Effect of an Herbal/Botanical Supplement on Recovery from Delayed Onset Muscle Soreness: A Randomized Placebo Controlled Trial

Background: We examined the effects of a proprietary herbal/botanical supplement (StemSport, Stemtech, San Clemente, CA.) suggested to increase circulating stem cells, decrease inflammation, and attenuate exercise induced muscle damage on recovery from delayed onset muscle soreness (DOMS). Methods: Sixteen subjects (male = 7, female = 9; age 23.8 ± 10 years; height 171.9 ± 10 cm, mass 72.2 ± 15 kg) were randomized in a crossover, double-blind, placebo controlled trial to receive a placebo or StemSport supplement (6150 mg/day) for 14 days. DOMS was induced on day 7 for both placebo and active conditions in the non-dominant elbow flexor group with repeated eccentric repetitions. Muscle swelling (biceps girth), elbow flexor isometric strength (hand held dynamometer), muscle pain/tenderness (visual analog scale), range of motion (active elbow flexion and extension), and inflammation (hsCRP, IL6, and TNF-ɑ) were measured at baseline and at 24 h, 48 h, 72 h, and 168 h (1 week) post eccentric exercise. The crossover washout period was \u3e= 14 days. Results: No significant condition-by-time interactions between placebo and StemSport supplementation were observed with regard to measures of pain (p = 0.59), tenderness (p = 0.71), isometric strength (p = 0.32), elbow flexion (p = 0.45), muscle swelling (p = 0.90), or inflammation (p \u3e 0.90). Decrements in elbow extension range of motion 48 h post-exercise were less after StemSport supplementation (Δ elbow extension 48 h post; StemSport, -2.0 deg; placebo, -10 deg; p = 0.003). Conclusions: These data suggest that compared to placebo, StemSport supplementation does not improve outcome measures related to muscle recovery after acute upper-arm induced DOMS

Exercise Intensity Modulates Glucose-Stimulated Insulin Secretion when Adjusted for Adipose, Liver and Skeletal Muscle Insulin Resistance

<div><p>Little is known about the effects of exercise intensity on compensatory changes in glucose-stimulated insulin secretion (GSIS) when adjusted for adipose, liver and skeletal muscle insulin resistance (IR). Fifteen participants (8F, Age: 49.9±3.6yr; BMI: 31.0±1.5kg/m²; VO₂peak: 23.2±1.2mg/kg/min) with prediabetes (ADA criteria, 75g OGTT and/or HbA_1c) underwent a time-course matched Control, and isocaloric (200kcal) exercise at moderate (MIE; at lactate threshold (LT)), and high-intensity (HIE; 75% of difference between LT and VO₂peak). A 75g OGTT was conducted 1 hour post-exercise/Control, and plasma glucose, insulin, C-peptide and free fatty acids were determined for calculations of skeletal muscle (1/Oral Minimal Model; SM_IR), hepatic (HOMA_IR), and adipose (ADIPOSE_IR) IR. Insulin secretion rates were determined by deconvolution modeling for GSIS, and disposition index (DI; GSIS/IR; DI_SMIR, DI_HOMAIR, DI_ADIPOSEIR) calculations. Compared to Control, exercise lowered SM_IR independent of intensity (<i>P</i><0.05), with HIE raising HOMA_IR and ADIPOSE_IR compared with Control (<i>P</i><0.05). GSIS was not reduced following exercise, but DI_HOMAIR and DI_ADIPOSEIR were lowered more following HIE compared with Control (<i>P</i><0.05). However, DI_SMIR increased in an intensity based manner relative to Control (<i>P</i><0.05), which corresponded with lower post-prandial blood glucose levels. Taken together, pancreatic insulin secretion adjusts in an exercise intensity dependent manner to match the level of insulin resistance in skeletal muscle, liver and adipose tissue. Further work is warranted to understand the mechanism by which exercise influences the cross-talk between tissues that regulate blood glucose in people with prediabetes.</p></div

Effect of exercise intensity on multi-organ insulin resistance.

<p>Data are expressed as mean ± SEM. OMM = oral minimal model was calculated from plasma glucose and insulin to measure skeletal muscle insulin resistance. Homeostatic model of insulin resistance (HOMR-IR) was calculated as fasting PG x fasting PI to depict hepatic insulin resistance. Adipose-IR was calculated as fasting FFA x fasting PI to determine adipose insulin resistance. *Compared to Control, P<0.05. ^Compared to MIE, P<0.05.</p

Effect of exercise intensity on β-cell function.

<p>Data are expressed as mean ± SEM. DI = disposition index and was used to characterize pancreatic β-cell function. Skeletal muscle DI was calculated as AUC of ISR/Glucose x oral glucose minimal model. Hepatic DI was estimated as AUC of ISR/Glucose x HOMA-IR. Adipose DI was determined as AUC of ISR/Glucose x Adipose-IR. *Compared to Control, <i>P</i><0.05. ^Compared to MIE, <i>P</i><0.05.</p

Subject Characteristics.

<p>Subject Characteristics.</p

Effect of exercise intensity on glucose-stimulated insulin secretion.

<p>Data are expressed as mean ± SEM. ISR = insulin secretion rate derived from deconvolution of plasma C-peptide. GSIS = glucose-stimulated insulin secretion rate (ISR; total AUC C-peptide divided by total AUC Glucose). *Compared to Control, P<0.05.</p

The metabolic syndrome, hypertriglyceridemic waist, and cardiometabolic risk factor profile in obese women

The hypertriglyceridemic waist (HTGW) and metabolic syndrome (MS) are associated with increased cardiometabolic risk. We evaluated the impact of the HTGW on cardiometabolic risk factors in obese women diagnosed with the MS. Thirty-six abdominally obese women with the MS as defined by the International Diabetes Federation (IDF) [(mean (SD); age 49 (11) y, ht 165 (6) cm, wt 95 (16) kg] participated. The HTGW was defined as follows: a waist circumference ≥80 cm and triglycerides ≥1.7 mM. Unpaired t-tests and Analysis of Covariance (ANCOVA) were employed to detect mean differences between women with MS plus or minus HTGW. Women with the MS plus HTGW had higher total cholesterol (16%, p=0.015), VLDL-cholesterol (97%, p<0.001), non-HDL-cholesterol (16%, p=0.002), insulin (40%, p=0.043), and abdominal visceral fat (24%, p=0.100), and lower total HDL-cholesterol (6%, p=0.024), HDL(3) (11%, p=0.031) and Quantitative Insulin Sensitivity Check Index (QUICKI) (5%, p=0.068) compared with women with the MS minus HTGW. Thus, the presence of the HTGW was accompanied by a worsened cardiometabolic risk factor profile in these obese women with the MS. In particular, women with the MS plus HTGW were more insulin resistant compared to women with the MS minus HTGW. In conclusion, the presence of the HTGW in obese women with the MS exacerbates insulin resistance and cardiometabolic risk factors