Scholarly Work - Health & Human Development

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    Creatine supplementation does not reduce muscle damage or enhance recovery from resistance exercise
    (2007-11) Rawson, E.S.; Conti, M.P.; Miles, Mary
    Previous studies have shown that creatine supplementation reduces muscle damage and inflammation following running but not following high-force, eccentric exercise. Although the mechanical strain placed on muscle fibers during high-force, eccentric exercise may be too overwhelming for creatine to exert any protective effect, creatine supplementation may protect skeletal muscle stressed by a resistance training challenge that is more hypoxic in nature. The purpose of this study was to examine the effects of short-term creatine supplementation on markers of muscle damage (i.e., strength, range of motion, muscle soreness, muscle serum protein activity, C-reactive protein) to determine whether creatine supplementation offers protective effects on skeletal muscle following a hypoxic resistance exercise test. Twenty-two healthy, weight-trained men (19–27 years) ingested either creatine or a placebo for 10 days. Following 5 days of supplementation, subjects performed a squat exercise protocol (5 sets of 15–20 repetitions at 50% of 1 repetition maximum [1RM]). Assessments of creatine kinase (CK) and lactate dehydrogenase activity, high-sensitivity C-reactive protein, maximal strength, range of motion (ROM), and muscle soreness (SOR) with movement and palpation were conducted pre-exercise and during a 5-day follow up. Following the exercise test, maximal strength and ROM decreased, whereas SOR and CK increased. Creatine and placebo-supplemented subjects experienced significant decreases in maximal strength (creatine: 13.4 kg, placebo: 17.5 kg) and ROM (creatine: 2.4°, placebo: 3.0°) immediately postexercise, with no difference be-tween groups. Following the exercise test, there were significant increases in SOR with movement and palpation (p < 0.05 at 24, 48, and 72 hours postexercise), and CK activity (p < 0.05 at 24 and 48 hours postexercise), with no differences between groups at any time. These data suggest that oral creatine supplementation does not reduce skeletal muscle damage or enhance recovery following a hypoxic resistance exercise challenge.
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    Apolipoprotein A1 genotype affects the change in high density lipoprotein cholesterol subfractions with exercise training.
    (2006-03) Ruaño, G.; Seip, R.L.; Windemuth, Andreas; Zöllner, S.; Tsongalis, Gregory J.; Otvos, J.; Ordovas, J.M.; Bilbie, C.; Miles, Mary; Zoeller, Robert F.; Visich, Paul S.; Gordon, P.M.; Angelopoulos, T.J.; Pescatello, Linda S.; Moyna, Niall M.; Thompson, P.D.
    High density lipoprotein cholesterol (HDL-C) is a primary risk factor for cardiovascular disease. Apolipoprotein A-1 (apoA1) is the major HDL-associated apolipoprotein. The −75 G/A single nucleotide polymorphism (SNP) in the apolipoprotein A1 gene (APOA1) promoter has been reported to be associated with HDL-C concentrations as well as HDL-C response to dietary changes in polyunsaturated fat intake. We examined the effect of this APOA1 SNP on exercise-induced changes in HDL subfraction distribution. From a cohort of healthy normolipidemic adults who volunteered for 6 months of supervised aerobic exercise, 75 subjects were genotyped for the −75 G/A SNP. Of these, 53 subjects were G homozygotes (G/G) and 22 were A carriers (A/G and A/A). HDL subfractions were measured by nuclear magnetic resonance (NMR) spectroscopy by adding categories HDL-C 1 + 2 for the small subfraction, and HDL-C 3 + 4 + 5 for the large. The change in total HDL-C after exercise was 0.8 ± 7.2 mg/dL (+1.7%), and was not statistically significant. HDL subfraction amounts also did not significantly change with exercise training in the total cohort or in G homozygotes or A carriers. The amount of the large HDL subfraction increased in the G homozygotes and decreased in the A carriers (mean ± S.E.M., 1.8 ± 6.6 mg/dL versus −6.1 ± 2.3 mg/dL, p < 0.0005). In contrast, the amount of the small HDL subfraction decreased in G homozygotes and increased in A carriers (−1.3 ± 6.6 mg/dL versus 4.7 ± 1.2 mg/dL, p < 0.005). These results show that genetic variation at the APOA1 gene promoter is associated with HDL subfraction redistribution resulting from exercise training.
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    Apolipoprotein E genotype and changes in serum lipids and maximal oxygen uptake with exercise training
    (W.B. Saunders Co, 2004) Thompson, P.D.; Tsongalis, Gregory J.; Seip, R.L.; Bilbie, C.; Miles, Mary; Zoeller, Robert F.; Visich, Paul S.; Gordon, P.M.; Angelopoulos, T.J.; Pescatello, Linda S.; Bausserman, L.; Moyna, Niall M.
    Physical activity improves lipid levels by altering triglyceride (TG) metabolism. Apolipoprotein E (Apo E) facilitates TG clearance by mediating lipoprotein binding to hepatic receptors, but Apo E also has less defined roles in skeletal muscle and nervous tissue. This study examined if variants in Apo E genotype affect the lipid and physiologic response to exercise training. Seven centers genetically screened 566 individuals to recruit 120 subjects into 6 gender-specific cohorts equal for the most common Apo E genotypes: E2/3, E3/3, and E3/4. Anthropometics, exercise capacity (Vo2max), serum lipids, and post heparin (PH) plasma lipase activities were measured before and after 6 months of supervised exercise training. Difference in the response (Δ) to training among the Apo E genotypes was the primary outcome variable. Differences in pretraining serum lipids among the Apo E genotypes mimicked those observed in population studies: TGs were slightly higher in E2/3 subjects, whereas low-density lipoprotein (LDL)-cholesterol (C) was lower (P = not significant [NS] ). TGs decreased 11% with training for the entire cohort (P < .0001) and 7%, 12%, and 14% for the Apo E 2/3, 3/3 and 3/4 groups, respectively (P = NS for Δ). LDL-C did not change in the entire cohort, but decreased slightly in the 2/3 and 3/3 subjects and increased 4% in the 3/4 group (P = NS for Δ). High-density lipoprotein (HDL)-C increased 2% for the entire cohort (P = .06) due to a 6% increase in the 3/3 group (P = .07 for Δ). Total cholesterol (TC)/HDL and LDL/HDL decreased with training in the 2/3 and 3/3 groups, but increased in the 3/4 subjects and these responses differed among the genotypes (P < .05 for Δ). Vo2max increased 9% to 10% for the entire cohort, but only 5% in the 3/3 subjects versus 13% in the 2/3 and 3/4 groups and these differences were significantly different among the genotypes (P < .01 for Δ). This is the first prospective study to demonstrate that the serum lipid response to exercise training differs by Apo E genotype in a pattern consistent with known metabolic differences among the variants. Surprisingly, Apo E genotype also affected the increase in aerobic capacity produced by exercise training possibly via undefined effects on nerve and skeletal muscle function.
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    Apolipoprotein E genotype and sex influence C-reactive protein levels regardless of exercise training status
    (W.B. Saunders Co, 2008) Miles, Mary; Lowndes, J.; Sivo, S.; Seip, R.L.; Angelopoulos, T.J.
    C-reactive protein (CRP) is a marker for systemic inflammation and increased cardiovascular disease risk. Regular exercise may decrease CRP. Apolipoprotein E (apo E) has 3 common genotype variants—E2/3, 3/3, and 3/4—that modulate lipid metabolism and may have other metabolic physiologic roles, including some evidence that the genotype affects CRP levels. We assessed fasting serum CRP in 117 (male = 51, female = 66) healthy adults who volunteered for a 6-month aerobic exercise program. Both pre- and posttraining measurements were available in 71 (male = 31, female = 40) subjects. At baseline and follow-up, the numbers of subjects in the 3 groups were approximately equal: 2/3, n = 33 and 20; 3/3, n = 41 and 26; and 3/4, n = 43 and 25. At baseline, CRP levels differed by apo E genotype: means ± SD were 2.84 ± 2.18, 2.59 ± 2.34, and 1.90 ± 2.13 mg/L for E2/3, 3/3, and 3/4 subjects, respectively (3/4 vs 2/3, P b .05). In women, CRP was higher than that in men (3.14 ± 2.49 vs 2.12 ± 2.13 mg/L, P b .006). Exercise failed to affect CRP in the entire cohort (2.68 ± 2.38 vs 2.52 ± 2.48 mg/L) or in any apo E genotype group, and the apo E genotype effect observed at baseline persisted after training. In a largely white study cohort, CRP is higher in apo E3/3 than in 3/4 subjects and in women compared with men, but remains unchanged by 6 months of standard aerobic exercise training of the volume and higher intensity promoted by national organizations to reduce cardiovascular disease risk. How apo E genotype affects CRP is not known.
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    Cytokine production by stimulated mononuclear cells did not change with aging in apparently healthy, well-nourished women
    (Elsevier, 2001) Ahluwalia, N.; Mastro, A.M.; Ball, R.; Miles, Mary; Rajendra, R.; Handte, G.
    Aging is often associated with a dysregulation of the immune system. We examined mitogen-stimulated production of interleukin (IL)-2 and proinflammatory cytokines, IL-1β and IL-6, in apparently healthy and generally well-nourished old versus young women. Subjects were screened for health using the SENIEUR protocol and a panel of laboratory tests for inflammation, as well as for the adequacy of nutritional status using criteria related to undernutrition, and protein, iron, vitamin B12, and folate status. Young (n=26, age: 20–40 years) and old (n=44, age: 62–88 years) cohorts did not differ on the number of circulating monocytes, granulocytes, B (CD19+) cells, and T (CD3+, CD4+, and CD8+) cells. No differences (P>0.10) were seen between the two age groups in IL-2, IL-1β and IL-6 levels in whole blood cultures at 48 h after stimulation with PHA (5 mg/l). Furthermore, no age-related differences were noted in the absolute amounts (pg) of IL-1β and IL-6 after normalizing for circulating monocytes, B cells, or T cells (P>0.10). Similarly, no age-related decline in absolute amount of IL-2 (pg) after normalizing for circulating T cells was noted (P>0.10). Thus, contrary to most previous reports, our results do not support an increase in the production of proinflammatory cytokines IL-1β and IL-6, and a reduced production of IL-2 with aging when health and nutritional status are maintained. These findings support our previous results of no change in monocyte function and few alterations in acquired immune response in a carefully selected group of healthy and well-nourished elderly women.
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    Carbohydrate Influences Interleukin-6 but not C-reactive Protein or Creatine Kinase Following a 32-km Mountain Trail Race
    (Human Kinetics, 2005) Miles, Mary; Walker, E.E.; Conant, S.B.; Hogan, S.P.; Kidd, J.R.
    Attenuation of exercise-induced interleukin-6 (IL-6) responses by carbohydrate (CHO) has been demonstrated in studies comparing controlled doses (≥ 0.9 g · kg–1 · h–1) to placebo, but not in studies of voluntary intake. This study sought to determine if attenuation of the IL-6 response during a 32.2-km mountain trail race occurs for high compared to low ad libitum CHO intakes. IL-6, C-reactive protein (CRP), and creatine kinase activity (CK) were analyzed from blood samples collected 12 h pre-, 0, 4, and 24 h post-race. Subjects were grouped into low (n =14, 0.4 ± 0.1 g · kg–1· h–1) and high (n =18, 0.8 ± 0.2 g · kg–1 · h–1) CHO intake groups. IL-6 0 h post-race (P < 0.05) was higher in the low (40.2 ± 22.7 pg · mL–1) compared to the high CHO group (32.7 ± 22.1 pg · mL–1). CRP and CK both increased post-race, but no differences were observed between groups. Attenuation of exercise-induced IL-6 is apparent across a range of CHO intakes.
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    Effect of Carbohydrate Intake During Recovery from Eccentric Exercise on Interleukin-6 and Muscle Damage Markers
    (Human Kinetics, 2007) Miles, Mary; Pearson, Sherri Diane; Andring, J.M.; Kidd, J.R.; Volpe, S.L.
    The purpose of this investigation was to determine whether carbohydrate supplementation during the first 2 d postexercise recovery influenced the inflammation (IL-6, C-reactive protein [CRP], and cortisol) and muscle-damage responses. Eight participants performed a high-force eccentric elbow-flexion exercise to induce muscle soreness and inflammation and then consumed carbohydrate (0.25 g·kg–1·h–1) or an equal volume of placebo during hours 0–12 and 24–36 postexercise in a double-blind, crossover protocol. Muscle soreness; midbrachial arm circumference; blood glucose, IL-6, CRP, cortisol, and creatine-kinase (CK) activity; and maximal force production were measured preexercise and 4, 8, 12, 24, 48, and 120 h postexercise. Plasma IL-6 increased, F(5) = 5.27, P < 0.05, 8 h postexercise, with no difference between carbohydrate and placebo conditions. Changes in muscle soreness, arm circumference, strength, and serum CK activity were consistent with small amounts of muscle damage and did not differ between conditions. The authors conclude that carbohydrate supplementation during recovery from soreness-inducing exercise does not influence the delayed IL-6 response temporally linked to inflammation or indications of muscle damage. Thus, increased carbohydrate consumption at levels consistent with recommendations for replenishing glycogen stores does not impair or promote the immune and muscle responses.
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    Diurnal Variation, Response to Eccentric Exercise, and Association of Inflammatory Mediators with Muscle Damage Variables
    (American Physiological Society, 2008) Miles, Mary; Andring, J.M.; Pearson, Sherri Diane; Gordon, L.K.; Kasper, C.; Depner, Chris M.; Kidd, J.R.
    This investigation determined whether inflammatory mediators 1) have diurnal variations, 2) respond to high-force eccentric exercise, and 3) associate with markers of muscle damage after high-force eccentric exercise. College-aged men and women (n 51) completed exercise (3 15 maximal eccentric elbow flexor actions using 1 arm) and control conditions in random order. Blood was collected preexercise and 4, 8, 12, 24, 48, and 96 h postexercise. Additional measures included maximal isometric force and midbiceps arm circumference (to detect swelling). Serum and plasma were analyzed for soluble tumor necrosis factor receptor-1 (sTNFR1), IL-6, C-reactive protein, cortisol, and creatine kinase (CK) activity. Relative to the 7:00 AM point in the control condition, diurnal decreases were measured at 12:00 PM and 4:00 PM for IL-6 and at 12:00 PM, 4:00 PM, and 8:00 PM for sTNFR1 and cortisol. sTNFR1, IL-6, CK, swelling, and soreness were higher in the exercise compared with the control condition. The largest of the inflammatory mediator responses was measured for IL-6 8 h postexercise in the exercise (3.00 3.59 pg/ml) relative to the control condition (1.15 0.99 pg/ml). The IL-6 response (time-matched exercise control concentration) at 8 h associated (r 0.282) with muscle soreness at 24 and 96 h, and the cortisol response at 8 h associated (r 0.285) with swelling at 8, 24, and 96 h. Thus soreness and swelling, but not CK and strength loss, had a low association with the inflammatory response following eccentric exercise.
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