Parents and children from 38 families were submitted to a cold-stress and maximal treadmill test. The number of subjects varied depending on the measurements. Plasma epinephrine and norepinephrine, blood pressure and heart rate were measured before, during and after a cold hand immersion test (in a water bath at 5 °C for 2 min), as well as before and after maximal exercise (modified Balke). Scores were adjusted for the effects of age and sex through multiple-regression procedures (age + sex + age × sex + age2 + age3), yielding residuals which were submitted to analysis. Characteristic variations during cold stress were observed. Maximal exercise yielded a mean aerobic power of 43 ml/kg min–1 (SD =10), a mean maximal heart rate of 192 (SD = 10) and a mean maximal blood lactate of 65 mg/100 ml (SD = 23). Family resemblances in cold stress and maximal exercise adaptive reactions were investigated by comparison of between-family over within-family means of squares. In response to the cold stress, there were indications of family lines in induced changes for systolic blood pressure, epinephrine, and total catecholamines at 1 min after the test (p ≤ 0.05). Furthermore, parent-child correlations were significant and reached 0.38 for epinephrine, 0.28 for norepinephrine, and 0.34 for total catecholamines. Familial concentrations could not be detected before or 8 min after the cold stress. There are no indications of family resemblance in plasma catecholamine concentrations following exposure to maximal-exercise stress. It is concluded that genetic variation is probably contributing only moderately to catecholamine changes under cold stress and very little under exercise stress.
Muscle genetic variants and relationship with performance and trainability. Med. Sci. Sports Exerc, Vol. 21, No. 1, pp. 71-77, 1989. Samples were obtained in a maximum of 295 males and females from the vastus lateralis muscle and proteins fractionated by thin-layer isoelectric focusing. Muscle creatine kinase (CKM) and adenylate kinase (myokinase) (AK1M) were studied for the presence of variants. Six individuals exhibited a CKM variant described here for the first time, for a frequency of the variant gene of 1%. For AK1M, 21 individuals were heterozygotes for an inherited variant protein, an allele frequency of 3.5%. CKM (N=5) and AK1M (N=18) variant individuals were paired with control subjects who had the common CKM or AK1M muscle phenotype and compared for several performance indicators. There was no significant difference between the CKM and AK1M common and variant phenotypes for any of the performance measurements. However, the CKM variant subjects tended to be more effective than controls in a 90-min performance test (by about 22%) and had less percent decline over 60 s in force generation (by about 26%). In a subsequent experiment, a few variant subjects could be compared to controls in terms of response to exercise training. Although trends were observed, the CKM and AK1M variant subjects had a response to training generally comparable to that of the nonvariant individuals. While human variation in performance and trainability cannot be accounted for by the genetic polymorphism of the two kinase enzymes, the trends in the data suggest that allelic variation at these two gene loci may be of some functional significance.
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No abstract is provided for this article.
No abstract is provided for this article.
Obesity is a common condition with delayed and usually late-onset consequences. Since the prevalence of obesity is high and still growing, it is important to understand who is at risk for becoming obese and for what reasons, so that preventive measures can be implemented. This is particularly important in the light of the dramatic increase in the prevalence of excess body mass in relation to height in children and adolescents during the past 30 years.1 Unfortunately, it is still not possible to determine which children will be obese as adults, which will be affected by the conditions commonly associated with . . .
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