Pre-exercise Baseline Research Articles

Naloxone does not affect the cardiovascular and sympathetic adjustments to static exercise in humans

Previous studies suggested that endogenous opiates may attenuate the cardiovascular and sympathetic adjustments to static exercise. We tested whether this effect originates from exercising skeletal muscle. Eight men performed 2 min of static handgrip (30% maximum) followed by 2 min of posthandgrip muscle ischemia after three interventions: 1) control, 2) intra-arterial injection of naloxone HCl (60 micrograms) or vehicle (saline) in the exercising arm, and 3) systemic infusion of naloxone (4 mg) or vehicle. Naloxone and vehicle trials were performed double blind on separate days. Preexercise baseline muscle sympathetic nerve activity (burst frequency), heart rate, and blood pressure were similar across interventions on either day. During static handgrip, control, intra-arterial, and systemic administration of vehicle and naloxone elicited similar increases in total muscle sympathetic nerve activity (58 +/- 24 vs. 68 +/- 26, 146 +/- 49 vs. 132 +/- 42, 137 +/- 54 vs. 164 +/- 44%, respectively), heart rate (9 +/- 2 vs. 8 +/- 3, 16 +/- 3 vs. 16 +/- 2, 20 +/- 4 vs. 19 +/- 3 beats/min, respectively), and mean arterial pressure (22 +/- 4 vs. 21 +/- 4, 29 +/- 5 vs. 26 +/- 3, 28 +/- 4 vs. 27 +/- 4 mmHg, respectively). Additionally, there were no differences between vehicle and naloxone trials during posthandgrip muscle ischemia. Thus, contrary to previous reports, we conclude that the endogenous opiate peptide system does not modulate cardiovascular and sympathetic responses to brief periods of static exercise or muscle ischemia in humans.

Effect of acute resistance exercise on postexercise energy expenditure and resting metabolic rate.

Two separate experiments were performed to determine the effect of acute resistive exercise on postexercise energy expenditure in male subjects previously trained in resistive exercise. In experiment 1, after measurement of their resting metabolic rate (RMR) at 0700 h and their ingestion of a standardized meal at 0800 h, seven subjects (age range 22-40 yr) beginning at 1400 h completed a 90-min weight-lifting protocol. Postexercise metabolic rate (PEMR) was measured continuously for 2 h after exercise and compared with a preexercise baseline. RMR was measured the following morning 15 h after completion of the workout. In experiment 2, six different men (age range 20-35 yr) completed a similar experimental protocol as well as a control condition on a separate day in which metabolic rate was measured for 2 h after a period of quiet sitting. For both experiments, PEMR remained elevated for the entire 2-h measured recovery period, with the average oxygen consumption for the last 6 min elevated by 11-12%. RMR measured the morning after exercise was 9.4% higher in experiment 1 and 4.7% higher in experiment 2 than on the previous day. In experiment 2, the postabsorptive respiratory exchange ratio was significantly lower the morning after the exercise bout. Strenuous resistive exercise may elevate PEMR for a prolonged period and may enhance postexercise lipid oxidation.

Effect of low and high intensity exercise on circulating growth hormone in men.

We hypothesized that circulating GH would increase only if a threshold of work intensity [corresponding to the anaerobic or lactate threshold (LT)] was exceeded. Ten healthy male volunteers (18-35 yr) first performed ramp-type progressive cycle-ergometer exercise to determine the LT and the maximal oxygen uptake. On subsequent mornings after an overnight fast, each subject performed bouts of 1, 5, and 10 min constant work rate exercise of either high intensity (above LT) or low intensity (below LT). A 1-h interval separated exercise bouts. Gas exchange (breath-by-breath), GH, immunoreactive insulin, glucose, lactate, pyruvate, and epinephrine and norepinephrine were measured at regular intervals. After the 10-min bouts of high compared with low intensity exercise, lactate was 7.2 +/- 3.7 mmol/L vs. 1.4 +/- 1.3, P less than 0.05; epinephrine was 1,113 +/- 519 pmol/L vs. 496 +/- 273, P less than 0.05; and norepinephrine was 7.89 +/- 3.45 nmole/L vs. 2.83 +/- 1.34, P less than 0.05. GH did not increase significantly from preexercise baseline during low intensity exercise (e.g., GH after 10-min low intensity exercise changed from baseline values by 1.5 +/- 2.0 micrograms/L, NS). Although lactate was elevated after 5-min of high intensity exercise, peak GH was significantly elevated (mean increase above baseline of 7.7 +/- 2.4 micrograms/L, P less than 0.05) only after 10 min of high intensity exercise (increases in 9 of 10 subjects). The GH increase occurred despite simultaneous increases in both IRI and glucose. A minimum duration of 10 min, high intensity exercise consistently increased circulating GH in adult males.

Nedocromil sodium inhibits the early and late asthmatic response to exercise

A double-blind, crossover study was carried out to investigate the effect of nedocromil sodium on the dual asthmatic response to exercise challenge. Nineteen patients with a late response to bicycle exercise were randomly treated on two study days with 4 mg nedocromil sodium or a matched placebo aerosol, 30 min before commencing exercise. Peak flow was measured before exercise, at intervals up to 60 min after exercise, then hourly for up to 13 h. In 12 of the 19 patients an early reaction to exercise occurred. In 8 of these 12 patients the early reaction could be inhibited by nedocromil sodium (p less than 0.01) although in half of these patients placebo was also shown to be protective. In the case of the late reaction after exercise challenge, 4-13 h after exercise challenge, nine patients were clearly protected by pretreatment with nedocromil sodium (p less than 0.01) when the fall in peak expiratory flow rate was related to the pre-exercise baseline, four patients showed an equal protective effect of placebo and nedocromil sodium, whilst the others were not protected. When the late asthmatic response (fall in peak expiratory flow rate) after exercise challenge was related to control diurnal peak flow values, the number of responses was reduced; the protective effect of nedocromil sodium remained.

Anxiety and Intense Running Exercise in the Presence and Absence of Interpersonal Competition

The purposes of this study were to evaluate the effects of intense running exercise in the presence and absence of interpersonal competition on both (a) pre-exercise anxiety levels and (b) alterations in anxiety as a consequence of the exercise. Seven females and 10 males performed a 5-mile run over the same outdoor course on two separate days. In one condition the subjects ran in a road-race in which intense exercise was combined with interpersonal competition. In the second condition, exercise of the same intensity (84% VO2max) and duration was completed, but interpersonal competition was absent. Cognitive (State-Trait Anxiety Inventory; STAI) and somatic (Body Awareness Scale; BAS) aspects of anxiety were measured 15 min before and after exercise as well as on a separate day under non-stressful, baseline conditions. A main effect for the Trials factor was found using repeated measures ANOVA [Condition (presence/absence of interpersonal competition) X Gender X Trials (baseline/pre-exercise/post-exercise)], and post-hoc analysis revealed that post-exercise state anxiety and body awareness levels were both reduced compared to pre-exercise baseline values. Condition and Gender main effects were not significant nor were any of the interaction effects. Pre-exercise STAI and BAS levels were found to be significantly (p less than .01) elevated above baseline values. However, while post-exercise STAI scores were significantly (p less than .01) below the baseline STAI level, the post-exercise BAS values did not fall below the corresponding baseline level.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of GR32191, a potent thromboxane receptor antagonist, on exercise induced bronchoconstriction in asthma.

Previous work suggests a role for mast cell derived mediators in exercise induced asthma. The contribution of newly generated contractile prostaglandins to exercise induced asthma was assessed by using a potent and orally active thromboxane (TP1) receptor antagonist, GR32191. The effect of 120 mg GR32191 on exercise induced asthma was observed in 12 asthmatic subjects. For the exercise challenge the subjects performed six minutes of treadmill exercise, breathing dry air at a work load that had previously been shown to induce a fall in FEV1 of 25% or more from the pre-exercise baseline. No effect of GR32191 on pre-exercise baseline airway calibre was evident. There was no significant difference in the mean maximum percentage fall in FEV1 from baseline after exercise between drug and placebo (placebo 30.2%, GR32191 day 31.6%). It is concluded that the thromboxane antagonist GR32191 has no effect on exercise induced asthma. This suggests that prostaglandins, including PGD2, that act via the thromboxane receptor do not have an important role in exercise induced asthma.

Intra-arterial blood pressure monitoring in the evaluation of the hypertensive athlete

To compare the blood pressure (BP) changes during a long-distance run with those during bicycle ergometry, nine normotensive and 18 hypertensive joggers were studied by means of ambulatory intra-arterial monitoring. In all subjects the ergometric test caused a progressive increase in systolic and little change in diastolic BP. Exertional BP levels were closely related to pre-exercise baseline values (P less than 0.001). A different BP pattern was observed during track running, as a sharp rise in systolic BP reaching maximum values 2-4 min after the start was recorded. Subsequently, systolic BP progressively declined throughout the run, only to increase again during the final sprint. Diastolic BP fell markedly at the onset of the run and then remained substantially stable throughout. A poor relationship was observed between the BP values at peak exercise and baseline levels (P less than 0.05) as the normotensives showed a significantly higher BP response than the hypertensives. On the contrary, during the ergometric test a parallel increase in BP was recorded in the normotensive and the hypertensive joggers. No correlation was found between the BP response to track running and to bicycle ergometry. These results indicate that the BP response to a standard stress test is not predictive of the BP changes determined by a long-distance run. The BP increase with strenuous effort seems to be reduced in hypertensive individuals, probably because of latent impairment of cardiac performance.

Effect of β-Adrenoceptor Blockade on Exercise-Induced Plasma Catecholamine Concentration-Heart Rate Response Relationship

We examined the chronotropic and sympathoadrenal responses to a strenuous exercise in eight normal subjects receiving placebo and carteolol, a nonselective beta-adrenoceptor blocker. Plasma catecholamines were measured with high-performance liquid chromatography with electrochemical detection (HPLC-ECD). Mean plasma norepinephrine (NE) and epinephrine (E) concentrations attained at 0.5 and 2 min after exercise were significantly (p less than 0.001-0.05) greater in the carteolol trial than in the placebo trial and approached concentrations fairly similar to preexercise baseline values by 15 min after cessation of exercise in the two trials. The postexercise plasma NE and E concentration-chronotropic response relationships were shifted to the right in the carteolol as compared with the placebo phase. The maximal postexercise NE concentrations measured during the placebo trial correlated significantly with beta-adrenoceptor blockade (p less than 0.05, r = 0.74), whereas the relationship between E concentrations and beta-adrenoceptor blockade did not reach significant level in this small group of study subjects. The results suggest that beta-adrenoceptor blockade increases plasma concentrations of both NE and E during an earlier postexercise period and may cause a greater reflex sympathetic activation as compared with the adrenal response. However, the mechanism(s) remains unclear. Whether the exercise-induced NE rather than E would participate more predominantly in the chronotropic response to beta-adrenoceptor blockade requires further studies.

Effectiveness of a Portable Face Mask in Attenuating Exercise-Induced Asthma

Recent investigations have demonstrated that exercise-induced asthma (EIA) can be prevented by inspiration of warm, fully humidified air during exercise. We evaluated the success of a surgical face mask, used to retain warm, humidified, expired air, in preventing EIA in ten asthmatic children. subjects underwent six minutes of exercise on a treadmill during two sessions, in one session breathing room air and in another wearing a mask covering the nose and mouth. On the control day, average group forced expiratory volume in 1 s (FEV1) and maximal midexpiratory flow rate (MMEF) decreased from the preexercise baseline value to 66% and 47% of baseline, respectively, at six minutes; on the mask day, FEV1 and MMEF were 91% and 82% of the baseline values (increased in all subjects). A simple face mask may be an inexpensive, nonpharmacologic alternative for alleviation of EIA.

Reactivity of normal airways to short-term exercise.

Reactivity of airways to short-term exercise was tested once in 15 healthy subjects and repeated on eight of the group using Stead-Wells and Wedge spirometers and body plethysmograph. The pulmonary function tests were performed at rest and shortly after exercise, and the data were studied by means of a randomized block analysis of variance. It was demonstrated that overall post-exercise pulmonary functions were not statistically different from the pre-exercise baseline.

Heat and water loss from the airways and exercise-induced asthma.

Exercise-induced asthma was studied in 8 asthmatics using various conditions of inspired air during exercise. The exercise consisted of walking on a treadmill for 10 min, with a speed and grade elevation adjusted to achieve the target heart rate of approximately 90% of predicted maximum. Pulmonary function tests were performed pre- and post-exercise to determine exercise-induced asthma. With inspired air at 23 degrees C and 15% relative humidity (RH), the post-exercise forced expiratory volume in a sec (FEV1), maximal mid-expiratory flow rate (MMEF), and specific airway conductance (SGaw) decreased to an average of 69, 59 and 38% of the pre-exercise baseline, respectively. In contrast, the exercise-induced asthma was clearly prevented in all subjects by using inspired air at 37 degrees C and 100% RH, when the post-exercise FEV1, MMEF, and SGaw were 99, 100 and 91% of the baseline, respectively. Inspiration of warm, dry air or humid, room air reduced but did not prevent exercise-induced asthma. The results indicate that the primary stimulus for exercise-induced asthma may be heat loss and/or water loss from the airways during exercise.