An appreciable volume of human clinical data supports increased dietary protein for greater gains from resistance training, but not all findings are in agreement. We recently proposed "protein spread theory" and "protein change theory" in an effort to explain discrepancies in the response to increased dietary protein in weight management interventions. The present review aimed to extend "protein spread theory" and "protein change theory" to studies examining the effects of protein on resistance training induced muscle and strength gains. Protein spread theory proposed that there must have been a sufficient spread or % difference in g/kg/day protein intake between groups during a protein intervention to see muscle and strength differences. Protein change theory postulated that for the higher protein group, there must be a sufficient change from baseline g/kg/day protein intake to during study g/kg/day protein intake to see muscle and strength benefits. Seventeen studies met inclusion criteria. In studies where a higher protein intervention was deemed successful there was, on average, a 66.1% g/kg/day between group intake spread versus a 10.2% g/kg/day spread in studies where a higher protein diet was no more effective than control. The average change in habitual protein intake in studies showing higher protein to be more effective than control was +59.5% compared to +6.5% when additional protein was no more effective than control. The magnitudes of difference between the mean spreads and changes of the present review are similar to our previous review on these theories in a weight management context. Providing sufficient deviation from habitual intake appears to be an important factor in determining the success of additional protein in enhancing muscle and strength gains from resistance training. An increase in dietary protein favorably effects muscle and strength during resistance training.

A large volume of human clinical data supports increased dietary protein for favorable changes to body composition, but not all data are conclusive. The aim of this review is to propose two theories, “protein spread theory” and “protein change theory” in an effort to explain discrepancies in the literature. Protein spread theory proposed that there must have been a sufficient spread or % difference in g/kg/day protein intake between groups during a protein intervention to see body composition and anthropometric differences. Protein change theory postulated that for the higher protein group, there must be a sufficient change from baseline g/kg/day protein intake to during study g/kg/day protein intake to see body composition and anthropometric benefits. Fifty-one studies met inclusion criteria. In studies where a higher protein intervention was deemed successful there was, on average, a 58.4% g/kg/day between group protein intake spread versus a 38.8% g/kg/day spread in studies where a higher protein diet was no more effective than control. The average change in habitual protein intake in studies showing higher protein to be more effective than control was +28.6% compared to +4.9% when additional protein was no more effective than control. Providing a sufficient deviation from habitual intake appears to be an important factor in determining the success of additional protein in weight management interventions. A modest increase in dietary protein favorably effects body composition during weight management interventions.

Previous studies reported that diets high in simple carbohydrates could increase blood pressure in rodents. We hypothesized that the converse, a low-carbohydrate/high-fat diet, might reduce blood pressure. Six-week-old spontaneously hypertensive rats (SHR; n = 54) and Wistar-Kyoto rats (WKY; n = 53, normotensive control) were fed either a control diet (C; 10% fat, 70% carbohydrate, 20% protein) or a low-carbohydrate/high-fat diet (HF; 20% carbohydrate, 60% fat, 20% protein). After 10 wk, SHR-HF had lower (P < 0.05) mean arterial pressure than SHR-C (148 ± 3 vs. 159 ± 3 mmHg) but a similar degree of cardiac hypertrophy (33.4 ± 0.4 vs. 33.1 ± 0.4 heart weight/tibia length, mg/mm). Mesenteric arteries and the entire aorta were used to assess vascular function and endothelial nitric oxide synthase (eNOS) signaling, respectively. Endothelium-dependent (acetylcholine) relaxation of mesenteric arteries was improved (P < 0.05) in SHR-HF vs. SHR-C, whereas contraction (potassium chloride, phenylephrine) was reduced (P < 0.05). Phosphorylation of eNOSSer1177 increased (P < 0.05) in arteries from SHR-HF vs. SHR-C. Plasma glucose, insulin, and homoeostatic model of insulin assessment were lower (P < 0.05) in SHR-HF vs. SHR-C, whereas peripheral insulin sensitivity (insulin tolerance test) was similar. After a 10-h fast, insulin stimulation (2 U/kg ip) increased (P < 0.05) phosphorylation of AktSer473 and S6 in heart and gastrocnemius similarly in SHR-C vs. SHR-HF. In conclusion, a low-carbohydrate/high-fat diet reduced blood pressure and improved arterial function in SHR without producing signs of insulin resistance or altering insulin-mediated signaling in the heart, skeletal muscle, or vasculature.

We hypothesized that a low carbohydrate ‐ high fat (LC) diet will attenuate blood pressure (BP) and cardiac hypertrophy in spontaneously hypertensive rats (SHR). SHR (6 wk old, n=54) and Wistar Kyoto rats (WKY, 6 wk old, n=53; normotensive control) were fed control (C, 70% carbohydrate, 10% fat, 20% protein) or LC diet (20% carbohydrate, 60% fat, 20% protein). After 10 wk mean arterial BP was 11 mmHg lower (p<0.05) in SHR‐LC vs. SHR‐C, however, cardiac S6K phosphorylation was augmented (p<0.05) and heart:tibia length was unchanged. Compared to SHR‐C, mesenteric arteries of SHR‐LC had improved (p<0.05) endothelium dependent (acetylcholine) & independent (sodium nitroprusside) relaxation, reduced (p<0.05) contraction (potassium chloride, phenylephrine), and increased (p<0.05) eNOSSer1177 phosphorylation. Plasma glucose was similar among all groups. Insulin was lower (p<0.05) in rats fed LC vs. C. SHR‐LC had greater (p<0.05) peripheral insulin sensitivity (insulin tolerance test) vs. WKY‐C. Insulin stimulated (10h fast, 2U/kg IP) phosphorylation of AktSer473 and S6 in heart and gastrocnemius was not altered SHR‐ LC vs. C. In conclusion, an LC diet reduced blood pressure and improved arterial function without producing insulin resistance or altering insulin mediated signaling in heart and skeletal muscle.