Beta-endorphin immunoreactivity during high-intensity exercise with and without opiate blockade

Nine highly fit men [mean (SE) maximum oxygen uptake, : 63.9 (1.7) ml·kg^–1·min^–1; age 27.6 (1.6) years] were studied during two treadmill exercise trials to determine plasma β-endorphin immunoreactivity during intense exercise (80% ). A double-blind experimental design was used, and subjects performed the two exercise trials in counterbalanced order. Exercise trials were 30 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (1.2 mg; 3 cm³) and the other after receiving a placebo (0.9% NaCl saline; 3 cm³). Prior to each experimental trial, a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Thereafter, each subject received either a naloxone or placebo bolus injection. Blood samples were also collected after 10, 20 and 30 min of continuous exercise. β-Endorphin was higher (P<0.05) during exercise when compared to pre-exercise in both trials. However, no statistically significant difference was found (P>0.05) between exercise time points within either experimental trial. β-endorphin immunoreactivity was greater (P<0.05) in the naloxone than in the placebo trial during each exercise sampling time point [10 min: 63.7 (3.9) pg·ml^–1 vs 78.7 (3.8) pg·ml^–1; 20 min: 68.7 (4.1) pg·ml^–1 vs 83.8 (4.3) pg·ml^–1; 30 min: 71.0 (4.3) pg·ml^–1 vs 82.5 (3.2) pg·ml^–1]. These data suggest that intense exercise induces significant increases in β-endorphin that are maintained over time during steady-rate exercise. Exercise and naloxone had an interactive effect on β-endorphin release that warrants further investigation. Electronic Publication     

Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Local and systemic effects on blood lactate concentration during exercise with small and large muscle groups

To evaluate the relationship between lactate release and [lac]_art and to investigate the influence of the catecholamines on the lactate release, 14 healthy men [age 25±3 (SE) year] were studied by superimposing cycle on forearm exercise, both at 65% of their maximal power reached in respective incremental tests. Handgrip exercise was performed for 30 min at 65% of peak power. In addition, between the tenth and the 22nd minute, cycling with the same intensity was superimposed. The increase in venous lactate concentration ([lac]_ven) (rest: 1.3±0.4 mmol·l⁻¹; 3rd min: 3.9±0.8 mmol·l⁻¹) begins with the forearm exercise, whereas arterial lactate concentration ([lac]_art) remains almost unchanged. Once cycling has been added to forearm exercise (COMB), [lac]_art increases with a concomitant increase in [lac]_ven (12th min: [lac]_art, 3.2±1.3 mmol·l⁻¹; [lac]_ven, 5.7±2.2 mmol·l⁻¹). A correlation between oxygen tension (P_vO₂) and [lac]_ven cannot be detected. There is a significant correlation between [lac]_art and norepinephrine ([NE]) (y=0.25x+1.2; r=0.815; p<0.01) but no correlation between lactate release and epinephrine ([EPI]) at moderate intensity. Our main conclusion is that lactate release from exercising muscles at moderate intensities is neither dependent on P_vO₂ nor on [EPI] in the blood.     

Sympathetic control of the forearm blood flow in man during brief isometric contractions

Summary Experiments were performed to assess the possible neurally mediated constriction in active skeletal muscle during isometric hand-grip contractions. Forearm blood flow was measured by venous occlusion plethysmography on 5 volunteers who exerted a series of repeated contractions of 4 s duration every 12 s at 60% of their maximum strength of fatigue. The blood flows increased initially, but then remained constant at 20–24 ml·min⁻¹·100 ml⁻¹ throughout the exercise even though mean arterial blood pressure reached 21–23 kPa (160–170 mm Hg). When the same exercise was performed after arterial infusion of phentolamine, forearm blood flow increased steadily to near maximal levels of 38.7±1.4 ml·min⁻¹·100 ml⁻¹. Venous catecholamines, principally norepinephrine, increased throughout exercise, reaching peak values of 983±258 pg·ml⁻¹ at fatigue. Of the vasoactive substances measured, the concentration of K⁺ and osmolarity in venous plasma also increased initially and reached a steady-state during the exercise but ATP increased steadily throughout the exercise. These data indicate a continually increasing α-adrenergic constriction to the vascular beds in active muscles in the human forearm during isometric exercise, that is only partially counteracted by vasoactive metabolites.     

Involvement of muscarinic cholinergic and α2-adrenergic mechanisms in growth hormone secretion during exercise in humans

The purpose of this study was to examine the role of muscarinic cholinergic and α₂-adrenergic mechanisms in growth hormone (GH) secretion during exercise in humans. The GH responses induced during moderate-intensity exercise (using a cycle ergometer at 60% maximal oxygen uptake, V˙O_2max, for 30 min) without treatment (control) and after the administration of a muscarinic cholinergic antagonist (atropine 1 mg) or after an α₂-adrenergic antagonist (yohimbine 15 mg) were compared in seven healthy men. Although, serum GH concentration had increased significantly after exercise in the control experiment [mean peak GH concentration 52.64 (SEM 18.60) ng · ml⁻¹], the increase was suppressed by the administration of either atropine [mean peak GH concentration 8.64 (SEM 7.47)  ng · ml⁻¹] or yohimbine [mean peak GH concentration 17.50 (SEM 7.89) ng · ml⁻¹]. The area under the curve of serum GH concentration against time was significantly lower in the experiment using these drugs [with atropine, mean area 458 (SEM 409) ng · ml⁻¹ · min], with yohimbine mean area 946 (SEM 435) ng · ml⁻¹ · min] than in the control experiment [mean area 3135 (SEM 1098) ng · ml⁻¹ · min]. These results suggest that muscarinic cholinergic and α₂-adrenergic mechanisms are involved in GH secretion during exercise in humans. Accepted: 9 March 2000     

Levels of serum creatine kinase and myoglobin in women after two isometric exercise conditions

Summary The purpose of this study was to measure serum creatine kinase (CK) activity and serum myoglobin (MG) concentrations in women after two unilateral isometric knee extension exercises. Forty maximal voluntary contractions (MVC) were held for 10 s, with either a 5 s (10∶5) or 20 s 10∶20 exercise (349.4±66.1 mU · ml⁻¹) and 6 h and MG values were measured pre, 0, 3, 6, and 18 h post exercise. For CK, the highest post exercise values were observed at 6 h following the 10∶20 exercise (349.4±66.1 mU · ml⁻¹) and 6 h following the 10∶5 exercise (194.1±18.6 mU · ml⁻¹). For MG, the highest values were found 3 h after the 10∶20 exercise (148.9±61.7 ng · ml⁻¹) and 6 h after the 10∶5 exercise (67.3±10.9 ng · ml⁻¹). Serum CK and MG levels were significantly greater (p<0.01) after the 10∶20 exercise bout. The data demonstrate that CK and MG values for women increase significantly after isometric exercise. Since greater tension levels were maintained during the 10∶20 exercise it is hypothesized that increased serum CK and MG values after isometric exercise may be related to the tension generated by the contracting muscle.     

Effect of short-term endurance training on exercise capacity,haemodynamics and atrial natriuretic peptide secretion in heart transplant recipients

Exercise tolerance of heart transplant patients is often limited. Central and peripheral factors have been proposed to explain such exercise limitation but, to date, the leading factors remain to be determined. We examined how a short-term endurance exercise training programme may improve exercise capacity after heart transplantation, and whether atrial natriuretic peptide (ANP) release may contribute to the beneficial effects of exercise training by minimizing ischaemia and/or cardiac and circulatory congestion through its vasodilatation and haemoconcentration properties. Seven heart transplant recipients performed a square-wave endurance exercise test before and after 6 weeks of supervised training, while monitoring haemodynamic parameters, ANP and catecholamine concentrations. After training, the maximal tolerated power and the total mechanical work load increased from 130.4 (SEM 6.5) to 150.0 (SEM 6.0) W (P < 0.05) and from 2.05 (SEM 0.1) to 3.58 (SEM 0.14) kJ · kg⁻¹ (P < 0.001). Resting heart rate decreased from 100.0 (SEM 3.4) to 92.4 (SEM 3.5) beats · min⁻¹ (P < 0.05) but resting and exercise induced increases in cardiac output, stroke volume, right atrial, pulmonary capillary wedge, systemic and pulmonary artery pressures were not significantly changed by training. Exercise-induced decrease of systemic vascular resistance was similar before and after training. After training arterio-venous differences in oxygen content were similar but maximal lactate concentrations decreased from 6.20 (SEM 0.55) to 4.88 (SEM 0.6) mmol · 1⁻¹ (P < 0.05) during exercise. Similarly, maximal exercise noradrenaline concentration tended to decrease from 2060 (SEM 327) to 1168 (SEM 227) pg · ml⁻¹. A significant correlation was observed between lactate and catecholamines concentrations. The ANP concentration at rest and the exercise-induced ANP concentration did not change throughout the experiment [104.8 (SEM 13.1) pg · ml⁻¹ vs 116.0 (SEM 13.5) pg · ml⁻¹ and 200.0 (SEM 23.0) pg · ml⁻¹ vs 206.5 (SEM 25.9) pg · ml⁻¹ respectively]. The results of this study suggested that the significant improvement in exercise capacity observed after this short-term endurance training period may have arisen mainly through peripheral mechanisms, associated with the possible decrease in plasma catecholamine concentrations and reversal of muscle deconditioning and/or prednisone-induced myopathy.     

Diurnal variation in the salivary melatonin responses to exercise: relation to exercise-mediated tachycardia

Salivary melatonin concentration is an established marker of human circadian rhythmicity. It is thought that melatonin is relatively robust to the masking effects of exercise. Nevertheless, the extent and even the direction of exercise-related change is unclear, possibly due to between-study differences in the time of day exercise is completed. Therefore, we aimed to compare melatonin responses between morning and afternoon exercise, and explore the relationships between exercise-related changes in melatonin and heart rate. At 08:00 and 17:00 hours, seven male subjects (mean ± SD age, 27 ± 5 years) completed 30 min of cycling at 70% peak oxygen uptake followed by 30 min of rest. Light intensity was maintained at ~150 lx. Salivary melatonin (ELISA) and heart rate were measured at baseline, 15 min during exercise, immediately post-exercise and following 30 min recovery. Melatonin was ≈15 pg ml⁻¹ higher in the morning trials compared with the afternoon (P = 0.030). The exercise-related increase in melatonin was more pronounced (P = 0.024) in the morning (11.1 ± 8.7 pg ml⁻¹) than in the afternoon (5.1 ± 5.7 pg ml⁻¹). The slope of the heart rate–melatonin relationship was significantly (P = 0.020) steeper in the morning (0.12 pg ml⁻¹ beats⁻¹ min⁻¹) than in the afternoon (0.03 pg ml⁻¹ beats⁻¹ min⁻¹). In conclusion, we report for the first time that the masking effect of moderate-intensity exercise on melatonin is approximately twice as high in the morning than the afternoon. The much steeper relationship between heart rate and melatonin changes in the morning raises the possibility that time of day alters the relationships between exercise-mediated sympathetic nervous activity and melatonin secretion.     

High levels of circulating angiotensin II shift the open-loop baroreflex control of splanchnic sympathetic nerve activity,heart rate and arterial pressure in anesthetized rats

Although an acute arterial pressure (AP) elevation induced by intravenous angiotensin II (ANG II) does not inhibit sympathetic nerve activity (SNA) compared to an equivalent AP elevation induced by phenylephrine, there are conflicting reports as to how circulating ANG II affects the baroreflex control of SNA. Because most studies have estimated the baroreflex function under closed-loop conditions, differences in the rate of input pressure change and the magnitude of pulsatility may have biased the estimation results. We examined the effects of intravenous ANG II (10 μg kg⁻¹ h⁻¹) on the open-loop system characteristics of the carotid sinus baroreflex in anesthetized and vagotomized rats. Carotid sinus pressure (CSP) was raised from 60 to 180 mmHg in increments of 20 mmHg every minute, and steady-state responses in systemic AP, splanchnic SNA and heart rate (HR) were analyzed using a four-parameter logistic function. ANG II significantly increased the minimum values of AP (67.6 ± 4.6 vs. 101.4 ± 10.9 mmHg, P < 0.01), SNA (33.3 ± 5.4 vs. 56.5 ± 11.5%, P < 0.05) and HR (391.1 ± 13.7 vs. 417.4 ± 11.5 beats/min, P < 0.01). ANG II, however, did not attenuate the response range for AP (56.2 ± 7.2 vs. 49.7 ± 6.2 mmHg), SNA (69.6 ± 5.7 vs. 78.9 ± 9.1%) or HR (41.7 ± 5.1 vs. 51.2 ± 3.8 beats/min). The maximum gain was not affected for AP (1.57 ± 0.28 vs. 1.20 ± 0.25), SNA (1.94 ± 0.34 vs. 2.04 ± 0.42%/mmHg) or HR (1.11 ± 0.12 vs. 1.28 ± 0.19 beats min⁻¹ mmHg⁻¹). It is concluded that high levels of circulating ANG II did not attenuate the response range of open-loop carotid sinus baroreflex control for AP, SNA or HR in anesthetized and vagotomized rats.     

The effects of whole body vibration and exercise on fibrinolysis in men

Whole body vibration (WBV) is a novel modality that has been demonstrated to enhance muscular and cardiovascular functions reported to increase fibrinolytic activity. The purpose of this study was to examine the fibrinolytic response to WBV and exercise in men. Twenty healthy males (23.8 ± 0.9 years, 25.6 ± 0.2 kg m⁻²) participated in the study. Each subject performed three trials in randomized order separated by 1 week: exercise (X), vibration (V) and vibration + exercise (VX). Exercise sessions consisted of 15 min of unloaded squatting at a rate of 20 per minute. Vibration sessions were conducted on a WBV platform vibrating for 15 min. Tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI-1) were assessed at baseline and immediately after each condition. The increase in tPA activity was significantly greater in VX (0.87 ± 0.35 to 3.21 ± 1.06 IU ml⁻¹) compared to X (0.71 ± 0.36 to 2.4 ± 1.13 IU ml⁻¹) or V (0.83 ± 0.25 to 1.00 ± 0.37 IU ml⁻¹) conditions, and greater in the X condition compared to the V condition. PAI-1 activity decreased significantly more in the VX (6.54 ± 5.53 to 4.89 ± 4.13 IU ml⁻¹) and X (9.76 ± 8.19 to 7.48 ± 7.11 IU ml⁻¹) conditions compared to the V (5.68 ± 3.53 to 5.84 ± 3.52 IU ml⁻¹) condition. WBV does not augment fibrinolytic activity in healthy men. However, WBV combined with squatting exercise increases fibrinolytic activity more than exercise alone.     

The effect of citrate loading on exercise performance,acid-base balance and metabolism

Summary Nine subjects ( 65±2 ml·kg⁻¹·min⁻¹, mean±SEM) were studied on two occasions following ingestion of 500 ml solution containing either sodium citrate (C, 0.300 g·kg⁻¹ body mass) or a sodium chloride placebo (P, 0.045 g·kg⁻¹ body mass). Exercise began 60 min later and consisted of cycle ergometer exercise performed continuously for 20 min each at power outputs corresponding to 33% and 66% , followed by exercise to exhaustion at 95% . Pre-exercise arterialized-venous [H⁺] was lower in C (36.2±0.5 nmol·l⁻¹; pH 7.44) than P (39.4±0.4 nmol·l⁻¹; pH 7.40); the plasma [H⁺] remained lower and [HCO ₃ ⁻ ] remained higher in C than P throughout exercise and recovery. Exercise time to exhaustion at 95% was similar in C (310±69 s) and P (313±74 s). Cardiorespiratory variables (ventilation, , , heart rate) measured during exercise were similar in the two conditions. The plasma [citrate] was higher in C at rest (C, 195±19 μmol·l⁻¹; P, 81±7 μmol·l⁻¹) and throughout exercise and recovery. The plasma [lactate] and [free fatty acid] were not affected by citrate loading but the plasma [glycerol] was lower during exercise in C than P. In conclusion, sodium citrate ingestion had an alkalinizing effect in the plasma but did not improve endurance time during exercise at 95% . Furthermore, citrate loading may have prevented the stimulation of lipolysis normally observed with exercise and prevented the stimulation of glycolysis in muscle normally observed in bicarbonate-induced alkalosis.     

Maximal voluntary hyperpnoea increases blood lactate concentration during exercise

Ventilatory work during heavy endurance exercise has not been thought to influence systemic lactate concentration. We evaluated the effect of maximal isocapnic volitional hyperpnoea upon arterialised venous blood lactate concentration ([lac⁻]_B) during leg cycling exercise at maximum lactate steady state (MLSS). Seven healthy males performed a lactate minimum test to estimate MLSS, which was then resolved using separate 30 min constant power tests (MLSS=207±8 W, mean ± SEM). Thereafter, a 30 min control trial at MLSS was performed. In a further experimental trial, the control trial was mimicked except that from 20 to 28 min maximal isocapnic volitional hyperpnoea was superimposed on exercise. Over 20–28 min minute ventilation, oxygen uptake, and heart rate during the control and experimental trials were 87.3±2.4 and 168.3±7.0 l min⁻¹ (P<0.01), the latter being comparable to that achieved in the maximal phase of the lactate minimum test (171.9±6.8 l min⁻¹), 3.46±0.20 and 3.83 ± 0.20 l min⁻¹ (P<0.01), and 158.5±2.7 and 166.8±2.7 beats min⁻¹ (P<0.05), respectively. From 20 to 30 min of the experimental trial [lac⁻]_B increased from 3.7±0.2 to 4.7±0.3 mmol l⁻¹ (P<0.05). The partial pressure of carbon dioxide in arterialised venous blood increased approximately 3 mmHg during volitional hyperpnoea, which may have attenuated the [lac⁻]_B increase. These results show that, during heavy exercise, respiratory muscle work may affect [lac⁻]_B. We speculate that the changes observed were related to the altered lactate turnover in respiratory muscles, locomotor muscles, or both.     

Angiotensin II induced reduction of peritubular capillary diameter in the rat kidney

Summary Large peritubular capillaries were infused consecutively (20 nl · min⁻¹) in random sequence with isotonic saline and angiotensin II (20–80 ng · ml⁻¹). The diameters of the infused capillaries were measured, without knowledge of the infusate used, from colour photographs of the infused area. Angiotensin II induced a significant (p<0.001) decrease in capillary diameter (Δ=−1.2±0.2 (SE) μm and Δ=−2.1±0.2 (SE) μm with 20 ng · ml⁻¹ and 80 ng · ml⁻¹ angiotensin II infusates, respectively). This decrease was shown to be independent of external tubular compression: separate experiments in which the surrounding tubules were collapsed by injection of oil blocks yielded similar results. The possibility that the observed reduction in diameter was caused by an angiotensin II induced change in capillary permeability to the staining solution was excluded, since the angiotensin II effect was unchanged when fluorescent dextran (mol. wt. 150000) was substituted for lissamin green. These experiments indicate that peritubular capillaries contract actively when infused with angiotensin II.     

Effects of acute carbohydrate supplementation during sessions of high-intensity intermittent exercise

Abs tract The present study evaluated the acute effects of carbohydrate supplementation on heart rate (HR), rate of perceived exertion (RPE), metabolic and hormonal responses during and after sessions of high-intensity intermittent running exercise. Fifteen endurance runners (26 ± 5 years, 64.5 ± 4.9 kg) performed two sessions of intermittent exercise under carbohydrate (CHO) and placebo (PLA) ingestion. The sessions consisted of 12 × 800 m separated by intervals of 1 min 30 s at a mean velocity corresponding to the previously performed 3-km time trial. Both the CHO and PLA sessions were concluded within ∼28 min. Blood glucose was significantly elevated in both sessions (123.9 ± 13.2 mg dl⁻¹ on CHO and 147.2 ± 16.3 mg dl⁻¹ on PLA) and mean blood lactate was significantly higher in the CHO (11.4 ± 4.9 mmol l⁻¹) than in the PLA condition (8.4 ± 5.1 mmol l⁻¹) (P < 0.05). The metabolic stress induced by the exercise model used was confirmed by the elevated HR (∼182 bpm) and RPE (∼18 on the 15-point Borg scale) for both conditions. No significant differences in plasma insulin, cortisol or free fatty acids were observed during exercise between the two trials. During the recovery period, free fatty acid and insulin concentrations were significantly lower in the CHO trial. Supplementation with CHO resulted in higher lactate associated with lipolytic suppression, but did not attenuate the cortisol, RPE or HR responses.     

Changes in blood lactate and respiratory gas exchange measures in sports with discontinuous load profiles

This study compares two different sport events (orienteering = OTC; tennis = TEC) with discontinuous load profiles and different activity/recovery patterns by means of blood lactate (LA), heart rate (HR), and respiratory gas exchange measures (RGME) determined via a portable respiratory system. During the TEC, 20 tennis-ranked male subjects [age: 26.0 (3.7) years; height: 181.0 (5.7) cm; weight: 73.2 (6.8) kg; maximal oxygen consumption (V˙O₂max): 57.3 (5.1) ml·kg⁻¹·min⁻¹] played ten matches of 50 min. During the OTC, 11 male members of the Austrian National Team [age: 23.5 (3.9) years; height: 183.6 (6.8) cm; weight: 72.4 (3.9) kg; V˙O₂max: 67.9 (3.8) ml·kg⁻¹·min⁻¹] performed a simulated OTC (six sections; average length: 10.090 m). In both studies data from the maximal treadmill tests (TT) were used as reference values for the comparison of energy expenditure of OTC and TEC. During TEC, the average V˙O₂ was considerably lower [29.1 (5.6) ml^·kg^−1·min⁻¹] or 51.1 (10.9)% of VO₂max and 64.8.0 (13.3)% of V˙O₂ determined at the individual anaerobic threshold (IAT) on the TT. The short high-intensity periods (activity/recovery = 1/6) did not result in higher LA levels [average LA of games: 2.07 (0.9) mmol·l⁻¹]. The highest average V˙O₂ value for a whole game was 47.8 ml·kg^−1·min⁻¹ and may provide a reference for energy demands required to sustain high-intensity periods of tennis predominately via aerobic mechanism of energy delivery. During OTC, we found an average V˙O₂ of 56.4 (4.5) ml·kg⁻¹·min⁻¹ or 83.0 (3.8)% of V˙O₂max and 94.6 (5.2)% of V˙O₂ at IAT. In contrast to TEC, LA were relatively high [5.16 (1.5) mmol·l⁻¹) although the average V˙O₂ was significantly lower than V˙O₂ at IAT. Our data suggest that portable RGEM provides valuable information concerning the energy expenditure in sports that cannot be interpreted from LA or HR measures alone. Portable RGEM systems provide valuable assessment of under- or over-estimation of requirements of sports and assist in the optimization and interpretation of training in athletes. Electronic Publication     

Cardiorespiratory responses to fatiguing dynamic and isometric hand-grip exercise

In occupational work, continuous repetitive and isometric actions performed with the upper extremity primarily cause local muscle strain and musculoskeletal disorders. They may also have some adverse effects on the cardiorespiratory system, particularly, through the elevation of blood pressure. The aim of the present study was to compare peak cardiorespiratory responses to fatiguing dynamic and isometric hand-grip exercise. The subjects were 21 untrained healthy men aged 24–45 years. The dynamic hand-grip exercise (DHGE) was performed using the left hand-grip muscles at the 57 (SD 4)% level of each individual's maximal voluntary contraction (MVC) with a frequency of 51 (SD 4) grips · min^−l. The isometric hand-grip exercise (IHGE) was done using the right hand at 46 (SD 3)% of the MVC. The endurance time, ventilatory gas exchange, heart rate (HR) and blood pressure were mea- sured during both kinds of exercise. The mean endurance times for DHGE and IHGE were different, 170 (SD 62) and 99 (SD 27) s, respectively (P < 0.001). During DHGE the mean peak values of the breathing frequency [20 (SD 6) breaths · min⁻¹] and tidal volume [0.89 (SD 0.34) l] differed significantly (P < 0.01) from peak values obtained during IHGE [15 (SD 5) breaths · min⁻¹, and 1.14 (SD 0.32) l, respectively]. The corresponding peak oxygen consumptions, pulmonary ventilations, HR and systolic blood pressures did not differ, and were 0.51 (SD 0.06) and 0.46 (SD 0.11) l · min⁻¹, 17.1 (SD 3.0) and 16.7 (SD 4.7) l · min⁻¹, 103 (SD 18) and 102 (SD 17) beats · min⁻¹, and 156 (SD 17) and 161 (SD 17) mmHg, respectively. The endurance times of both DHGE and IHGE were short (<240 s). The results indicate that the peak responses for the ventilatory gas exchange, HR and blood pressure were similar during fatiguing DHGE and IHGE, whereas the breathing patterns differed significantly between the two types of exercise. The present findings emphasize the importance of following ergonomic design principles in occupational settings which aim to reduce the output of force, particularly in tasks requiring isometric and/or one-sided repetitive muscle actions. Accepted: 16 February 2000     

Blood lactate responses in incremental exercise as predictors of constant load performance

Summary Seven trained male cyclists ( =4.42±0.23 l·min⁻¹; weight 71.7±2.7 kg, mean ± SE) completed two incremental cycling tests on the cycle ergometer for the estimation of the “individual anaerobic threshold” (IAT). The cyclists completed three more exercises in which the work rate incremented by the same protocol, but upon reaching selected work rates of approximately 40, 60 and 80% , the subjects cycled for 60 min or until exhaustion. In these constant load studies, blood lactate concentration was determined on arterialized venous ([La⁻]a_v) and deep venous blood ([La⁻]_v) of the resting forearm. The a_v-v lactate gradient across the inactive forearm muscle was −0.08 mmol·l⁻¹ at rest. After 3 min at each of the constant load work rates, the gradients were +0.05, +0.65* and +1.60* mmol·l⁻¹ (*P<0.05). The gradients after 10 min at these same work rates were −0.09, +0.24 and +1.03* mmol·l⁻¹. For the two highest work rates taken together, the lactate gradient was less at 10 min than 3 min constant load exercise (P<0.05). The [La⁻]a_v was consistently higher during prolonged exercise at both 60 and 80% than that observed at the same work rate during progressive exercise. At the highest work rate (at or above the IAT), time to exhaustion ranged from 3 to 36 min in the different subjects. These data showed that [La⁻] uptake across resting muscle continued to increase to work rates above the IAT. Further, the greater a_v-v lactate gradient at 3 min than 10 min constant load exercise supports the concept that inactive muscle might act as a passive sink for lactate in addition to a metabolic site.     

Intense hypoxic cycle exercise does not alter lung density in competitive male cyclists

We tested the hypothesis that intense short duration hypoxic exercise would result in an increase in extravascular lung water (EVLW), as evidenced by an increase in lung density. Using computed tomography (CT), baseline lung density was obtained in eight highly trained male cyclists (mean ± SD: age = 28 ± 8 years; height = 180 ± 9 cm; mass = 71.6 ± 8.2 kg; = 65.0 ± 5.2 ml kg min⁻¹). Subjects then completed an intense hypoxic exercise challenge on a cycle ergometer and metabolic data, HR and %S_pO₂ were recorded throughout. While breathing 15% O₂, subjects performed five 3 km cycling intervals (mean power, 286 ± 20 W; HR = 91 ± 4% HR_max) separated by 5 min of recovery. From a resting hypoxic S_pO₂ of 92 ± 4%, subjects further desaturated during exercise to 76 ± 3%. CT scans were repeated 76 ± 10 min (range 63–88 min) following the completion of exercise. There was no change in lung density from pre (0.18 ± 0.02 g ml⁻¹) to post-exercise (0.18 ± 0.04 g ml⁻¹). The substantial reduction in S_pO₂ may be explained by a number of potential mechanisms, including decreased pulmonary diffusion capacity, alveolar hypoventilation, reduced red cell transit time, ventilation/perfusion inequality or a temperature and pH induced rightward-shift in the oxyhaemoglobin dissociation curve. Alternatively, the integrity of the blood gas barrier may have been disrupted without any measurable increase in lung density.     

Extracellular pH defense against lactic acid in untrained and trained altitude residents

The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Δ) in lactic acid ([La]), [HCO₃ ⁻], pH and PCO₂ in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (β _nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃ ⁻] · ΔpH⁻¹) amounted to 40 ± 2 (SEM) and 28 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.01). During recovery β _nbi decreased to 20 (UT) and 16 (TR) mmol l⁻¹ (P < 0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Δ[La]. β _bi amounted to 37–41 mmol l⁻¹ being lower than at sea level. The large exercise β _nbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower β _nbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders β _nbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO₃ ⁻]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.     

Circulating reverse triiodothyronine in humans during exercise

Summary Circulating thyroxine (T₄), triiodothyronine (T₃) and reverse triiodothyronine (rT₃) as well as blood lactate and glucose concentrations were measured in a group of 12 trained volunteer subjects prior to and after swimming 0.18 or 0.9 km, to determine if increase in metabolic activity was accompanied by diversion of T₄ monodeiodination from the active (T₄ to T₃) to the inactive (T₄ to rT₃) pathway. The resting T₄, T₃, and rT₃ levels were 8.5 Μg·100 ml⁻¹, 108 ng·100 ml⁻¹, and 57 ng·100 ml⁻¹, respectively, whereas after 0.18 km of swimming the corresponding levels were 9.5 Μg·100 ml⁻¹, 135 ng. 100 ml⁻¹ and 70 ng·100 ml⁻¹. After 0.9 km of swimming, T₄, T₃, and rT₃ levels were 9.0 Μg·100 ml⁻¹, 126 ng·100 ml⁻¹, and 66 ng·100 ml⁻¹, respectively. The swimming was accompanied by hemoconcentration and increase in blood lactate but not in glucose concentrations. In two other investigations thyroid hormones were measured prior to and after 60 or 90 min of moderate exercise on a bicycle ergometer. This exercise had no effect on circulating thyroid hormone levels. Free thyroxine (FT₄) concentration and thyroxine binding globulin (TBG) capacity were unaltered after exercise. In conclusion, brief strenuous swimming or moderate bicycle exercise had minor or no effect on thyroid hormone concentrations when consideration was given to the attendant hemoconcentration. Even when exercise induced small T₃ and rT₃ changes were noted, they were in the same direction (increase) thus demonstrating a lack of diversion of peripheral T₄ monodeiodination. Investigations partially supported by NIH grant AG-01613 and the Narveen Medical Research Foundation, St. Louis, Missouri, USA