Biomedical subjects

S E Gordon

Publications and source records attributed to S E Gordon.

At least 55 records · Page 3Linked to original sources

PubMed1995

Subunit interactions in coordination of Ni2+ in cyclic nucleotide-gated channels.

Cyclic nucleotide-gated (CNG) channels present a unique model for studying the molecular mechanisms of channel gating. We have studied the mechanism of potentiation of expressed rod CNG channels by Ni2+ as a first step toward understanding the channel gating process. Here we report that coordination of Ni2+ between histidine residues (H420) on adjacent channel subunits occurs when the channels are open. Mutation of H420 to lysine completely eliminated the potentiation by Ni2+ but did not markedly alter the apparent cGMP affinity of the channel, indicating that the introduction of positive charge at the Ni(2+)-binding site was not sufficient to produce potentiation. Deletion or mutation of most of the other histidines present in the channel did not diminish potentiation by Ni2+. We studied the role of subunit interactions in Ni2+ potentiation by generating heteromultimeric channels using tandem dimers of the rod CNG channel sequence. Injection of single heterodimers in which one subunit contained H420 and the other did not (wt/H420Q or H420Q/wt) resulted in channels that were not potentiated by Ni2+. However, coinjection of both heterodimers into Xenopus oocytes resulted in channels that exhibited potentiation. The H420 residues probably occurred predominantly in nonadjacent subunits when each heterodimer was injected individually, but, when the two heterodimers were coinjected, the H420 residues could occur in adjacent subunits as well. These results suggest that the mechanism of Ni2+ potentiation involves intersubunit coordination of Ni2+ by H420. Based on the preferential binding of Ni2+ to open channels, we suggest that alignment of H420 residues of neighboring subunits into the Ni(2+)-coordinating position may be associated with channel opening.

Amino Acid Sequence↗

PubMed1995

Modulation of the cGMP-gated ion channel in frog rods by calmodulin and an endogenous inhibitory factor.

1. Outer segment patches excised in the light were used to investigate the effects of exogenous calmodulin and an endogenous inhibitory factor on the cGMP-gated channel of frog rods. 2. Calmodulin shifted to the right the dose-response relation for activation of the channels by 8-Br-cGMP, but did not change the maximum current or the form of the relation. Reversal of this effect by removal of calmodulin was accelerated by brief exposure to saturating [8-Br-cGMP]. Inhibition by calmodulin required calcium and gave as much as a 5-fold decrease in current for an [8-Br-cGMP] functionally comparable to the presumed physiological [cGMP]. 3. Exposure to low [Ca2+]i (tens of nanomolar) appeared to irreversibly remove or inactivate an endogenous channel inhibitory factor from the patches, increasing the current at low [8-Br-cGMP]. Like calmodulin, this factor slowed the voltage-dependent channel-gating kinetics and did not change the maximum current. However, unlike calmodulin, the endogenous factor remained stably associated with the patches at high [Ca2+]i (1 microM), even with exposure to saturating [8-Br-cGMP]. 4. After the low-Ca2+ treatment increased the current, calmodulin reduced the current to about the same level as it had before the low-Ca2+ treatment, giving a larger fractional suppression. Furthermore, patches with high initial sensitivity to 8-Br-cGMP had small low-Ca2+ effects and large calmodulin effects, while the reverse was true for patches with low initial agonist sensitivity. 5. Application of trypsin to the intracellular surface of the patch prevented the responses to calmodulin and to low [Ca2+]i, suggesting involvement of a cytoplasmic portion of the channel. However, trypsin also reduced the total agonist-induced patch current. 6. Our results are consistent with a model in which calmodulin and an endogenous calcium-binding protein compete for the same site, inhibiting channel opening or cGMP binding. The tight association of the endogenous factor with the channel even at relatively low [Ca2+]i suggests that in the transducing rod it may inhibit the channels most of the time in darkness and in dim light, preventing any potential inhibitory effects of calmodulin. The endogenous factor would be expected to leave the channel only in bright or prolonged light, when the [Ca2+]i is thought to be very low.

Animals↗

PubMed1995

Localization of regions affecting an allosteric transition in cyclic nucleotide-activated channels.

Sensory transduction in olfactory receptors and photoreceptors is mediated by cyclic nucleotide-activated ion channels. We have studied the gating mechanism in olfactory and rod channels expressed in Xenopus oocytes. We report that the differences in cyclic nucleotide affinity and efficacy between these channels resulted from sequence differences outside the cyclic nucleotide-binding domain, especially in the amino-terminal domain, influencing the free energy of the closed to open allosteric conformational change. In addition, Ni2+ inhibited activation of the olfactory channel, decreasing both the maximum current and the apparent affinity for cyclic nucleotides. Ni2+ exerted its effect by binding preferentially to the closed configuration of the channel, thereby destabilizing the opening conformational change. We have localized this inhibition to a single histidine (H396) following the last transmembrane segment, suggesting a role for this region in channel gating.

Allosteric Regulation↗

PubMed1995

A histidine residue associated with the gate of the cyclic nucleotide-activated channels in rod photoreceptors.

Ion channels directly activated by the binding of cGMP mediate the electrical response to light in rod photoreceptors. Here, we identify a region of the channel associated with the activation gate using potentiation by intracellular Ni2+. Low concentrations of Ni2+ caused a dramatic increase in the response of rod channels expressed in Xenopus oocytes to both cGMP and cAMP. Whereas saturating cAMP normally activated less than 1% of the channels, Ni2+ increased the cAMP potency nearly 50-fold. Ni2+ did not produce potentiation in the related channel from the olfactory epithelium. We localized the Ni(2+)-binding site to a histidine residue in the putative intracellular mouth of the rod channel (H420). We propose a mechanism for potentiation in which Ni2+ binds to H420 primarily when the channel is open, stabilizing the open conformation. These experiments suggest that H420 is associated with the activation gate.

Animals↗

PubMed1995

Diacylglycerol analogs inhibit the rod cGMP-gated channel by a phosphorylation-independent mechanism.

The electrical response to light in retinal rods is mediated by cyclic nucleotide-gated, nonselective cation channels in the outer segment plasma membrane. Although cGMP appears to be the primary light-regulated second messenger, cellular levels of other substances, including Ca2+ and phosphatidylinositol-4,5-bisphosphate, are also sensitive to the level of illumination. We now show that diacylglycerol (DAG) analogs reversibly suppress the cGMP-activated conductance in excised patches from frog rod outer segments. This suppression did not require nucleoside triphosphates, indicating that a phosphorylation reaction was not involved. DAG was more effective at low than at high [cGMP]: with 50 microM 8-Br-cGMP, the DAG analog 1,2-dioctanoyl-sn-glycerol (1,2-DiC8) reduced the current with an IC50 of approximately 22 microM (Hill coefficient, 0.8), whereas with 1.2 microM 8-Br-cGMP, only approximately 1 microM 1,2-DiC8 was required to halve the current. DAG reduced the apparent affinity of the channels for cGMP: 4 microM 1,2-DiC8 produced a threefold increase in the K1/2 for channel activation by 8-Br-cGMP, as well as a threefold reduction in the maximum current, without changing the apparent stoichiometry or cooperativity of cGMP binding. Inhibition by 1,2-DiC8 was not relieved by supersaturating concentrations of 8-Br-cGMP, suggesting that DAG did not act by competitive inhibition of cGMP binding. Furthermore, DAG did not seem to significantly reduce single-channel conductance. A DAG analog similar to 1,2-DiC8--1,3-dioctanoyl-sn-glycerol (1,3-DiC8)--suppressed the current with the same potency as 1,2-DiC8, whereas an ethylene glycol of identical chain length (DiC8-EG) was much less effective. Our results suggest that DAG allosterically interferes with channel opening, and raise the question of whether DAG is involved in visual transduction.

Ambystoma↗

PubMed1995

Effects of multibuffer supplementation on acid-base balance and 2,3-diphosphoglycerate following repetitive anaerobic exercise.

The purpose of this investigation was to determine the effects of a 3.5-day dietary multibuffer supplement (containing predominantly inorganic phosphate, or Pi, along with bicarbonate and carnosine, i.e., PhosFuel) on repetitive (four trials separated by 2 min rest) Wingate test (WT) performances and whole blood 2,3-diphosphoglycerate (2,3-DPG) concentrations in 10 recreationally trained road cyclists (T) and 10 normally active but untrained (UT) men. A 2-week washout period was utilized between experimental sessions. Venous blood samples were obtained via cannula once before exercise (baseline), immediately post each WT, and 3 min after the final WT (recovery). The data indicate that this supplement does not affect acid-base status with following intense anaerobic exercise and does not improve repetitive WT performance. However, the supplement does enhance post-exercise levels of 2,3-DPG and the 2,3-DPG/Hb ratio in recreationally trained cyclists while improving acute recovery of peak power in these men.

2,3-Diphosphoglycerate↗

PubMed1995

Compatibility of high-intensity strength and endurance training on hormonal and skeletal muscle adaptations.

Thirty-five healthy men were matched and randomly assigned to one of four training groups that performed high-intensity strength and endurance training (C; n = 9), upper body only high-intensity strength and endurance training (UC; n = 9), high-intensity endurance training (E; n = 8), or high-intensity strength training (ST; n = 9). The C and ST groups significantly increased one-repetition maximum strength for all exercises (P < 0.05). Only the C, UC, and E groups demonstrated significant increases in treadmill maximal oxygen consumption. The ST group showed significant increases in power output. Hormonal responses to treadmill exercise demonstrated a differential response to the different training programs, indicating that the underlying physiological milieu differed with the training program. Significant changes in muscle fiber areas were as follows: types I, IIa, and IIc increased in the ST group; types I and IIc decreased in the E group; type IIa increased in the C group; and there were no changes in the UC group. Significant shifts in percentage from type IIb to type IIa were observed in all training groups, with the greatest shift in the groups in which resistance trained the thigh musculature. This investigation indicates that the combination of strength and endurance training results in an attenuation of the performance improvements and physiological adaptations typical of single-mode training.

Adaptation, Physiological↗

PubMed1995

Responses of IGF-I to endogenous increases in growth hormone after heavy-resistance exercise.

The purpose of this study was to examine the effects of a heavy-resistance exercise protocol known to dramatically elevate immunoreactive growth hormone (GH) on circulating insulin-like growth factor I (IGF-I) after the exercise stimulus. Seven men (23.1 +/- 2.4 yr) volunteered to participate in this study. Each subject was asked to perform an eight-station heavy-resistance exercise protocol consisting of 3 sets of 10 repetition maximum resistances with 1-min rest between sets and exercises followed by a recovery day. In addition, a control day followed a nonexercise day to provide baseline data. Pre- and postexercise (0, 15, and 30 min) blood samples were obtained and analyzed for lactate, creatinine kinase, GH, and IGF-I. Postexercise values for lactate and GH were significantly (P < 0.05) elevated above preexercise and resting baseline values. The highest mean GH concentration after the heavy-resistance exercise protocol was 23.8 +/- 11.8 micrograms/l, observed at the immediate postexercise time point. Significant increases in creatine kinase were observed after the exercise protocol and during the recovery day. No significant relationships were observed between creatine kinase and IGF-I concentrations. No significant changes in serum IGF-I concentrations were observed with acute exercise or between the recovery and control days. Thus, these data demonstrate that a high-intensity bout of heavy-resistance exercise that increases circulating GH did not appear to affect IGF-I concentrations over a 24-h recovery period in recreationally strength-trained and healthy young men.

Adult↗

PubMed1994

Endocrine responses to overreaching before and after 1 year of weightlifting.

Nine elite male junior weightlifters (mean age 17.6 +/- 0.3 yrs) performed weightlifting tests before (Test 1) and after (Test 2) 1 week of increased training volume (overreaching) and repeated the protocol after 1 year of their training program. Strength increased by Year 2 (p < 0.05) but did not change during either week of increased training volume. The 1-week overreaching stimulus resulted in attenuated exercise-induced testosterone concentrations during Year 1, but augmented exercise-induced testosterone concentrations during Year 2. Testosterone concentrations at 7 a.m. decreased for only Year 1. For both years, the 1-week overreaching stimulus increased cortisol at 7 a.m, indicative of the increased training volumes. Testosterone/cortisol was not affected by increased training volume for either year. One year of chronic weightlifting and prior exposure to the overreaching stimulus appears to decrease the detrimental effects of stressful training on the endocrine system.

Adaptation, Physiological↗

PubMed1994

Effect of acid-base balance on the growth hormone response to acute high-intensity cycle exercise.

To investigate the effect of acid-base balance on serum human growth hormone (hGH) concentration after an acute high-intensity anaerobic exercise bout, 10 untrained but normally active men [age, 24.6 +/- 1.5 (SE) yr] participated in a randomized double-blind counterbalanced experiment. Each subject reported in a fasted state at the same time of day for two experimental sessions separated by 1 wk. For each session, subjects were administered a decaffeinated tea solution containing either 0.3 g NaHCO3/kg body wt [alkalosis (ALK)] or 0.04 g NaCl/kg body wt [control (CTRL)] over a 45-min ingestion period. Venous blood samples were obtained before [baseline (BL)] and 75 min after the ingestion period, as well as postexercise at 0, 5, 10, 15, 20, and 30 min. The exercise task immediately followed the preexercise blood draw and consisted of 90 s of maximal-effort cycle ergometry against an opposing force of 0.49 N (0.05 kg)/kg body wt. There were no differences between the ALK and CTRL conditions in mean or peak power output or total work during the exercise task. Whole blood pH was significantly (P < or = 0.05) elevated in ALK above CTRL at all time points except BL. Postexercise serum hGH concentration significantly increased above BL at 10, 15, 20, and 30 min in CTRL and at 20 and 30 min in ALK. The hGH concentration was significantly lower in ALK than in CTRL at 15, 20, and 30 min postexercise. These data indicate that an increase in blood hydrogen ion concentration may be partly responsible for the hGH response to acute high-intensity anaerobic exercise.

Acid-Base Equilibrium↗

PubMed1994

Skeletal muscle adaptations during early phase of heavy-resistance training in men and women.

An 8-wk progressive resistance training program for the lower extremity was performed twice a week to investigate the time course for skeletal muscle adaptations in men and women. Maximal dynamic strength was tested biweekly. Muscle biopsies were extracted at the beginning and every 2 wk of the study from resistance-trained and from nontrained (control) subjects. The muscle samples were analyzed for fiber type composition, cross-sectional area, and myosin heavy chain content. In addition, fasting blood samples were measured for resting serum levels of testosterone, cortisol, and growth hormone. With the exception of the leg press for women (after 2 wk of training) and leg extension for men (after 6 wk of training), absolute and relative maximal dynamic strength was significantly increased after 4 wk of training for all three exercises (squat, leg press, and leg extension) in both sexes. Resistance training also caused a significant decrease in the percentage of type IIb fibers after 2 wk in women and 4 wk in men, an increase in the resting levels of serum testosterone after 4 wk in men, and a decrease in cortisol after 6 wk in men. No significant changes occurred over time for any of the other measured parameters for either sex. These data suggest that skeletal muscle adaptations that may contribute to strength gains of the lower extremity are similar for men and women during the early phase of resistance training and, with the exception of changes in the fast fiber type composition, that they occur gradually.

Adaptation, Physiological↗

PubMed1993

Effects of different heavy-resistance exercise protocols on plasma beta-endorphin concentrations.

To examine the changes of plasma beta-endorphin (beta-EP) concentrations in response to various heavy-resistance exercise protocols, eight healthy male subjects randomly performed each of six heavy-resistance exercise protocols, which consisted of identically ordered exercises carefully designed to control for the repetition maximum (RM) resistance (5 vs. 10 RM), rest period length (1 vs. 3 min), and total work (joules). Plasma beta-EP, ammonia, whole blood lactate and serum cortisol, creatine kinase, urea, and creatinine were determined preexercise, midexercise, immediately postexercise, and at various time points after the exercise session (5 min-48 h), depending on the specific blood variable examined. Only the high total work-exercise protocol [1 min rest, 10 RM load (H10/1)] demonstrated significant increases in plasma beta-EP and serum cortisol at midexercise and 0, 5, and 15 min postexercise. Increases in lactate were observed after all protocols, but the largest increases were observed after the H10/1 protocol. Within the H10/1 protocol, lactate concentrations were correlated (r = 0.82, P < 0.05) with plasma beta-EP concentrations. Cortisol increases were significantly correlated (r = 0.84) with 24-h peak creatine kinase values. The primary finding of this investigation was that beta-EP responds differently to various heavy-resistance exercise protocols. In heavy-resistance exercise, it appears that the duration of the force production and the length of the rest periods between sets are key exercise variables that influence increases in plasma beta-EP and serum cortisol concentrations. Furthermore the H10/1 protocol's significant challenge to the acid-base status of the blood, due to marked increases in whole blood lactate, may be associated with mechanisms modulating peripheral blood concentrations of beta-EP and cortisol.

Adult↗

PubMed1993

Changes in hormonal concentrations after different heavy-resistance exercise protocols in women.

Nine eumenorrheic women (age 24.11 +/- 4.28 yr) performed each of six randomly assigned heavy-resistance protocols (HREPs) on separate days during the early follicular phase of the menstrual cycle. The HREPs consisted of two series [series 1 (strength, S) and series 2 (hypertrophy, H)] of three protocols, each using identically ordered exercises controlled for load [5 vs. 10 repetitions maximum (RM)], rest period length (1 vs. 3 min), and total work (J) within each three-protocol series. Blood measures were determined pre-, mid- (after 4 of 8 exercises), and postexercise (0, 5, 15, 30, 60, 90, 120 min and 24 and 48 h). In series 1, a significant (P < 0.05) reduction in growth hormone (GH) was observed at 90 min postexercise for all three protocols. In series 2, the 10-RM protocol with 1-min rest periods (H10/1) produced significant increases above rest in GH concentrations at 0, 5, and 15 min postexercise, and the H10/1 and H5/1 protocols demonstrated significant reductions at 90 and 120 min postexercise. Cortisol demonstrated significant increases in response to the S10/3 protocol at 0 min, to the H10/1 protocol at midexercise and at 0 and 5 min postexercise, and to the H5/1 protocol at 5 and 15 min postexercise. No significant changes were observed in total insulin-like growth factor I, total testosterone, urea, or creatinine for any of the HREPs. Significant elevations in whole blood lactate and ammonia along with significant reductions in blood glucose were observed. Hormonal and metabolic blood variables measured in the early follicular phase of the menstrual cycle varied in response to different HREPs. The most dramatic increases above resting concentrations were observed with the H10/1 protocol, indicating that the more glycolytic HREPs may stimulate greater GH and cortisol increases.

Adult↗

PubMed1992

Protein phosphatases modulate the apparent agonist affinity of the light-regulated ion channel in retinal rods.

Ion channels directly activated by cGMP mediate the light response in retinal rods. Several components of the enzyme cascade controlling cGMP concentration are regulated, but there are no accepted mechanisms for modulation of the response of the channel to cGMP. Here we report evidence that in excised patches an endogenous protein phosphatase converts the channel from a state with low cGMP sensitivity to a state with almost 3 orders of magnitude higher sensitivity in the predicted physiological range of cGMP concentration. The action of this endogenous phosphatase was blocked by specific serine/threonine phosphatase inhibitors (microcystin-LR, okadaic acid, and calyculin A). An increase in apparent agonist affinity also was produced by addition of purified protein phosphatase 1. In contrast, protein phosphatase 2A decreased apparent agonist affinity, suggesting that two phosphorylation sites may regulate the agonist sensitivity of the channel in a reciprocal manner. This regulation may be involved in fine-tuning the light response or in light or dark adaptation.

Animals↗

PubMed1991

Endogenous anabolic hormonal and growth factor responses to heavy resistance exercise in males and females.

To examine endogenous anabolic hormonal responses to two different types of heavy resistance exercise protocols (HREPs), eight male and eight female subjects performed two randomly assigned protocols (i.e. P-1 and P-2) on separate days. Each protocol consisted of eight identically ordered exercises carefully designed to control for load, rest period length, and total work (J) effects. P-1 utilized a 5 RM load, 3-min rest periods and had lower total work than P-2. P-2 utilized a 10 RM load, 1-min rest periods and had a higher total work than P-1. Whole blood lactate and serum glucose, human growth hormone (hGH), testosterone (T), and somatomedin-C [SM-C] (i.e. insulin-like growth factor 1, IGF-1) were determined pre-exercise, mid-exercise (i.e. after 4 of the 8 exercises), and at 0, 5, 15, 30, and 60 min post-exercise. Males demonstrated significant (p less than 0.05) increases above rest in serum T values, and all serum concentrations were greater than corresponding female values. Growth hormone increases in both males and females following the P-2 HREP were significantly greater at all time points than corresponding P-1 values. Females exhibited significantly higher pre-exercise hGH levels compared to males. The P-1 exercise protocol did not result in any hGH increases in females. SM-C demonstrated random significant increases above rest in both males and females in response to both HREPs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗

PubMed1991

Effects of high-intensity cycle exercise on sympathoadrenal-medullary response patterns.

Plasma proenkephalin peptide F immunoreactivity and catecholamines were examined on separate days in nine healthy males before and after maximal exercise to exhaustion at four intensities [36, 55, 73, and 100% of maximal leg power (MLP)] by use of a computerized cycle ergometer. The mean duration of 36, 55, 73, and 100% MLP was 3.31, 0.781, 0.270, and 0.1 min, respectively. All intensities were greater than those eliciting peak O2 uptake for the individual subjects. Blood samples were obtained before, immediately after exercise, and 5 and 15 min after exercise. Significant (P less than 0.05) increases in plasma peptide F immunoreactivity (i.e., from mean resting value of 0.18 to 0.43 pmol/ml) were observed immediately after exercise at 36% MLP. Significant increases in plasma epinephrine were observed immediately after exercise at 36% MLP (i.e., from mean resting value of 2.22 to 3.11 pmol/ml) and 55% MLP (i.e., from mean resting value of 1.67 to 2.98 pmol/ml) and 15 min after exercise at 100% MLP (i.e., from mean resting value of 1.92 to 3.88 pmol/ml). Significant increases for plasma norepinephrine were observed immediately after exercise (36, 55, 73, and 100% MLP), 5 min after exercise (36, 55, and 73% MLP), and 15 min after exercise (36% MLP). Increases in whole blood lactate were observed at all points after exercise for 36, 55, and 73% MLP and 5 min after exercise for 100% MLP. These data show that brief high-intensity exercise results in differential response patterns of catecholamines and proenkephalin peptide F immunoreactivity.

Adrenal Medulla↗

PubMed1991

Plasma changes in beta-endorphin to acute hypobaric hypoxia and high intensity exercise.

The purpose of this study was to examine the immediate post-exercise effects of acute exposure to a simulated altitude of 4,300 m on plasma concentrations of beta-endorphin (beta-EP) and associated changes of adrenocorticotropin (ACTH), and cortisol to high intensity cycle exercise (i.e., stages of 90 and 100% peak Vo2). Exercise intensities were assigned relative to peak O2 uptake both under sea level conditions and under acute hypobaric hypoxic conditions. Plasma beta-EP concentrations significantly increased from pre- to immediately post-exercise at both 90 and 100% peak Vo2 in both the sea level and acute hypobaric hypoxic trials. No associated exercise-induced changes were observed for ACTH or cortisol pre- to immediately post-exercise at either sea level or during hypoxic conditions. Exercise at acute hypobaric hypoxia elicited no significantly different responses in plasma beta-EP, ACTH, or cortisol than those elicited by the same relative exercise intensities under normobaric normoxic conditions. Additionally, no changes in the beta-EP/ACTH molar ratio for exercise or between conditions were observed. These data indicate that acute simulated high altitude exposure neither diminishes nor augments the physiological stimuli involved with high relative exercise intensity activation mechanisms of these hormones.

Adaptation, Physiological↗

PubMed1990

The effects of graded exercise on plasma proenkephalin peptide F and catecholamine responses at sea level.

The purpose of this study was to evaluate the effects of graded treadmill exercise on plasma preproenkephalin peptide F immunoreactivity and concomitant catecholamine responses at sea level (elevation, 50 m). Few data exist regarding the sea-level responses of plasma peptide F immunoreactivity to exercise. thirty-five healthy men performed a graded exercise test on a motor-driven treadmill at the relative exercise intensities of 25, 50, 75, and 100% of maximum oxygen consumption (VO2max). Significant (P less than 0.05) increases above rest were observed for plasma peptide F immunoreactivity and norepinephrine at 75 and 100% of the VO2 max and at 5 min into recovery. Significant increases in plasma epinephrine were observed at 75 and 100% of VO2max. Whole blood lactate significantly increased above resting values at 50, 75, and 100% of the VO2max and at 5 min into recovery. These data demonstrate that exercise stress increases plasma peptide F immunoreactivity levels at sea level. While the exercise response patterns of peptide F immunoreactivity are similar to catecholamines and blood lactate responses, no bivariate relationships were observed. These data show that sea-level response patterns to graded exercise are similar to those previously observed at moderate altitude (elevation, 2200 m).

Adult↗