Biomedical subjects

C Foster

Publications and source records attributed to C Foster.

At least 73 records · Page 4Linked to original sources

PubMed1998

Monitoring training in athletes with reference to overtraining syndrome.

PURPOSE: Overtraining is primarily related to sustained high load training, often coupled with other stressors. Studies in animal models have suggested that unremittingly heavy training (monotonous training) may increase the likelihood of developing overtraining syndrome. The purpose of this study was to extend our preliminary observations by relating the incidence of illnesses and minor injuries to various indices of training. METHODS: We report observations of the relationship of banal illnesses (a frequently cited marker of overtraining syndrome) to training load and training monotony in experienced athletes (N = 25). Athletes recorded their training using a method that integrates the exercise session RPE and the duration of the training session. Illnesses were noted and correlated with indices of training load (rolling 6 wk average), monotony (daily mean/standard deviation), and strain (load x monotony). RESULTS: It was observed that a high percentage of illnesses could be accounted for when individual athletes exceeded individually identifiable training thresholds, mostly related to the strain of training. CONCLUSIONS: These suggest that simple methods of monitoring the characteristics of training may allow the athlete to achieve the goals of training while minimizing undesired training outcomes.

Adult↗

PubMed1998

Physiological and pathological aspects of exercise left ventricular function.

Measures of left ventricular function during exercise provide information that is more accurate than the exercise ECG in the diagnosis of coronary artery disease, supportive of the data provided by myocardial perfusion studies, and of great prognostic significance. We review basic methods for evaluating left ventricular function during exercise and responses to various types of exercise, including incremental exercise and exercise training conditions. Additionally, we review changes in both incremental exercise test responses and responses to training in various pathological conditions. Case reports are included to illustrate the utility of measuring left ventricular function during exercise.

Coronary Circulation↗

PubMed1997

Characterization of in vitro and in vivo platelet responses to thrombin and thrombin receptor-activating peptides in guinea pigs.

Guinea pig platelets are similar to human platelets in their responsiveness to thrombin receptor-activating peptides and other agonists. Therefore, guinea pigs anesthetized with Inactin (90 mg/kg i.p.) were used to assess in vivo activities of thrombin and thrombin receptor-activating peptides (TRAPs) using 111 In-labeled platelets and a microcomputer-based system. The aggregatory responses are expressed as percent change for a 20 min period over basal radioactivity (AUC). Reversible accumulation of platelets occurred in the pulmonary microcirculation in response to stimuli. Human thrombin (50 and 100 U/kg i.v.) caused a dose-related platelet accumulation. Responses of similar magnitude were induced by SFLLRN (TRAP-(1-6)) and Ala-Phe(p-F)-Arg-Cha-HArg-Tyr-NH2 (high-affinity thrombin receptor-activating peptide, 0.03, 0.1 and 0.3 mg/kg i.v.). High-affinity thrombin receptor-activating peptide, a new synthetic oligopeptide agonist, is about 3-fold more potent than TRAP-(1-6), a wild-type sequence. Similarly, high-affinity thrombin receptor-activating peptide is about 4 times more potent than TRAP-(1-6) in the radioligand binding study using platelet membrane. By comparison, high-affinity thrombin receptor-activating peptide manifested an aggregatory activity (EC60 = 1.2 microM) about 15 times more potent than that of TRAP-(1-6)(EC60 = 18.6 microM) in washed guinea pig platelets. The intrapulmonary platelet aggregation in response to thrombin, TRAP-(1-6) and high-affinity thrombin receptor-activating peptide was characterized by long duration (approximately 30 min); a reduction in response (18-54%) tended to occur with repeated challenges, presumably due to desensitization and consumption. The response to thrombin (100 U/kg) was greatly inhibited by (D)-Phe-Pro-Arg-chloromethyl ketone (PPACK), a potent thrombin inhibitor (250 micrograms/kg + 6 micrograms/kg per min i.v. x 30): AUC, 150 +/- 552 vs. 7171 +/- 1052 in the control period (n = 8, P < 0.05). The response to high-affinity thrombin receptor-activating peptide (0.03 mg/kg), which acts on thrombin receptor directly, was not affected by PPACK. It is concluded that guinea pigs are an appropriate preparation for evaluation of in vivo activity of thrombin inhibitors as well as thrombin receptor agonists and antagonists.

Amino Acid Chloromethyl Ketones↗

PubMed1997

Left ventricular function during exercise testing and training.

Left ventricular function (LVEF) deteriorates during incremental exercise (GXT) in patients with ischemia (+ISCH). Left ventricular (LV) functional response during steady-state exercise, typical of that used in exercise training, are unknown. We compared LVEF in patients with documented coronary heart disease (CHD) who either had (+) or did not have (-) ISCH, and in healthy volunteers (CONTROL) during GXT and steady state. First pass RNA was performed during upright cycle GXT at rest (R), at the ventilatory threshold (VT), and at maximal exercise (Max); and during steady state at the workload associated with VT after 10, 20, and 30 min of exercise. RNA allowed measurement of ejection fraction (EF) and wall motion (WM); ISCH was mild, angina being relieved by momentary reductions in workload during steady state. Although +ISCH demonstrated the expected deterioration in LV function during GXT (decreased EF, abnormal WM)(EF = 58 to 56 to 54%), there was no evidence for progressive deterioration of LV function during steady state despite the presence of mild ISCH (56 to 56 to 54 to 54%). In -ISCH and CONTROL there were normal responses of EF during GXT (43 to 51 to 51% and 59 to 65 to 61%) and steady state (43 to 51 to 53 to 51% and 59 to 65 to 68 to 69%). We conclude that mild ischemia may be tolerated during steady-state exercise at levels consistent with exercise training without progressive deterioration of LV function.

Adult↗

PubMed1997

Comparison of free range and graded exercise testing.

Previous studies with athletes have demonstrated greater physiologic responses during free range (FR) compared with graded (GXT) exercise testing. Since the sensitivity of clinical exercise testing depends upon the magnitude of physiologic responses, we sought to determine whether FR might provoke greater responses than GXT in nonathletic individuals and patients. Healthy, physically active nonathletes and clinically stable CHD patients (N = 12) performed GXT on cycle ergometer (15 W + 15 W.min-1) and FR (minimal time for 75 kJ task) on a cycle ergometer. A starting power output was recommended for FR, but the patients were free to pedal at their own rates. During FR, VO2max (36.5 +/- 10.1 vs 34.1 +/- 9.4 mL.min-1.kg-1), HRmax (156 +/- 25 vs 144 +/- 27 beats.min-1), double product (31.4 +/- 4.9 vs 29.1 +/- 5.9) and VEmax (111 +/- 26 vs 94 +/- 17 L.min-1) were all significantly greater than during cycle GXT. The mean peak power output during GXT (180 +/- 45 W) was not significantly different than the mean power output during FR (204 +/- 45 W). During FR, successive "0.5 mile laps" (approximately 12.5 kJ) were accomplished at power outputs of 217 +/- 45, 217 +/- 52, 192 +/- 60, 194 +/- 65, 199 +/- 63, and 207 +/- 63 W. No patient experienced angina or ECG changes during either FR or GXT. The patients uniformly reported that FR felt like "hurrying" in the real world. Some patients had to make large reductions in their power output in mid ride to allow recovery from a too aggressive start, much as they would in the real world. We conclude that FR exercise provides a clinically useful method of exercise testing that is not only more like real world exercise patterns but also provokes greater physiologic responses than are achievable during conventional GXT.

Adult↗

PubMed1997

Binding of a thrombin receptor tethered ligand analogue to human platelet thrombin receptor.

A thrombin receptor-radioligand binding assay was developed using [3H]A(pF-F)R(ChA)(hR)Y-NH2 ([3H]haTRAP), a high affinity thrombin receptor-activating peptide (TRAP), and human platelet membranes. Scatchard analysis of saturation binding data indicated that [3H]haTRAP bound to platelet membranes with a Kd of 15 nM and a Bmax of 5.2 pmol/mg of protein. The binding was reduced by GPPNHP, a nonmetabolizable GTP analogue. Various TRAPs and a TRAP antagonist, but not other receptor agonists, displaced [3H]haTRAP from the binding sites. SFLLRN-NH2, a thrombin receptor-tethered ligand analogue, and [3H]haTRAP exhibited competitive binding for the same binding sites. The relative affinity of these peptides for the binding site paralleled their EC50 or IC50 values for platelet aggregation. These data indicate that [3H]haTRAP binds specifically and saturably to the functioning G protein-linked thrombin (tethered ligand) receptor in human platelet membranes.

Dose-Response Relationship, Drug↗

PubMed1997

Twenty-year follow-up of aerobic power and body composition of older track athletes.

The purpose was to determine the aerobic power (maximal oxygen uptake) and body composition of older track athletes after a 20-yr follow-up (T3). At 20 yr, 21 subjects [mean ages: 50.5 +/- 8.5 yr at initial evaluation (T1), 60.2 +/- 8.8 yr at 10-yr follow-up (T2), and 70.4 +/- 8.8 yr at 20-yr follow-up (T3)] were divided into three intensity groups: high (H; remained elite; n = 9); moderate (M; continued frequent moderate-to-rigorous endurance training; n = 10); and low (L; greatly reduced training; n = 2). All groups decreased in maximal oxygen uptake at each testing point (H, 8 and 15%; M, 13 and 14%; and L, 18 and 34% from T1 to T2 and T2 to T3, respectively). Maximal heart rate showed a linear decrease of approximately 5-7 beats.min-1.decade-1 and was independent of training status. Body weight remained stable for the H and M groups and percent fat increased approximately 2-2.5%/decade. Although fat-free weight decreased at each testing point, there was a trend for those who began weight-training exercise to better maintain it. Cross-sectional analysis at T3 showed that leg strength and bone mineral density were generally maintained from age 60 to 89 yr. Those who performed weight training had a greater arm region bone mineral density than those who did not. These longitudinal data show that the physiological capacities of older athletes are reduced despite continued vigorous endurance exercise over a 20-yr period (approximately 8-15%/decade). Changes in body composition appeared to be less than those shown for the healthy sedentary population and were related to changes in training habits.

Aged↗

PubMed1997

Ultrasonic nebulization of albuterol is no more effective than jet nebulization for the treatment of acute asthma in children.

STUDY OBJECTIVE: Nebulizer systems used to generate therapeutic aerosols vary in their ability to deliver medication to the airway. In a recent study in 17 adults with stable asthma, albuterol given using an ultrasonic nebulizer (UN) appeared to produce greater bronchodilatation than the same dose of albuterol given by a jet nebulizer (JN). The purpose of this study was to determine if the UN used in that study would produce a better bronchodilator response in children with acute asthma than the JN system that has been in use at Cardinal Glennon Children's Hospital. DESIGN: Randomized, prospective, unblinded study. SETTING: An urban university children's hospital emergency department. PARTICIPANTS: One hundred thirteen children, aged 7 to 16 years, who presented for treatment of acute moderately severe asthma completed this study. INTERVENTIONS: After randomization and exclusion of dropouts, 46 children received albuterol by UN and 67 were treated by JN. MEASUREMENTS: Pulmonary function tests (PFTs) by spirometry, pulse oximetry, and symptom score at baseline and at 15 and 30 min following a single prescribed treatment. RESULTS: PFT on entry to the study was the same in both groups (FEV1; p>0.97). The change in FEV1 after therapy (UN+0.22 L vs JN+0.37 L) was significant (p<0.05) and favored JN. There was no difference in the improvement in pulmonary function between JN and UN therapy in children with an initial FEV1/FVC > 75% predicted but when FEV1/FVC < 75%, the improvement in FEV1 again favored the JN (UN+0.2 vs JN+0.47; p<0.05). CONCLUSION: For the treatment of acute exacerbations of asthma in children, there is no greater bronchodilator response when albuterol is administered by a UN than by a JN.

Acute Disease↗

PubMed1997

Isolation and characterization of liver epithelial cell lines from wild-type and mutant TgN737Rpw mice.

The Tg737 gene encodes a tetratricopeptide repeat containing protein that, when disrupted in TgN737Rpw mutant mice, results in pleiotropic phenotypes that include the proliferation of epithelial cells. In the kidney and liver, this causes a phenotype that resembles autosomal recessive polycystic kidney disease. In the liver, the affected epithelial cells morphologically and immunologically resemble oval cells. Here we describe the isolation, culture, and characterization of epithelial cell lines derived from the livers of wild-type, heterozygous, and homozygous TgN737Rpw mice. Essentially homogeneous cell cultures were established and the expression of liver markers was examined by reverse transcriptase polymerase chain reaction and by immunohistochemistry. All of the cell lines reacted to the A6 antibody that was raised against mouse oval cells and expressed markers seen in oval cells. Cells transplanted into the interscapular fat pads of isogenic mice formed well defined ductular structures. Furthermore, in transfection experiments, we have demonstrated the involvement of Tg737 in cellular proliferation.

Adipose Tissue↗

PubMed1997

Training and overtraining: an overview and experimental results in endurance sports.

Overtraining can be defined as "training-competition > > recovery imbalance", that is assumed to result in glycogen deficit, catabolic > anabolic imbalance, neuroendocrine imbalance, amino acid imbalance, and autonomic imbalance. Additional non-training stress factors and monotony of training exacerbate the risk of a resulting overtraining syndrome. Short-term overtraining called overreaching which can be seen as a normal part of athletic training, must be distinguished from long-term overtraining that can lead to a state described as burnout, staleness or overtraining syndrome. Persistent performance incompetence, persistent high fatigue ratings, altered mood state, increased rate of infections, and suppressed reproductive function have been described as key findings in overtraining syndrome. An increased risk of overtraining syndrome may be expected around 3 weeks of intensified/prolonged endurance training at a high training load level. Heavy training loads may apparently be tolerated for extensive periods of time if athletes take a rest day every week and use alternating hard and easy days of training. Persistent performance incompetence and high fatigue ratings may depend on impaired or inhibited transmission of ergotropic (catabolic) signals to target organs, such as: (I) decreased neuromuscular excitability, (II) inhibition of alpha-motoneuron activity (hypothetic), (III) decreased adrenal sensitivity to ACTH (cortisol release) and increased pituitary sensitivity to GHRH (GH release) resulting in a counter-regulatory shift to a more anabolic endocrine responsibility, (IV) decreased beta-adrenoreceptor density (sensitivity to catecholamines), (V) decreased intrinsic sympathetic activity, and (VI) intracellular protective mechanisms such as increased synthesis of heat-shock proteins (HSP 70) represent a complex strategy against an overload-dependent cellular damage.

Adrenal Glands↗

PubMed1996

Commentary: ethics of clinical research without patients' consent.

What makes a research project ethical? A series of criteria need to be satisfied. Difficulties arise when only some of them can be satisfied or, as in the case of this trial, when two of them are mutually exclusive. The criteria are that the research is aimed at obtaining a desirable end, that the research subjects will not be harmed by being in the trial, and that the research subjects are consulted before going enrolled into the research.

Clinical Trials as Topic↗

PubMed1996

Cumulative experience of percutaneous epididymal sperm aspiration (PESA) with intracytoplasmic sperm injection.

OBJECTIVE: Our objective was to evaluate the recovery rate of spermatozoa from the epididymis using a percutaneous aspiration technique and to assess the fertilisation rate after intracytoplasmic sperm injection. MATERIALS AND METHODS: Fifty-four patients with azoospermia had a total of 59 cycles at IVF with intracytoplasmic sperm injection (ICSI). The cause of the azoospermia was failed vasectomy reversal in 23 cases, congenital absence of the vas in 22 cases, partial testicular failure in 5 cases, and retrograde ejaculation in 2 cases, while the remaining 2 patients had erectile disorders. RESULTS: A total of 741 oocytes was collected and 521 metaphase II oocytes were subsequently microinjected. Normal fertilisation occurred in 274 oocytes (52.6%), and of these, 234 cleaved (85.4%). In 54 cycles, embryo transfer of more than one embryo occurred (91.5%) and a total of 155 embryos was replaced. The pregnancy rate was 30.5% per cycle and 33.3% per embryo transfer. The implantation rate was 14.2%; failure of fertilisation occurred in two cycles, while in three other cycles the embryos did not cleave. CONCLUSIONS: Percutaneous epididymal sperm aspiration can be used successfully to retrieve sperm in men with azoospermia due to obstructive, or nonobstructive, disorders. The technique is simple, cost-effective, and associated with fewer complications than an open microsurgical operation.

Adult↗

PubMed1996

Predicting functional capacity during treadmill testing independent of exercise protocol.

Clinically useful estimates of VO2max from treadmill tests (GXT) may be made using protocol-specific equations. In many cases, GXT may proceed more effectively if the clinician is free to adjust speed and grade independent of a specific protocol. We sought to determine whether VO2max could be predicted from the estimated steady-state VO2 of the terminal exercise stage. Seventy clinically stable individuals performed GXT with direct measurement of VO2. Exercise was incremented each minute to optimize clinical examination. Measured VO2max was compared to the estimated steady-state VO2 of the terminal stage based on ACSM equations. Equations for walking or running were used based on the patient's observed method of ambulation. The measured VO2max was always less than the ACSM estimate, with a regular relationship between measured and estimated VO2max. No handrail support: VO2max = 0.869.ACSM -0.07; R2 = 0.955, SEE = 4.8 ml.min-1.kg-1 (N = 30). With handrail support: VO2max = 0.694.ACSM + 3.33; R2 = 0.833, SEE = 4.4 ml.min-1.kg-1 (N = 40). The equations were cross-validated with 20 patients. The correlation between predicted and observed values was r = 0.98 and 0.97 without and with handrail support, respectively. The mean absolute prediction error (3.1 and 4.1 ml.min-1.kg-1) were similar to protocol-specific equations. We conclude that VO2max can be predicted independent of treadmill protocol with approximately the same error as protocol-specific equations.

Adult↗

PubMed1996

Athletic performance in relation to training load.

Athletic performance generally is thought to improve with increases in training load. However, few data exist showing the quantitative relationship between training load and performance. We followed 56 athletes (16 runners; 40 cyclists/speed skaters) during 12 weeks of training. We recorded index performances (3.2 km time trial or 5 or 10 km bicycle ergometry) after 6 weeks of baseline training and 6 weeks of a self-selected training increases. Training load was quantitated as the product of intensity (global rating of perceived exertion (RPE)) and the duration (time) of each training session. Load was expressed as the weekly average over the 6 weeks preceding each index performance. We also recorded the duration of high intensity training (RPE>5, hard) (inten). From 6 to 12 weeks, performance improved 12.95 +/- 3.83 to 12.66 +/- 3.00 min (p < .01). Training time (345 +/- 282 to 355 +/- 273 min/wk) and inten (61 +/- 88 to 71 +/- 91 min/wk) did not change significantly, although RPE (3.8 +/- 0.7 to 4.0 +/- 0.8) and load (1242 +/- 957 to 1386 +/- 978) increased significantly. No strong correlations existed between changes in performance and changes in any training measure (TIME, r = -0.031, RPE, r = -0.039, LOAD, r = 0.29, INTEN, r = 0.025.) Data suggest that improved performance in events of 7-20 minutes duration in response to intensified training is primarily dependent upon increases in total load and overall RPE during training and; that a 10-fold increase in training load may be associated with an approximately 10% improvement in performance. These data suggest the possibility of understanding the training responses of athletes on a quantitative basis.

Adult↗

PubMed1996

Oval cell proliferation associated with the murine insertional mutation TgN737Rpw.

The Tg737 gene was identified by its direct association with a transgene-induced insertion mutation in the mouse. This mutation causes pleiotropic phenotypes including a syndrome similar to autosomal recessive polycystic kidney disease in humans. This syndrome, in addition to renal cyst formation, includes the presence of an invariably associated liver abnormality. The liver pathology in TgN737Rpw mice is characterized by a biliary hyperplasia that includes the proliferation of cells that morphologically and immunologically resemble oval cells, a liver progenitor cell. This abnormality is first observed at approximately 5 days of age in the portal region and then progresses into the periportal regions. Additionally, the formation and proliferation of dysplastic ductular structures are observed from the onset of the phenotype. Serum chemistry indicated that the primary defect is likely to be of biliary origin, and hepatic function appears normal in the mutant mice. Therefore, this mutation is unlike other causes of oval cell proliferation in that the hepatic parenchyma is relatively unaffected. The identification of the Tg737 gene associated with this mutation suggests that it functions in regulating the proliferation/differentiation of oval cells within the liver, which further indicates that this gene may function in pathological conditions that include oval cell proliferation, such as hepatocellular carcinogenesis.

Animals↗

PubMed1995

Cyclic nucleotide phosphodiesterase isozymes in rat mesangial cells.

We characterized cyclic nucleotide phosphodiesterases isolated from rat mesangial cells and assessed their roles in regulating cellular cyclic nucleotide levels. Three peaks of phosphodiesterase activity were eluted by a linear sodium acetate gradient from a Q Sepharose column loaded with the mesangial cell extract. The first peak activity was stimulated by Ca(2+)-calmodulin and inhibited by calmodulin-stimulated phosphodiesterase inhibitors but not by a selective cGMP specific phosphodiesterase V inhibitor. The second, minor activity peak was stimulated by cyclic GMP and inhibited by EHNA [erythro-9-(2-hydroxy-3-nonyl)-adenine], a selective inhibitor of cyclic GMP-stimulated phosphodiesterase II. The last peak activity was not inhibited by cyclic GMP but selectively inhibited by rolipram [4-(3-cyclopentyloxy-4-methoxyphenyl)-2-pyrrolidene] or Ro 20-1724 [4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone], inhibitors of cyclic AMP specific, cyclic GMP insensitive phosphodiesterase IV. Based on their order of chromatographic elution, kinetic properties and sensitivity to allosteric agents and inhibitors, the peak 1, 2 and 3 correspond to phosphodiesterase I, II and IV. The basal cyclic GMP level was raised more effectively by selective inhibitor of phosphodiesterase I than phosphodiesterase II. In contrast, the atrial natriuretic factor-induced cyclic GMP elevation was potentiated more effectively by selective inhibitors of phosphodiesterase II than phosphodiesterase I. The forskolin-induced cyclic AMP increase was greatly potentiated by selective phosphodiesterase IV inhibitors but not by other phosphodiesterase inhibitors. These data suggest that phosphodiesterase I and II are responsible for cyclic GMP hydrolysis whereas phosphodiesterase IV is mainly responsible for cyclic AMP hydrolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Nitric oxide regulates angiotensin II receptors in vascular smooth muscle cells.

The objective of this study was to determine whether an enhanced generation of nitric oxide (NO) causes regulation of angiotensin II receptors in vitro using rat vascular smooth muscle cells in culture. Chronic treatment of cells with a series of NO-generating drugs, sodium nitroprusside, S-nitroso-N-acetylpenicillamine and isosorbide dinitrate for 18h dose and time-dependently decreased [125I]-angiotensin II binding to cells without any significant change in affinity. Induction of nitric oxide synthase following lipopolysaccharide (10 and 100 ng/ml) treatment of cells for 18 h increased basal nitric oxide synthase activity with a concomitant increase of nitrite and cyclic cGMP levels in the conditioned media. LPS treatment significantly (P < 0.05) decreased [125I]-angiotensin II binding to these cells, an effect that was significantly (P < 0.05) attenuated in the presence of NG-nitro-L-arginine methyl ester. In contrast, treatment of cells with atrial natriuretic factor, dibutyryl cGMP, 8-bromo-cGMP, NaNO2 or NaNO3 failed to significantly alter the affinity or number of [125I]-angiotensin II binding sites. These results suggest that NO regulates angiotensin II receptors in vitro through a cGMP-independent mechanism.

Amino Acid Oxidoreductases↗

PubMed1995

Effects of specific versus cross-training on running performance.

The cross-training (XT) hypothesis suggests that despite the principle of specificity of training, athletes may improve performance in one mode of exercise by training using another mode. To test this hypothesis we studied 30 well-trained individuals (10 men, 20 women) in a randomized longitudinal trail. Subjects were evaluated before and after 8 weeks of enhanced training (+10%/week), accomplished by adding either running (R) or swimming (XT) to baseline running, versus continued baseline running (C). Both R (-26.4s) and XT (-13.2s) improved time trial (3.2 km) performance, whereas C did not (-5.4s). There were no significant changes during treadmill running in maximum oxygen uptake (VO2peak; -0.2, -6.0, and +2.7%), steady state submaximal VO2 at 2.68 m.s-1 (-1.2, -3.3 and +0.2 ml.kg-1.min-1), velocity at VO2peak (+0.05, +0.25 and +0.09 m.s-1) or accumulated O2 deficit (+11.2, -6.1 and +9.4%) in the R, XT or C groups, respectively. There was a significant increase in velocity associated with a blood lactate concentration of 4 mmol.l-1 in R but not in XT or C (+0.32, +0.07 and +0.08 m.s-1). There were significant changes in arm crank VO2peak (+5%) and arm crank VO2 at 4 mmol.l-1 (+6.4%) in XT. There was no significant changes in arm crank VO2peak (+1.3 and -7.7%) or arm crank VO2 at 4 mmol.l-1 (+0.8 and +0.4%) in R or C, respectively. The data suggest that muscularly non-similar XT may contribute to improved running performance but not to the same degree as increased specific training.

Adult↗