Resistance Exercise Selectively Mobilizes Monocyte Subsets: Role of Polyphenols.

PURPOSE: To examine the impact of polyphenol supplementation on the recruitment, mobilization, and activation of monocyte subsets after resistance exercise. METHODS: Thirty-eight recreationally active males (22.1 ± 3.1 yr; 173.9 ± 7.9 cm; 77.8 ± 14.5 kg) were assigned to 28 d of polyphenol blend (PPB) supplementation, placebo (PL), or control (CON). Blood samples were obtained before (PRE) postresistance exercise, immediately (IP) postresistance exercise, 1 h (1H) postresistance exercise, 5 h (5H) postresistance exercise, 24 h (24H) postresistance exercise, and 48 h (48H) postresistance exercise (PPB/PL) or rest (CON). Fine-needle biopsies were obtained from the vastus lateralis at PRE, 1H, 5H, and 48H. Circulating concentrations of macrophage chemoattractant protein-1 (MCP-1) and fractalkine, as well as intramuscular MCP-1 were analyzed via multiplex assay. Changes in the proportions and expression of CD11b on monocyte subsets were assessed via flow cytometry. RESULTS: Circulating MCP-1 increased in PPB and PL at IP with further increases at 5H. Intramuscular MCP-1 was increased at 1H, 5H, and 48H in all groups. Classical monocyte proportions were reduced in PPB and PL at IP, and increased at 1H. Nonclassical monocytes were increased in PPB and PL at IP, whereas intermediate monocytes were increased at IP, and reduced at 1H. Intermediate monocytes were increased in PPB at 24H and 48H. CD11b expression was reduced on PPB compared with PL and CON at PRE on intermediate and nonclassical monocytes. CONCLUSIONS: Resistance exercise may elicit selective mobilization of intermediate monocytes at 24H and 48H, which may be mediated by tissue damage. Additionally, polyphenol supplementation may suppress CD11b expression on monocyte subsets at rest.

Polyphenol supplementation alters intramuscular apoptotic signaling following acute resistance exercise.

The purpose of this study was to examine the effects of 28-days of supplementation with an aqueous proprietary polyphenol blend (PPB) sourced from Camellia sinensis on intramuscular apoptotic signaling following an acute lower-body resistance exercise protocol and subsequent recovery. Untrained males (n = 38, 21.8 ± 2.7 years, 173.4 ± 7.9 cm, 77.6 ± 14.6 kg) were randomized to PPB (n = 14), placebo (PL; n = 14) or control (CON; n = 10). Participants completed a lower-body resistance exercise protocol comprised of the squat, leg press, and leg extension exercises. Skeletal muscle microbiopsies were obtained from the vastus lateralis preexercise (PRE), 1-h (1HR), 5-h (5HR), and 48-h (48HR) post-resistance exercise. Apoptotic signaling pathways were quantified using multiplex signaling assay kits to quantify total proteins (Caspase 3, 8, 9) and markers of phosphorylation status (JNK, FADD, p53, BAD, Bcl-2). Changes in markers of muscle damage and intramuscular signaling were analyzed via separate repeated measures analysis of variance (ANOVA). Change in Bcl-2 phosphorylation at 1H was significantly greater in PL compared to CON (P = 0.001). BAD phosphorylation was significantly elevated at 5H in PL compared to PPB (P = 0.015) and CON (P = 0.006). The change in JNK phosphorylation was significantly greater in PPB (P = 0.009), and PL (P = 0.017) compared to CON at 1H, while the change for PL was elevated compared to CON at 5H (P = 0.002). A main effect was observed (P < 0.05) at 1H, 5H, and 48H for p53 and Caspase 8, with Caspase 3 and Caspase 9 elevated at 48H. These data indicate that chronic supplementation with PPB alters apoptotic signaling in skeletal muscle following acute muscle-damaging resistance exercise.

Comparison of Two ß-Alanine Dosing Protocols on Muscle Carnosine Elevations.

OBJECTIVE: ß-alanine (BA) is a nonproteogenic amino acid that combines with histidine to form carnosine. The amount taken orally in individual doses, however, is limited due to symptoms of paresthesia that are associated with higher doses. The use of a sustained-release formulation has been reported to reduce the symptoms of paresthesia, suggesting that a greater daily dose may be possible. The purpose of the present study was to determine whether increasing the daily dose of BA can result in a similar increase in muscle carnosine in a reduced time. METHODS: Eighteen men and twelve women were randomized into either a placebo (PLC), 6-g BA (6G), or 12-g BA (12G) groups. PLC and 6G were supplemented for 4 weeks, while 12G was supplemented for 2 weeks. A resting blood draw and muscle biopsy were obtained prior to (PRE) and following (POST) supplementation. Plasma and muscle metabolites were measured by high-performance liquid chromatography. The loss in peak torque (ΔPT) was calculated from maximal isometric contractions before and after 250 isokinetic kicks at 180°·sec-1 PRE and POST. RESULTS: Both 12G (p = 0.026) and 6G (p = 0.004) increased muscle carnosine compared to PLC. Plasma histidine was decreased from PRE to POST in 12G compared to PLC (p = 0.002) and 6G (p = 0.001), but no group x time interaction (p = 0.662) was observed for muscle histidine. No differences were observed for any hematological measure (e.g., complete blood counts) or in symptoms of paresthesia among the groups. Although no interaction was noted in ΔPT, a trend (p = 0.073) was observed. CONCLUSION: Results of this investigation indicate that a BA supplementation protocol of 12 g/d-1, using a sustained-release formulation, can accelerate the increase in carnosine content in skeletal muscle while attenuating paresthesia.

Post-resistance exercise ingestion of milk protein attenuates plasma TNFα and TNFr1 expression on monocyte subpopulations.

Attenuating TNFα/TNFr1 signaling in monocytes has been proposed as a means of mitigating inflammation. The purpose of this study was to examine the effects of a milk protein supplement on TNFα and monocyte TNFr1 expression. Ten resistance-trained men (24.7 ± 3.4 years; 90.1 ± 11.3 kg; 176.0 ± 4.9 cm) ingested supplement (SUPP) or placebo (PL) immediately post-exercise in a randomized, cross-over design. Blood samples were obtained at baseline (BL), immediately (IP), 30-min (30P), 1-h (1H), 2-h (2H), and 5-h (5H) post-exercise to assess plasma concentrations of myoglobin; tumor necrosis factor-alpha (TNFα); and expression of tumor necrosis factor receptor 1 (TNFr1) on classical, intermediate, and non-classical monocytes. Magnitude-based inferences were used to provide inferences on the true effects of SUPP compared to PL. Plasma TNFα concentrations were "likely attenuated" (91.6% likelihood effect) from BL to 30P in the SUPP group compared with PL (d = 0.87; mean effect: 2.3 ± 2.4 pg mL-1). TNFr1 expressions on classical (75.9% likelihood effect) and intermediate (93.0% likelihood effect) monocytes were "likely attenuated" from BL to 2H in the SUPP group compared with PL (d = 0.67; mean effect: 510 ± 670 RFU, and d = 1.05; mean effect: 2500 ± 2300 RFU, respectively). TNFr1 expression on non-classical monocytes was "likely attenuated" (77.6% likelihood effect) from BL to 1H in the SUPP group compared with PL (d = 0.69; mean effect: 330 ± 430 RFU). Ingestion of a milk protein supplement immediately post-exercise appears to attenuate both plasma TNFα concentrations and TNFr1 expression on monocyte subpopulations in resistance-trained men.

Effects of a 10-Week Introductory Judo Course on Postural Control During a Bilateral Reactionary Gripping Task.

This study examined the effect of a 10-week introductory judo course on postural control during a bilateral reactionary gripping task using different stance conditions. A total of 20 volunteers were divided into experimental (JDO) and control (CON) groups. Countermovement jump was measured and center of pressure variables were evaluated while performing a bilateral reactionary gripping task under different stance conditions during pre- and posttesting. No interactions were observed for the center of pressure variables (p > .05), while both countermovement jump power (+165.4 W; p = .036) and height (+3.5 cm; p = .018) significantly improved in the JDO group following the 10-week course. Results indicate that 10 weeks of an introductory judo course has no effect on postural control while performing a bilateral reactionary gripping task using different stance conditions.

The Effect of Post-Resistance Exercise Amino Acids on Plasma MCP-1 and CCR2 Expression.

The recruitment and infiltration of classical monocytes into damaged muscle is critical for optimal tissue remodeling. This study examined the effects of an amino acid supplement on classical monocyte recruitment following an acute bout of lower body resistance exercise. Ten resistance-trained men (24.7 ± 3.4 years; 90.1 ± 11.3 kg; 176.0 ± 4.9 cm) ingested supplement (SUPP) or placebo (PL) immediately post-exercise in a randomized, cross-over design. Blood samples were obtained at baseline (BL), immediately (IP), 30-min (30P), 1-h (1H), 2-h (2H), and 5-h (5H) post-exercise to assess plasma concentrations of monocyte chemoattractant protein 1 (MCP-1), myoglobin, cortisol and insulin concentrations; and expressions of C-C chemokine receptor-2 (CCR2), and macrophage-1 antigen (CD11b) on classical monocytes. Magnitude-based inferences were used to provide inferences on the true effects of SUPP compared to PL. Changes in myoglobin, cortisol, and insulin concentrations were similar between treatments. Compared to PL, plasma MCP-1 was "very likely greater" (98.1% likelihood effect) in SUPP at 2H. CCR2 expression was "likely greater" at IP (84.9% likelihood effect), "likely greater" at 1H (87.7% likelihood effect), "very likely greater" at 2H (97.0% likelihood effect), and "likely greater" at 5H (90.1% likelihood effect) in SUPP, compared to PL. Ingestion of SUPP did not influence CD11b expression. Ingestion of an amino acid supplement immediately post-exercise appears to help maintain plasma MCP-1 concentrations and augment CCR2 expression in resistance trained men.

Protein supplementation does not alter intramuscular anabolic signaling or endocrine response after resistance exercise in trained men.

The mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway appears to be the primary regulator of muscle protein synthesis. A variety of stimuli including resistance exercise, amino acids, and hormonal signals activate mTORC1 signaling. The purpose of this study was to investigate the effect of a protein supplement on mTORC1 signaling following a resistance exercise protocol designed to promote elevations in circulating hormone concentrations. We hypothesized that the protein supplement would augment the intramuscular anabolic signaling response. Ten resistance-trained men (age, 24.7 ± 3.4 years; weight, 90.1 ± 11.3 kg; height, 176.0 ± 4.9 cm) received either a placebo or a supplement containing 20 g protein, 6 g carbohydrates, and 1 g fat after high-volume, short-rest lower-body resistance exercise. Blood samples were obtained at baseline, immediately, 30 minutes, 1 hour, 2 hours, and 5 hours after exercise. Fine-needle muscle biopsies were completed at baseline, 1 hour, and 5 hours after exercise. Myoglobin, lactate dehydrogenase, and lactate concentrations were significantly elevated after resistance exercise (P < .0001); however, no differences were observed between trials. Resistance exercise also elicited a significant insulin, growth hormone, and cortisol response (P < .01); however, no differences were observed between trials for insulin-like growth factor-1, insulin, testosterone, growth hormone, or cortisol. Intramuscular anabolic signaling analysis revealed significant elevations in RPS6 phosphorylation after resistance exercise (P = .001); however, no differences were observed between trials for signaling proteins including Akt, mTOR, p70S6k, and RPS6. The endocrine response and phosphorylation status of signaling proteins within the mTORC1 pathway did not appear to be altered by ingestion of supplement after resistance exercise in resistance-trained men.

Muscle strength and hypertrophy occur independently of protein supplementation during short-term resistance training in untrained men.

Short-term resistance training has consistently demonstrated gains in muscular strength, but not hypertrophy. Post-resistance training protein ingestion is posited to augment the acute anabolic stimulus, thus potentially accelerating changes in muscle size and strength. The purpose of this investigation was to examine the effects of 4 weeks of resistance training with protein supplementation on strength and muscle morphology changes in untrained men. Participants (mean ± SD; N = 18; age, 22.0 ± 2.5 years; body mass index, 25.1 ± 5.4 kg · m(-2)) were randomly assigned to a resistance training + protein group (n = 9; whey (17 g) + colostrum (3 g) + leucine (2 g)) or a resistance training + placebo group (n = 9). One-repetition maximum (1RM) strength in the leg press (LP) and leg extension (LE) exercises, maximal isometric knee extensor strength (MVIC), and muscle morphology (thickness (MT), cross-sectional area (CSA), pennation angle) of the dominant rectus femoris (RF) and vastus lateralis (VL) was assessed before and after training. Participants performed LP and LE exercises (3 × 8-10; at 80% 1RM) 3 days/week for 4 weeks. Data were analyzed using 2-way ANOVA with repeated measures. Four weeks of resistance training resulted in significant increases in LP (p < 0.001), LE (p < 0.001), MVIC (p < 0.001), RF MT (p < 0.001), RF CSA (p < 0.001), VL MT (p < 0.001), and VL CSA (p < 0.001). No between-group differences were observed. Although nutrition can significantly affect training adaptations, these results suggest that short-term resistance training augments muscle strength and size in previously untrained men with no additive benefit from postexercise protein supplementation.

ß-Hydroxy-ß-methylbutyrate (HMB)-free acid attenuates circulating TNF-α and TNFR1 expression postresistance exercise.

The purpose of this study was to examine the effect of ß-hydroxy-ß-methylbutyrate-free acid (HMB-FA) and cold-water immersion (CWI) on circulating concentrations of TNF-α and monocyte TNF-α receptor 1 (TNFR1) expression. Forty resistance-trained men (22.3 ± 2.4 yr) were randomized into four groups [placebo (PL), HMB-FA, CWI, and HMB-FA-CWI] and performed an acute, intense exercise protocol (four sets of up to 10 repetitions of the squat, dead lift, and split squat). Participants also performed four sets of up to 10 repetitions of the squat at 24 and 48 h following the initial exercise bout. Blood was sampled before exercise (PRE), immediately postexercise (IP), and 30 min, 24 h, and 48 h postexercise (30P, 24P, and 48P, respectively). Circulating TNF-α was assayed, and TNFR1 expression on CD14+ monocytes was measured by flow cytometry. The exercise protocol significantly elevated TNF-α in only PL (P = 0.006) and CWI (P = 0.045) IP. Mean percent changes show that TNF-α significantly increased from PRE to IP for only PL and CWI groups (P < 0.05), whereas the percent change of TNF-α for HMB-FA and HMB-FA-CWI was not significant. TNFR1 expression was elevated in PL (P = 0.023) and CWI (P = 0.02) at 30P compared with PRE, whereas both HMB-FA-treated groups did not increase significantly. In conclusion, HMB-FA attenuated circulating TNF-α IP and TNFR1 expression during recovery compared with PL and CWI. HMB-FA supplementation may attenuate the initial immune response to intense exercise, which may reduce recovery time following intense exercise.