear differences between plant protein and animal protein are found in observational studies, and trials comparing plant versus animal protein are lacking. Different protein sources may lower BP via different mechanisms, which might explain divergent findings. Potential harms of high protein diets are not confirmed in recent trials in healthy persons. SUMMARY: Increasing dietary protein intake or decreasing carbohydrate intake within reasonable limits may be beneficial for BP. The most and least beneficial protein sources still need to be determined.

Protein supplementation lowers blood pressure in overweight adults: effect of dietary proteins on blood pressure (PROPRES), a randomized trial.

BACKGROUND: Dietary protein intake may help to manage blood pressure (BP) and prevent complications associated with elevated BP. OBJECTIVE: The objective of this study was to determine whether 4 wk of increased protein intake (∼25% compared with ∼15% of energy intake that isoenergetically replaces carbohydrate intake) lowers office and daytime BP compared with increased carbohydrate intake. DESIGN: A randomized, double-blind, parallel study compared consumption of 3 × 20 g protein/d (20% pea, 20% soy, 30% egg, and 30% milk-protein isolate) with 3 × 20 g maltodextrin/d. Protein or maltodextrin were isoenergetically substituted for a sugar-sweetened drink. Primary outcomes were office and daytime BP. A total of 99 men and women [age range: 20-70 y; BMI (in kg/m²): 25-35] with untreated elevated BP (BP ≥130/85 and <160/100 mm Hg) were randomly assigned. Ninety-four completers (51 subjects in the maltodextrin group, 43 subjects in the protein group) were included in the analyses. RESULTS: Office systolic blood pressure (SBP) and diastolic blood pressure (DBP) were 4.9 ± 1.7 mm Hg (P = 0.005) and 2.7 ± 1.3 mm Hg (P = 0.05) lower, respectively, in the protein group. Daytime SBP was 4.6 ± 1.7 mm Hg lower in the protein group (P = 0.006), whereas daytime DBP did not differ between groups (P = 0.37). Urinary sodium excretion was higher in the maltodextrin group (P = 0.004). CONCLUSION: Increased protein intake, at the expense of maltodextrin, lowers BP in overweight adults with upper-range prehypertension and grade 1 hypertension. This trial was registered at www.trialregister.nl as NTR 1362.