Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow.

To test the hypothesis that heightened sympathetic outflow precedes and predicts the magnitude of the growth hormone (GH) response to acute exercise (Ex), we studied 10 men [age 26.1 +/- 1.7 (SE) yr] six times in randomly assigned order (control and 5 Ex intensities). During exercise, subjects exercised for 30 min (0900-0930) on each occasion at a single intensity: 25 and 75% of the difference between lactate threshold (LT) and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT). Mean values for peak plasma epinephrine (Epi), plasma norepinephrine (NE), and serum GH concentrations were determined [Epi: 328 +/- 93 (SE), 513 +/- 76, 584 +/- 109, 660 +/- 72, and 2,614 +/- 579 pmol/l; NE: 2. 3 +/- 0.2, 3.9 +/- 0.4, 6.9 +/- 1.0, 10.7 +/- 1.6, and 23.9 +/- 3.9 nmol/l; GH: 3.6 +/- 1.5, 6.6 +/- 2.0, 7.0 +/- 2.0, 10.7 +/- 2.4, and 13.7 +/- 2.2 microg/l for 0.25, 0.75, 1.0, 1.25, and 1.75LT, respectively]. In all instances, the time of peak plasma Epi and NE preceded peak GH release. Plasma concentrations of Epi and NE always peaked at 20 min after the onset of Ex, whereas times to peak for GH were 54 +/- 6 (SE), 44 +/- 5, 38 +/- 4, 38 +/- 4, and 37 +/- 2 min after the onset of Ex for 0.25-1.75LT, respectively. ANOVA revealed that intensity of exercise did not affect the foregoing time delay between peak NE or Epi and peak GH (range 17-24 min), with the exception of 0.25LT (P < 0.05). Within-subject linear regression analysis disclosed that, with increasing exercise intensity, change in (Delta) GH was proportionate to both DeltaNE (P = 0.002) and DeltaEpi (P = 0.014). Furthermore, within-subject multiple-regression analysis indicated that the significant GH increment associated with an antecedent rise in NE (P = 0.02) could not be explained by changes in Epi alone (P = 0.77). Our results suggest that exercise intensity and GH release in the human may be coupled mechanistically by central adrenergic activation.     

Gender governs the relationship between exercise intensity and growth hormone release in young adults.

We previously reported that in young adult males growth hormone (GH) release is related to exercise intensity in a linear dose-response manner (Pritzlaff et al. J Appl Physiol 87: 498-504, 1999). To investigate the effects of gender and exercise intensity on GH release, eight women (24.3 +/- 1.3 yr, 171 +/- 3.2 cm height, 63.6 +/- 8.7 kg weight) were each tested on six randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (Ex + recovery or C). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex, subjects exercised for 30 min (0900-0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest, at LT, and at 25 and 75% of the difference between LT and peak O2 uptake. No differences were observed among conditions for baseline IGHC. To determine whether total (Ex + recovery) IGHC changed with increasing exercise intensity, slopes associated with individual linear regression models were subjected to a Wilcoxon signed-rank test. To test for gender differences, data in women were compared with the previously published data in men. A Wilcoxon ranked-sums two-tailed test was used to analyze the slopes and intercepts from the regression models. Total IGHC increased linearly with increasing exercise intensity. The slope and intercept values for the relationship between total IGHC and exercise intensity were greater in women than in men. Deconvolution analysis (0700-1300 h) revealed that, regardless of gender, increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and summed GH production rate, with no changes in GH secretory pulse frequency or apparent half-life of elimination. Exercise reduced the half-duration of GH secretory burst in men but not in women. Gender comparisons revealed that women had greater basal (nonpulsatile) GH secretion across all conditions, more frequent GH secretory pulses, a greater GH secretory pulse amplitude, a greater production rate, and a trend for a greater mass of GH secreted per pulse than men. We conclude that, in young adults, the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern. For each incremental increase in exercise intensity, the fractional stimulation of GH secretion is greater in women than in men.     

Catecholamine release, growth hormone secretion, and energy expenditure during exercise vs. recovery in men.

We examined the relationship between energy expenditure (in kcal) and epinephrine (Epi), norepinephrine (NE), and growth hormone (GH) release. Ten men [age, 26 yr; height, 178 cm; weight, 81 kg; O(2) uptake at lactate threshold (LT), 36.3 ml. kg(-1). min(-1); peak O(2) uptake, 49.5 ml. kg(-1). min(-1)] were tested on six randomly ordered occasions [control, 5 exercise: at 25 and 75% of the difference between LT and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT) (0900-0930)]. From 0700 to 1300, blood was sampled and assayed for GH, Epi, and NE. Carbohydrate (CHO) expenditure during exercise and fat expenditure during recovery rose proportionately to increasing exercise intensity (P = 0.002). Fat expenditure during exercise and CHO expenditure during recovery were not affected by exercise intensity. The relationship between exercise intensity and CHO expenditure during exercise could not be explained by either Epi (P = 1.00) or NE (P = 0.922), whereas fat expenditure during recovery increased with Epi and GH independently of exercise intensity (P = 0. 028). When Epi and GH were regressed against fat expenditure during recovery, only GH remained statistically significant (P < 0.05). We conclude that a positive relationship exists between exercise intensity and both CHO expenditure during exercise and fat expenditure during recovery and that the increase in fat expenditure during recovery with higher exercise intensities is related to GH release.     

Effects of gender on exercise-induced growth hormone release.

We examined gender differences in growth hormone (GH) secretion during rest and exercise. Eighteen subjects (9 women and 9 men) were tested on two occasions each [resting condition (R) and exercise condition (Ex)]. Blood was sampled at 10-min intervals from 0600 to 1200 and was assayed for GH by chemiluminescence. At R, women had a 3.69-fold greater mean calculated mass of GH secreted per burst compared with men (5.4 +/- 1.0 vs. 1.7 +/- 0.4 microg/l, respectively) and higher basal (interpulse) GH secretion rates, which resulted in greater GH production rates and serum GH area under the curve (AUC; 1,107 +/- 194 vs. 595 +/- 146 microg x l(-1) x min, women vs. men; P = 0.04). Compared with R, Ex resulted in greater mean mass of GH secreted per burst, greater mean GH secretory burst amplitude, and greater GH AUC (1,196 +/- 211 vs. 506 +/- 90 microg x l(-1) x min, Ex vs. R, respectively; P < 0.001). During Ex, women attained maximal serum GH concentrations significantly earlier than men (24 vs. 32 min after initiation of Ex, respectively; P = 0.004). Despite this temporal disparity, both genders had similar maximal serum GH concentrations. The change in AUC (adjusted for unequal baselines) was similar for men and women (593 +/- 201 vs. 811 +/- 268 microg x l(-1) x min), but there were significant gender-by-condition interactive effects on GH secretory burst mass, pulsatile GH production rate, and maximal serum GH concentration. We conclude that, although women exhibit greater absolute GH secretion rates than men both at rest and during exercise, exercise evokes a similar incremental GH response in men and women. Thus the magnitude of the incremental secretory GH response is not gender dependent.     

The impact of sex and exercise duration on growth hormone secretion.

Previous research clearly indicates a linear relationship between exercise intensity and growth hormone (GH) release and that this relationship is influenced by sex. The present study examined the GH response to increasing exercise duration in young men and women. Fifteen healthy subjects (8 men and 7 women) completed three randomly assigned exercise sessions (30, 60, and 120 min) at 70% of peak oxygen consumption. Blood samples were collected every 10 min beginning 30 min before exercise, for a total of 240 min. Total integrated GH concentration (IGHC) increased with increasing exercise duration for men and women (601, 1,394, and 2,360 microg/l.4 h; 659, 1,009 and 1,243 microg/l.4 h for 30, 60, and 120 min of exercise, respectively). Regression analysis revealed that IGHC (logarithmically transformed) was significantly influenced by exercise duration (logarithmically transformed) (120 min > 60 min > 30 min) and that a significant sex-dependent effect was present even after adjustments for fitness level and percent body fat (men > women). The slope of the regression line was greater for men than for women (1.003 vs. 0.612; P = 0.013), but the average height of the regression line was greater for women (7.287 vs. 6.595; P < 0.001). Although GH secretory pulse half-duration was greater in women (P = 0.001), and GH half-life was greater in men (P = 0.001), they were not affected by exercise duration. The total mass of GH secreted during exercise increased with exercise duration (P < 0.001) but was not affected by sex (P = 0.137). Results from the present investigation indicate that when exercise intensity is constant, exercise duration significantly increases IGHC and that this relationship is sex dependent.     

Oral arginine attenuates the growth hormone response to resistance exercise.

This study investigated the combined effect of resistance exercise and arginine ingestion on spontaneous growth hormone (GH) release. Eight healthy male subjects were studied randomly on four separate occasions [placebo, arginine (Arg), placebo + exercise (Ex), arginine + exercise (Arg+Ex)]. Subjects had blood sampled every 10 min for 3.5 h. After baseline sampling (30 min), subjects ingested a 7-g dose of arginine or placebo (blinded, randomly assigned). On the exercise days, the subject performed 3 sets of 9 exercises, 10 repetitions at 80% one repetition maximum. Resting GH concentrations were similar on each study day. Integrated GH area under the curve was significantly higher on the Ex day (508.7 +/- 169.6 min.ng/ml; P < 0.05) than on any of the other study days. Arg+Ex (260.5 +/- 76.8 min.ng/ml) resulted in a greater response than the placebo day but not significantly greater than the Arg day. The GH half-life and half duration were not influenced by the stimulus administered. The GH secretory burst mass was larger, but not significantly, on the Arg, Ex, and Arg+Ex day than the placebo day. Endogenous GH production rate (Ex > Arg+Ex > Arg > placebo) was greater on the Ex and Arg+Ex day than on the placebo day (P < 0.05) but there were no differences between the Ex and Arg+Ex day. Oral arginine alone (7 g) stimulated GH release, but a greater GH response was seen with exercise alone. The combined effect of arginine before exercise attenuates the GH response. Autonegative feedback possibly causes a refractory period such that when the two stimuli are presented there will be suppression of the somatotrope.     

Growth hormone and muscle function responses to skeletal muscle ischemia.

We examined the effects of ischemia (ISC) alone and with low-intensity exercise (ISC+EX) on growth hormone (GH) and muscle function responses. Nine men (22 +/- 0.7 yr) completed 3 study days: an ISC day (thigh cuff inflated five times, 5 min on, 3 min off), an ISC+EX day [knee extension at 20% maximal voluntary contraction (MVC) with ISC], and a control day. MVCs and submaximal contraction tasks (15 and 30% MVC) were performed before and following the perturbations. Surface electromyogram signals were collected from thigh muscles and analyzed for median frequency and root mean square alterations. Blood samples were collected every 10 min (190 min total) and analyzed for GH concentrations. Peak GH concentrations and GH area under the curve were highest (P < 0.01) on the ISC+EX day (7.5 microg/l and 432 microg.l(-1).min(-1), respectively) compared with the ISC (0.9 microg/l and 76.4 microg.l(-1).min(-1)), and CON (1.1 microg/l and 83.8 microg.l(-1).min(-1)) days. A greater GH pulse amplitude, mass/pulse, and production rate were also observed on the ISC+EX day (P < 0.05). Following the intervention, force production decreased on the ISC and ISC+EX days by 16.1 and 55.8%, respectively, and did not return to baseline values within 5 min of recovery. During the submaximal contractions, median frequency shifted to lower frequencies for most of the muscles examined, and root mean square electromyogram was consistently elevated for ISC+EX day. In conclusion, ISC coupled with resistance exercise acutely increases GH levels and reduces MVC, whereas ISC alone decreases force capacity, without alterations in GH levels.     

Gender differences in glucose kinetics and substrate oxidation during exercise near the lactate threshold.

The purpose of this investigation was to determine plasma glucose kinetics and substrate oxidation in men and women during exercise relative to the lactate threshold (LT). Subjects cycled for 25 min at 70 and 90% of O(2) uptake (VO(2)) at LT (70 and 90% LT, respectively). Plasma glucose appearance (R(a)) and disappearance (R(d)) were determined with a primed constant infusion of [6,6-(2)H]glucose. There were no significant differences in glucose R(a) between men [22.6 +/- 1.9 and 39.9 +/- 3.9 micromol x kg fat-free mass (FFM)(-1) x min(-1) for 70 and 90% LT, respectively] and women (22.3 +/- 2.7 and 33.9 +/- 5.7 micromol x kg FFM(-1) x min(-1) for 70 and 90% LT, respectively). Similarly, there were no significant differences in glucose R(d) between men (21.2 +/- 1.9 and 38.1 +/- 3.7 micromol x kg FFM(-1) x min(-1) for 70 and 90% LT, respectively) and women (21.3 +/- 2.8 and 33.3 +/- 5.6 micromol x kg FFM(-1) x min(-1) for 70 and 90% LT, respectively). Although there were no differences between genders in the relative contribution of carbohydrate (CHO) to total energy expenditure, the relative contribution of muscle glycogen to total CHO oxidation (75.8 +/- 3.2 and 64.2 +/- 8.0% for men and women, respectively, at 70% LT and 75.1 +/- 2.6 and 60.1 +/- 11.2% for men and women, respectively, at 90% LT) was lower in women. Consequently, the relative contribution of blood glucose to total CHO oxidation was significantly higher in women. These results indicate that although plasma glucose R(a) and R(d) are similar in men and women, the relative contribution of muscle glycogen and blood glucose is significantly different in women during moderate-intensity exercise relative to LT.     

Effects of glutamine supplementation, GH, and IGF-I on glutamine metabolism in critically ill patients

During critical illness glutamine deficiency may develop. Glutamine supplementation can restore plasma concentration to normal, but the effect on glutamine metabolism is unknown. The use of growth hormone (GH) and insulin-like growth factor I (IGF-I) to prevent protein catabolism in these patients may exacerbate the glutamine deficiency. We have investigated, in critically ill patients, the effects of 72 h of treatment with standard parenteral nutrition (TPN; n = 6), TPN supplemented with glutamine (TPNGLN; 0.4 g x kg(-1) x day(-1), n = 6), or TPNGLN with combined GH (0.2 IU. kg(-1). day(-1)) and IGF-I (160 microg x kg (-1) x day(-1)) (TPNGLN+GH/IGF-I; n = 5) on glutamine metabolism using [2-(15)N]glutamine. In patients receiving TPNGLN and TPNGLN+GH/IGF-I, plasma glutamine concentration was increased (338 +/- 22 vs. 461 +/- 24 micromol/l, P < 0.001, and 307 +/- 65 vs. 524 +/- 71 micromol/l, P < 0.05, respectively) and glutamine uptake was increased (5.2 +/- 0.5 vs. 7.4 +/- 0.7 micromol x kg(-1) x min(-1), P < 0.05 and 5.2 +/- 1.1 vs. 7.6 +/- 0.8 micromol x kg(-1) x min(-1), P < 0.05). Glutamine production and metabolic clearance rates were not altered by the three treatments. These results suggest that there is an increased requirement for glutamine in critically ill patients. Combined GH/IGF-I treatment with TPNGLN did not have adverse effects on glutamine metabolism.     

Effect of different muscle shortening velocities during prolonged incremental cycling exercise on the plasma growth hormone, insulin, glucose, glucagon, cortisol, leptin and lactate concentrations.

BACKGROUND: Strenuous exercise was reported to involve the alteration in the release of some "stress" hormones such as growth hormone (GH), cortisol, catecholamines and appropriate adjustment of energy metabolism but the relative contribution of these hormones to metabolic response, to cycling exercise performed at different muscle shortening velocities, has not been clarified. AIMS: The purpose of this experiment was to assess the effect of applying different pedalling rates during a prolonged incremental cycling exercise test on the changes in the plasma levels of growth hormone, cortisol, insulin, glucagon and leptin in humans. Material and METHODS: Fifteen healthy non-smoking men (means +/- SD: age 22.9 +/- 2.4 years; body mass 71.9 +/- 8.2 kg; height 178 +/- 6 cm; with VO2max of 3.896 +/- 0.544 1 x min(-1), assessed in laboratory tests, were subjects in this study. The subjects performed in two different days a prolonged incremental exercise tests at two different pedalling rates, one of them at 60 and another at 120 rev x min(-1). During this tests the power output has increased by 30 W every 6 minutes. The tests were stopped when the subject reached about 70 % of the VO2max. RESULTS AND CONCLUSIONS: We have found that choosing slow or fast pedalling rates (60 or 120 rev min(-1)), while generating the same external mechanical power output, had no effect on the pattern of changes in plasma cortisol, insulin, glucagon, glucose and leptin concentrations. But, generation of the same external mechanical power output at 120 rev min(-1) causes more stepper increase (p < 0.01) in the plasma growth hormone concentration [GH]pl and plasma lactate concentrations [La]pl when compared to that observed during cycling at 60 rev x min(-1). We have also found that the onset of a significant increase in [GH]pl during cycling at 60 rev x min(-1) was not accompanied by significant increase in [La]pl. While during cycling at 120 rev x min(-1) the onset of a significant increase in [La]pl occurred without increase in [GH]pl, but with continuation of exercise when plasma [La]pl increased, there was also a parallel rise in plasma [GH]pl, as reported before. This results indicates that the increase in [GH]pl during exercise is not closely related to the increase in [La]pl.     

Age is an important determinant of the growth hormone response to sprint exercise in non-obese young men

BACKGROUND: The factors that regulate the growth hormone (GH) response to physiological stimuli, such as exercise, are not fully understood. The aim of the present study is to determine whether age, body composition, measures of sprint performance or the metabolic response to a sprint are predictors of the GH response to sprint exercise in non-obese young men. METHODS: Twenty-seven healthy, non-obese males aged 18-32 years performed an all-out 30-second sprint on a cycle ergometer. Univariate linear regression analysis was employed to evaluate age-, BMI-, performance- and metabolic-dependent changes from pre-exercise to peak GH and integrated GH for 60 min after the sprint. RESULTS: GH was elevated following the sprint (change in GH: 17.0 +/- 14.2 microg l(-1); integrated GH: 662 +/- 582 min microg l(-1)). Performance characteristics, the metabolic response to exercise and BMI were not significant predictors of the GH response to exercise. However, age emerged as a significant predictor of both integrated GH (beta = -0.547, p = 0.003) and change in GH (beta = -0.448, p = 0.019) after the sprint. CONCLUSION: In non-obese young men, age is a more important predictor of GH following sprint exercise than BMI, sprint performance or the metabolic response to sprint exercise.     

The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men.

A single 30-s sprint is a potent physiological stimulus for growth hormone (GH) release. However, repeated bouts of sprinting attenuate the GH response, possibly due to negative feedback via elevated systemic free fatty acids (FFA). The aim of the study was to use nicotinic acid (NA) to suppress lipolysis to investigate whether serum FFA can modulate the GH response to exercise. Seven nonobese, healthy men performed two trials, consisting of two maximal 30-s cycle ergometer sprints separated by 4 h of recovery. In one trial (NA), participants ingested NA (1 g 60 min before, and 0.5 g 60 and 180 min after sprint 1); the other was a control (Con) trial. Serum FFA was not significantly different between trials before sprint 1 but was significantly lower in the NA trial immediately before sprint 2 [NA vs. Con: mean (SD); 0.08 (0.05) vs. 0.75 (0.34) mmol/l, P < 0.05]. Peak and integrated GH were significantly greater following sprint 2 compared with sprint 1 in the NA trial [peak GH: 23.3 (7.0) vs. 7.7 (11.9) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 316 (527) microg.l(-1).60 min(-1), P < 0.05] and compared with sprint 2 in the Con trial [peak GH: 23.3 (7.0) vs. 5.2 (2.3) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 206 (118) microg.l(-1).60 min(-1), P < 0.05]. In conclusion, suppressing lipolysis resulted in a significantly greater GH response to the second of two sprints, suggesting a potential role for serum FFA in negative feedback control of the GH response to repeated exercise.     

Nonuniform effects of endurance exercise training on vasodilation in rat skeletal muscle.

Endurance exercise training (Ex) has been shown to increase maximal skeletal muscle blood flow. The purpose of this study was to test the hypothesis that increased endothelium-dependent vasodilation is associated with the Ex-induced increase in muscle blood flow. Furthermore, we hypothesized that enhanced endothelium-dependent dilation is confined to vessels in high-oxidative muscles that are recruited during Ex. To test these hypotheses, sedentary (Sed) and rats that underwent Ex (30 m/min x 10% grade, 60 min/day, 5 days/wk, 8-12 wk) were studied using three experimental approaches. Training effectiveness was evidenced by increased citrate synthase activity in soleus and vastus lateralis (red section) muscles (P < 0.05). Vasodilatory responses to the endothelium-dependent agent acetylcholine (ACh) in situ tended to be augmented by training in the red section of gastrocnemius muscle (RG; Sed: control, 0.69 +/- 0.12; ACh, 1.25 +/- 0.15; Ex: control, 0.86 +/- 0.17; ACh, 1.76 +/- 0.27 ml x min(-1) x 100 g(-1) x mmHg(-1); 0.05 < P < 0.10 for Ex vs. Sed during ACh). Responses to ACh in situ did not differ between Sed and Ex for either the soleus muscle or white section of gastrocnemius muscle (WG). Dilatory responses of second-order arterioles from the RG in vitro to flow (4-8 microl/min) and sodium nitroprusside (SNP; 10(-7) through 10(-4) M), but not ACh, were augmented in Ex (vs. Sed; P < 0.05). Dilatory responses to ACh, flow, and SNP of arterioles from soleus and WG muscles did not differ between Sed and Ex. Content of the endothelial isoform of nitric oxide synthase (eNOS) was increased in second-order, fourth-order, and fifth-order arterioles from the RG of Ex; eNOS content was similar between Sed and Ex in vessels from the soleus and WG muscles. These findings indicate that Ex induces endothelial adaptations in fast-twitch, oxidative, glycolytic skeletal muscle. These adaptations may contribute to enhanced skeletal muscle blood flow in endurance-trained individuals.     

Human lung density is not altered following normoxic and hypoxic moderate-intensity exercise: implications for transient edema.

The purpose of this study was to examine the effects of exercise on extravascular lung water as it may relate to pulmonary gas exchange. Ten male humans underwent measures of maximal oxygen uptake (Vo2 max) in two conditions: normoxia (N) and normobaric hypoxia of 15% O2 (H). Lung density was measured by quantified MRI before and 48.0 +/- 7.4 and 100.7 +/- 15.1 min following 60 min of cycling exercise in N (intensity = 61.6 +/- 9.5% Vo2 max) and 55.5 +/- 9.8 and 104.3 +/- 9.1 min following 60 min cycling exercise in H (intensity = 65.4 +/- 7.1% hypoxic Vo2 max), where Vo2 max = 65.0 +/- 7.5 ml x kg(-1) x min(-1) (N) and 54.1 +/- 7.0 ml x kg(-1) x min(-1) (H). Two subjects demonstrated mild exercise-induced arterial hypoxemia (EIAH) [minimum arterial oxygen saturation (SaO2 min) = 94.5% and 93.8%], and seven subjects demonstrated moderate EIAH (SaO2 min = 91.4 +/- 1.1%) as measured noninvasively during the Vo2 max test in N. Mean lung densities, measured once preexercise and twice postexercise, were 0.177 +/- 0.019, 0.181 +/- 0.019, and 0.173 +/- 0.019 g/ml (N) and 0.178 +/- 0.021, 0.174 +/- 0.022, and 0.176 +/- 0.019 g/ml (H), respectively. No significant differences (P > 0.05) were found in lung density following exercise in either condition or between conditions. Transient interstitial pulmonary edema did not occur following sustained steady-state cycling exercise in N or H, indicating that transient edema does not result from pulmonary capillary leakage during sustained submaximal exercise.     

Overnight responses of the circulating IGF-I system after acute, heavy-resistance exercise.

This study evaluated the individual components of the insulin-like growth factor I (IGF-I) system [i.e., total and free IGF-I, insulin-like growth factor binding protein (IGFBP)-2 and -3, and the acid-labile subunit (ALS)] in 10 young, healthy men (age: 22 +/- 1 yr, height: 177 +/- 2 cm, weight: 79 +/- 3 kg, body fat: 11 +/- 1%) overnight for 13 h after two conditions: a resting control (Con) and an acute, heavy-resistance exercise protocol (Ex). The Ex was a high-volume, multiset exercise protocol that alternated between 10- and 5-repetition maximum sets with 90-s rest periods between sets. The Ex was performed from 1500 to 1700; blood was obtained immediately postexercise and sampled throughout the night (every 10 min for the first hour and every hour thereafter) until 0600 the next morning. For the first hour, significant differences (P < or = 0.05) were only observed for IGFBP-3 (Ex: 3,801 > Con: 3,531 ng/ml). For the overnight responses, no differences were observed for total or free IGF-I or IGFBP-3, whereas IGFBP-2 increased (Ex: 561 > Con: 500 ng/ml) and ALS decreased (Ex: 35 < Con: 39 microg/ml) after exercise. The results from this study suggest that the impact that resistance exercise exerts on the circulating IGF-I system is not in the alteration of the amount of IGF-I but rather of the manner in which IGF-I is partitioned among its family of binding proteins. Thus acute, heavy-resistance exercise can lead to alterations in the IGF-I system that can be detected in the systemic circulation.     

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O2 uptake (VO2 peak) = 56.4 +/- 2.8 ml x kg(-1) x min(-1); mean +/- SE]. Subjects exercised on a cycle ergometer at >or=90% VO2 peak) to exhaustion (13.2 +/- 0.8 min), during which time arterial O2 saturation (Sa(O2)) fell from 97.7 +/- 0.1% at rest to 91.9 +/- 0.9% (range 84-94%) at end exercise, primarily because of changes in blood pH (7.183 +/- 0.017) and body temperature (38.9 +/- 0.2 degrees C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O2 fraction (Fi(O2)) = 0.25-0.31] that prevented EIAH (Sa(O2) = 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at Fi(O2) 0.21, the mean force response across 1-100 Hz decreased 33 +/- 5% compared with only 15 +/- 5% when EIAH was prevented (P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at Fi(O2) 0.21 (Sa(O2) = 95.3 +/- 0.7%), the decrease in evoked force was exacerbated by 35% (P < 0.05) in response to further desaturation induced via Fi(O2) 0.17 (Sa(O2) = 87.8 +/- 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (-6 +/- 1% DeltaSa(O2) from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.     

Epinephrine infusion during moderate intensity exercise increases glucose production and uptake

The glucoregulatory response to intense exercise [IE, >80% maximum O(2) uptake (VO(2 max))] comprises a marked increment in glucose production (R(a)) and a lesser increment in glucose uptake (R(d)), resulting in hyperglycemia. The R(a) correlates with plasma catecholamines but not with the glucagon-to-insulin (IRG/IRI) ratio. If epinephrine (Epi) infusion during moderate exercise were able to markedly stimulate R(a), this would support an important role for the catecholamines' response in IE. Seven fit male subjects (26 +/- 2 yr, body mass index 23 +/- 0.5 kg/m(2), VO(2 max) 65 +/- 5 ml x kg(-1) x min(-1)) underwent 40 min of postabsorptive cycle ergometer exercise (145 +/- 14 W) once without [control (CON)] and once with Epi infusion [EPI (0.1 microg x kg(-1) x min(-1))] from 30 to 40 min. Epi levels reached 9.4 +/- 0.8 nM (20x rest, 10x CON). R(a) increased approximately 70% to 3.75 +/- 0.53 in CON but to 8.57 +/- 0.58 mg x kg(-1) x min(-1) in EPI (P < 0.001). Increments in R(a) and Epi correlated (r(2) = 0.923, P 相似文献   

Validity of pulse oximetry during maximal exercise in normoxia, hypoxia, and hyperoxia.

During exercise, pulse oximetry is problematic due to motion artifact and altered digital perfusion. New pulse oximeter technology addresses these issues and may offer improved performance. We simultaneously compared Nellcor N-395 (Oxismart XLTM) pulse oximeters with an RS-10 forehead sensor (RS-10), a D-25 digit sensor (D-25), and the Ivy 2000 (Masimo SETTM)/LNOP-Adt digit sensor (Ivy) to arterial blood oxygen saturation (Sa(O(2))) by cooximetry. Nine normal subjects, six athletes, and four patients with chronic disease exercised to maximum oxygen consumption (VO(2 max)) under various conditions [normoxia, hypoxia inspired oxygen fraction (FI(O(2))) = 0.125; hyperoxia, FI(O(2)) = 1.0]. Regression analysis for normoxia and hypoxic data was performed (n = 161 observations, Sa(O(2)) = 73-99.9%), and bias (B) and precision (P) were calculated. RS10 offered greater validity than the other two devices tested (y = 1.009x - 0.52, R(2) = 0.90, B+/-P = 0.3 +/- 2.5). Finger sensors had low precision and a significant negative bias (D-25: y = 1.004x - 2.327, R(2) = 0.52, B+/-P = -2.0 +/- 7.3; Ivy: y = 1.237x - 24.2, R(2) = 0.78, B+/-P = -2.0 +/- 5.2). Eliminating measurements in which heart rate differed by >10 beats/min from the electrocardiogram value improved precision minimally and did not affect bias substantially (B+/-P = 0.5 +/- 2.0, -1.8 +/- 8.4, and -1.25+/-4.33 for RS-10, D-25, and Ivy, respectively). Signal detection algorithms and pulse oximeter were identical between RS-10 and D-25; thus the improved performance of the forehead sensor is likely because of sensor location. RS-10 should be considered for exercise testing in which pulse oximetry is desirable.     

Oxidation of combined ingestion of glucose and fructose during exercise.

The purpose of the present study was to examine whether combined ingestion of a large amount of fructose and glucose during cycling exercise would lead to exogenous carbohydrate oxidation rates >1 g/min. Eight trained cyclists (maximal O(2) consumption: 62 +/- 3 ml x kg(-1) x min(-1)) performed four exercise trials in random order. Each trial consisted of 120 min of cycling at 50% maximum power output (63 +/- 2% maximal O(2) consumption), while subjects received a solution providing either 1.2 g/min of glucose (Med-Glu), 1.8 g/min of glucose (High-Glu), 0.6 g/min of fructose + 1.2 g/min of glucose (Fruc+Glu), or water. The ingested fructose was labeled with [U-(13)C]fructose, and the ingested glucose was labeled with [U-(14)C]glucose. Peak exogenous carbohydrate oxidation rates were approximately 55% higher (P < 0.001) in Fruc+Glu (1.26 +/- 0.07 g/min) compared with Med-Glu and High-Glu (0.80 +/- 0.04 and 0.83 +/- 0.05 g/min, respectively). Furthermore, the average exogenous carbohydrate oxidation rates over the 60- to 120-min exercise period were higher (P < 0.001) in Fruc+Glu compared with Med-Glu and High-Glu (1.16 +/- 0.06, 0.75 +/- 0.04, and 0.75 +/- 0.04 g/min, respectively). There was a trend toward a lower endogenous carbohydrate oxidation in Fruc+Glu compared with the other two carbohydrate trials, but this failed to reach statistical significance (P = 0.075). The present results demonstrate that, when fructose and glucose are ingested simultaneously at high rates during cycling exercise, exogenous carbohydrate oxidation rates can reach peak values of approximately 1.3 g/min.