Adiposity attenuates muscle quality and the adaptive response to resistance exercise in non-obese, healthy adults.

BACKGROUND: Emerging data have revealed a negative association between adiposity and muscle quality (MQ). There is a lack of research to examine this interaction among young, healthy individuals, and to evaluate the contribution of adiposity to adaptation after resistance exercise (RE). OBJECTIVE: The purpose of this investigation was to examine the influence of subcutaneous adipose tissue (SAT) on muscle function among non-obese individuals before and after RE. DESIGN: Analyses included 634 non-obese (body mass index <30 kg m(-2)) subjects (253 males, 381 females; age=23.3 ± 5.2 years). SAT and muscle mass (magnetic resonance imaging-derived SAT and biceps muscle volume), isometric and dynamic biceps strength, and MQ (strength/muscle volume), were analyzed at baseline and after 12 weeks of unilateral RE. RESULTS: At baseline, SAT was independently associated with lower MQ for males (ß=-0.55; P<0.01) and females (ß=-0.45; P<0.01), controlling for body mass and age. Adaptation to RE revealed a significant negative association between SAT and changes for strength capacity (ß=-0.13; p=0.03) and MQ (ß=-0.14; P<0.01) among males. No attenuation was identified among females. Post-intervention SAT remained a negative predictor of MQ for males and females (ß=-0.47; P<0.01). CONCLUSIONS: The findings reveal that SAT is a negative predictor of MQ among non-obese, healthy adults, and that after 12 weeks of progressive RE this association was not ameliorated. Data suggest that SAT exerts a weak, negative influence on the adaptive response to strength and MQ among males.

Leptin responses to long-term cardiorespiratory exercise training without concomitant weight loss: a prospective study.

AIM: The aims of the present study were to examine 1) whether changes in circulating leptin levels occur in response to six months of aerobic exercise training (ET) without concomitant weight loss; 2) whether there is a different response with respect to gender; and 3) the relationship between age and leptin and whether this relationship has any impact on the response to ET without weight-loss. METHODS: Thirty-eight healthy, sedentary men and women (age 38.43+/-2.24, range 18-59 years) participated in 6 months of supervised, moderate intensity (ET) performed 4 days per week. Maintenance of usual dietary practices were encouraged to minimize weight-loss. Participants were evaluated for circulating fasting leptin, body mass, body fat percentage and maximal aerobic power (VO2max) prior to and after ET. RESULTS: There was no decrease in body weight or leptin concentration (17.69+/-2.67 vs 16.85+/-3.12 ng dL(-1)). Gender did not affect the response to exercise training. The bivariate correlation between leptin and age was not significant, but the relationship reached significance after controlling for body fat percentage and VO2max (r = -0.358, P < 0.05). Age did not affect the response of leptin concentration to ET. CONCLUSION: It is probable that changes in leptin concentration reported previously with ET may be attributable to concomitant weight loss, but age does not play a role in how leptin responds to ET.

Plasma renin activity and albumin excretion in teenage type I diabetic subjects. A prospective study.

Plasma renin activity (PRA) may be high among teenage and young adult insulin-dependent diabetic subjects. Supine PRA and stimulated PRA were therefore measured in 50 female and 50 male diabetic subjects, 13-20 years old, diagnosed before the age of 16. Fifty percent have been restudied after 4.6 +/- 0.2 (mean +/- SEM) years. Initially, 43% had high PRA (supine 4.0 +/- 0.37, stimulated 12.02 +/- 0.8 ng/ml/hr angiotensin I), 45% had normal activity (supine 2.89 +/- 0.26, stimulated 6.47 +/- 0.34 ng/ml/hr/angiotensin I), and 12% had low activity (supine 1.57 +/- 0.05, stimulated 3.09 +/- 0.08 ng/ml/hr/angiotensin I). Levels were directly associated with prepubertal duration of diabetes and were inversely associated with duration of diabetes after onset of puberty but not with total duration or patient age. Within 4.6 +/- 0.2 years the percentage of subjects with high PRA fell to 13%, and the percentage of those with low PRA rose to 35%. Initially 51% of the cohort had normal albumin excretion rates (AER) at rest and during exercise equal to or less than 10 micrograms/min/m2; 32% had elevated rates only during exercise of 39 +/- 5 micrograms/min/m2; 13% had elevated rates at rest of 41 +/- 8 micrograms/min/m2 and during exercise of 116 +/- 21 micrograms/min/m2; and 4% had clinical proteinuria at rest and during each exercise period equal to or greater than 150 micrograms/min/m2. After 5 years, 58% continued to have normal AER, or their AER improved.(ABSTRACT TRUNCATED AT 250 WORDS)

Accurate assessment of body composition in obese females.

Although several generalized regression equations exist for body composition assessment the accuracy of these equations for special populations is uncertain. This study examined the ability to predict body composition variables from girth measurements in obese women. Girth measurements were taken on 156 obese women at abdomen 1 and abdomen 2 (mean value of the two was used), buttocks, and right thigh. Stepwise multiple-regression analysis generated on 110 randomly assigned subjects yielded the following equations: density (g/cc) = -0.00020(mean abdomen) - 0.00032(wt) + 0.00039(ht) + 0.97783 (R = 0.76, SEE = +/- 0.00061); % fat = 0.11077(mean abdomen) - 0.17666(ht) + 0.14354(wt) + 51.03301 (R = 0.76, SEE = +/- 2.9); fat wt (kg) = 0.62039(wt) - 0.17844(ht) + 0.09495(mean abdomen) + 5.88874 (R = 0.96, SEE = +/- 2.9); and lean body wt (kg) = 0.37939(wt) + 0.17898(ht) - 0.09494(mean abdomen) - 6.00423 (R = 0.89, SEE = +/- 3.0). Data from the remaining 46 women were used for cross-validation. These equations were valid, with validity coefficients for fat weight and lean body weight of r = 0.92 (SE = +/- 3.3 kg) and r = 0.86 (SE = +/- 3.3 kg), respectively, with no significant mean differences between actual and predicted values. The use of girth measurements is a simple and practical method of estimating fat weight and lean body weight in obese women.

Release of luteinizing hormone and growth hormone after recovery from maximal exercise.

Pulsatile properties of luteinizing hormone (LH) and growth hormone (GH) release were evaluated in 19 eumenorrheic untrained females [mean age 31.1 +/- 1.1 yr, height 165.2 +/- 1.4 cm, weight 64.8 +/- 2.1 kg, peak oxygen uptake (Vo2) 41.6 +/- 1.4 (SE) ml.kg-1.min-1] during the early follicular phase of the menstrual cycle (days 3-4 after the onset of menses). Each subject was studied during two consecutive menstrual cycles under each of two conditions in random order: 1) no formal exercise for 72 h (C) and 2) 12-24 h after two maximal exercise bouts (peak Vo2/lactate threshold treadmill evaluation and a 3,200-m time-trial run or a maximal Vo2 inclined treadmill test) performed on consecutive days (EX). Blood sampling was performed every 10 min for 12 h. LH and GH pulsatile parameters were identified and characterized by the Cluster pulse detection algorithm. No significant differences were noted in the number of peaks, peak amplitude, interpeak interval, peak increment, or 12-h integrated concentrations between C and EX for LH or GH. We conclude that maximal exercise protocols typically used for exercise evaluation do not have an effect on the pulsatile characteristics of LH or GH release in untrained women during the early follicular phase of the menstrual cycle if 12-24 h of recovery are allowed before evaluation of the pulsatile secretion of gonadotropins or GH.

Durability of the reproductive axis in eumenorrheic women during 1 yr of endurance training.

Menstrual cycle (MC) alterations occur in some endurance-training women. We hypothesized that a prospective running program would evoke alterations in MC phase lengths and in the physiological frequency of pulses of luteinizing hormone (LH) and/or diminish 24-h integrated serum LH concentrations in some women. In addition, we postulated that women who train more intensively (above the lactate threshold) would show alterations in gonadotropin release earlier in the training program or to a greater degree. To test these hypotheses, we examined the effects of different exercise intensities on physiological and endocrine responses. Twenty-three healthy eumenorrheic gynecologically mature (postmenarchal age 17.8 +/- 0.9 yr) untrained women undertook a 1-yr training program at one of two exercise intensities, one at a velocity corresponding to the lactate threshold (LT) and the other halfway between that of LT and peak running velocity, or served as controls. Training distance was the same in each exercise group. Physiological measurements were repeated every four MC to track changes in fitness and readjust training velocities. The lengths of the MC and the follicular and luteal phases were determined from hormonal concentrations. Body composition, nutritional intake, and pulsatile release of LH were determined. The women ran approximately 790 miles. Each group improved physiologically, with the greater than LT group improving to a greater degree. A less than 2-day decrease in the luteal phase length was observed only in the greater than LT group. No significant changes for any parameter of pulsatile LH release were noted between exercise groups. No significant changes in nutritional intake and only small changes in body composition were noted in either exercise group despite the added energy expenditure of exercise. We conclude that a progressive exercise program of moderate distance and intensity does not adversely affect the robust reproductive system of gynecologically mature eumenorrheic women.

Perceptual responses and blood lactate concentration: effect of training state.

The present study investigated the effect of training state on ratings of perceived exertion obtained at the lactate threshold (LT) and fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM. Runners (N = 20) and nonrunners (N = 29) completed a progressive horizontal treadmill (TM) running test which allowed identification of the TM velocities associated with the LT and FBLC. Runners attained significantly higher TM velocities, greater VO2, greater VE, greater heart rate, and a lower ventilatory equivalent for oxygen (VE/VO2) at each exercise intensity, with the exceptions of heart rate at 4.0 mM and VE/VO2 at the LT. Compared to nonrunners, runners also attained higher VO2, VE, and heart rate relative to peak values at LT and 2.0, 2.5, and 4.0 mM. Despite these relative and absolute physiological differences, there were no differences between groups in local, central, or overall ratings of perceived exertion (RPE) (Borg scale) at any condition. The data from both groups were combined to give the following means and SD for overall RPE during horizontal running: at the LT-11.0 +/- 2.0, and at FBLC of 2.0 mM-13.7 +/- 2.1, 2.5 mM-14.5 +/- 1.8, and 4.0 mM-16.5 +/- 2.3.

Effect of exercise modality on ratings of perceived exertion at various lactate concentrations.

The effect of exercise modality on the relationship between ratings of perceived exertion (RPE), blood lactate concentration, oxygen uptake (VO2), and heart rate (HR) was examined in 29 untrained male subjects who completed counterbalanced VO2max/lactate threshold (LT) protocols on a cycle ergometer (CE) and treadmill (TM). Heart rate, VO2, and RPE were determined at power outputs corresponding to LT and fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM and during maximal exercise. A repeated measures ANOVA indicated that, despite significant differences across exercise modality in HR and VO2 at LT, FBLC, and maximal exercise, no significant differences in RPE were found between exercise modalities during leg exercise. Mean (+/- SD) respective values for overall RPE at LT and FBLC of 2.0 mM, 2.5 mM, 4.0 mM, and max were 10.2 (2.2), 13.1 (2.1), 14.1 (2.3), 15.9 (2.3), and 18.8 (1.3) for the CE and 10.8 (1.9), 13.8 (1.8), 14.6 (1.6), 16.2 (2.6), and 18.5 (1.5) for the TM. It was concluded that exercise modality does not affect the perception of exertion at LT, FBLC, or maximal exercise and that a strong relationship exists between RPE and blood lactate concentrations.

Perceived exertion during hypobaric hypoxia in low- and moderate-altitude natives.

Ratings of perceived exertion (RPE) were examined in six low- (LAN) and eight moderate- (MAN) altitude natives during exercise at their residence (home) altitude (366 m and 2,200 m, respectively) and 1-4 wk later following 2-d decompression to 4,270 m (447 mm Hg). Cardiorespiratory, plasma lactate, and differentiated RPE measures were obtained at exercise intensities representing 35, 55, 75, 85, and 100% VO2peak. In general, cardiorespiratory and plasma lactate values were similar in LAN and MAN at their residence altitudes and during hypobaric hypoxia. However, the decrease in VCO2 was greater (P < 0.05) in LAN than MAN. At their residence altitudes, both LAN and MAN reported local RPE values that were greater (P < 0.05) than central ratings at the moderate to high exercise intensities. At 447 mm Hg, central and local RPE were similar in LAN. However, there was a significant correlation between acute mountain sickness (AMS) symptoms and central RPE (r = 0.875) across the five exercise intensities in LAN. The differences between the central and local RPE noted in MAN during their residence testing also persisted at 447 mm Hg. Thus, differentiated ratings of perceived exertion were similar in MAN at their residence altitude and at 4,270 m, but not in LAN subjects. Several factors, including AMS, may have contributed to this group difference in the RPE response.

Leptin and leptin receptor genetic variants associate with habitual physical activity and the arm body composition response to resistance training.

PURPOSE: We investigated the influence of Leptin (LEP) and leptin receptor (LEPR) SNPs on habitual physical activity (PA) and body composition response to a unilateral, upper body resistance training (RT) program. METHODS: European-derived American volunteers (men=111, women=131, 23.4 ± 5.4 yr, 24.4 ± 4.6 kg·m(-2)) were genotyped for LEP 19 G>A (rs2167270), and LEPR 326 A>G (rs1137100), 668 A>G (rs1137101), 3057 G>A (rs1805096), and 1968 G>C (rs8179183). They completed the Paffenbarger PA Questionnaire. Arm muscle and subcutaneous fat volumes were measured before and after 12 wk of supervised RT with MRI. Multivariate and repeated measures ANCOVA tested differences among phenotypes by genotype and gender with age and body mass index as covariates. RESULTS: Adults with the LEP 19 GG genotype reported more kcal/wk in vigorous intensity PA (1273.3 ± 176.8, p=0.017) and sports/recreation (1922.8 ± 226.0, p<0.04) than A allele carriers (718.0 ± 147.2, 1328.6 ± 188.2, respectively). Those with the LEP 19 GG genotype spent more h/wk in light intensity PA (39.7 ± 1.6) than A allele carriers (35.0 ± 1.4, p=0.03). In response to RT, adults with the LEPR 668 G allele gained greater arm muscle volume (67,687.05 ± 3186.7 vs. 52,321.87 ± 5125.05 mm(3), p=0.01) and subcutaneous fat volume (10,599.89 ± 3683.57 vs. -5224.73 ± 5923.98 mm(3), p=0.02) than adults with the LEPR 668 AA genotype, respectively. CONCLUSION: LEP19 G>A and LEPR 668 A>G associated with habitual PA and the body composition response to RT. These LEP and LEPR SNPs are located in coding exons likely influencing LEP and LEPR function. Further investigation is needed to confirm our findings and establish mechanisms for LEP and LEPR genotype and PA and body composition associations we observed.

Skeletal muscle lipoprotein lipase: molecular regulation and physiological effects in relation to exercise.

LPL directs the body wide distribution of fatty acids derived from circulating triglycerides. This is accomplished by tissue-specific regulation. In adipose tissue, LPLA per gram is higher than in muscle tissue. Eating increases adipose tissue LPLA and may increase blood flow. Exercise greatly increases SM blood flow and LPLA over a longer time frame as compared to the effect of eating on adipose tissue LPLA. The regulation of LPLA occurs at several levels and is better understood in adipose tissue models. In muscle, the study of regulation has been neglected. LPL expression in muscle may be more complex than in adipose tissue owing to the changes in blood flow and metabolism associated with contractile activity, as well as to other factors intrinsic to contraction, such as electrical events and cellular deformation. Sixty to 90 minutes of continuous leg exercise at 60% of VO2 max induces muscle LPL expression, increases LPL mRNA in humans with 4 hours of exercise, and raises immunoreactive mass by 8 hours post-exercise. Within 24 hours, both LPL and mRNA and mass have returned to normal levels. Increased muscle LPL mass following exercise may serve to replenish intramyofibral stores of triglyceride, which are depleted with endurance exercise and are greater in aerobically-trained individuals as compared to untrained individuals. The post-exercise increase in muscle LPL mass coincides with the post-exercise acute fall in circulating triglycerides typically observed in subjects capable of exercising for 60-90 minutes at 60% of VO2 max. The low fasting triglyceride levels often seen in highly trained individuals are due in part to their high levels of muscle LPLA. Both the physiological mediator and the molecular mediator of the exercised-induced induction of muscle LPL expression are known. Hopefully, the next decade will see careful studies aimed at better defining the molecular physiology of LPL expression in muscle.

Exercise induces human lipoprotein lipase gene expression in skeletal muscle but not adipose tissue.

Lipoprotein lipase (LPL) is regulated by exercise in humans, but the effects of exercise on LPL expression in different tissues and the molecular mechanisms involved are unclear. We assessed the effects of 5-13 consecutive days of supervised exercise on tissue LPL expression as well as fasting plasma lipids and lipoproteins in 32 sedentary, weight-stable adult men. In skeletal muscle, exercise training increased the mean LPL mRNA level by 117% (P = 0.037), LPL protein mass by 53% (P = 0.038), and total LPL enzyme activity by 35% (P = 0.025). In adipose tissue, mean LPL mRNA, protein mass, and activity did not change. Exercise decreased triglycerides [from 172 +/- 4.3 to 127 +/- 3.2 (SE) mg/dl, P = 0.002], total cholesterol (from 188 +/- 1.2 to 181 +/- 1.0 mg/dl, P = 0.011), and very low-density lipoprotein-cholesterol (from 30.1 +/- 0.9 to 22.0 +/- 0.8, P = 0.004) and increased high-density lipoprotein cholesterol (HDL-C; from 43.4 +/- 0.35 to 45.0 +/- 0.37, P = 0.030) and HDL2-C (from 6.6 +/- 0.21 to 7.7 +/- 0.19, P = 0.021). Changes in muscle but not adipose tissue heparin-releasable LPL activity were inversely correlated (r = -0.435, P < 0.034) with changes in triglycerides. These data suggest the existence of an exercise stimulus intrinsic to skeletal muscle, which raises LPL activity in part by pretranslational mechanisms, a process that contributes to the improvement in circulating lipids seen with physical activity.

Postprandial lipemia in subjects with hypobetalipoproteinemia and a single intestinal allele for apoB-48.

Hypobetalipoproteinemia in many kindreds is associated with truncated forms of apoB-100. Mutations of the apoB gene specifying more than 20 different carboxyl terminal truncations of apoB have been identified ranging in length from apoB-2 to apoB-89. Truncations longer than apoB-48 appear to be secreted only by liver, while truncations shorter than apoB-48 are secreted by liver as well as intestine. Thus, intestines of subjects heterozygous for truncations > apoB-48 contain two alleles producing apoB-48, while intestines of heterozygotes with truncations < apoB-48 contain only one allele producing apoB-48. Our aims were to assess whether intestinal fat absorption differed from normal in subjects with apoB-truncation-associated hypobetalipoproteinemia and whether fat absorption in heterozygotes with apoB < 48 differed from heterozygotes with apoB > 48. Ten subjects heterozygous for apoB > 48 (apoBs -89, -75, -54, -52), six heterozygous for apoB < 48 (apoBs -46, -40, -31) and a group of 16 controls matched for age, sex, body mass index characteristics, and eating similar diets were given identical fat meals containing vitamin A. Plasma triglycerides in whole plasma and retinyl palmitate in chylomicron and non-chylomicron (remnant) fractions were analyzed at zero time and over the next 14 hours. Fasting vitamins A and E also were quantified. Fasting plasma levels of vitamin E were lower in heterozygotes (536 +/- 198 mg/l for apoB > 48 vs. 372 +/- 155 for apoB < 48) versus controls (1162 +/- 441), but were not different when corrected for differences in LDL-C. Plasma vitamin A levels (uncorrected) were not different. Meal responses were characterized in terms of peak concentrations and areas under the curves (after subtraction of minimum points). These indices of fat absorption were comparable in all apoB phenotype groups suggesting that one allele specifying the intestinal production of apoB-48 is sufficient for normal fat absorption.

Absence of left ventricular hypertrophy in elite college basketball players.

Left ventricular dimensions of 11 successful male college basketball players engaged in pre-season conditioning (mean age, 20.3 years) and 13 tall healthy male controls (mean age, 21.6 years) were studied by echocardiography. Left ventricular internal dimension (LVIDd, mm), posterior wall thickness (PWT, mm), septal thickness (ST, mm), and calculated left ventricular mass (LV mass, g) in the athletes were within or only slightly in excess of echocardiographic normal limits and mean values were not significantly different from the control group. LVIDd (mm/m2 body surface area) was significantly lower in the athletes. However, five guard-type players displayed significantly greater mean values for PWT and LV mass compared to six taller forwards/centers with linear body builds. It was concluded that left ventricular hypertrophy is not a common characteristic of college basketball players. It was hypothesized that cardiac dimensions of young men may vary independently of gross body size in relation to somatotype or other anthropometric variables.

Effect of short-term recombinant growth hormone administration on plasma lipoproteins in elderly adults.

To characterize the effects of recombinant human growth hormone (rhGH) on plasma lipids and lipoproteins, rhGH was administered daily at a dose of 40 micrograms.kg-1 (Genentech) for 14 days in 7 healthy elderly male (67.4 +/- 1.9 years, 75.8 +/- 2.6 kg) adults. Six other healthy males (63.9 +/- 0.7 years, 77.8 +/- 3.8 kg) served as concurrent controls. Total plasma cholesterol (TC), triglycerides (TG), very-low-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, very-low-density lipoprotein-TG (VLDL-TG) and apolipoprotein AI and apolipoprotein B were determined after an overnight fast before and after the 14-day period of rhGH administration. Subcutaneous rhGH administration was physiologically effective, as shown by a threefold increase in insulin-like growth factor-I (from 110.8 +/- 8.2 to 355.5 +/- 41.6 ng.ml-1; p < 0.05). Plasma fasting insulin also increased from 38.0 +/- 6.5 to 129.9 +/- 43.8 mumol.l-1 (p < 0.05) at the end of the 14 days of rhGH treatment. With respect to plasma lipid/lipoprotein changes, rhGH administration increased plasma TG levels (from 1.5 +/- 0.3 to 2.2 +/- 0.4 mmol.l-1; p < 0.05) and VLDL-TG (from 1.1 +/- 0.3 to 1.8 +/- 0.4 mmol.l-1; p < 0.05), but did not change TC (from 5.0 +/- 0.4 to 5.2 +/- 0.3 mmol.l-1) or any other lipid/lipoprotein variables measured. No significant lipid changes were noted in the control group over the 14-day period. These data suggest that short-term rhGH treatment significantly alters plasma variables of TG profile, perhaps by altering metabolic parameters (i.e. synthesis and/or clearance rates) of VLDL metabolism.

The effect of training intensity on ratings of perceived exertion.

We examined the effects of intensity of training on ratings of perceived exertion (RPE) at the lactate threshold (LT), fixed blood lactate concentrations (FBLC) of 2.0, 2.5 and 4.0 mM and peak in 25 untrained eumenorrheic women (mean +/- SD: age = 30.9 +/- 4.1 yrs; height = 165.7 +/- 5.9 cm; weight = 65.5 +/- 7.6 kg) who completed one year of run training. Subjects were recruited as sedentary controls or were randomly assigned to one of two training groups: 1) at the lactate threshold (at LT) or 2) above the lactate threshold (greater than LT). The at LT group trained at velocity LT and the greater than LT group trained at the velocity midway between velocity LT and peak velocity. Training subjects were reevaluated every fourth menstrual cycle and training intensity was adjusted. The control group was reassessed at menstrual cycle 12. Before training no among group differences were observed for VO2 or velocity at LT, FBLC and peak. Both training groups increased VO2 at LT, FBLC and peak as a result of training (p less than 0.05), with the greater than LT group exhibiting greater improvement than the at LT group (VO2 at LT, FBLC of 2.0, 2.5 and 4.0 mM and peak increased by 6.4, 5.3, 5.1, 4.0 and 4.7 ml/kg.min-1 for at LT and by 10.4, 9.2, 8.6, 5.1 and 5.9 ml/kg.min-1 for greater than LT; p less than 0.05). Similar findings were observed for the velocity associated with these lactate concentrations. No pre/post differences were observed in VO2 or velocity for the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Apolipoprotein E genotyping methods for the clinical laboratory.

To select the best method for detecting apolipoprotein E (apo E) genotypes determined by the three common alleles epsilon 2, epsilon 3 and epsilon 4, we compared the radiolabeled allele-specific oligonucleotide (ASO) probe assay and the nonisotopic restriction isotyping assay. Leukocytic DNA was extracted from the blood of 93 patients after which the region containing two mutation points coding amino acid residues 112 and 158 was amplified by using the polymerase chain reaction (PCR). Amplified DNA fragments were spotted on nylon membranes, then hybridized for the ASO probe assay. The amplified DNA fragments were also digested with restriction endonuclease Hhal, followed by polyacrylamide gel electrophoresis for the restriction isotyping assay. The apo E genotypes determined by both methods for every specimen studied were in complete agreement. Although the radiolabeled ASO probe method was 10 times more sensitive than restriction isotyping on polyacrylamide gel, the two were comparable in accuracy. Additionally, because it is simpler to perform, is less time consuming, and is less expensive, we conclude that the restriction isotyping assay is the more suitable of these two methods for use in a clinical laboratory.

Induction of human skeletal muscle lipoprotein lipase gene expression by short-term exercise is transient.

Exercise increases skeletal muscle lipoprotein lipase (LPL) expression, but the time course of this response is not known. In the present study, we examined the time course of the LPL response to both short-term and acute exercise and measured circulating levels of putative regulators of muscle LPL. Nine adults underwent short-term exercise training (60-90 min of stationary cycling at 55-70% of leg ergometer peak oxygen uptake on 5 consecutive days). Five vastus lateralis biopsies were performed: before training, 20 h after the fourth bout (immediately before the 5th bout), and 0.2, 4, and 8 h after the fifth bout. After four bouts of exercise in 4 days, there was no increase in LPL mass or LPL mRNA exactly 20 h after the fourth bout. However, when tissues were sampled closer to the exercise bout on the 5th day, transient increases were seen. On day 5, LPL mRNA increased by 127% (P < 0.05) at 4 h postexercise and was followed by an increase in LPL mass of 93% (P < 0.05) at 8 h postexercise. Serum triglycerides decreased by 23% (P < 0.05) during the protocol. Two nonexercising subjects showed no consistent change in LPL mRNA or mass. Acute exercise transiently increased levels of norepinephrine (9-fold) and epinephrine (5-fold) and reduced insulin levels. Acute exercise preceded by four daily bouts of exercise induces a transient rise in LPL mRNA followed by rise in LPL mass, suggesting that these responses are temporally related. This induction of LPL gene expression may result from dynamic changes in serum catecholamines, plasma insulin, or events intrinsic to muscle contraction itself.

Adrenocortical responses to maximal exercise in moderate-altitude natives at 447 Torr.

Serum hydrocortisone and aldosterone (Aldo) responses to maximal exercise were examined in six low-altitude natives (LAN) (373 m or less, aged 19-25 yr) and eight moderate-altitude natives (MAN) (1,830-2,200 m, aged 19-23 yr) at their residence (home) altitudes (740 and 587 Torr, respectively) and later in a hypobaric chamber at a simulated altitude of 4,270 m (447 Torr). After 2 days at their respective residence altitude and in the chamber, each subject exercised to voluntary exhaustion on the bicycle ergometer. Fluid intake was similar in both groups at all testing locations. Preexercise 24-h urinary Aldo was lower in both groups at 447 Torr but only significantly reduced in the LAN group. In general, the changes in maximum exercise cardiorespiratory variables were twice as large in LAN as in MAN subjects going from residence altitude to 447 Torr. Both serum hydrocortisone and Aldo concentrations were increased (P less than 0.01) after exercise in both groups at residence altitude and 447 Torr. Aldo was lower (P less than 0.05) postexercise at 447 Torr than at residence altitude in both groups, but this decrease was more pronounced (P less than 0.01) in the LAN group. Thus it appears that high-altitude Aldo concentrations are more like resident altitude values in MAN than in LAN subjects.

Effects of training specificity on the lactate threshold and VO2 peak.

We examined the effects of training specificity on the lactate threshold (LT) and VO2peak. Sixteen male subjects completed VO2peak/LT protocols on the cycle ergometer (CE) and treadmill (TM) before and after a training program. The subjects were assigned to run training (N = 5), cycle training (N = 6), and control groups (N = 5). Subjects trained 4 day/week for 10 weeks at approximately 89% of pre-training VO2peak. Results indicated that run training increased VO2 at LT (VO2LT) within both the CE and TM protocols (17.9 to 22.5 ml/kg.min-1 for CE, 22.7 to 36.0 ml/kg.min-1 for TM, p less than 0.05) with the 58.5% increase in VO2LT for TM being greater than the 30.3% increase for CE (p less than 0.05). Cycle training resulted in a 38.7% increase in CE VO2LT (19.7 to 27.4 ml/kg.min-1, p less than 0.05) with no significant improvement in TM VO2LT (23.6 to 24.0 ml/kg.min-1). Similar increases in VO2peak were observed for CE and TM protocols for both cycle and run training groups (VO2peak increased by 11.9 to 20.7% in both CE and TM regardless of training mode). No changes were observed in the control group for any variable. The present data suggest that increases in LT resulting from training may be specific to the mode of exercise.