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Endurance exercise training does not alter lipolytic or adipose tissue blood flow sensitivity to epinephrine.

We evaluated the relationship between lipolysis and adipose tissue blood flow (ATBF) in response to epinephrine and the effect of endurance exercise training on these responses. Five healthy untrained men underwent a four-stage incremental epinephrine infusion (0.00125, 0.005, 0.0125, and 0.025 microgram. kg fat free mass(-1). min(-1)) plus hormonal clamp before and after 16 wk of cycle ergometry exercise training. Whole body glycerol and free fatty acid (FFA) rates of appearance (R(a)) in plasma were determined by stable isotope methodology, and ATBF was assessed by (133)Xe clearance. After each training session, subjects were fed the approximate number of calories expended during exercise to prevent changes in body weight. Glycerol R(a), FFA R(a), and ATBF increased when plasma epinephrine concentration reached 0.8 nM, but at plasma epinephrine concentrations >1.6 nM ATBF plateaued, whereas lipolysis continued to increase. Exercise training increased peak oxygen uptake by 24 +/- 7% (2.9 +/- 0.2 vs. 3.6 +/- 0.1 l/min; P < 0. 05) but did not alter body weight [70.5 +/- 3.8 vs. 72.0 +/- 3.8 kg; P = nonsignificant (NS)] or percent body fat (18.4 +/- 1.6 vs. 17.8 +/- 1.9%; P = NS). Lipolytic and ATBF responses to epinephrine were also the same before and after training. We conclude that the lipolytic and ATBF responses to epinephrine are coordinated when plasma epinephrine concentration is </=1.6 nM, but that at higher epinephrine concentrations, lipolysis continues to increase while ATBF remains constant. Endurance exercise training does not change lipolytic or ATBF sensitivity to epinephrine infusion in vivo during resting conditions.

Adipose Tissue↗

Effects of exercise training on vasomotor reactivity of porcine coronary arteries.

The purpose of this study was to determine whether exercise training induces changes in the contractile behavior of proximal coronary arteries. Female Yucatan miniature swine were either exercise trained (ET) on a motor-driven treadmill or allowed to remain sedentary (SED) for 16-22 wk. Responses to vasoactive compounds were evaluated in vitro using coronary arterial rings (approximately 2 mm diam) isolated from ET and SED pigs. Each ring was stretched to the apex of the length-active tension relationship. Concentration-response relationships for isometric contractions evoked with KCl (5-100 mM), prostaglandin F2 alpha (PGF2 alpha; 10(-8)-3 x 10(-5) M), acetylcholine (ACh; 10(-9)-10(-4) M), and endothelin (10(-10)-10(-7) M) were similar in arteries from SED and ET pigs. In contrast, arteries from the ET group developed 50-60% less maximal tension in response to norepinephrine (NE; 10(-6)-10(-4) M) than did controls. Vasodilator responses of rings precontracted with either KCl or PGF2 alpha were evaluated with adenosine (ADO; 10(-9)-10(-4) M), isoproterenol (10(-9)-10(-4) M), forskolin (10(-9)-10(-4) M), and sodium nitroprusside (NP; 10(-10)-10(-4) M). Vasodilator responses were similar in SED and ET groups for all agents except ADO and NP; arteries from ET pigs were more sensitive to ADO and less sensitive to NP. The ET-induced alterations in vasomotor responses to NE and ADO appear to be due to changes in vascular smooth muscle because they were still present after removal of endothelium. We conclude that chronic exercise training in pigs induces selective alterations in NE and ADO receptor-second messenger coupling and/or postreceptor-related events in epicardial coronary vascular smooth muscle.

Animals↗

Effects of exercise training on aerobic fitness in African-American females.

Physical inactivity, a primary risk factor for cardiovascular disease, is more prevalent within the African-American population. Unfortunately, only a few investigators have documented the effects of exercise training studies on cardiovascular fitness in this cohort. Therefore, the purpose of this study was to examine the effects of a six-week endurance exercise training program on aerobic fitness (VO2peak) in African-American females. Twenty-five women (16 treatment, 9 controls, mean age 23.1+/-3.9) participated in the study. The six-week exercise training protocol consisted of exercising three times a week on a cycle ergometer between 60-70% VO2peak for 20 minutes. No significant changes in aerobic fitness were observed in the control group. However, the relative and absolute VO2peak significantly increased by 18% and 19%, respectively, in the treatment group, 21.7+/-2.6 to 25.6+/-2.8 mL x kg(-1) x min(-1) (P<.01) and 1.77+/-2.7 to 2.11+/-3.8 L x min(-1) (P<.01). The maximal heart rates and respiratory exchange ratios were not significantly different between pre- and post-training, suggesting that similar efforts were given. These results document the fact that significant increases in aerobic fitness are possible with a moderate exercise training regime in an African-American female population.

Adult↗

Limb muscle dysfunction in COPD: effects of muscle wasting and exercise training.

PURPOSE: Lower-limb muscle weakness has often been reported in COPD, and contributes to exercise intolerance. Controversial information is available regarding upper-limb muscle adaptations and the influence of muscle wasting on muscle weakness. We investigated leg and arm muscle function in 59 stable COPD patients (GOLD stage III) with preserved fat-free mass (FFM) and in 28 patients with reduced FFM relative to age- and sex-matched healthy control subjects and studied the effects of 8 wk of whole-body exercise training. METHODS: FFM was measured with bioelectrical impedance analysis. Isokinetic quadriceps (F-leg) and biceps strength (F-arm), as well as quadriceps (E-leg) and biceps endurance (E-arm) were determined with a Biodex dynamometer. Exercise training consisted of cycle ergometry, treadmill walking, weight training, and gymnastics during 5 d.wk. RESULTS: F-leg (76.2 +/- 3.6 vs 118.2 +/- 6.3 N.m, P < 0.001) and F-arm (25.6 +/- 1.3 vs 38.1 +/- 2.1 N.m, P < 0.001) were significantly and similarly reduced in the COPD patient group compared with controls. Also, E-leg (-2.13 +/- 0.12 vs -1.61 +/- 0.11, P < 0.01), but not E-arm (-2.72 +/- 0.11 and -2.47 +/- 0.13 NS), was decreased in patients. F-leg (62.4 +/- 4.3 vs 82.8 +/- 4.7 N.m, P < 0.01), but not F-arm or muscle endurance, was reduced in FFM-depleted compared with non-FFM-depleted patients. Whereas after training F-leg and E-leg significantly increased by 20% in the whole COPD group, biceps muscle function remained unchanged. CONCLUSION: Lower- and upper-limb muscle dysfunction was observed in COPD patients, irrespective of the presence of FFM depletion. Generalized muscle weakness suggests systemic muscular involvement, although the preserved arm endurance and the poor response of arm performance to exercise training is indicative for intrinsic differences in muscular adaptations between leg and arm muscles.

Case-Control Studies↗

Cardioprotective effects of exercise training on myofilament calcium activation in ovariectomized rats.

The risks associated with hormone replacement therapy, especially cardiac diseases in postmenopausal women, have prompted extensive studies for other preventive or therapeutic alternatives. We investigated the cardioprotective effects of exercise training on the changes in cardiac myofilament Ca2+ activation in 10-wk-old ovariectomized rats. The exercise groups were subjected to a 9-wk running program on a motor-driven treadmill 1 wk after surgery. The relationship between pCa (-log molar free Ca2+ concentration) and myofibrillar MgATPase activity of exercise-sham myofibrils or exercise-ovariectomized myofibrils was the same and could not be distinguished from that of sedentary-sham control hearts. In contrast, a significant suppression in maximum MgATPase activity and a leftward shift of pCa50 (half-maximally activating pCa) in the pCa-ATPase activity relationship were detected in sedentary-ovariectomized rats. Exercise training also prevented the shift in myosin heavy chain (MHC) isoforms toward beta-MHC in ovariectomized hearts. The upregulation of beta1-adrenergic receptors in the left ventricular membranes of ovariectomized rat hearts, as measured by receptor binding and immunoblot analyses, was no longer observed in exercise-ovariectomized hearts. Immunoblot analyses of heat shock protein (HSP) 72, an inducible form of HSP70, demonstrated a significant downregulation in ovariectomized hearts. Exercise training in ovariectomized rats completely reversed the expression of HSP72 to the same level as sham controls. Our results clearly indicate the cardioprotective effects of exercise training on changes in cardiac myofilament Ca2+ activation in ovariectomized rats. Alterations in expression of beta1-adrenergic receptors and HSP72 may, in part, play a mechanistic role in the cardioprotective effects.

Actin Cytoskeleton↗

Effects of gradual coronary artery occlusion and exercise training on gene expression in swine heart.

Gradual occlusion (O) of the swine left circumflex coronary artery (LCX) with an ameroid occluder results in complete O within 3 weeks, collateral vessel development, and compensatory hypertrophy. The purpose of this investigation was to determine the independent and combined effects of O and exercise training (E) on gene expression in the swine heart. Adult Yucatan miniature swine were assigned to one of the following groups (n=6-9/group): sedentary control (S), exercise-trained (E), sedentary swine subjected to LCX occlusion (SO), and exercise-trained swine with LCX occlusion (EO). Exercise consisted of progressive treadmill running conducted 5 d/wk for 16 weeks. Gene expression was studied in myocardium isolated from the collateral-dependent left ventricle free wall (LV) and the collateral-independent septum (SEP) by RNA blotting. E and O each stimulated cardiac hypertrophy independently (p<0.001) with no interaction. O but not E increased atrial natriuretic factor expression in the LV, but not in the SEP. E decreased the expression of beta-myosin heavy chain in the LV, but not in the SEP. E retarded the expression of collagen III mRNA in SEP; but not in the LV. Exercise training and coronary artery occlusion each stimulate cardiac hypertrophy independently and induce different patterns of gene expression.

Animals↗

Regional changes in reactive hyperemic blood flow during exercise training: time-course adaptations.

BACKGROUND: Few studies have examined the time-course of localized exercise training on regional blood flow in humans. The study examined the influence of handgrip exercise training on forearm reactive hyperemic blood flow and vascular resistance in apparently healthy men. METHODS: Forearm blood flow and vascular resistance were evaluated, in 17 individuals [Age: 22.6 +/- 3.5], in both arms, at rest and following 5 minutes of arterial occlusion, using strain gauge plethysmography, prior to training (V1) and every week thereafter (V2-5) for 4 weeks. Handgrip exercise was performed in the non-dominant arm 5 d/wk for 20 minutes at 60% of maximum voluntary contraction, while the dominant arm served as control. RESULTS: Resting HR, BP, and forearm blood flow and vascular resistance were not altered with training. The trained arm handgrip strength and circumference increased by 14.5% (p = 0.014) and 1.56% (p = 0.03), respectively. ANOVA tests revealed an arms by visit interaction for the trained arm for reactive hyperemic blood flow (p = 0.02) and vascular resistance (p = 0.009). Post-hoc comparison demonstrated increased reactive hyperemic blood flow (p = 0.0013), and decreased post-occlusion vascular resistance (p = 0.05), following the 1st week of training, with no significant changes in subsequent visits. CONCLUSION: The results indicate unilateral improvements in forearm reactive hyperemic blood flow and vascular resistance following 1 week of handgrip exercise training and leveled off for the rest of the study.

Journal Article↗

Effect of weight training exercise and treadmill exercise on post-exercise oxygen consumption.

Effect of weight training exercise and treadmill exercise on postexercise oxygen consumption. Med. Sci. Sports Exerc., Vol. 30, No. 4, pp. 518-522, 1998. To compare the effect of weight training (WT) and treadmill (TM) exercise on postexercise oxygen consumption (VO2), 15 males (mean +/- SD) age = 22.7 +/- 1.6 yr; height = 175.0 +/- 6.2 cm; mass = 82.0 +/- 14.3 kg) performed a 27-min bout of WT and a 27-min bout of TM exercise at matched rates of VO2. WT consisted of performing two circuits of eight exercises at 60% of each subject's one repetition maximum with a work/rest ratio of 45 s/60 s. Approximately 5 d after WT each subject walked or jogged on the TM at a pace that elicited an average VO2 matched with his mean value during WT. VO2 was measured continuously during exercise and the first 30 min into recovery and at 60 and 90 min into recovery. VO2 during WT (1.58 L.min-1) and TM exercise (1.55 L.min-1) were not significantly (P > 0.05) different; thus the two activities were matched for VO2. Total oxygen consumption during the first 30 min of recovery was significantly higher (P < 0.05) as a result of WT (19.0 L) compared with that during TM exercise (12.7 L). However, VO2 values at 60 (0.32 vs 0.29 L.min-1), and 90 min (0.33 vs 0.30 L.min-1) were not significantly different (P > 0.05) between WT and TM exercise, respectively. The results suggest that, during the first 30 min following exercise. WT elicits a greater elevated postexercise VO2 than TM exercise when the two activities are performed at matched VO2 and equal durations. Therefore, total energy expenditure as a consequence of WT will be underestimated if based on exercise VO2 only.

Adult↗

Exercise training reduces the acute inflammatory response associated with claudication.

BACKGROUND: recent research has shown that episodes of claudication may be associated with a systemic inflammatory response that causes injury to the vascular endothelium. As claudicants are often directed to undertake regular walking exercises there has been a concern that this may accelerate endothelial injury. AIMS: the aim of our study was to assess the baseline markers of ischaemia-reperfusion injury (IRI) in claudicants and controls after acute treadmill exercise and to then examine the effect of a 3 month supervised exercise-training programme, on these markers, in the claudicant group. METHODS: forty-six claudicants and 22 age-matched controls undertook acute treadmill exercise. Neutrophil activation, degranulation, free radical damage and antioxidants were measured (by flow cytometry, ELISA, and chemiluminescence) at rest and at 5, 30 and 60 min post-exercise. Claudicants were then recruited into an intensive 3 month supervised exercise programme (SEP) after which the same parameters of IRI were reassessed at different time points, at 3 and 6 months. RESULTS: resting markers of IRI were similar in both groups. Exercise had no effect on the control group. Immediately after exercise, claudicants developed significant neutrophil activation and degranulation with free radical damage. This effect decreased sequentially after 3 months of exercise training. CONCLUSION: this study for the first time demonstrates that the exercise training of claudicants is beneficial, not only in terms of improving their walking distance, but also by decreasing the injurious effects of IRI that occur during claudication. Exercise training should be an essential part of the medical management of the majority of claudicants.

Adult↗

Apoptotic adaptations from exercise training in skeletal and cardiac muscles.

The effect of exercise on apoptosis in postmitotic tissues is not known. In this study, we investigated the effect of regular moderate physical activity (i.e., exercise training) on the extent of apoptosis in rat skeletal and cardiac muscles. Adult Sprague Dawley rats were trained (TR) 5 days weekly for 8 wk on treadmill. Sedentary rats served as controls (CON). An ELISA was used to detect mono- and oligonucleosome fragmentation as an indicator of apoptosis. Bcl-2, Bax, Apaf-1, AIF, cleaved PARP, cleaved caspase-3, cleaved/active caspase-9, heat shock protein (HSP)70, Cu/Zn-SOD, and Mn-SOD protein levels were determined by Western analyses. Bcl-2 and Bax transcript contents were estimated by RT-PCR. A spectrofluorometric assay was used to determine caspase-3 activity. DNA fragmentation in ventricles of the TR group decreased by 15% whereas that in soleus of the TR group tended to decrease (P=0.058) when compared with CON group. Protein contents of Bcl-2, HSP70, and Mn-SOD increased in both soleus and ventricle muscles of TR animals when compared with CON animals. Apaf-1 protein content in the soleus of TR animals was lower than that of CON animals. Bcl-2 mRNA levels increased in both ventricle and soleus muscles of TR animals, and Bax mRNA levels decreased in the soleus of TR animals when compared with CON animals. Furthermore, HSP70 protein content was negatively correlated to Bax mRNA content and was positively correlated to Bcl-2 protein and mRNA contents. Mn-SOD protein content was negatively correlated to the apoptotic index, and caspase-3 activity and was positively correlated to Bcl-2 transcript content and HSP70 protein content. These data suggest that exercise training attenuates the extent of apoptosis in cardiac and skeletal muscles.

Animals↗

Effects of resistive training on lipoprotein-lipid profiles: a comparison to aerobic exercise training.

A recent surge of cross-sectional and longitudinal studies dealing with resistive training and lipid profiles have produced conflicting results. The majority of cross-sectional studies demonstrate a reduced HDL cholesterol level or elevated total cholesterol to HDL ratio in strength trained athletes as compared with endurance trained athletes. Because of selection biases from many of these studies, there is a lack of control for factors that may influence lipids and lipoproteins, such as age, body composition, diet, and anabolic-androgenic steroid use. Most investigators have reported improved lipoprotein-lipid profiles from resistive training programs. However, many of these studies have design flaws or limitations that make their conclusions questionable. The most serious design flaws include the combination of no control group and only one blood sample taken before and after training, the use of subjects who have low risk profiles, and the lack of control for dietary effects. In a recent study in which we attempted to control for these factors, no changes in lipid profiles were observed after 20 wk of resistive training among individuals at risk for coronary heart disease (CHD). A group serving as reference controls who participated in aerobic-type exercise training during the same time period reduced their plasma triglyceride levels but did not alter their cholesterol or lipoprotein levels. No changes in any lipids or lipoproteins were observed in a group of inactive controls. Thus, resistive training does not appear to alter lipoprotein-lipid profiles among individuals at risk for CHD.

Adolescent↗

Chronic endurance exercise training: a condition of inadequate blood pressure regulation and reduced tolerance to LBNP.

We review the hypotheses presented to account for the anecdotal and literature-based reports that chronic endurance exercise training reduces orthostatic tolerance. The findings from cross-sectional investigations of unfit subjects and endurance athletes are examined, as well as limited data from recent investigations of the changes in orthostatic tolerance and blood pressure regulation that occur after 8 d to 8 months of endurance exercise training. Statistical models have not found wide variations in maximal aerobic power (VO2max) to contribute to the prediction of orthostatic responses. However, research data are generally consistent that the orthostatic tolerance of athletes whose VO2max exceeds 65 ml.kg-1.min-1 is lower than that of sedentary control subjects. These two findings suggest that it is exercise training, rather than VO2max, that reduces orthostatic tolerance. Findings from a recent longitudinal investigation corroborate this theory. We conclude that at least four factors associated with exercise training contribute to the development of orthostatic intolerance. These include: a) increased limb compliance (although its effect is likely to be trivial), b) eccentric ventricular hypertrophy, and c) increases in total blood volume, which may attenuate cardiopulmonary baroreflex responsiveness, shift ventricular function to a steeper portion of the ventricular compliance curve, and increase the inhibitory effect of cardiopulmonary baroreceptors on carotid baroreflex responsiveness; and d) an independent effect that reduces carotid and aortic baroreflex responsiveness. These mechanisms mimic changes observed in pathological states such as heart failure and hypertension. Our conclusions are best summarized by Greenleaf et al. (J. Appl. Physiol. 51:298-305, 1981): ""Trained men can run, but they cannot stand.''

Adaptation, Physiological↗

Effects of exercise training on the biosynthesis of prostacyclin and thromboxane in rats.

The effects of exercise training on eicosanoid levels were studied in male Wistar rats. One-month-old rats were trained on a drum exerciser at an intensity of around 70% of maximal oxygen consumption for 10 weeks (60 min day-1, 5 days week-1) after familiarization. Some animals of the same age did not exercise and served as a control. Two days after training, several blood vessels, including thoracic aortae, inferior vena cavae, external iliac arteries, external iliac veins, common carotid arteries and jugular veins, were excised and incubated for 10 min. Basal release of prostacyclin from these vessels was determined using [125I]radio-immunoassay (RIA) of 6-keto-PGF1 alpha. The levels of plasma prostacyclin and urinary metabolites of prostacyclin and thromboxane were also determined by RIA. Our results showed that trained animals had lower body weight and urine 11-dehydro-thromboxane B2 levels than the controls (P < 0.001 and P < 0.05, respectively). In contrast, urinary 2,3-dinor-6-keto-PGF1 alpha level was elevated after training (P < 0.05). Nonetheless, prostacyclin levels in plasma and from various dissected vessel segments, except thoracic aorta, did not change significantly after training. These findings suggest that exercise training may affect endogenous eicosanoid levels by increasing the basal release of prostacyclin and reducing the basal thromboxane level.

6-Ketoprostaglandin F1 alpha↗

Ventricular ectopy frequency and complexity not altered by exercise training in coronary disease patients.

To assess the effect of exercise training on ventricular ectopy in coronary artery disease patients, 21 patients with coronary disease had 24-hour ambulatory electrocardiograph recordings done at entry into a cardiac rehabilitation program and after 6 months' exercise training. Mean frequency of premature ventricular contractions was not significantly changed, being 9.7 +/- 33.0/h before and 13.2 +/- 94.3/h after training. 9 demonstrated an increased, 9 a decreased, and 3 an unchanged frequency. Lown grade of ventricular ectopy was similarly not consistently changed with training.

Arrhythmias, Cardiac↗

Adaptations to exercise training and contraction-induced muscle injury in animal models of muscular dystrophy.

This article reviews the current status of exercise training and contraction-induced muscle-injury investigations in animal models of muscular dystrophy. Most exercise-training studies have compared the adaptations of normal and dystrophic muscles with exercise. Adaptation of diseased muscle to exercise occurs at many levels, starting with the extracellular matrix, but also involves cytoskeletal architecture, muscle contractility, repair mechanisms, and gene regulation. The majority of exercise-injury investigations have attempted to determine the susceptibility of dystrophin-deficient muscles to contraction-induced injury. There is some evidence in animal models that diseased muscle can adapt and respond to mechanical stress. However, exercise-injury studies show that dystrophic muscles have an increased susceptibility to high mechanical forces. Most of the studies involving exercise training have shown that muscle adaptations in dystrophic animals were qualitatively similar to the adaptations observed in control muscle. Deleterious effects of the dystrophy usually occur only in older animals with advanced muscle fiber degeneration or after high-resistive eccentric training. The main limitations in applying these conclusions to humans are the differences in phenotypic expression between humans and genetically homologous animal models and in the significant biomechanical differences between humans and these animal models.

Adaptation, Physiological↗

Exercise training and clenbuterol reduce insulin resistance of obese Zucker rats.

This study compared the effects of aerobic exercise training and chronic administration of the selective beta 2-adrenergic agonist clenbuterol on whole body and skeletal muscle insulin resistance in obese (fa/fa) Zucker rats. Obese rats were randomly assigned to training, clenbuterol, or sedentary control groups. Lean littermates served as a second control group. After 4-5 wk of treatment, an oral glucose tolerance test was performed, followed 1 wk later by hindlimb perfusion, during which time the rates of glucose uptake and 3-O-methyl-D-glucose (3-MG) transport were assessed in the presence of a submaximal (500 microU/ml) insulin concentration. Training resulted in a significant increase in citrate synthase and cytochrome oxidase activity in the recruited muscles. Clenbuterol induced a large increase in muscle mass but provoked a significant decrease in oxidative enzyme activity and beta-adrenergic receptor density. Both treatments increased glucose tolerance and reduced the postglucose insulin response, with the improvements being more pronounced in the clenbuterol group. However, only exercise training improved insulin-stimulated hindlimb muscle glucose uptake (11.37 +/- 0.65, 8.73 +/- 0.77, and 8.27 +/- 0.41 mumol.g-1.h-1 for trained, clenbuterol, and sedentary control groups, respectively) and 3-MG transport. These results suggest that aerobic exercise training attenuated the insulin-resistant condition in the obese Zucker rat by a mechanism other than or in addition to beta 2-adrenergic receptor activation.

3-O-Methylglucose↗

Effects of exercise training on bone remodeling, insulin-like growth factors, and bone mineral density in postmenopausal women with and without hormone replacement therapy.

The purpose of this study was to determine the effects of 12 months of weight bearing and resistance exercise on bone mineral density (BMD) and bone remodeling (bone formation and bone resorption) in 2 groups of postmenopausal women either with or without hormone replacement therapy (HRT). Secondary aims were to characterize the changes in insulin-like growth factors-1 and -2 (IGF-1 and -2) and IGF binding protein 3 (IGFBP3) in response to exercise training. Women who were 3-10 years postmenopausal (aged 40-65 years) were included in the study. Women in the HRT and no HRT groups were randomized into the exercise intervention, resulting in four groups: (1) women not taking HRT, not exercising; (2) those taking HRT, not exercising; (3) those exercising, not taking HRT; and (4) women exercising, taking HRT. The number of subjects per group after 1 year was 27, 21, 25, and 17, respectively. HRT increased BMD at most sites whereas the combination of exercise and HRT produced increases in BMD greater than either treatment alone. Exercise training alone resulted in modest site-specific increases in BMD. Bone remodeling was suppressed in the groups taking HRT regardless of exercise status. The bone remodeling response to exercise training in women not taking HRT was not significantly different from those not exercising. However, the direction of change suggests an elevation in bone remodeling in response to exercise training, a phenomenon usually associated with bone loss. No training-induced differences in IGF-1, IGF-2, IGF-l:IGF-2 (IGF-1 : IGF-2), and IGFBP3 were detected.

Adult↗

Effects of non-specific vs individualized exercise training protocols on aerobic, anaerobic and strength performance in severely obese subjects during a short-term body mass reduction program.

The purpose of the present study was to compare aerobic, anaerobic and strength performance changes induced by two short-term (3-week) body mass reduction programs based on the same low-calory diet (1200-1500 kcal/day), nutritional education and psychological counseling, but entailing different exercise training protocols. An individualized, low-volume and moderate-intensity exercise training (IET) was contrasted with a non-specific, high-volume, low-intensity exercise training (NET). Thirty obese in-patients (12 males, 18 females; mean age +/- SD: 33.9 +/- 9.4 yr, range: 19-51yr; mean BMI: 40.5 +/- 3.8 kg/m2, range: 35.3-51.4 kg/m2) were randomly divided in two gender-matched groups of 15 subjects each undergoing a different exercise training protocol. Maximum oxygen uptake (VO2max) determined with a submaximal indirect test on a bicycle ergometer, lower limb maximum power output (W(max)) determined with the jumping method, global motor capabilities determined by analysis of locomotor pattern during a short (8 m) running, maximum strength (1-RM) of upper and lower limb muscle groups determined with isotonic machines were tested before and after the program. Adherence to an individual exercise activity and maintenance of body weight (bw) loss were evaluated with a telephonic interview 6 months after the completion of the program. In both groups a significant (p < 0.001) and comparable weight loss was observed (IET: -4.27%; NET: -4.17%). In both groups VO2max and W(max) increased significantly (p < 0.05-0.001) when expressed relatively to body mass, while in absolute terms they were significantly (p < 0.001) improved only in IET group. 1-RM in all tested muscle groups was significantly increased in both IET and NET subjects (p < 0.001-0.01), but improvements were significantly greater in IET as compared with NET (p < 0.05-0.001). The analysis of locomotor pattern during the short running indicated that IET subjects significantly improved their global motor capabilities (p < 0.05-0.001), while no change was observed in NET group. After 6 months, IET subjects reported a level of spontaneously chosen physical activity significantly higher (p < 0.05) than NET subjects, displaying a trend of further decrease in bw. It was concluded that, although no difference in bw loss was appreciated between the two studied groups and significant improvements were found also in subjects performing NET protocol, the IET protocol offers better overall results in terms of muscle performance and physical fitness, with a possibly stronger motivation to subsequent exercise activity.

Adult↗