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PubMed2004

VEGF receptor antagonism blocks arteriogenesis, but only partially inhibits angiogenesis, in skeletal muscle of exercise-trained rats.

Both collateral vessel enlargement (arteriogenesis) and capillary growth (angiogenesis) in skeletal muscle occur in response to exercise training. Vascular endothelial growth factor (VEGF) is implicated in both processes. Thus we examined the effect of a VEGF receptor (VEGF-R) inhibitor (ZD4190, AstraZeneca) on collateral-dependent blood flow in vivo and collateral artery size ex vivo (indicators of arteriogenesis) and capillary contacts per fiber (CCF; an index of angiogenesis) in skeletal muscle of both sedentary and exercise-trained rats 14 days after bilateral occlusion of the femoral arteries. Total daily treadmill run time increased appreciably from approximately 70 to approximately 100 min (at 15-20 m/min, twice per day) and produced a large (approximately 75%, P < 0.01) increase in calf muscle blood flow and a greater size of the collateral artery (wall cross-sectional area). ZD4190, which previously has been shown to inhibit the activity of VEGF-R2 and -R1 tyrosine kinase in vitro (IC50 = 30 and 700 nM, respectively), completely blocked the increase in collateral-dependent blood flow and inhibited collateral vessel enlargement. Thus exercise-stimulated collateral arteriogenesis appears to be completely dependent on VEGF-R signaling. Interestingly, enhanced mRNA expression of the VEGF family ligand placental growth factor (2- to 3.5-fold), VEGF-R1 (approximately 2-fold), and endothelial nitric oxide synthase (2- to 3.5-fold) in an isolated collateral artery implicates these factors as important in arteriogenesis. Training of ischemic muscle also induced angiogenesis, as shown by an increase (approximately 25%, P < 0.01) in CCF in white gastrocnemius muscle. VEGF-R inhibition only partially blocked (P < 0.01) but did not eliminate the increase (P < 0.01) in capillarity. Our findings indicate that VEGF-R tyrosine kinase activity is essential for collateral arteriogenesis and important for the angiogenesis induced in ischemic muscle by exercise training; however, other angiogenic stimuli are also important for angiogenesis in flow-limited active muscle.

Animals↗

PubMed2003

Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes.

AIM/HYPOTHESIS: We determined the effect of exercise training on insulin sensitivity and muscle lipids (triglyceride [TG(m)] and long-chain fatty acyl CoA [LCACoA] concentration) in patients with Type 2 diabetes. METHODS: Seven patients with Type 2 diabetes and six healthy control subjects who were matched for age, BMI, % body fat and VO(2)peak participated in a 3 days per week training program for 8 weeks. Insulin sensitivity was determined pre- and post-training during a 120 min euglycaemic-hyperinsulinaemic clamp and muscle biopsies were obtained before and after each clamp. Oxidative enzyme activities [citrate synthase (CS), beta-hydroxy-acyl-CoA (beta-HAD)] and TG(m) were determined from basal muscle samples pre- and post training, while total LCACoA content was measured in samples obtained before and after insulin-stimulation, pre- and post training. RESULTS: The training-induced increase in VO(2)peak (approximately 20%, p<0.01) was similar in both groups. Compared with control subjects, insulin sensitivity was lower in the diabetic patients before and after training (approximately 60%; p<0.05), but was increased to the same extent in both groups with training (approximately 30%; p<0.01). TG(m) was increased in patients with Type 2 diabetes (170%; p<0.05) before, but was normalized to levels observed in control subjects after training. Basal LCACoA content was similar between groups and was unaltered by training. Insulin-stimulation had no detectable effect on LCACoA content. CS and beta-HAD activity were increased to the same extent in both groups in response to training ( p<0.001). CONCLUSION/INTERPRETATION: We conclude that the enhanced insulin sensitivity observed after short-term exercise training was associated with a marked decrease in TG(m) content in patients with Type 2 diabetes. However, despite the normalization of TG(m )to levels observed in healthy individuals, insulin resistance was not completely reversed in the diabetic patients.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2004

Effects of short-period exercise training and orlistat therapy on body composition and maximal power production capacity in obese patients.

We examined the effects of weight loss induced by diet-orlistat (DO) and diet-orlistat combined with exercise (DOE) on maximal work rate production (Wmax) capacity in obese patients. Total of 24 obese patients were involved in this study. Twelve of them were subjected to DO therapy only and the remaining 12 patients participated in a regular aerobic exercise-training program in addition to DO therapy (DOE). Each patient performed two incremental ramp exercise tests up to exhaustion using an electromagnetically-braked cycle ergometer: one at the onset and one at the end of the 4th week. DOE therapy caused a significant decrease in total body weight: 101.5+/-17.4 kg (basal) vs 96.3+/-17.3 kg (4 wk) associated with a significant decrease in body fat mass: 45.0+/-10.5 kg (basal) vs 40.9+/-9.8 kg (4 wk). DO therapy also resulted in a significant decrease of total body weight 94.9+/-14.9 kg (basal) vs 91.6+/-13.5 kg (4 wk) associated with small but significant decreases in body fat mass: 37.7+/-5.6 kg (basal) to 36.0+/-6.2 kg (4 wk). Weight reduction achieved during DO therapy was not associated with increased Wmax capacity: 106+/-32 W (basal) vs 106+/-33 W (4 wk), while DOE therapy resulted in a markedly increased Wmax capacity: 109+/-39 W (basal) vs 138+/-30 W (4 wk). DO therapy combined with aerobic exercise training resulted in a significant reduction of fat mass tissue and markedly improved the aerobic fitness and Wmax capacities of obese patients. Considering this improvement within such a short period, physicians should consider applying an aerobic exercise-training program to sedentary obese patients for improving their physical fitness and thereby reduce the negative outcomes of obesity.

Adolescent↗

PubMed1999

Short-term heart rate variability changes after exercise training in subjects following myocardial infarction.

Heart rate variability reflects the activity of autonomic nervous system. The aim was to evaluate the value of short-term spectral analysis of heart rate for monitoring the effects of exercise training on the autonomic nervous system in subjects following myocardial infarction. Short-term spectral analysis of heart rate variability was performed during standardised supine-standing-supine test in a group of 29 clinically stable patients after myocardial infarction and the same test was repeated after 2 months of exercise training (ergometry or rapid walking). Each subject exercised at 60-80% of his maximal performance for 30 minutes once a day. Short-term spectral analysis of heart rate variability was assessed in the frequency range of 0.02-0.5 Hz involving very low frequency (VLF, 0.02-0.05 Hz), low frequency (LF, 0.05-0.15 Hz) and high frequency (HF, 0.15-0.5 Hz) spectral bands. The influence of exercise training on the autonomic nervous system was registered in the physically active group (n = 16) as a decrease in sympathetic response to standardised orthostatic load. In conclusions the regular exercise influenced an altered neural autonomic regulation of heart rate in post-infarction patients shown by a decrease in sympathetic activity in the short-term heart rate variability. This method enables monitoring of the effects of physical training on the autonomic nervous system in patients following myocardial infarction.

Echocardiography↗

PubMed2000

Prior exercise training increases collateral-dependent blood flow in rats after acute femoral artery occlusion.

We evaluated whether prior training would improve collateral blood flow (BF) to the calf muscles after acute-onset occlusion of the femoral artery. Exercise training was performed in the absence of any vascular occlusion. Adult male Sprague-Dawley rats ( approximately 325 g) were kept sedentary (n = 14), limited to cage activity, or exercise trained (n = 14) for 6 wk by treadmill running. Early in the day of measurement, animals were surgically prepared for BF determination, and the femoral arteries were occluded bilaterally. Four to five hours later, collateral BF was determined twice during treadmill running with the use of (141)Ce and (85)Sr microspheres: first, at a demanding speed and, second, after a brief rest and at a higher speed. The absence of any further increase in BF at the higher speed indicated that maximal collateral BF was measured. Prior training increased calf muscle BF by approximately 70% compared with sedentary animals; however, absolute BF remained below values previously observed in animals with a well-developed collateral vascular tree. Thus prior training appeared to optimize the use of the existing collateral circuit. This implies that altered vasoresponsiveness induced in normal nonoccluded vessels with exercise training serves to improve collateral BF to the periphery.

Acute Disease↗

PubMed2006

[Left ventricular remodeling in ischemic heart disease patients with signs and symptoms of chronic heart failure: an impact of the long-term exercise training].

Our study aimed at determining the effects of long-term exercise training on cardiorespiratory function and left ventricular remodeling in ischemic heart disease patients with the evidence of chronic heart failure, who had undergone a successful coronary angioplasty. One hundred thirty-five patients were entered into one-year study: 70 patients were assigned to the long-term exercise training group, and the remaining 65 persons--to the control group. All the patients were subjected to ergospirometry and echocardiography at study entry and at 6 and 12 months. At the outset, both groups showed no significant difference (P>0.05) in terms of ergospirometry findings. However, after 6 months, the rehabilitation group demonstrated significant changes (P<0.05) in exercise time, double product, RQ, AT VO2, VE/VO2, while the control group displayed no significant changes. After 12 months, the patients of rehabilitation group showed further increase in exercise time (from 5.6+/-1.9 min to 6.5+/-2.1 min) and AT VO2 (from 17.3+/-7.2 ml/kg/min to 20.8+/-5.4 ml/kg/min) indices (P<0.05). Those of double product and VE/VO2 decreased slightly when compared with findings at 6 months. RQ remained virtually at the same level, but significantly differed from the corresponding indices at the outset. Echocardiography performed at the entry and at 6 and 12 months revealed significant changes in systolic left ventricular function among the patients of rehabilitation group: wall movement index, ejection fraction as well as the left atrial long axis and left ventricular wall thickness. Echocardiographic changes indicate a positive impact of complex rehabilitative measures on systolic left ventricular function as evidenced by the ejection fraction and wall movement index values, as well as by regression of left ventricular wall thickness and left atrial long axis. Ergospirometry findings allow us to propose that the adequate choice of rehabilitative tools favorably affects the cardiovascular system, and this is reflected in exercise time and AT VO2 indices.

Angioplasty, Balloon, Coronary↗

PubMed2002

Long- and medium-chain fatty acid oxidation is increased in exercise-trained human skeletal muscle.

The purpose of this study was to test the hypothesis that skeletal muscle fatty acid oxidation is enhanced by increased entry into the mitochondria with exercise training. Muscle was obtained from young ( approximately 24 years) sedentary (n = 13) and endurance-trained (n = 10) volunteers and oxidation studied by measuring (14)CO(2) production from labeled medium-chain (MCFA) or long-chain (LCFA) fatty acids in muscle homogenate preparations. LCFA (palmitate) oxidation was (P <.05) approximately 34% higher in the trained than sedentary subjects (26.9 +/- 3.0 v 17.8 +/- 1.3 nmol CO(2)/g x h). MCFA (octanoate) oxidation was also about 26% higher (P <.05) in the trained subjects (21.7 +/- 2.1 v 16.1 +/- 2.0 nmol CO(2)/g x h). To examine the roles of carnitine-mediated transport and mitochondrial content, we also measured carnitine palmitoyltransferase I (CPT1), carnitine octanoyl transferase (COT), and citrate synthase (CS) activities. CPT1 and CS activity were significantly (P <.05) higher (approximately 25%) in the endurance-trained subjects; there was no difference in COT activity. These data suggest that adaptations at the level of CPT1 and processes distal to this step may contribute to increases in LCFA or MFCA oxidation with exercise training. In contrast, carnitine-mediated transport (COT) does not appear to contribute to an enhancement in MCFA oxidation with exercise training.

Adult↗

PubMed2005

Myocardial hypoperfusion/reperfusion tolerance with exercise training in hypertension.

The purpose of this study was to examine whether exercise training, superimposed on compensated-concentric hypertrophy, could increase myocardial hypoperfusion-reperfusion (H/R) tolerance. Female Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) (age: 4 mo; N = 40) were placed into a sedentary (SED) or exercise training (TRD) group (treadmill running; 25 m/min, 1 h/day, 5 days/wk for 16 wk). Four groups were studied: WKY-SED (n = 10), WKY-TRD (n = 10), SHR-SED (n = 10), and SHR-TRD (n = 10). Blood pressure and heart rate were determined, and in vitro isolated heart performance was measured with a retrogradely perfused, Langendorff isovolumic preparation. The H/R protocol consisted of a 75% reduction in coronary flow for 17 min followed by 30 min of reperfusion. Although the rate-pressure product was significantly elevated in SHR relative to WKY, training-induced bradycardia reduced the rate-pressure product in SHR-TRD (P < 0.05) without an attenuation in systolic blood pressure. Heart-to-body weight ratio was greater in both groups of SHR vs. WKY-SED (P < 0.001). Absolute and relative myocardial tolerance to H/R was greater in WKY-TRD and both groups of SHR relative to WKY-SED (P < 0.05). Endurance training superimposed on hypertension-induced compensated hypertrophy conferred no further cardioprotection to H/R. Postreperfusion 72-kDa heat shock protein abundance was enhanced in WKY-TRD and both groups of SHR relative to WKY-SED (P < 0.05) and was highly correlated with absolute left ventricular functional recovery during reperfusion (R2= 0.86, P < 0.0001). These data suggest that both compensated hypertrophy associated with short-term hypertension and endurance training individually improved H/R and that increased postreperfusion 72-kDa heat shock protein abundance was, in part, associated with the cardioprotective phenotype observed in this study.

Animals↗

PubMed1994

Exercise-training enhances fat-free mass preservation during diet-induced weight loss: a meta-analytical finding.

A meta-analysis was performed to examine how exercise training and gender influence the composition of diet-induced weight loss. The groups did not differ with respect to either the amount of body weight lost (mean = -10 +/- 1.4 kg) or fat mass lost (mean = -8 +/- 1.1 kg). However, exercise training significantly (P < 0.05) reduced the amount of body weight lost as fat-free mass compared to dietary restriction only (DO) for the same sex. The percentage of weight lost as fat-free mass for diet-plus-exercise (DPE) subjects was approximately half (P < 0.05) of that for DO subjects of the same sex (DO males = 28 +/- 4% of weight lost as fat-free mass; DPE males = 13 +/- 6%, DO females = 24 +/- 2%, DPE females = 11 +/- 3%). These data provide evidence that exercise training reduces the amount of body weight lost as fat-free mass during diet-induced weight loss. In addition, sex differences do not seem to exist with respect to the composition of diet-induced weight loss.

Adult↗

PubMed1997

Induction of nitric oxide synthase mRNA in coronary resistance arteries isolated from exercise-trained pigs.

The purpose of this study was to develop a method by which endothelial cell nitric oxide synthase (ecNOS) mRNA expression could be measured in single coronary resistance arteries and to test the hypothesis that ecNOS gene expression is upregulated by exercise training. Yucatan miniature swine were randomly assigned to exercise-trained (ET; n = 5) or sedentary (Sed; n = 4) groups for 16 wk. Individual coronary resistance arteries (50-100 microns) were dissected, frozen in liquid nitrogen, and homogenized in a LiCl buffer, mRNA was isolated from each vessel, and ecNOS gene expression was assessed using reverse transcriptase (RT)-polymerase chain reaction (PCR) standardized by coamplifying ecNOS with glyceraldehyde 3-phosphate dehydrogenase (GAPHD). The ecNOS-to-GAPDH amplicon ratio was significantly greater in coronary resistance arteries isolated from ET pigs than in Sed controls. On the basis of these data, it is concluded that RT-PCR can be used on single coronary resistance arteries to assess cell-specific mRNA expression and that ecNOS gene expression is upregulated by exercise training in porcine coronary resistance arteries.

Animals↗

PubMed1988

Exercise training attenuates baroreflex regulation of nerve activity in rabbits.

Baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) during changes in arterial pressure were examined in conscious rabbits before and after 8 wk of treadmill endurance exercise training. Exercise-induced bradycardia (decreased HR at rest and at identical workloads) was used to document a cardiovascular training effect. At 29.4 m/min, 20% grade, posttraining HR was significantly lower than pretraining values (295 +/- 6 beats/min vs. 361 +/- 8 beats/min, P less than 0.05). Rabbits were instrumented with an occluder around the inferior vena cava (IVCO), arterial and venous catheters, and recording electrodes around renal sympathetic nerves. Baroreflex-mediated changes in HR and RSNA to a 25-mmHg decrease and increase in mean arterial pressure (MAP) were obtained by inflating the IVCO or progressive infusion of phenylephrine, respectively. After training, the range (maximum response minus minimum response) of baroreflex control of RSNA and HR was significantly attenuated (209 +/- 12 vs. 413 +/- 14% and 123 +/- 16 vs. 162 +/- 8 beats/min). In addition, the slope of baroreflex control of HR and RSNA was significantly attenuated after training (4.17 +/- 0.35 vs. 8.32 +/- 0.23%/mmHg and 2.57 +/- 0.4 vs. 4.14 +/- 0.4 beats.min-1.mmHg-1). These data demonstrate that endurance exercise training significantly attenuated baroreflex control of HR and RSNA in conscious rabbits.

Animals↗

PubMed1990

Microvascular injury after ischemia and reperfusion in skeletal muscle of exercise-trained rats.

Ischemia and reperfusion in skeletal muscle is associated with increases in total vascular resistance (Rt) and the microvascular permeability to plasma proteins. To determine whether exercise training can attenuate ischemia and reperfusion-induced microvascular injury in skeletal muscle, intact (with skin) and skinned, maximally vasodilated (papaverine), isolated hindquarters of control (C) and exercise-trained (ET) rats were subjected to ischemia (intact 120 min; skinned 60 min) followed by 60 min of reperfusion. ET rats ran on a motorized treadmill at 32 m/min (8% grade), 2 h/day for 12 wk, whereas the C rats were cage confined. Before ischemia, ET hindquarters had higher isogravimetric flow, lower Rt, and similar solvent drag reflection coefficients (sigma f) compared with C. During reperfusion in intact hindquarters, flow was higher (P less than 0.05) and Rt tended to be lower (15 +/- 2 vs. 25 +/- 5 mmHg.ml-1.min.100 g; P less than 0.1) in ET compared with C; however, in skinned hindquarters flow and Rt (14 +/- 2 vs. 13 +/- 2 mmHg.ml-1.min.100 g) were not different between C and ET. During reperfusion, sigma f was reduced (P less than 0.05) in both intact (C 0.68 +/- 0.03; ET 0.68 +/- 0.02) and skinned (C 0.66 +/- 0.03; ET 0.68 +/- 0.03) hindquarters, indicative of an increased microvascular permeability to plasma proteins. These results indicate that exercise training did not attenuate the microvascular injury (increased Rt and decreased sigma f) associated with ischemia and reperfusion in rat skeletal muscle.

Animals↗

PubMed1992

Influence of exercise training soon after myocardial infarction on regional myocardial perfusion and resting left ventricular function.

There is scant information regarding the effect of exercise training begun soon after hospital discharge for myocardial infarction (MI) with respect to subsequent improvement in exercise tolerance, enhancement of regional myocardial perfusion, or left ventricular function. Accordingly, 19 post-MI patients (mean age 53 +/- 7 years) underwent treadmill exercise quantitative thallium-201 (Tl-201) scintigraphy and rest radionuclide angiography (RNA) prior to and after 12 weeks of thrice-weekly exercise training which was targeted to 70-85% of maximum exercise heart rate achieved. Training was begun at 25 +/- 3 days after hospital discharge. Eight Tl-201 scan segments were each scored from 1-6 points based upon uptake and washout criteria with 6 being the most severe defect (greater than 50% reduction in Tl-201 events with no delayed redistribution). When matched to the pretraining peak workload on exercise testing, 12 weeks of training significantly lessened heart rate (120 +/- 4 to 97 +/- 4, p less than 0.001), peak systolic blood pressure (142 +/- 6 to 129 +/- 5 mmHg, p less than 0.01), and significantly reduced double product [17.2 +/- 10.8 to 12.7 +/- 9 (x10(3), p less than 0.001]. Training was associated with a reduction of exercise-induced ST depression or angina (42 to 16%) which was not statistically significant. The mean resting by RNA ejection fraction was 50 +/- 3% prior to training and 51 +/- 3% after training. There was no significant change in overall Tl-201 defect score or the number of defect regions per patient scan comparing pre- and post-training scintigrams.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Circulation↗

PubMed2001

Effects of aerobic exercise training on 24 hr profile of heart rate variability in female athletes.

BACKGROUND: The aim of this study was to investigate the effects of exercise training on autonomic regulation of heart rate under daily life conditions. METHODS: Twenty-six healthy female athletes (age 24.5 +/- 1.9 yrs) involved in regular physical activity were recruited during a period of yearly rest and randomly assigned to a five-week aerobic exercise training program (n = 13) or to a non-exercise control group (n = 13). MEASURES: Before and after the five-week training, all subjects underwent a bycicle ergometer stress test and a 24-hour dynamic ECG monitoring. Autonomic regulation of heart rate has been investigated by means of both time and frequency domain analyses of heart rate variability (HRV). Spectral analysis of R-R interval variability (autoregressive algorithm) provided markers of sympathetic (low frequency, LF, 0.10 Hz) and parasympathetic (high frequency, HF, 0.25 Hz) modulation of the sinus node. RESULTS: Trained subjects showed a reduced heart rate response to submaximal workload. Before training there was no significant difference between the two groups. After training resting heart rate did not significantly differ between trained and untrained subjects. No significant differences were observed in the different time domain indexes of heart rate variability. The day-night difference in SD and SDRR were significantly less in the trained as compared to the untrained group. Normalized LF and HF components did not significantly differ between trained and untrained subjects, during the awake period. The decrease in the LF and the increase in the HF component during nighttime were significantly less in the trained group. The LF/HF ratio was significantly decreased during the night in the untrained group whereas it was not significantly different from the awake state in the trained group. CONCLUSIONS: These findings of the relative night-time increase in LF and the decrease in the day-night difference in time domain indexes of heart rate variability suggest that, in young female athletes, exercise training is able to induce an increase in the sympathetic modulation of the sinus node which may coexist with signs of relatively reduced, or unaffected, vagal modulation.

Adult↗

PubMed2000

Cellular adaptations in fat tissue of exercise-trained miniature swine: role of excess energy intake.

This study examined the influence of energy expenditure and energy intake on cellular mechanisms regulating adipose tissue metabolism. Twenty-four swine were assigned to restricted-fed sedentary, restricted-fed exercise-trained, full-fed sedentary, or full-fed exercise-trained groups. After 3 mo of treatment, adipocytes were isolated and adipocyte size, adenosine A(1) receptor characteristics, and lipolytic sensitivity were measured. Swine were infused with epinephrine during which adipose tissue extracellular adenosine, plasma fatty acids, and plasma glycerol were measured. Results revealed that adipocytes isolated from restricted-fed exercised swine had a smaller diameter, a lower number of A(1) receptors, and a greater sensitivity to lipolytic stimulation, compared with adipocytes from full-fed exercised swine. Extracellular adenosine levels were transiently increased on infusion of epinephrine in adipose tissue of restricted-fed exercised but not full-fed exercised swine. These results suggest a role for adenosine in explaining the discrepancy between in vitro and in vivo lipolysis findings and underscore the notion that excess energy intake dampens the lipolytic sensitivity of adipocytes to beta-agonists and adenosine, even if accompanied by exercise training.

Adaptation, Physiological↗

PubMed2002

Effect of short-term exercise training on insulin-stimulated PI 3-kinase activity in middle-aged men.

The purpose of this study was to determine whether the improved insulin action with short-term exercise training in middle-aged individuals is associated with enhanced phosphatidylinositol (PI) 3-kinase activity in skeletal muscle. Nine men of ages 50-70 yr were studied before and after 7 consecutive days of supervised exercise (60 min/day, 70% peak O2 consumption). Insulin sensitivity was measured with a euglycemic hyperinsulinemic glucose clamp in the sedentary condition and 15-17 h after the final exercise session. Anti-phosphotyrosine-associated PI 3-kinase activity was determined from muscle samples obtained in the fasted condition and after 60 min of insulin infusion during the clamp. With exercise, the glucose infusion rate increased (P < 0.001) by 33%, indicating enhanced insulin action (mean +/- SE, 6.6 +/- 0.6 vs. 8.7 +/- 0.8 mg x kg(-1) x min(-1)). Short-term exercise training did not, however, increase insulin-stimulated (insulin stimulated/fasting) PI 3-kinase activity (1.8 +/- 0.8 vs. 1.8 +/- 0.7-fold stimulation with insulin pre- vs. posttraining, respectively). There was also no change in insulin-stimulated protein kinase B activity (1.3 +/- 0.1 vs. 1.4 +/- 0.2-fold stimulation with insulin) with training. These data suggest that insulin action is enhanced with short-term exercise training via an adaptation distal to PI 3-kinase in middle-aged, insulin-resistant individuals.

Aged↗

PubMed2003

Negative energy balance plays a major role in the IGF-I response to exercise training.

Circulating IGF-I is correlated with fitness, but results of prospective exercise training studies have been inconsistent, showing both increases and decreases in IGF-I. We hypothesized that energy balance, often not accounted for, is a regulating variable such that training plus an energy intake deficit would cause a reduction in IGF-I, whereas training plus energy intake excess would lead to an increased IGF-I. To test this, 19 young, healthy men completed a 7-day strenuous exercise program in which they were randomly assigned to either a positive energy balance [overfed (OF), n = 10] or negative energy balance [underfed (UF), n = 9] group. IGF-I (free and total), insulin, and IGF-binding protein-1 were measured before, during, and 1 wk after the training. Weight decreased in the UF subjects and increased in the OF subjects. Free and total IGF-I decreased substantially in the UF group (P < 0.0005 for both), but, in the OF group, IGF-I remained unchanged. The UF group also demonstrated an increase in IGF-binding protein-1 (P < 0.027), whereas glucose levels decreased (P < 0.0005). In contrast, insulin was reduced in both the OF and UF exercise-training groups (P < 0.044). Finally, within 7 days of the cessation of the diet and training regimen, IGF-I and IGF-binding protein-1 in the UF group returned to preintervention levels. We conclude that energy balance during periods of exercise training influences circulating IGF-I and related growth mediators. Exercise-associated mechanisms may inhibit increases in IGF-I early in the course of a training protocol, even in overfed subjects.

Adolescent↗

PubMed1998

A randomized comparison of exercise training in patients with normal vs reduced ventricular function.

BACKGROUND: Exercise training is recommended after myocardial infarction (MI) or bypass surgery in order to improve exercise tolerance. In some patients, the decrement in exercise capacity secondary to deconditioning and the left ventricular stunning associated with MI or coronary artery bypass graft (CABG) spontaneously improves after the event. However, the impact of the status of the left ventricle on these improvements is unknown. METHODS: Sixty-seven patients 1 month after MI or CABG were randomized to a training (n=34; age, 59+/-7 years) or a control group (n=33; age, 55+/-6 years). Forty-two patients had an ejection fraction >50% (22 in the training group and 20 in the control group), and 25 patients had an ejection fraction <40% (12 in the exercise group and 13 in the control group). After stabilization for approximately 1 month after the event, patients in the exercise group underwent 8 weeks of twice daily exercise at a residential rehabilitation center, while control patients received usual care. Initially and after 8 weeks, patients in both groups underwent maximal exercise testing with gas exchange and lactate analysis. RESULTS: Exercise training increased peak oxygen consumption (VO2) only in the reduced ejection fraction group (19.4+/-3.0 to 23.9+/-4.8 mL/kg/min; p<0.05); the exercise group with normal ventricular function did not change significantly. Changes in VO2 at the lactate threshold paralleled those of peak VO2 for both groups. Conversely, control patients with normal ventricular function increased peak VO2 spontaneously (20.8+/-3.9 to 24.8+/-3.5 mL/kg/min; p<0.01), whereas control patients with reduced ventricular function did not improve peak VO2. CONCLUSION: These data suggest that patients with depressed left ventricular function strongly benefit from rehabilitation, whereas most patients with preserved left ventricular function following MI or CABG tend to improve spontaneously 1 to 3 months after the event.

Coronary Artery Bypass↗