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Quantitative thermal perception thresholds relative to exposure to vibration.

OBJECTIVES: To assess the risk of disturbed thermal perception relative to exposure to vibration, to investigate a possible exposure-response relation and to analyse a possible relation between thermal perception and sensory symptoms. METHODS: The study was based on a cross section of 123 male workers exposed to vibration and 62 male workers who were not exposed. Thermal perception of cold, warmth, and heat pain was bilaterally determined from the thenar eminence by the method of limits. Perception of cold and warmth were also tested in the second digit. Personal energy equivalent exposure to vibration was measured for all subjects. Vibration was measured in accordance with International Standards Organisation (ISO) 5349 and assessed separately for the left and right hand. RESULTS: Combining exposure times and intensities gave the left hand an 0.80 exposure to vibration compared with the right. The risk of having contracted reduced thermal perception was increased at all test sites. The risk was higher for the thenar measurements than the finger measurements. A yearly extra contribution of 4000 mh/s(2) in cumulative exposure increases the risk of contracting a wider neutral zone by 18% (95% confidence interval (95% CI) 1.06 to 1.32) for the right and 18% (1.05 to 1.32) for the left hand side. Subjects with symptoms of nocturnal paraesthesia had a rate ratio (95% CI) of 2.80 (1.17 to 6.67) for the right hand and 2.72 (1.12 to 6.63) for the left hand for increased neutral zones at the thenar eminence. CONCLUSIONS: The results indicate thermal sensory impairment related to cumulative exposure to vibration. The effect appeared at vibration levels below the current guiding standard. Quantitative sensory testing of thermal perception offers the chance to assess this specific hazard to the peripheral sensorineural system associated with hand intensive work entailing vibration.

Adult↗

Assessment of work performance in asthma for determination of cardiorespiratory fitness and training capacity.

In view of the lack of objective information on work performance in asthma, a progressive incremental exercise test was carried out in 44 subjects with mild to moderate asthma and 64 normal, healthy subjects matched for habitual activity, to compare cardiorespiratory fitness and to determine the relative contribution of airflow obstruction to exercise limitation. The two groups achieved similar maximum heart rates (mean (SD) 176(12) and 175(10) beats/min). After allowance for confounding factors the asthmatic subjects had a lower maximum oxygen consumption (VO2 max) (by 199 ml min-1) than control subjects. Having asthma also accounted for a significant reduction in anaerobic threshold (125 ml min-1) and oxygen pulse (0.805 ml/beat). There was no correlation of FEV1 with VO2 max, anaerobic threshold, or oxygen pulse either before or after bronchodilator. The dyspnoea index (VE/MVV%) was increased in the asthmatic subjects at peak exercise, but was less than 60% in all subjects at a workload that produced 75% of the predicted maximum heart rate. Thus the asthmatic subjects had a maximum heart rate similar to that of normal subjects but the low VO2 max, anaerobic threshold, and oxygen pulse suggest suboptimal fitness, which was not directly due to airflow obstruction. All had sufficient ventilatory reserve to allow toleration of training at a work intensity adequate to permit improvements in cardiovascular fitness.

Adult↗

Cross-adaptive responses to different forms of leg training: skeletal muscle biochemistry and histochemistry.

The influence of a program of high intensity training and of a combined program of high intensity training and prolonged submaximal training on adaptations to the vastus lateralis muscle was investigated in two groups of elite athletes. The high intensity training (H) consisted of ice hockey practices and games over a 14-week period while the combined program (HI-LO) included the addition of supplementary sessions of cycling, three times per week, progressively increasing from 30 to 45 min per session and at an intensity of 70% VO2max. Determinations of enzyme activities representative of energy supplying pathways revealed no change in 3-hydroxyacl CoA dehydrogenase (HADH), total phosphorylase (PHOSP), phosphofructokinase (PFK), lactate dehydrogenase (LDH), and a 7% increase (p less than 0.05) in succinate dehydrogenase (SDH). The addition of the supplementary program caused no further adaptation in the metabolic profile. Similarly, neither the HI nor the HI-LO program induced any alteration in the percentage fibre type (slow twitch (ST) vs. fast twitch (FT) or the subtypes (FTa, FTb, FTc). Reductions in the size (p less than 0.05) of ST fibres were noted for both the HI and the HI-LO training programs. In contrast, increases in capillarization (p less than 0.05) were found for both the ST (23%) and FTa (32%) fibres for the HI-LO program whereas a reduction in capillarization (21%) occurred in the FTa fibres as a result of HI training only. It is concluded that metabolic differentiation does not appear to occur in a manner consistent with the conditions of energy expenditure at least for high intensity work.

Adaptation, Physiological↗

Gender differences in cardiovascular and metabolic responses to cold and exercise.

This study was conducted because of the paucity of information concerning gender differences in the cardiovascular and metabolic responses to cold stress. Lightly clad men (n = 8) and women (n = 8) were tested in 21 and 5 degrees C environments during a 20-min rest, followed by 20 min each of 50, 100, and 150 W of exercise. At 21 degrees C there was no gender differences in VO2 or cardiac output. Cold lowered skin temperature more in women than in men, but women demonstrated no differences in heart rate, stroke volume, or VO2 at 5 and 21 degrees C. The women's noradrenaline levels in the cold were higher than comparable 21 degrees C data at rest and 50 W and increased with work intensity in both tests. In contrast, men had a lower heart rate, higher stroke volume, and higher VO2 throughout the 5 degrees C treatment compared with 21 degrees C. The men's noradrenaline response to 5 degrees C was similar to that of women at rest and 50 W, but the level subsequently declined at 100 and 150 W. Thus, the women do not show a heart rate-stroke volume shift in either resting or exercising states in cold environments. Furthermore, the data fail to support that either skin cooling or changes in noradrenaline cause the bradycardia and enhanced stroke volume seen in men.

Adult↗

Endurance training reduces the contraction-induced interleukin-6 mRNA expression in human skeletal muscle.

Contracting skeletal muscle expresses large amounts of IL-6. Because 1) IL-6 mRNA expression in contracting skeletal muscle is enhanced by low muscle glycogen content, and 2) IL-6 increases lipolysis and oxidation of fatty acids, we hypothesized that regular exercise training, associated with increased levels of resting muscle glycogen and enhanced capacity to oxidize fatty acids, would lead to a less-pronounced increase of skeletal muscle IL-6 mRNA in response to acute exercise. Thus, before and after 10 wk of knee extensor endurance training, skeletal muscle IL-6 mRNA expression was determined in young healthy men (n = 7) in response to 3 h of dynamic knee extensor exercise, using the same relative workload. Maximal power output, time to exhaustion during submaximal exercise, resting muscle glycogen content, and citrate synthase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity were all significantly enhanced by training. IL-6 mRNA expression in resting skeletal muscle did not change in response to training. However, although absolute workload during acute exercise was 44% higher (P < 0.05) after the training period, skeletal muscle IL-6 mRNA content increased 76-fold (P < 0.05) in response to exercise before the training period, but only 8-fold (P < 0.05, relative to rest and pretraining) in response to exercise after training. Furthermore, the exercise-induced increase of plasma IL-6 (P < 0.05, pre- and posttraining) was not higher after training despite higher absolute work intensity. In conclusion, the magnitude of the exercise-induced IL-6 mRNA expression in contracting human skeletal muscle was markedly reduced by 10 wk of training.

3-Hydroxyacyl CoA Dehydrogenases↗

Role of epinephrine for muscular glycogenolysis and pancreatic hormonal secretion in running rats.

We have previously shown that during swimming muscular glycogen breakdown was diminished and plasma glucagon and insulin were lower and higher, respectively, in adrenodemedullated rats compared to controls. These findings might be due to a lower work intensity or higher efficiency in adrenodemedullated rats than in controls. Furthermore, they might be due to either an acute or a chronic influence of epinephrine. Rats were adrenodemedullated (DM) or sham-operated (C). They were chronically cannulated and either rested or ran in a metabolism chamber for 45 min. Running DM rats had either saline (DM-S) or epinephrine (normalizing the concentration in plasma) (DM-E) infused. During running, oxygen uptake was identical in C and DM rats. Muscular glycogen breakdown was similar in DM-E and C rats and higher than in DM-S rats. Blood glucose, lactate, and heart rate increased in C and DM-E, but not in DM-S rats. In spite of the differences in blood glucose, plasma insulin was the same in all groups and plasma glucagon increased identically in all running rats. Plasma FFA and liver glycogen were similar in all groups. In conclusion. in running rats, epinephrine exerts an acute enhancing effect on muscular glycogenolysis, glucagon secretion, and heart rate and an acute depressing effect on insulin secretion.

Adrenal Medulla↗

Effects of age and training status on heart rate recovery after peak exercise.

Previous studies have shown that the kinetics of heart rate (HR) recovery are delayed in older individuals after exercise. This study was designed to determine whether this observation held when the variables of physical fitness and work intensity were controlled. Twenty male subjects were categorized into four groups (n = 5) according to age and fitness level (peak O2 consumption ml. kg-1.min-1): young trained (YT) 24 +/- 2 yr, 63 +/- 3 ml.kg-1. min-1; old trained (OT) 51 +/- 2 yr, 57 +/- 3 ml.kg-1.min-1; young untrained (YU) 25 +/- 3 yr, 44 +/- 2 ml.kg-1.min-1; old untrained (OU) 57 +/- 4 yr, 36 +/- 4 ml.kg-1.min-1. Bicycle ergometry exercise was performed in incremental stages to a maximally tolerated level of exertion, and HR was monitored continuously postexercise. Regression analysis of the fast (15-120 s) and initial slow (120-240 s) phases of recovery showed no effect of age on HR recovery when comparing YT vs. OT and YU vs. OU. Trained subjects, irrespective of age, demonstrated a significantly faster HR recovery than untrained subjects which was particularly marked during fast-phase recovery (P less than 0.005). These results indicate that the slower HR recovery previously reported in older subjects may be due to a failure to control for variables that influence recovery HR.

Adult↗

Vasopressin contributes to the cardiovascular response to dynamic exercise.

Vasopressin is a powerful vasoconstrictor that is released into the systemic circulation during exercise. We tested the hypothesis that this peptide contributes to the cardiovascular response during treadmill exercise in the pig. Seventeen miniswine were instrumented with epicardial electrocardiogram leads, left atrial and aortic catheters, and a left ventricular pressure transducer for measurement of heart rate (HR), regional blood flow, arterial blood pressure (MAP), and myocardial contractility [first derivative of left ventricular pressure (dP/dt) at 40 mmHg developed pressure] at rest and during exercise. At a work intensity of 80% of each animal's maximal HR reserve, exercise-induced increases in MAP, HR, dP/dt at 40 mmHg developed pressure, and cardiac output were measured. On a separate day, the workload performed by each animal was replicated in the presence of selective vasopressin V1-receptor inhibition using the specific V1 antagonist, [d(CH2)5Tyr(Me)]arginine vasopressin (10-14 micrograms/kg iv). During exercise, MAP was lower (96 +/- 3 vs. 104 +/- 2 mmHg) and cardiac output was higher (13.5 +/- 0.6 vs. 12.6 +/- 1.0 l/min) in the presence of V1-receptor blockade than during unblocked conditions, respectively. Furthermore, we observed an attenuation of exercise-induced decreases in blood flow to the colon. Increases in vascular resistance in the stomach, small intestine, colon, and pancreas also were diminished by V1-receptor inhibition. However, HR and myocardial contractile responses to exercise were not affected. These results suggest that vasopressin contributes to increases in MAP and to the redistribution of cardiac output during dynamic exercise in the miniswine.

Animals↗

Humid heat acclimation does not elicit a preferential sweat redistribution toward the limbs.

We tested the hypothesis that local sweat rates would not display a systematic postadaptation redistribution toward the limbs after humid heat acclimation. Eleven nonadapted males were acclimated over 3 wk (16 exposures), cycling 90 min/day, 6 days/wk (40 degrees C, 60% relative humidity), using the controlled-hyperthermia acclimation technique, in which work rate was modified to achieve and maintain a target core temperature (38.5 degrees C). Local sudomotor adaptation (forehead, chest, scapula, forearm, thigh) and onset thresholds were studied during constant work intensity heat stress tests (39.8 degrees C, 59.2% relative humidity) conducted on days 1, 8, and 22 of acclimation. The mean body temperature (Tb) at which sweating commenced (threshold) was reduced on days 8 and 22 (P < 0.05), and these displacements paralleled the resting thermoneutral Tb shift, such that the Tb change to elicit sweating remained constant from days 1 to 22. Whole body sweat rate increased significantly from 0.87 +/- 0.06 l/h on day 1 to 1.09 +/- 0.08 and 1.16 +/- 0.11 l/h on days 8 and 22, respectively. However, not all skin regions exhibited equivalent relative sweat rate elevations from day 1 to day 22. The relative increase in forearm sweat rate (117 +/- 31%) exceeded that at the forehead (47 +/- 18%; P < 0.05) and thigh (42 +/- 16%; P < 0.05), while the chest sweat rate elevation (106 +/- 29%) also exceeded the thigh (P < 0.05). Two unique postacclimation observations arose from this project. First, reduced sweat thresholds appeared to be primarily related to a lower resting Tb, and more dependent on Tb change. Second, our data did not support the hypothesis of a generalized and preferential trunk-to-limb sweat redistribution after heat acclimation.

Acclimatization↗

Exercise training-induced hypervolemia in greyhounds: role of water intake and renal mechanisms.

The purpose of this study was to determine if the chronic hypervolemia that accompanies endurance exercise training is due only to an increase in the rate of water intake or if there were contributions from renal mechanisms. Four greyhound dogs, previously sedentary for 3 yr, were utilized. During the 28-day experiment each dog was trained on a treadmill ergometer for 14 consecutive days at 65% of its pretraining maximal work intensity. After training, plasma volume increased 472 ml (27.5%, P less than 0.05). The rate of water intake increased 328 ml/day (33%, P less than 0.05), whereas urine output increased 87 ml/day (20.8%, P less than 0.05). The mean resting 24-h values for clearance of sodium increased 0.29 ml/min (90.3%, P less than 0.05), and clearance of potassium decreased 1.51 ml/min (16.1%, NS). Glomerular filtration rate, free water clearance, and osmotic clearance were not significantly altered. These data suggest that the primary mechanism for the exercise training-induced hypervolemia in dogs is a net positive water balance via increased water consumption without significant contribution from an increase in renal water reabsorption.

Animals↗

Factors associated with vasopressin release in exercising swine.

This study examined the effect of dynamic exercise on vasopressin release in the miniswine and factors that may elicit this response (n = 15). Thus lysine vasopressin (LVP), the catecholamines epinephrine and norepinephrine (EPI and NE), plasma renin activity (PRA), and plasma volume, Na+, and osmolality were measured before and during treadmill running at work intensities of 60, 80, and 100% of each swine's maximal heart rate reserve (HRR). LVP increased in a progressive manner similar to that of humans, ranging from 5.9 +/- 0.4 pg/ml before exercise to 30.1 +/- 4.5 pg/ml during maximal exercise. EPI, NE, and PRA [an index of angiotensin II (ANG II) activity] demonstrated a pattern of response comparable to LVP. Although these hormones can influence the release of LVP, only PRA displayed a strong correlation with LVP (r = 0.84). When ANG II synthesis was blocked (captopril, 1-3 mg/kg, intra-atrial injection) during exercise (80% HRR), plasma LVP was reduced from 9.9 +/- 0.6 to 7.5 +/- 0.6 pg/ml (P < 0.05). In addition, moderate-to-strong correlations were found between plasma concentrations of LVP and plasma osmolality (r = 0.79) and body temperature (r = 0.78). Plasma LVP also correlated with decreases in plasma volume (r = 0.84). These data suggest that the miniswine model is a good one for studying vasopressin effects during exercise and that ANG II appears to be a particularly strong stimulus for the release of this hormone.

Angiotensin-Converting Enzyme Inhibitors↗

Effect of autonomic blockade on power spectrum of heart rate variability during exercise.

To validate power spectral analysis of heart rate variability (HRV) as an autonomic indicator during exercise, ten males performed four identical progressive cycling tests during infusions of saline, esmolol (beta 1-blocker), glycopyrrolate (muscarinic blocker), or both drugs. Power spectra were constructed from the recorded electrocardiogram by Fourier algorithm and integrated for low-frequency power (LF) and high-frequency power (HF). Four different LF bands (0.004-0.1, 0.004-0.15, 0.05-0.1, and 0.05-0.15 Hz) and two different HF bands (0.1-1.0 and 0.15-1.0 Hz) were evaluated. The parasympathetic index, HF, decreased exponentially with workload and was attenuated by glycopyrrolate and combined treatments with both HF frequency bands measured. Whereas some sympathetic indexes (LF/total power and LF/HF) did reflect expected increases in sympathetic nerve activity associated with progressive increases in work intensity, none of the measured increases responded appropriately to autonomic blockade. It is concluded that HRV is a valid technique for noninvasive measurement of parasympathetic tone during exercise, but its validity as a measure of sympathetic tone during exercise is equivocal.

Adrenergic beta-Antagonists↗

Interstitial K(+) in human skeletal muscle during and after dynamic graded exercise determined by microdialysis.

Interstitial K(+) concentrations were measured during one-legged knee-extensor exercise by use of microdialysis with probes inserted in the vastus lateralis muscle of the subjects. K(+) in the dialysate was measured either by flame photometry or a K(+)-sensitive electrode placed in the perfusion outlet. The correction for fractional K(+) recovery was based on the assumption of identical fractional thallium loss. The interstitial K(+) was 4. 19 +/- 0.09 mM at rest and increased to 6.17 +/- 0.19, 7.48 +/- 1.18, and 9.04 +/- 0.74 mM at 10, 30, and 50 W exercise, respectively. The individual probes demonstrated large variations in interstitial K(+), and values >10 mM were obtained. The observed interstitial K(+) was markedly higher than previously found for venous K(+) concentrations at similar work intensities. The present data support a potential role for interstitial K(+) in regulation of blood flow and development of fatigue.

Adult↗

Muscle angiogenic growth factor gene responses to exercise in chronic renal failure.

Patients with chronic renal failure (CRF) have impaired exercise capacity even after erythropoietin treatment. We recently showed that although this is explained in part by reduced convective O(2) delivery to muscles, there is also an impairment of O(2) transport from muscle capillaries to the mitochondria. Given the importance of the capillary surface area for capillary mitochondrial O(2) transport and reports of reduced capillarity in CRF, we hypothesized that the angiogenic gene response to exercise is impaired in such patients. Six patients with CRF and six control subjects matched for age, size, and sedentary lifestyle exercised on a single occasion for 1 h at similar work intensities averaging 50% of maximal capacity. Exercise was confined to the knee extensors of a single leg by means of a specially designed leg-kick ergometer. A percutaneous biopsy of the quadriceps was taken within 30 min of cessation of exercise and compared with a similar biopsy done at different times without any prior exercise for 24 h. Conventional Northern blots were prepared and probed for vascular endothelial growth factor (VEGF; the major putative angiogenic growth factor for muscle), basic fibroblast growth factor (bFGF), and transforming growth factor (TGF)-beta(1). Data during both rest and exercise were successfully obtained in four subjects of each group. We also assessed muscle capillarity and mitochondrial oxidative capacity to relate to these changes. Mitochondrial oxidative capacity was normal, whereas capillary number per fiber was 12% lower than in normal subjects. VEGF mRNA abundance was increased after exercise by about one order of magnitude, with no reduction in response in CRF. For bFGF and TGF-beta(1), exercise elicited no response in either group. Reduced muscle capillarity in CRF does not, therefore, stem from reduced transcription of VEGF. To the extent that VEGF is important to exercise-induced angiogenesis in muscle, we suspect a posttranscriptional aberration in this response occurs in CRF to explain reduced capillarity.

Adolescent↗

Effect of acute and established anemia on O2 transport at rest, submaximal and maximal work.

Effects of acute and maintained isovolemic anemia on oxygen transport was studied during rest and exercise in normal males. Following 34% reduction in hemoglobin concentration (Hb), supine and standing Q rose acutely by 56% and 20%, respectively, but returned nearly to the control value by 10-14 days, producing a decrease in PVO2. Redistribution of blood flow appeared to compensate significantly for the decrease in systemic oxygen transport. 2,3-Diphosphoglycerate rose by 18%, in vivo PO2 at half-saturation of hemoglobin (P50) rose by approximately 2 mm over 7-9 days and probably afforded some compensation. The relationship between VO2 and external work intensity was independent of Hb. During exercise, Q/VO2 and VE/VO2 were increased in acute anemia, but PVO2, for a given VO2, decreased below control levels. After 10-14 days the relative increase in VE with exercise persisted; the increase in Q was less pronounced; and PVO2 was further decreased. With both acute and extablished anemia maximal exercise capacity and maximal VO2 (VO2 max) decreased in proportion to the Hb reduction.

Acute Disease↗

Plasma renin activity, vasopressin concentration, and urinary excretory responses to exercise in men.

Plasma vasopressin concentration (PAVP), renal function, and effectors of vasopressin release were evaluated in male volunteers during running at heart rates of 0, 35, 70, and 100% of maximum after 10 h abstinence from water (normal hydration) and at 100% after ingestion of 300 ml water. Plasma renin activity (PRA) and PAVP were linearly correlated and correlated to work intensity over all observations. Changes in PAVP were not correlated with changes in plasma osmolality (POSMOL) and plasma volume (PV) over all observations. Furthermore, despite similar changes in POSMOL, PV, PRA, body weight, mean arterial pressure, and plasma lactate concentration, the increase in PAVP after maximal exercise was greater during normal hydration than the water-supplemented state. Decreased urine flow observed in association with exercise was characterized by increased free water and decreased osmotic and creatinine clearances. Thus increased PAVP associated with exercise appears not to play a role in the concomitant antidiuresis. Vasopressin stimuli are probably variable at different times during exercise and may include factors other than those measured.

Adult↗

Dynamics of cardiac, respiratory, and metabolic function in men in response to step work load.

Stroke volume, heart rate, cardiac output, tidal volume, respiratory frequency, minute ventilation, end-tidal tensions of O2 and CO2, O2 uptake, CO2 output, and respiratory exchange ratio were measured simultaneously in healthy male volunteers before, during, and after upright bicycle exercise from 0 to 360 and 720 kpm/min. The circulatory variables were determined continuously once per 20 cardiac cycles and the respiratory variables breath by breath using separate computer-based systems in which an impedance pneumograph and an impedance cardiograph were incorporated. Stroke volume, heart rate, and cardiac output started to increase without measurable delay at the onset of exercise. Stroke volume increased by 20% from resting control value in response to the mildest exercise and essentially leveled off with a further increase in work load. Time constant for cardiac output increased with the increasing work load. Time constant for minute ventilation was much longer than that for cardiac output and independent of work intensity. A good synchronization between the ventilation and cardiac output responses at an initial period of transitions from rest to exercise and from exercise to rest seems to support the concept of cardiodynamic hyperpnea.

Adult↗

Cutaneous vascular response to exercise and acute hypoxia.

Six normal young men were studied during 50 min of moderate exercise (100-137 W) that included one 15-min (protocol 1) or two 10-min periods of breathing 11-12% O2 (in N2) (protocol 2). Absolute work intensity was kept constant for each subject, but relative severity increased during hypoxia owing to reduction in maximum O2 uptake. Our question was whether hypoxia causes cutaneous vasoconstriction; this in turn should cause a rise in esophageal temperature (Tes) and a shift in the forearm skin blood flow (SkBF)-Tes relationship. In all subjects forearm blood flow (FBF) (venous occlusion plethysmography) rose throughout exercise and Tes tended to stabilize. Neither 10- nor 15-min periods of hypoxia caused systematic changes in FBF or Tes or their relationship to each other. We conclude that hypoxia equivalent to that incurred at 4,500-5,000 m does not significantly alter the short-term regulation of SkBF and body temperature during moderate exercise. Net cutaneous vasoconstriction is not elicited by arterial chemoreflexes under these conditions.

Adult↗