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Several studies are conducted to examine the various changes induced in the coagulation factors in the older adults because of any form of exercise training, as the coagulation cascade plays a very important role in the development of a cardiovascular disease (CVD). The results show that endurance training highly affects the coagulation cascade, as it reduces the coagulation activity in the common pathway at rest by increasing the activation potential of the intrinsic pathway.

Background: A common functional missense mutation [Ala54Thr of the fatty acid-binding protein 2 gene (FABP2)] has previously been studied for associations with glucoregulation, postprandial lipemia, and lipid oxidation rates. However, most of those studies have not accounted for the interactive and potentially confounding effects of habitual physical activity and diet. Objective: We tested the hypothesis that, in sedentary nondiabetic subjects following a low-fat diet, Thr54 FABP2 carriers have lower glucoregulatory function, greater postprandial lipemia, and greater lipid oxidation rates than do their Ala54 FABP2-homozygous counterparts. Design: Men and women (n = 122) aged 50-75 y who were following a low-fat diet were genotyped and underwent oral-glucose-tolerance tests. A subgroup (n = 36) also underwent postprandial lipemia tests with lipid oxidation rate measurements. Results: Thr54 carriers were less likely to have normal glucose tolerance (P = 0.05) and had higher fasting glucose concentrations (P = 0.003) than did Ala54 homozygotes. In Thr54 carriers, the insulin sensitivity index was lower (P = 0.02), and the fasting insulin and the oral-glucose-tolerance test insulin area under the curve were higher (P = 0.05 and 0.03, respectively) than in Ala54 homozygotes. FABP2 genotype was not associated with fasting or postprandial lipemia test triacylglycerol or free fatty acids (P [greater than or equal to] 0.22 for all), but postprandial lipid oxidation rates were higher (P = 0.01), which suggests that fat absorption is higher in Thr54 carriers than in Ala54 homozygotes. Conclusions: In sedentary nondiabetic persons following a low-fat diet, FABP2 Thr54 carriers have lower glucose tolerance and lower insulin action than do Ala54-homozygous persons. Furthermore, FABP Thr54 carriers have higher lipid oxidation rates, which may be the mechanism of glucoregulatory dysfunction. KEY WORDS Postprandial lipemia, fatty acid-binding protein, insulin action, glucose tolerance, genotype, lipid oxidation

The 2005 update of the human gene map for physical performance and health related fitness phenotypes are presented. It is shown that little progress is made in the 12 months with respect to the genetic basis of human variation in performance and health-related fitness.

OBJECTIVE--Physical inactivity and increased adiposity contribute to insulin resistance; less is known, however, about the relative contributions of these factors in older adults. The aim of this study was to [...]

Research shows that higher bone mineral density is linked to prolonged physical activity at the low-to-moderate level in postmenopausal women. Data were obtained from 23 endurance-trained athletes, 20 active nonathletic women, and 20 sedentary women.

This article examines the effects of an intense resistive exercise session on blood pressure levels during the following day. Findings indicate that resistive exercise did not significantly influence subsequent blood pressure levels in sedentary or trained subjects.

A study to test the effect of aerobic exercise training on glucose-stimulated insulin responses in those who are middle-aged and older has been carried out over 9 months using moderate-intensity aerobic exercise training in 17 men. It was found that the decrease in glucose-stimulated insulin secretion with aerobic exercise training is mediated, at least in part, by reductions in abdominal fat. Regular physical exercise may prevent or ameliorate conditions associated with hyperinsulinemia.

This study compares the hemodynamics and cardiac output of postmenopausal women athletes and their sedentary peers while performing maximal treadmill exercise. Results indicate that postmenopausal women athletes have greater cardiac outputs and higher stroke volumes when compared to the control group.

Background and Purpose. The primary purpose of this study was to evaluate the effects of endurance training and detraining on the development of and recovery from fatigue induced by isokinetic exercise. It was our hypothesis that the rate of recovery from fatigue would correlate with maximal oxygen uptake ([Vo.sub.2]max). A secondary purpose was to determine whether changes in the development of fatigue and in the time course of recovery that occur with alterations in training status correlate with shifts in the proportions of type IIa and type IIb muscle fibers. Subjects and Methods. Four subjects with no regular endurance exercise training participated in a 12-week program of intense endurance exercise training, and 6 endurance-trained subjects stopped all exercise training for 12 weeks In addition, 11 subjects performed a single isokinetic fatigue test with recovery and a graded treadmill or bicycle ergometer test to determine [Vo.sub.2]max. Results. Maximal oxygen uptake increased 24% (SD = 10%) in response to the exercise training program and decreased 17% (SD = 6%) with detraining. The percentage of type IIa and type IIb muscle fibers changed with endurance training and detraining. The percentage of decline in torque during a 60-second isokinetic exercise test was unaffected by endurance training or detraining, however, there was a significant change in recovery of torque. Conclusion and Discussion. The results demonstrate a positive correlation (r = .75) between the percentage of reduction in torque at 30 seconds of recovery and the change in the proportion of type IIb fibers with both training and detraining. The results also demonstrate a high, negative correlation (r = -.84) between the percentage of reduction in torque at 30 seconds of recovery and [Vo.sub.2].max. These results suggest the recovery of muscle torque reflects both the training- and detraining-induced changes in the proportion of type IIa and type IIb muscle fibers and maximal aerobic exercise capacity [Sinacore DR, Coyle EF, Hagberg JM, Holloszy JO. Histochemical and physiological correlates of training- and detraining-induced changes in the recovery from a fatigue test Phys Ther. 1993,73:661-667], Key Words: Energy expenditure, Exercise, strengthening, Fatigue, Functional training and activities, Pulmonary, tests and measurements Tests of local muscle endurance able to detect changes induced by exercise training or detraining [...]

The most significant articles in exercise, fitness, and performance genomics and a brief overview of the first genome-wide association study of the genetic differences between exercisers and nonexercisers are reported. The findings recommended an urgent need to prioritize high-quality research designs and replication studies with large sample sizes.

A study was conducted to analyze whether p22phox (CYBA) polymorphisms C242T and A640G, is associated with changes in urinary 8-iso-prostaglandin [F.sub.2alpha]. Results concluded that C242T CYBA variant effects baseline levels of urinary 8-iso-PG[F.sub.2alpha] but not the aerobic exercise-induced responses.

A subset of the 2004 update of the human gene map project focueses on physical performance and health-related fitness phenotypes. Information on peer-reviewed papers on this topic published in 2004 is presented. The genes and markers for sedentary people, people beginning sports training and very seasoned athletes are discusses. These genes and markers are positioned on the genetic map of all autosomes and the X chromosome.

Circulating microRNAs (ci-miRs) are post-transcriptional regulators of gene expression released by cells into blood or other biofluids. Acute and chronic exercise have been shown to alter the profile of ci-miRs. The past few years have seen an upsurge in research detailing the exercise responses of ci-miRs and investigating their utility as biomarkers for various conditions. The functions of ci-miRs as paracrine/endocrine mediators of systemic adaptations to exercise training are also strongly suggested, but direct evidence is still lacking. The purpose of this review is to provide an update on recent advancements concerning ci-miRs in the field of exercise physiology.

ABSTRACTPurpose: Aggressive play in professional soccer, punished by referees with fouls and cards, carries increased injury risk. We compared fouls and cards in the English Premier League (EPL) with the next three divisions of English soccer over 17 seasons (2000/01–2016/17), to determine whether previously observed differences with other top European leagues are unique to the EPL or are characteristic of English professional soccer overall.Methods: Data from individual matches were obtained through online sources and season averages for each league were compared. Fouls and cards were also compared between home and away teams. Correlations with final league positions were examined.Results: Numbers of fouls and yellow cards per match did not substantially differ between leagues, with average differences of 3–3.8% and 6.1–14.0% (effect sizes (ηp2) < 0.01). Away teams consistently committed more fouls and yellow card offences than home teams in each league. Results were similar though less consistent for red cards. Number and rate of cards awarded to the opposition exhibited strongest correlations with final league position across leagues.Conclusions: Our results suggest similar rates of aggressive play among the top English soccer leagues, possibly due to standardized refereeing style. Consequently, contact injuries rates may be higher in English soccer.

Independent and combined associations with hormone replacement, cardiovascular fitness, and body composition OBJECTIVE -- The effects of combined physical activity and hormone replacement therapy (HRT) on insulin sensitivity in postmenopausal [...]

Objectives: To examine the contribution of adrenergic receptor (ADR) gene polymorphisms and their gene‐gene interactions to the variability of exercise training‐induced body fat response. Research Methods and Procedures: This was an intervention study that used a volunteer sample of 70 healthy, sedentary men (n= 29) and postmenopausal women (n= 41) 50 to 75 years of age, with a BMI ≤37 kg/m2, from the Washington, DC, metropolitan area. Participants completed 6 weeks of dietary stabilization (American Heart Association diet) before 24 weeks of supervised aerobic exercise training. Diet was maintained throughout the intervention. Change in percent total body fat, percent trunk fat, and fat mass by DXA in ADRgenotype groups (Glu12/Glu9α2b‐ADR, Trp64Arg β3‐ADR, and Gln27Glu β2‐ADR) at baseline and after 24 weeks of aerobic exercise training was measured. Results: In multivariate analysis (covariates: age, gender, and baseline value of phenotype), best fit models for percent total body and trunk fat response to exercise training retained main effects of all three ADRgene loci and the effects of each gene‐gene interaction (p= 0.009 and 0.003, respectively). Similarly, there was a trend for the fat mass response model (p= 0.03). The combined genetic factors explained 17.5% of the overall model variability for percent total body fat, 22% for percent trunk fat, and 10% for fat mass. Discussion: The body fat response to exercise training in older adults is associated with the combined effects of the Glu12/Glu9α2b‐, Trp64Arg β3‐, and Gln27Glu β2‐ADRgene variants and their gene‐gene interactions.

Plasma high-density lipoprotein cholesterol (HDL-C) levels are an important independent risk factor for cardiovascular disease (CVD) that can be modified through exercise training. However, levels of HDL-C and its subfractions and their response to standardized exercise training are highly variable among individuals. Such variability suggests that levels of HDL-C, its subfractions, and their response to exercise training may be influenced by genetic variation and the interaction of that genetic variation with physical activity. The endothelial lipase gene (LIPG) may influence HDL-C metabolism and has several recently identified genetic variants. We hypothesized that the LIPG Thr111Ile polymorphism would be associated with variation in HDL-C levels and its subfractions and their response to exercise training. Eighty-three sedentary, healthy 50- to 75-year-old subjects were weight-maintained on an American Heart Association Step 1 Diet and then studied before and after aerobic exercise training. Sample size varied according to outcome measure as complete data was not available for all subjects. Initial age, body composition, and maximum oxygen consumption (Vo2max) did not differ between LIPG genotype groups (CC, n = 41 to 44; CT/TT, n = 37 to 39). Initial total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) levels were not significantly different between groups. The CT/TT group had lower initial HDL2NMR-C (12 ± 1.0 v17 ± 1.1 mg/dL; P= .002) and integrated HDL1,2NMR-C (13 ± 1.0 v18 ± 1.1 mg/dL; P= .002) levels and somewhat higher initial levels of integrated HDL3,4,5-C (31 ± 2.2 v25 ± 2.3 mg/dL; P= .06). With exercise training, Vo2maxincreased, and body weight, total body fat, and visceral adipose tissue decreased similarly in both groups. With training, HDL-C levels increased twice as much (4.4 ± 0.8 v1.9 ± 0.9 mg/dL; P= .04), HDL3-C levels increased almost 2-fold greater (3.8 ± 0.7 v2.2 ± 0.6 mg/dL; P= .07), and HDL5NMR-C levels increased more than 4 times as much (2.2 ± 0.8 v0.5 ± 0.6 mg/dL; P= .08) in the CC compared to the CT/TT group. We conclude that the LIPG genotype is associated with interindividual variability in HDL-C and its subfractions and their response to exercise training.

Hypoxia-inducible factor 1 (HIF1) is a DNA transcription factor composed of two subunits, one of which is regulated by hypoxia (HIF1α, encoded by HIF1A). Genes regulated by HIF1 are involved in the processes of angiogenesis, erythropoiesis, and metabolism, making HIF1Aa candidate gene in establishing maximal oxygen consumption (V˙o2 max) before and after aerobic exercise training. The purpose of the present study was to screen HIF1Afor sequence variation and determine whether such variation is associated with V˙o2 maxbefore and after aerobic exercise training. A total of 233 Caucasian and African-American subjects were available for screening of HIF1Aand determination of allele frequencies, with 155 of those subjects used to study V˙o2 maxin relation to identified variants. We measured V˙o2 maxbefore and after 24 wk of aerobic exercise training. Screening revealed several rare and common polymorphisms in HIF1Awith race-specific allele frequencies. African Americans with AT or TT genotype at the A−2500T locus exhibited significantly lower baseline V˙o2 maxcompared with those of AA genotype (21.9 ± 0.99 vs. 25.1 ± 1.0, P= 0.03). An age by P582S (C/T) genotype interaction was observed in Caucasian subjects, such that those of CT or TT genotype exhibited significantly lower change in V˙o2 maxafter training than those of CC genotype when compared at ages 65 and 60 yr, but not at age 55 yr. No other significant differences were noted among genotype groups at the A−2500T, P582S, or T+140C sites. Based on these findings, we conclude that HIF1Asequence variation is associated with V˙o2 maxbefore and after aerobic exercise training in older humans.

The intestinal fatty acid binding protein (FABP2) gene is proposed as a candidate gene for diabetes because the protein it codes is involved in fatty acid (FA) absorption and metabolism and may, therefore, affect insulin sensitivity and glucose metabolism. Numerous studies have assessed FABP2 gene variants and their association with insulin resistance and type 2 diabetes. Some weak evidence indicates that the silent variants and those in the noncoding regions of the gene (codon 118, 3′ noncoding region, intron 2 trinucleotide repeat) might be associated with insulin resistance/type 2 diabetes. The most extensively studied variant is the missense Ala54Thr variation, which is common in diverse populations and results in increased FA absorption in vivo. Some evidence indicates that this variant may be associated with insulin sensitivity/type 2 diabetes. However, the large majority of studies assessing the potential association between the Ala54Thr FABP2 variant and insulin resistance/type 2 diabetes did not account for the independent and substantial effects of body composition, habitual physical activity (PA) levels, and diet on insulin resistance. We recently reported that there was an association between Ala54Thr FABP2 genotypes and insulin sensitivity after accounting for the independent effects of body composition and habitual PA levels on insulin sensitivity. Furthermore, others have demonstrated that Ala54Thr FABP2 may associate with insulin sensitivity, but only if individuals are consuming a high-fat diet. These results highlight the importance of including behavioral and environmental factors in the design of studies seeking to assess the impact of genes on physiological and clinical outcome phenotypes.

We sought to determine whether the M235T angiotensinogen (AGT) polymorphism, either interacting with habitual physical activity (PA) levels or independently, was associated with cardiovascular (CV) hemodynamics during maximal and submaximal exercise. Sixty-one healthy postmenopausal women (16 sedentary, 21 physically active, and 24 endurance athletes) had heart rate (HR), blood pressure (BP), cardiac output, stroke volume (SV), total peripheral resistance (TPR), and arteriovenous O2difference (a-vDo2) assessed during 40, 60, 80, and ∼100% of Vo2 maxtreadmill exercise. Vo2 maxdid not differ among AGT genotype groups; however, maximal HR was 14 beats/min higher in AGT TT than MM genotype women (P< 0.05). AGT TT genotype women also had 19 beats/min higher HR during ∼100% Vo2 maxexercise than AGT MM genotype women (P= 0.008). AGT genotype also interacted with habitual PA levels to associate with systolic BP and a-vDo2during ∼100% Vo2 maxexercise (both P< 0.01). AGT TT genotype women had 11 beats/min higher HR during submaximal exercise than MM genotype women (P< 0.05). AGT genotype interacted with habitual PA levels to associate with systolic BP during submaximal exercise (P= 0.009). AGT genotype, independently or interacting with habitual PA levels, did not associate significantly with diastolic BP, cardiac output, SV, or TPR during maximal or submaximal exercise. Thus this common genetic variant in the renin-angiotensin system appears to associate, both interactively with habitual PA levels and independently, with HR, systolic BP, and a-vDo2responses to maximal and submaximal exercise in postmenopausal women.

We sought to determine whether the angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism is associated with submaximal exercise cardiovascular hemodynamics. Postmenopausal healthy women (20 sedentary, 20 physically active, 22 endurance athletes) had cardiac output (acetylene rebreathing) measured during 40, 60, and 80%V˙o2 maxexercise. The interaction of ACE genotype and habitual physical activity (PA) level was significantly associated with submaximal exercise systolic blood pressure, with only sedentary women exhibiting differences among genotypes. No significant effects of ACE genotype or its interaction with PA levels was observed for submaximal exercise diastolic blood pressure. ACE genotype was significantly associated with submaximal exercise heart rate (HR) with ACE II having ∼10 beats/min higher HR than ACE ID/DD genotype women. ACE genotype did not interact significantly with habitual PA level to associate with submaximal exercise HR. ACE genotype was not independently, but was interactively with habitual PA levels, associated with differences in submaximal exercise cardiac output and stroke volume. For cardiac output, ACE II genotype women athletes had ∼25% greater cardiac output than ACE DD genotype women athletes, whereas for stroke volume genotype-dependent differences were observed in both the physically active and athletic women. ACE genotype was not significantly associated, either independently or interactively with habitual PA levels, with submaximal exercise total peripheral resistance or arteriovenous O2difference. Thus the common ACE locus polymorphic variation is associated with many submaximal exercise cardiovascular hemodynamic responses.

HAGBERG, J.M., G.E. MOORE, and R.E. FERRELL. Specific genetic markers of endurance performance and o2max. Exerc. Sport Sci. Rev., Vol. 29, No. 1, pp 15–19, 2001. Recent advances have revolutionized genetic studies of quantitative traits. Mitochondrial DNA and creatine kinase variations may influence o2max. Other data strongly suggest that angiotensin-converting enzyme genotype affects o2max and endurance performance capacity, but the mechanisms are unclear. A recent genome-wide scan study also has provided candidate loci requiring further study.

Apolipoprotein E (apo E) is important in plasma lipid metabolism and is a component of several plasma lipoprotein-lipid particles. Three major apo E isoforms are encoded by three common alleles at the APO E locus. The E2 allele is associated with lower and the E4 allele with higher total plasma cholesterol and LDL cholesterol levels compared with the E3 allele. Available data generally indicate that APO E2, and possibly E3, genotype individuals reduce plasma total and low-density lipoprotein (LDL) cholesterol levels more than APO E4 individuals with statin therapy. Some evidence also indicates that APO E2 individuals are more likely to respond favorably to gemfibrozil and cholestyramine. On the other hand, it appears that with probucol, APO E4 genotype individuals may improve plasma lipoprotein-lipid profiles more than APO E3 individuals. APO E2 and E3 genotype perimenopausal women appear to improve plasma lipoprotein-lipid profiles more with hormone replacement therapy than APO E4 women. On the other hand, low-fat diet interventions tend to reduce plasma LDL cholesterol and, perhaps, plasma total cholesterol levels more in APO E4 than in APO E2 or E3 individuals. Both cross-sectional and longitudinal studies generally indicate that APO E2 and E3 individuals improve plasma lipoprotein-lipid profiles more with exercise training than APO E4 individuals. Although these data are hardly definitive, they lend strong support for the possibility that in the near future individuals will be directed to what might be their optimal therapy for improving plasma lipoprotein-lipid profiles and cardiovascular disease risk based partially on APO E genotype.

We sought to determine the cardiovascular responses to increasing exercise intensities in postmenopausal women with different physical activity levels and hormone replacement therapy (HRT) status. Forty-four women (11 sedentary, 19 physically active, 14 master athletes; 24 not on HRT, 20 on HRT) completed treadmill exercise at 40, 60, 80, and 100% of maximal oxygen consumption. Oxygen consumption, heart rate, blood pressure, and cardiac output, determined via acetylene rebreathing, were measured at each exercise intensity. HRT did not affect cardiovascular hemodynamics. Stroke volume (SV) decreased significantly between 40 and 100% of maximal oxygen consumption in all groups, and the decrease did not differ among groups. The greater oxygen consumption of the athletes at each intensity was due to their significantly greater cardiac output, which was the result of a significantly greater SV, compared with both of the less active groups. The athletes had significantly lower total peripheral resistance at each exercise intensity than did the two less active groups. There were no consistent significant hemodynamic differences between the physically active and sedentary women. These results indicate that SV decreases in postmenopausal women as exercise intensity increases to maximum, regardless of their habitual physical activity levels or HRT status.

Relationships have frequently been found between angiotensin-converting enzyme (ACE) genotype and various pathological and physiological cardiovascular outcomes and functions. Thus we sought to determine whether ACE genotype affected maximal O2consumption (V˙o2 max) and maximal exercise hemodynamics in postmenopausal women with different habitual physical activity levels. Age, body composition, and habitual physical activity levels did not differ among ACE genotype groups. However, ACE insertion/insertion (II) genotype carriers had a 6.3 ml ⋅ kg−1⋅ min−1higher V˙o2 max(P< 0.05) than the ACE deletion/deletion (DD) genotype group after accounting for the effect of physical activity levels. The ACE II genotype group also had a 3.3 ml ⋅ kg−1⋅ min−1higher V˙o2 max(P< 0.05) than the ACE insertion/deletion (ID) genotype group. The ACE ID group tended to have a higher V˙o2 maxthan the DD genotype group, but the difference was not significant. ACE genotype accounted for 12% of the variation inV˙o2 maxamong women after accounting for the effect of habitual physical activity levels. The entire difference inV˙o2 maxamong ACE genotype groups was the result of differences in maximal arteriovenous O2difference (a-vDo2). ACE genotype accounted for 17% of the variation in maximal a-vDo2in these women. Maximal cardiac output index did not differ whatsoever among ACE genotype groups. Thus it appears that ACE genotype accounts for a significant portion of the interindividual differences inV˙o2 maxamong these women. However, this difference is the result of genotype-dependent differences in maximal a-vDo2and not of maximal stroke volume and maximal cardiac output.

Myostatin is a recently identified member of the transforming growth factor-β family of regulatory factors, also known as growth and differentiation factor 8 (GDF8). The nucleotide sequence of human myostatin was determined in 40 individuals. The invariant promoter contains a consensus MyoD binding site, and the coding sequence contains five missense substitutions in conserved amino acid residues (A55T, K153R, E164K, P198A, and I225T). Two of these, A55T in exon 1 and K153R in exon 2, are polymorphic in the general population with significantly different allele frequencies in Caucasians and African Americans (P< 0.001). Neither of the common polymorphisms had a significant impact on muscle mass response to strength training in either Caucasians or African Americans, although skewed allele frequencies preclude detection of small effects. These allelic variants provide markers for examining association between the myostatin gene and interindividual variation in muscle mass and differences in loss of muscle mass with aging.

This study was designed to characterize the changes in left ventricular performance induced by graded isometric exercise. Fourteen healthy subjects (12 men and 2 women), aged 19 to 27, performed handgrip isometric exercise at 20, 40, and 60 percent of their maximal voluntary contraction (MVC) with three minutes of rest interval between each contraction. Left ventricular performance was assessed by M-mode echocardiography at rest and during each isometric contraction. Left ventricular end-diastolic and end-systolic dimensions did not change significantly. Heart rate and blood pressure increased significantly during each level of isometric contraction. Left ventricular posterior wall thickness fell from 8.6 ± .4 (mean ± SE) to 7.1 ± .5 (P<0.01) and 6.5 ± .4 mm (P < 0.001) in response to 40 and 60 percent of MVC, respectively. Left ventricular wall thickness to radius ratio decreased progressively as systolic blood pressure increased which suggests increased wall tension. Fractional shortening remained unchanged during graded isometric exercise. However, mean velocity of circumferential fiber shortening (mVcf) increased from 1.08 ± 0.4 to 1.24 ± .05 circ/sec (P<0.005) in response to 60 percent of MVC. We conclude that the effect of isometric exercise on left ventricular performance depends, to some extent, on the relative strength of muscle contraction. In healthy subjects, isometric exercise of low intensity (<40 percent of MVC) does not generally result in depression of left ventricular function. Higher levels of isometric exercise may modestly enhance left ventricular performance despite a sudden increase in blood pressure.

The purpose of this study was to evaluate the effects of long-term exercise training on maximal aerobic exercise capacity, evidence of myocardial ischemia and plasma lipid-lipoprotein concentrations in patients with coronary artery disease. Nine men with coronary artery disease, aged 57 ± 2 years, who had completed 12 months of supervised intense exercise training were restudied after 6 additional years during which they continued to exercise. The first 12 months of training resulted in a 44% increase in maximal oxygen consumption ( VO2max) from 25.0 ± 1.3 to 35.9 ± 1.5 ml kg−1min−1(p < 0.001). The VO2max after 6 additional years (total 7 years) of intense training was 36.8 ± 2.4ml·kg−1min−1.

A 29-year-old woman had muscle weakness, low concentrations of carnitine in muscle and serum, and abnormally low urinary excretion of carnitine. During a fast, exercise capacity declined, ketone body concentrations rose, metabolic acidosis worsened, and she became hypoglycemic. After treatment with oral carnitine, serum carnitine content returned to normal and blood glucose was maintained during fasting, but ketone body concentrations in blood were even higher. Muscle carnitine content and exercise capacity did not improve. This patient demonstrated features of both systemic and muscle carnitine deficiency, suggesting that the current classification of carnitine-deficiency syndromes is inadequate.

Nine sedentary men (53 ± 3 yr) were studied before and after 6 d of endurance exercise training to determine the effects on maximal oxygen uptake (VO2 max), and on the heart rate, blood pressure, and metabolic responses to a standard bout of steady-state sub-maximal exercise. The subjects exercised approximately 1 h-d-1at about 68 of VO2 max. The 6-d protocol elicited no improvement in VO2 max, (2.50 ± 0.14 before vs 2.58 ± 0.15 1-min-1after training). Heart rates were significantly lower by 5 to 8 b-min-1, systolic blood pressures were reduced by 16 to 19 mm Hg, and blood lactate concentrations were 25 to 35 less at the same exercise intensities (60, 70, and 80 of VO2 max) after 6 d of exercise. Rate pressure product was about 15 lower at the same exercise intensity after 6 d of training (P<0.05). The respiratory exchange ratio during submaximal exercise was 0.02 to 0.04 units lower (P<0.05; P<0.01) after 6 d of exercise, indicating a shift in substrate utilization favoring fat oxidation. These findings suggest that short-term endurance training can induce heart rate, blood pressure, and metabolic adaptations to sub-maximal exercise before there is a significant increase in VO2 maxin sedentary, middle-aged men who are capable of vigorous exercise.

Studies assessing changes in maximal aerobic capacity (V˙o2 max) associated with aging have traditionally employed the ratio ofV˙o2 maxto body weight. Log-linear, ordinary least-squares, and weighted least-squares models may avoid some of the inherent weaknesses associated with the use of ratios. In this study we used four different methods to examine the age-associated decline inV˙o2 maxin a cross-sectional sample of 276 healthy men, aged 45–80 yr. Sixty-one of the men were aerobically trained athletes, and the remainder were sedentary. The model that accounted for the largest proportion of variance was a weighted least-squares model that included age, fat-free mass, and an indicator variable denoting exercise training status. The model accounted for 66% of the variance inV˙o2 maxand satisfied all the important general linear model assumptions. The other approaches failed to satisfy one or more of these assumptions. The results indicated thatV˙o2 maxdeclines at the same rate in athletic and sedentary men (0.24 l/min or 9%/decade) and that 35% of this decline (0.08 l ⋅ min−1⋅ decade−1) is due to the age-associated loss of fat-free mass.

Objective:To assess the effects of 1 and 7 consecutive days of exercise on glucose and insulin responses to an oral glucose challenge.

Eleven healthy men and women (63 ±1 years) participated in a 12-month endurance-training program to determine the effects of low-intensity and high-intensity training on glucose tolerance and plasma lipids in older persons. Plasma glucose, insulin, and C-peptide concentrations were measured for three hours after ingestion of 100 g of glucose and the total areas under the respective curves were calculated. Total plasma lipids and lipoprotein concentrations were determined during fasting. Maximal oxygen uptake increased 12% during six months of low-intensity training; a further 18% increase occurred during an additional six months of high-intensity training. Glucose tolerance, which was normal initially, was not significantly changed after training. However, the total area for insulin was 8% lower after low-intensity training, and 23% lower after high-intensity training, compared with before training. C-peptide concentrations were similarly reduced. Plasma lipid and lipoprotein concentrations were unchanged after low-intensity training, but high-intensity training resulted in an increase in high-density lipoprotein cholesterol and a reduction in triglycerides. These results demonstrate that older persons respond to prolonged, high-intensity endurance training with an increase in sensitivity to insulin and a favorable alteration in their plasma lipoprotein-lipid profile.(JAMA 1984;252:645-649)

To determine the relationship between lipid profiles and the type of weight training and to assess the effects of anabolic-androgenic steroids on lipids, bodybuilders and powerlifters of similar age, body fat, and testosterone levels were studied before and after androgen use. Before androgen administration powerlifters had lower levels of plasma high-density—lipoprotein cholesterol (HDL-C) and HDL2-C (38±2; 6±1 mg/dL; X ± SE, n=8) than bodybuilders (55 ±2; 12 ± 1 mg/dL; n=8) and runners of comparable age and body fat (47 ±2; 14±2 mg/dL; n=8), while levels of low-density—lipoprotein cholesterol (LDL-C) were higher in powerlifters 138±10 mg/dL) than in bodybuilders (104±7 mg/dL) and runners (110 ±6 mg/dL). Therefore, powerlifters had higher LDL-C/HDL-C ratios (3.7 ±0.3) than bodybuilders (2.0 ±0.2) and runners (2.4 ±0.2). Androgen use by eight bodybuilders and four powerlifters lowered values of both HDL-C and HDL2-C by 55% and raised values of LDL-C (61% ±10%) and LDL-C/HDL-C ratios (280%±40%). Therefore, the training regimen of bodybuilders is associated with a more favorable lipid profile than the training used by powerlifters. Androgen use by strength-trained athletes may increase their risk for coronary heart disease.(JAMA 1984;252:507-513)

The-response to a standardized exercise test was investigated in 12 volunteers and 13 patients with aches, cramps, and pains. In men, creatine kinase (CK) levels peaked (up to 1600 mU per milliliter) between 10 and 20 hours after exercise. High levels of blood lactate during exercise were related to the intensity of work and to high levels of CK after exercise. The patients could be divided into several groups: (1) those with no change in blood metabolites (psychogenic); (2) those with a disproportionate rise in CK (metabolic myopathies); (3) those with a disproportionate rise of lactate (mitochondrial abnormalities); and (4) in one patient with exercise-related pains, subnormal elevation of fatty acid levels. The correlation of changes in blood lactate, CK, and fatty acids may be useful, whereas an isolated measurement, even if outside the normal range, is often meaningless.

Exercise training elicits numerous beneficial adaptations in patients with coronary artery disease (CAD), but until 10 yr ago these adaptations were generally believed to be peripheral adaptations rather than improvements in myocardial blood supply. However, animal models of CAD have been shown to elicit improvements in myocardial blood flow and left ventricular performance with prolonged, intense exercise training. More recently we have provided electrocardiographic, echocardiographic, hemodynamic, and radionuclide evidence of central cardiovascular adaptations in patients with CAD after a year-long program of 1 h of exercise at 70–90 of VO2max5 d·wk-1. These training-induced adaptations are consistent with an improvement in myocardial oxygenation and concomitantly an enhanced left ventricular function in these patients. This program also resulted in improvements in glucose tolerance, insulin sensitivity, and plasma lipoprotein-lipid profile. We have also shown that these beneficial cardiovascular and metabolic adaptations are maintained during six additional years of training in patients with CAD. These results do not imply that all patients with CAD should initiate such an intense training program, but rather that, in selected patients undergoing a training stimulus well in excess of that conventionally prescribed for coronary patients, the training-induced adaptations may be substantially greater than previously believed.

POLLOCK, M. L., J. F. CARROLL, J. E. GRAVES, S. H. LEGGETT, R. W. BRAITH, M. LIMACHER, and J. M. HAGBERG. Injuries and adherence to walk/jog and resistance training programs in the elderly. Med. Sci. Sports Exerc., Vol. 23, No. 10, pp. 1194–1200, 1991. To evaluate the effects of 26 wk of aerobic and resistance training on the incidence of injury and program adherence in 70− to 79-yr-old men and women, 57 healthy volunteers (25 males, 32 females) were randomly assigned to a walk/jog (W/J, N= 21), strength (STREN, N= 23), or control (CONT, N= 13) group. Walk/jog training was for 30–45 min, 3 d. wk-1with intensity equal to 40–70 heart rate max reserve (HRmaxreserve) during the first 13 wk, and 75–85 HRmaxreserve for weeks 14–26. STREN training consisted of one set (10–12 repetitions) each of 10 variable resistance exercises performed to volitional fatigue. Forty-nine of the original participants completed the training program. Walk/jog training increased O2maxfrom 22.5 to 27.1 ml.kg-1.min-1(P± 0.05) while STREN and CONT showed no change. STREN improved significantly in chest press and leg extension strength (P± 0.05) while W/J and CONT showed no change. Adherence to training was 20/23 (87) and 17/21 (81) in STREN and W/J, respectively. One repetition maximum (1-RM) strength testing resulted in 11 injuries in the 57 subjects (19.3) while STREN training resulted in only two injuries in 23 subjects (8.7). Walk training during weeks 1–13 resulted in one injury in 21 subjects (4.8). Eight of 14 subjects (57) who began jogging intervals at week 14 incurred an injury: two of eight (25) of the men and all of the women (6 of 6). All W/J training injuries were to the lower extremity. Only one dropout occurred due to injury. The results showed that 70–79 yr olds make significant improvements in O2maxand strength with training, but because of injuries incurred during jogging and 1-RM strength testing, these activities should be used with caution.

SEALS, DOUGLAS R. and JAMES M. HAGBERG. The effect of exercise training on human hypertension: a review Med. Sci. Sports Exerc., Vol. 16, No. 3., pp. 207–215. 1984. Numerous sources of Information in both the medical and exercise physiology areas state that exercise training lowers blood pressure at rest and during submaximal exercise in normotensive and hypertensive individuals. Based on these statements, the medical community is currently recommending regular exercise as a non-pharmacological therapy for reducing blood pressure in hypertensive patients. The purpose of this review was to assess the existing literature in this area to determine whether a basis exists for this recommendation. Our findings indicate that most of the studies reviewed reported modest reductions in blood pressure (≤10 mmHg) at rest and during submaximal exercise after training. However, even the modest reductions in blood pressure reported in these studies must be interpreted with caution because of numerous methodological shortcomings and inadequate study design, most notably the omission of non-exercising hypertensive control groups. Therefore, the evidence available at the present time is inadequate to recommend exercise training as a non-pharmacological therapy in hypertension.

Patients with neuromuscular diseases have low levels of cardio vascular fitness and they fatigue rapidly during daily activities. The purpose of this investigation was to determine whether patients with slowly-progressive or non-progressive neuromuscular diseases could complete a 12-wk training program without untoward responses, and develop cardiovascular training adaptations. All eight patients completed the training program with better than 90 compliance. Resting creatine kinase and myoglobin in the group as a whole showed no change with training, though two patients did have definite elevations after training. Their VO2maxincreased by 25 ± 5 with training and their relative increase in Vo2maxwas not different from that of healthy subjects undergoing the same training. Heart rate reductions during submaximal exercise were somewhat delayed or non-existent in the two patients with Charcot-Marie-Tooth disease, a hereditary neuropathy. However, the six patients with myopathies had heart rate adaptations similar to those in healthy subjects. Thus, some patients with slowly-progressive or non-progressive neuromuscular diseases can undergo exercise training and in many cases demonstrate adaptations not differernt from those in healthy subjects. Patients with different diseases, however, need not respond uniformly, in terms of training adaptations or markers of muscle damage. Therefore, each disease must be considered individually.

Comparable effects of diet and exercise on body composition and lipoproteins in older men. Med. Sci, Sports Exerc., Vol. 26, No. 11, pp. 1307–1315, 1994. Changes in body composition, fat distribution and lipoprotein lipids in response to weight loss elicited by a 10-month program of hypocaloric diet (HD) therapy alone or combined with aerobic exercise training (AEXHD) were examined in sedentary obese older males. Body composition was assessed by hydrodensitometry and fat distribution was evaluated with skinfold thickness and circumference measures. The HD group underwent a dietary/behavioral modification program to reduce caloric intake. The AEXHD group underwent a similar dietary modification program combined with aerobic exercise training. Following completion of the study, 15 subjects from each group were individually pair matched based on age (57.1 ± 1.7 vs 61.3 ± 2.4 yrs) and their reduction in body mass (−7.6 ± 1.3 vs −8.0 ± 1.1 kg). Reductions in fat and fat-free mass and skinfold thickness and circumferences were similar in both groups. In both the AEXHD and HD groups there were significant reductions in the ratio of low-density lipoproteins to high-density lipoproteins (HDL-C) and triglycerides and a significant increase in HDL2-C. There were no differences in final values or absolute and relative changes in the various lipoprotein values between the two groups. These results suggest weight loss induced by diet alone or combined with aerobic exercise cause similar changes in body composition and lipoprotein lipids.

Men and women 70–79 yr of age (TV = 49) were studied to assess the effect of 6 months of resistance or endurance exercise training on their blood pressure, hemodynamic parameters, and pressor hormone levels. Resistance training consisted of one set of 8–12 repetitions on ten Nautilus®machines three times per week. The endurance training group progressed to training at 75–85 O2maxfor 35–45 min three times per week for the last 2 months of training. No changes in body weight or estimated lean body mass occurred; however, the sum of seven skinfolds, as an index of percent body fat, decreased in both exercise groups. Upper and lower body strength increased with resistance training, while O2maxincreased by 20 in the endurance training group. Blood pressure did not change with resistance training in individuals with normal or somewhat elevated blood pressures. Diastolic and mean blood pressure decreased significantly, by 5 and 4 mm Hg, with endurance training. Subjects with blood pressure > 140/90 reduced their systolic, diastolic, and mean blood pressure by 8,9, and 8 mm Hg, respectively, with endurance exercise training. Cardiac output, peripheral vascular resistance, and plasma levels of angiotensin I and II and epi- and norepinephrine did not change in any of the groups. Thus, resistance exercise training does not adversely affect, or reduce, blood pressure, while endurance exercise training produces modest reductions in blood pressure in 70–79-yr-old individuals with somewhat elevated blood pressures.

To determine whether expanded intravascular volumes contribute to the older athlete’s higher exercise stroke volume and maximal oxygen consumption (V˙o2 max), we measured peak upright cycle ergometry cardiac volumes (99mTc ventriculography) and plasma (125I-labeled albumin) and red cell (NaCr51) volumes in 7 endurance-trained and 12 age-matched lean sedentary men. The athletes had ∼40% higherV˙o2 maxvalues than did the sedentary men and larger relative plasma (46 vs. 38 ml/kg), red cell (30 vs. 26 ml/kg), and total blood volumes (76 vs. 64 ml/kg) (allP< 0.05). Athletes had larger peak cycle ergometer exercise stroke volume indexes (75 vs. 57 ml/m2,P< 0.05) and 17% larger end-diastolic volume indexes. In the total group,V˙o2 maxcorrelated with plasma, red cell, and total blood volumes (r= 0.61–0.70,P< 0.01). Peak exercise stroke volume was correlated directly with the blood volume variables (r= 0.59–0.67,P< 0.01). Multiple regression analyses showed that fat-free mass and plasma or total blood volume, but not red cell volume, were independent determinants ofV˙o2 maxand peak exercise stroke volume. Plasma and total blood volumes correlated with the stroke volume and end-diastolic volume changes from rest to peak exercise. This suggests that expanded intravascular volumes, particularly plasma and total blood volumes, contribute to the higher peak exercise left ventricular end-diastolic volume, stroke volume, and cardiac output and hence the higherV˙o2 maxin master athletes by eliciting both chronic volume overload and increased utilization of the Frank-Starling effect during exercise.

• Using bicycle ergometry with computerized respiratory gas exchange measurements, we compared exercise capacities in patients with various neuromuscular diseases to those in normal controls. As expected, male and female patients had significantly reduced maximum work capacities (kilopond-meters per minute per kilogram of body weight) and maximal oxygen consumptions. The oxygen cost of exercise was normal in the majority of patients, although some appeared to have abnormally high oxygen consumptions during exercise. Breathing patterns during exercise, particularly in regard to onset of hyperventilation, were similar in patients and controls.

HAGBERG, JAMES A. and EDWARD F. COYLE. Physiological determinants of endurance performance as studied in competitive racewalkers. Med. Sci. Sports Exerc., Vol. 15, No. 4, pp. 287–289, 1983. The physiological factors that relate to 20-km performance were studied in eight competitive racewalkers. The racewalking velocity at the blood lactate threshold (LT) during steady-state exercise was highly correlated to racewalking pace (r=0.94) and predicted performance times to within 0.6, which agrees with previous observations on runners. The two factors that contribute to velocity at LT are O2uptake at LT (o2at LT) and submaximal racewalking economy (measured as the o2at a standard velocity). Oxygen uptake at LT was significantly correlated (r=0.89) to performance in the racewalkers in the present investigation, which agrees with previous observations of runners. Submaximal economy was significantly correlated to performance in the racewalkers (r=0.82). Maximal oxygen uptake measured during racewalking was not significantly correlated (r=0.62) to performance. These data indicate that the velocity at LT correlates closely to performance in racewalkers and that the factor of submaximal economy, which partly determines velocity at LT, is related more to performance ability in racewalking than was previously observed in running.

We used riboflavin to treat a patient with lipid myopathy, reduced exercise capacity, intolerance to fasting, and reduced concentrations of carnitine in muscle and serum. Although carnitine concentrations did not change, exercise capacity doubled, and response to fasting improved. Muscle enzyme assay showed that palmityl CoA dehydrogenase activity with and without added flavin adenine dinucleotide (a riboflavin product) was normal. Another riboflavin derivative, electron transfer flavoprotein, could be the site of the defect.

OBJECTIVE: To determine the effects of 3 months of voluntary deconditioning on cardiac function in master athletes.