6 research outputs found

    Acute High Intensity Anaerobic Training and Rhabdomyolysis Risk

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    International Journal of Exercise Science 8(1) : 65-74, 2015. The current popularity of high intensity anaerobic training has caused concerns over the safety and prevalence of conditions such as rhabdomyolysis; thus it is important to understand the possible risks of participating in this type of activity. The purpose of this study was to determine the magnitude of muscle damage associated with a single high intensity anaerobic training session, and the relationship of this response to markers of fitness. Fifteen recreationally trained male participants (age 22.9 ± 4.3 y, mass 87.3 ± 15.6 kg, body fat 16.8 ± 6.4%, VO2 peak 50.1 ± 7.2 ml · kg-1 · min-1 ) completed a single anaerobic training session consisting of high intensity plyometrics and calisthenics. Prior to the exercise session, participants completed a maximal aerobic capacity test, body composition analysis, and a military physical fitness test (1 min push-ups, 54 ± 14; 1 min sit-ups, 45 ± 11; 1.5 mile run, 12:17 ± 0.067 min). Serum creatine kinase (CK) was measured prior to and 48 h following the exercise session. CK at 48 h (126.3 ± 68.9 U· L-1) did not reach the limits indicating rhabdomyolysis (~881-1479 U/L) but was elevated above resting (CK resting 90.5 ± 53.4). VO2 peak (L · m-1) had a positive correlation with CK levels (r = .51; p \u3c 0.05) but body mass or any other indicator of fitness did not correlate. An increase in serum CK levels occurred, but did not reach levels of rhabdomyolysis, suggesting that a single high intensity exercise session is safe for healthy individuals who exercise regularly

    Identification of Common Genetic Variants Influencing Spontaneous Dizygotic Twinning and Female Fertility.

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    Spontaneous dizygotic (DZ) twinning occurs in 1%-4% of women, with familial clustering and unknown physiological pathways and genetic origin. DZ twinning might index increased fertility and has distinct health implications for mother and child. We performed a GWAS in 1,980 mothers of spontaneous DZ twins and 12,953 control subjects. Findings were replicated in a large Icelandic cohort and tested for association across a broad range of fertility traits in women. Two SNPs were identified (rs11031006 near FSHB, p = 1.54 × 10(-9), and rs17293443 in SMAD3, p = 1.57 × 10(-8)) and replicated (p = 3 × 10(-3) and p = 1.44 × 10(-4), respectively). Based on ∼90,000 births in Iceland, the risk of a mother delivering twins increased by 18% for each copy of allele rs11031006-G and 9% for rs17293443-C. A higher polygenic risk score (PRS) for DZ twinning, calculated based on the results of the DZ twinning GWAS, was significantly associated with DZ twinning in Iceland (p = 0.001). A higher PRS was also associated with having children (p = 0.01), greater lifetime parity (p = 0.03), and earlier age at first child (p = 0.02). Allele rs11031006-G was associated with higher serum FSH levels, earlier age at menarche, earlier age at first child, higher lifetime parity, lower PCOS risk, and earlier age at menopause. Conversely, rs17293443-C was associated with later age at last child. We identified robust genetic risk variants for DZ twinning: one near FSHB and a second within SMAD3, the product of which plays an important role in gonadal responsiveness to FSH. These loci contribute to crucial aspects of reproductive capacity and health.Support for the Netherlands Twin Register was obtained from the Netherlands Organization for Scientific Research (NWO) and The Netherlands Organization for Health Research and Development (ZonMW) grants, 904-61-193,480-04-004, 400-05-717, Addiction-31160008, 911-09-032, Biobanking and Biomolecular Resources Research Infrastructure (BBMRI –NL, 184.021.007); Royal Netherlands Academy of Science Professor Award (PAH/6635) to DIB; European Research Council (ERC-230374 and ERC-284167); Rutgers University Cell and DNA Repository (NIMH U24 MH068457-06), the Avera Institute, Sioux Falls, South Dakota (USA) and the National Institutes of Health (NIH R01 HD042157-01A1). Part of the genotyping was funded by the Genetic Association Information Network (GAIN) of the Foundation for the National Institutes of Health and Grand Opportunity grants 1RC2 MH089951). We acknowledge support from VU Amsterdam and the Institute for Health and Care Research (EMGO+). The Berghofer Medical Research Institute (QIMR) study was supported by grants from the National Health and Medical Research Council (NHMRC) of Australia (241944, 339462, 389927, 389875, 389891, 389892, 389938, 443036, 442915, 442981, 496610, 496739, 552485, 552498, 1050208, 1075175). Dale R. Nyholt was supported by the Australian Research Council (ARC) Future Fellowship (FT0991022), NHMRC Research Fellowship (APP0613674) Schemes and by the Visiting Professors Programme (VPP) of the Royal Netherlands Academy of Arts and Sciences (KNAW). Allan F. McRae was supported by an NRMRC Career Development Fellowship (APP1083656). Grant W. Montgomery was supported by NIH grant (HD042157, a collaborative study of the genetics of DZ twinning) and NHMRC Fellowship (GNT1078399). The Minnesota Center for Twin and Family Research (MCTFR) was supported in part by USPHS Grants from the National Institute on Alcohol Abuse and Alcoholism (AA09367 and AA11886), and the National Institute on Drug Abuse (DA05147, DA13240, and DA024417). We would like to thank also 23andMe's consented research participants for contributing data on age at menarche for the FSHB gene locus and the Twinning Gwas Consortium (TGC). Co-authors from: Finland (Anu Loukola, Juho Wedenoja, Emmi Tikkanen, Beenish Qaiser), Sweden (Nancy Pedersen, Andrea Ganna), United kingdom King's College London (Department of Twin Research & Genetic Epidemiology: Pirro Hysi, Massimo Mangino), Institute of Psychiatry, Psychology & Neuroscience, Medical Research Council Social, Genetic and Developmental Psychiatry Centre (Eva Krapohl, Andrew McMillan).This is the author accepted manuscript. The final version is available from Elsevier via http://dx.doi.org/10.1016/j.ajhg.2016.03.00

    The Performance Effect of Early Versus Late Carbohydrate Feedings During Prolonged Exercise

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    Ingesting carbohydrate during prolonged exercise can increase time to fatigue and improve time trial performance at the end of exercise. The purpose of this study was to determine how the timing of isoenergetic carbohydrate feedings during prolonged cycling affects performance in a subsequent 10 km cycling performance trial. Recreationally trained male cyclists (n = 8, age 34.5 ± 8.3 y, mass 80.0 ± 6.3 kg, 16.0 ± 3.8% body fat, VO2 peak 4.54 ± 0.42 L · min-1 ) completed four experimental trials consisting of cycling continuously for two hours at 60% of VO2 peak, followed immediately by a self-paced 10 km performance trial. Participants consumed 250 mL of beverage every 15 minutes during the two hour exercise. The four conditions included no carbohydrate ingestion (PP), early carbohydrate ingestion (CP), late carbohydrate ingestion (PC), or carbohydrate ingestion throughout (CC). A total of 60 g of carbohydrate was given in all trials except PP. Trials were completed in a randomized, counterbalanced order. 10 km performance trial time to completion was faster in trials CC (17.70 ± 0.52 min) and PC (17.60 ± 0.62 min) as compared to trial PP (18.13 ± 0.52 min, p = 0.028 and p = 0.007, respectively) while trial CP (17.85 ± 0.58 min) was not different from trial PP (p = 0.178) . Blood variables mirrored performance results. These data indicate that carbohydrate ingestion late during exercise (CC and PC) can improve subsequent 10 km time trial performance while early ingestion (CP) does not

    Human skeletal muscle mRNA response to exercise in a hot environment

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    Mitochondrial adaptation is important for both maintaining optimal health as well as improving athletic The purpose of this investigation was to determine the effects of exercise in a hot environment on mitochondrial biogenesisrelated gene expression in human skeletal muscle. Recreationally-active males (n = 9, 25 ± 4 y, 179 ± 4 cm, 76.2 ± 8.0 kg, VO2 peak 4.39 ± 0.82 L · min-1, 13.4 ± 3.3% body fat) completed two experimental trials in which they cycled for 1 h at 60% of Wmax in an environmental temperature of either 20º C (N) or 33º C (H). Muscle biopsies were obtained from the vastus lateralis pre- and 3 h post-exercise for determination of gene expression. Relative oxygen consumption was higher during exercise in H (69.8 ± 4.7%) than N (64.5 ± 5.7%; p = 0.004), as was HR (H: 163 ± 9 bpm, N: 151 ± 9 bpm; p \u3c 0.001). There was a tendency for expression of PGC-1α to be lower following H than N (p = 0.083). Expression of ERRα (p = 0.009), GABPA (p = 0.010), MEF2A (p = 0.080), NRF-1 (p = 0.004), and VEGF (p = 0.004) was blunted following exercise in H as compared to N. Expression of PPARG, SIRT-1, and TFAM was unaffected by temperature or exercise (p = 0.305, p = 0.103, p = 0.410, respectively). These data demonstrate that exercise in a hot environment blunts expression of several genes related to mitochondrial biogenesis

    Dose-response of hypoxia on mitochondrial related gene expression

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    Mitochondrial function is increased in repeated short term exposure to hypoxia. However, chronic hypoxia exposure has been shown to decrease mitochondrial function. It is unknown if a dose-response relationship between mitochondrial gene expression and magnitude of hypoxia impacts this paradox in mitochondrial function between acute and chronic hypoxic exposure. PURPOSE: To determine the mitochondrial related gene response to incremental levels of hypoxia. METHODS: Recreationally-trained male cyclists completed a 60-minute ride at 70% of Wmax at an altitude of 975 m, followed by 6 h of recovery at four different simulated altitudes (0 m, 1667 m, 3333 m, or 5000 m). Blood O2 saturation was measured via pulse oximetry every hour during the 6 h recovery period. Muscle biopsies were obtained from the vastus lateralis pre- and 6 h post-exercise for analysis of mitochondrial related gene expression. RESULTS: Blood O2 saturation decreased with increasing simulated altitude during recovery (0 m: 98 ± 1%; 1667 m: 94 ± 1%; 3333 m: 90 ± 1%; 5000 m: 79 ± 2%; p \u3c 0.05). Expression of PGC-1α, HK, and SOD increased significantly with exercise (p \u3c 0.05), but were not different between trials. There was a tendency for expression of HIF-2α to increase with exercise, although this did not reach statistical significance (p = 0.089). CONCLUSION: These data demonstrate no dose-response relationship between magnitude of hypoxic exposure and mitochondrial gene expression. Therefore, the paradox of mitochondrial function in response to acute and chronic exposure to hypoxia cannot be explained by the magnitude of hypoxia
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