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Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

The plasticity of capillary orientation in response to combined hypoxic hypoxia and high activity levels was investigated in anterior tibialis muscle of Japanese waltzing mice (Mus wagneri rotans). Following 2 weeks of normobaric, normothermic hypoxia (PIO2 congruent to 87 Torr), muscles were perfusion-fixed in situ with glutaraldehyde and analyzed morphometrically. Muscles from hypoxic waltzers, HW, were compared with those from normoxic waltzers, NW, and normoxic control mice, N. At sarcomere lengths from 2.84 to 1.69 microns, tortuosity and branching increased capillary length 3 to 38%. When capillary orientation was related to sarcomere length, muscles from HW were not different from NW or N. At group-averaged sarcomere lengths of 2.22 microns (HW), 2.33 microns (NW) and 2.35 microns (N), tortuosity and branching contributed 16,20 and 18% respectively, to capillary length. We conclude that high activity levels under normoxic or hypoxic conditions in Japanese waltzing mice do not augment muscle capillary length by means of increased capillary tortuosity and/or branching.

The sustained high-energy turnover of cardiac muscle presents a formidable challenge to the O2 delivery systems. One major determinant of blood-tissue gas exchange potential is capillary surface area per volume of muscle fiber, Sv(c,f). Estimation of Sv(c,f) necessitates quantification of capillary orientation. Capillary geometry was analyzed systematically in subepi- (epi) and subendocardium (endo) of glutaraldehyde perfusion-fixed rat heart (n = 4). On 1-micron sections cut rigorously transverse and longitudinal to the muscle fiber axis we determined capillary number per fiber square millimeter on transverse, QA(0), and longitudinal, QA(pi/2), sections, capillary diameter, d(c), fiber cross-sectional area, a(f), and sarcomere length, l. Sv(c,f) was computed as pi.d(c).Jv(c,f), where Jv(c,f) is capillary length per fiber volume determined on the basis of a directional distribution model of capillary segments (Fisher axial). Analysis of capillary density, QA(alpha), in sections taken at angles alpha [from 0 to 90 degrees (pi/2) to fiber axis] showed that the Fisher axial distribution provides a good fit to capillary segment orientation in cardiac muscle. No systematic difference was found in fiber size (epi = 269.7 +/- 28.9, endo = 283.8 +/- 16.3 microns 2), capillary diameter (epi = 4.9 +/- 0.3; endo = 4.5 +/- 0.2 microns), Jv(c,f) (epi = 6,302 +/- 558; endo = 5,957 +/- 492 mm-2), or capillary surface per volume of muscle fiber (epi = 968.1 +/- 76.5; endo = 838.2 +/- 93.0 cm-1) between epi and endo. Contribution of capillary tortuosity and branching to Jv(c,f) ranged from 6-27% (epi) and 8-21% (endo) over the small ranges of l considered (epi = 2.09-2.23; endo = 2.04-2.17 microns).(ABSTRACT TRUNCATED AT 250 WORDS)

The tolerable work duration (t) for high-intensity cycling is well described as a hyperbolic function of power (W): W = (W'.t-1) + Wa, where Wa is the upper limit for sustainable power (lying between maximum W and the threshold for sustained blood [lactate] increase, theta lac), and W' is a constant which defines the amount of work which can be performed greater than Wa. As training increases the tolerable duration of high-intensity cycling, we explored whether this reflected an alteration of Wa, W' or both. Before and after a 7-week regimen of intense interval cycle-training by healthy males, we estimated ( ) theta lac and determined maximum O2 uptake (mu VO2); Wa; W'; and the temporal profiles of pulmonary gas exchange, blood gas, acid-base and metabolic response to constant-load cycling at and above Wa. Although training increased theta lac (24%), mu VO2 (15%) and Wa (15%), W' was unaffected. For exercise at Wa, a steady state was attained for VO2, [lactate] and pH both pre- and post-training, despite blood [norepinephrine] and [epinephrine] ([NE], [E]) and rectal temperature continuing to rise. For exercise greater than Wa, there was a progressive increase in VO2 (resulting in mu VO2 at fatigue), [lactate], [NE], [E] and rectal temperature, and a progressive decrease for pH. We conclude that the increased endurance capacity for high-intensity exercise following training reflects an increased W asymptote of the W-t relationship with no effect on its curvature; consequently, there is no appreciable change in the amount of work which can be performed above Wa.(ABSTRACT TRUNCATED AT 250 WORDS)

The four experiments summarized above demonstrate that there is a strong relationship between both measured muscle venous PO2 and calculated mean muscle capillary PO2 and VO2max. This is true for whole body or exercising muscle VO2max, and is seen both in isolated canine gastrocnemius and intact man. This behavior is exactly what would be expected if the diffusing properties for oxygen in skeletal muscle play a constraining role in setting maximum VO2. These data therefore support the hypothesis we advanced (Wagner, 1988a; Wagner, 1988b), that it is a quantitative integrative relationship between convective and diffusive phenomena that combine to set maximum VO2. A specific prediction of this integrative hypothesis (i.e., the non-uniqueness of VO2max as a function of convective oxygen delivery) was confirmed (Experiment 3). While at this point in time phenomena such as perfusion heterogeneity and muscle shunts cannot be quantitatively taken into account in such analyses, the remarkable concurrence between expectations of the hypothesis and experimental data continue to lend support to the basic idea that maximum VO2 is not limited by any single step of the oxygen transport pathway from atmosphere to mitochondria, but rather by the way in which each and every step combines with every other step to determine oxygen supply.

Exercise performed above the lactate threshold (OLa) produces a slowly-developing phase of oxygen uptake (VO2) kinetics which elevates VO2 above that predicted from the sub-OLa VO2-work rate relationship. This phenomenon has only been demonstrated, to date, in subjects who were relatively homogeneous with respect to fitness. This investigation therefore examined whether this behaviour occurred at a given absolute VO2 or whether it was a characteristic of supra-OLa exercise in a group of subjects with over a threefold range of OLa (990-3000 ml O2.min-1) and peak VO2 (1600-5260 ml O2.min-1). Twelve healthy subjects performed: 1) exhausting incremental cycle ergometer exercise for estimation of OLa (OLa) and peak VO2, and 11) a series of constant-load tests above and below OLa for determination of the VO2 profile and efficiency of work. During all tests expired ventilation, VO2 and carbon dioxide production were monitored breath-by-breath. The efficiency of work determined during incremental exercise (28.1 +/- 0.7%, means +/- SE, n = 12) did not differ from that determined during sub-OLa constant-load exercise (27.4 +/- 0.5%, p greater than 0.05). For constant-load exercise, VO2 rose above that predicted, from the sub-OLa VO2-work rate relationship, for all supra-OLa work rates. This was evident above 990 ml O2.min-1 in the least fit subject but only above 3000 ml O2.min-1 in the fittest subject. As a consequence the efficiency of work was reduced from 27.4 +/- 0.5% for sub-OLa exercise to 22.6 +/- 0.4% (p less than 0.05) at the lowest supra-OLa work rate (i.e. OLa + 20 W, on average).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of the latency, amplitude, and rise characteristics of the stapedius reflex as demonstrated on a strip recorder revealed abnormalities in patients with vestibular neuronitis and other vertigo syndromes. The findings in vestibular neuronitis, acute labyrinthitis, perilymphatic fistulas, Meniere's disease, cerebrovascular insufficiency, and metabolic vertigo are described. Alterations in the stapedius reflex included increase in latency, decrease in amplitude, stepping of the rise, and absence of the reflex. This study suggests that absence of the reflex can be associated with vertigo as well as with acoustic neuromas and other retrocochlear lesions. The findings of abnormalities in vestibular neuronitis support a brain-stem localization as the site of lesion in this disease.

The total capillary length available for blood-tissue transfer is determined by the number and orientation of the capillaries. Therefore, whether capillary tortuosity changes with exercise training has important implications for peripheral gas exchange. To determine the effects of exercise training on capillary orientation and capillary length per volume of muscle fiber [Jv(c,f)] female rats were trained by treadmill running (30 m/min, up to 60 min/day, 5 days/wk) for 4 wk. Muscles from control and trained rats were perfusion fixed at sarcomere lengths (l) ranging from 1.59 to 2.15 microns, and morphometric techniques were used to estimate capillary orientation and Jv(c,f). Training increased (P less than 0.05) musculus soleus oxidative capacity 35% [as estimated from citrate synthase activity: 24.7 +/- 1.4 to 34.7 +/- 1.0 (SE) mumol.g-1.min-1], capillary-to-fiber ratio 30% (2.17 +/- 0.06 to 2.83 +/- 0.05), and Jv(c,f) 32% (1,886 +/- 73 to 2,496 +/- 180 mm-2). Capillary tortuosity (as determined from comparisons of transverse and longitudinal sections) was a direct function of l in control and trained rats and contributed 17-73% of capillary length above that estimated from capillary counts on transverse sections. We conclude that capillary tortuosity in m. soleus is unchanged by training. Therefore, Jv(c,f) increases as a consequence of increased capillary number. M. soleus citrate synthase activity is best correlated with Jv(c,f) and not with capillary counts on transverse sections. We hypothesize that training-induced muscle changes of capillary geometry improve O2 delivery to skeletal muscle and may therefore alter the metabolic response (e.g., lactate accumulation) to exercise after training.(ABSTRACT TRUNCATED AT 250 WORDS)

1. At a given level of pulmonary gas exchange, ventilation (VE) is appreciably higher during isometric exercise than during isotonic exercise. It is presently not clear whether the resultant hypocapnia represents a compensatory hyperventilation for an arterial metabolic acidaemia or whether it might reflect a primary respiratory alkalaemia. 2. To resolve this issue, five subjects performed isometric leg exercise designed to induce exhaustion in ca. 5 min and, on a separate occasion, ca. 8 min. VE, CO2 output (VCO2), O2 uptake (VO2) and end-tidal gas tensions (PET,CO2, PET,O2) were measured breath-by-breath during exercise and recovery; arterialized venous blood (drawn from the dorsum of the heated hand) was sampled frequently and analysed for PCO2, PO2, pH, bicarbonate and lactate. These response profiles were compared with those resulting from exhausting bouts of isotonic leg exercise (cycle ergometry) of similar duration. 3. The isotonic exercise induced a metabolic (lactic) acidaemia with partial respiratory compensation. In contrast, isometric exercise consistently resulted in a respiratory alkalaemia, with little or no increase of blood [lactate]. At the end of the isometric exercise, VE fell abruptly and then rose again after a short interval (20 s, on average). This secondary stimulation presumably reflected the acid-base consequences of the increased blood [lactate] (3-5 mM, on average) which occurred in the recovery phase. 4. We therefore conclude that a primary respiratory alkalaemia occurs during isometric exercise, and that this results from ventilatory stimulation at a time when the 'exercise' metabolites are trapped within the contracting muscles as a consequence of impeded blood flow. The initial rapid reduction of ventilation which occurred at the cessation of the isometric exercise is consistent with a washing-out of 'hyperpnoea-inducing' metabolites from the muscles. Allowing for transit to the central circulation, the reduced ventilation is subsequently supplemented by a powerful humoral drive to breathe which results in a further hyperpnoea and secondary hypocapnia. Because of its latency, we hypothesize that this secondary hypocapnia is of peripheral chemoreceptor origin. 5. The ventilatory response profile for isometric exercise, and the subsequent recovery phase, supports the contention that both the exercising muscles and the peripheral chemoreceptors can be important sites for inducing hyperpnoea in humans.

Whether caloric restriction can alter the efficiency of muscular work raises important questions regarding the control of energetic coupling processes and the efficacy of exercise as a treatment for obesity. To address these issues, oxygen uptake (VO2) was determined at rest and during incremental cycle ergometry in 13 moderately obese (133 +/- 3% ideal body weight, means +/- SEM) women during weight maintenance and after 3 wk of caloric restriction (800 kcal/d). Work efficiency was calculated from the linear portion of the VO2-work rate relationship. Caloric restriction decreased body weight 4.0 +/- 0.4 kg (p less than 0.05), VO2 at rest 32 +/- 3 mL/min (p less than 0.05), and VO2 during unloaded (0 W) cycling 47 +/- 14 mL/min (p less than 0.05). However, work efficiency was unchanged (ie, -0.3 +/- 1.2%, NS). We conclude that, despite metabolic adaptations resulting in decreased energy expenditure at rest and during zero Watt cycling, acute caloric restriction does not alter work efficiency.

The effect of a pattern of exercise and dietary modifications, which was designed to produce alterations in the muscle glycogen content, on the capacity to perform anaerobic exercise was investigated. Six young male subjects worked to exhaustion on a bicycle ergometer at a supramaximal work load equivalent to 104 +/- 5% of VO2max after a normal diet, after a carbohydrate (CHO)-free diet following prolonged exhausting exercise, and after a high-CHO diet. This regimen has previously been shown to cause changes in the glycogen content of the working muscle. Mean work time for subjects on the first test was 4.87 +/- 1.07 min (mean +/- SD). After the low-CHO diet, the time for which work could be maintained was reduced in an increase to 3.32 +/- 0.93 min, whereas administration of the high-CHO diet resulted in an increase to 6.65 +/- 1.39 min. The resting blood lactate concentration was lower than normal following the low-CHO diet and higher than normal following the high-CHO diet. Post exercise blood lactate concentrations reached a peak between 2 and 6 min after exhaustion and again were lower (8.60 +/- 1.58 mmol/l) after the low-CHO diet and higher (12.86 +/- 1.42 mmol/l) after the high-CHO diet than after performing the same intensity of work to exhaustion on a normal diet (11.66 +/- 1.16 mmol/l). The rate of lactate accumulation appeared to be approximately the same during exercise under all three dietary conditions. If this is the case, it suggests that the alterations in endurance capacity do not result from changes in the rate of anaerobic glycolytic energy production, but possibly from a change in the total capacity of the system.

The potential for gas and metabolite exchange across the capillary bed is determined largely by the capillary length and surface area available for blood-tissue transfer. It has been suggested that chronic exposure to hypoxia increases capillary tortuosity; however, the degree of orientation of capillaries in muscles of sea level animals chronically exposed to hypoxia has never been quantified rigorously. An augmented capillary tortuosity would increase capillary length per volume of muscle fiber, Jv(c,f), irrespective of whether new capillaries are formed. To resolve this issue, female rats (278 +/- 5 g) were maintained for 5 months in a temperate environment at 3800 m (PIO2 = 91 Torr). Capillary tortuosity and Jv(c,f) were estimated from transverse and longitudinal sections in perfusion-fixed M. Soleus and M. Gastrocnemius. Values were compared with weight-matched controls (274 +/- 7 g). Neither capillary density (normalized to sarcomere length 2.1 microns, hypoxic = 1292 +/- 79, control = 1282 +/- 43 mm-2) nor capillary-to-fiber ratio (hypoxic = 2.50 +/- 0.15, control = 2.57 +/- 0.05) were changed after altitude exposure. Capillary tortuosity was a function of sarcomere length in all animals and this relationship was not changed by hypoxia. Capillary length per volume of muscle fiber was unchanged (hypoxic = 1541 +/- 72, control = 1531 +/- 44 mm-2) as was mean capillary diameter. We conclude that chronic exposure to 3800 m does not change capillary tortuosity or surface area in rat M. Soleus or M. Gastrocnemius.

The evidence for the existence of secondary endolymphatic hydrops in patients with perilymphatic fistulas is reviewed and the indications for treatment of such hydrops in patients with fistulas are discussed. The indications for and results of combined fistula repair by middle ear exploration and endolymphatic sac surgery in fifteen patients are presented. The preliminary results in these patients appear encouraging. Patients with recurrent perilymphatic fistulas, or with symptoms of attacks of spinning vertigo after fistula repair, and those who present with severe imbalance with findings of a perilymphatic fistula appear to be candidates for combined fistula and sac surgery.

Resting energy expenditure (REE), maximum oxygen uptake (VO2max), and body composition were measured in seven moderately obese women during 9 wk of dietary restriction (800 kcal/d). During weeks 4-6, subjects underwent exercise training (30 min cycling/d, 5 d/wk, at 70% VO2max). The first 3 wk of caloric restriction decreased REE by 13% (from 1437 +/- 76 to 1254 +/- 66 kcal/24 h, means +/- SEM, p less than 0.05). Exercise training increased VO2max (from 1717 +/- 108 to 1960 +/- 120 mL/min, means +/- SEM, p less than 0.05) but did not elevate the dietary-depressed REE (from 1254 +/- 66 to 1262 +/- 62 kcal/24 h). The greatest decrease in body fat (3.7 +/- 0.4 kg) occurred during exercise training, resulting in a small apparent increase in REE when expressed per kilogram total body weight. However, expressed per unit lean body mass, REE remained suppressed throughout the period of caloric restriction. We conclude that exercise training of sufficient intensity to substantially increase VO2max does not reverse the dietary-induced depression of REE.

A new application of the glycerin test in the diagnosis of post-traumatic perilymphatic fistulas is described. Temporary disappearance of abnormal responses to the fistula and Quix tests and improvement in the hearing occurred. The glycerin test was useful in confirming the diagnosis of post-traumatic perilymphatic fistula in 13 patients in whom fistulas were found at middle ear exploration.

Pulmonary gas exchange was studied in eight normal subjects both before and after 2 wk of altitude acclimatization at 3,800 m (12,470 ft, barometric pressure = 484 Torr). Respiratory and multiple inert gas tensions, ventilation, cardiac output (Q), and hemoglobin concentration were measured at rest and during three levels of constant-load cycle exercise during both normoxia [inspired PO2 (PIO2) = 148 Torr] and normobaric hypoxia (PIO2 = 91 Torr). After acclimatization, the measured alveolar-arterial PO2 difference (A-aPO2) for any given work rate decreased (P less than 0.02). The largest reductions were observed during the highest work rates and were 24.8 +/- 1.4 to 19.7 +/- 0.8 Torr (normoxia) and 22.0 +/- 1.1 to 19.4 +/- 0.7 Torr (hypoxia). This could not be explained by changes in ventilation-perfusion inequality or estimated O2 diffusing capacity, which were unaffected by acclimatization. However, Q for any given work rate was significantly decreased (P less than 0.001) after acclimatization. We suggest that the reduction in A-aPO2 after acclimatization is a result of more nearly complete alveolar/end-capillary diffusion equilibration on the basis of a longer pulmonary capillary transit time.

The onset and duration of positive responses to the glycerin test were studied in 28 patients with Menière's disease who had positive responses to the test. The responses were measured for three hours at 30-minute intervals after the ingestion of glycerin. Positive responses were found as early as 30 minutes after ingestion of glycerin. The responses had often become negative by two to three hours. Testing of patients with Menière's disease only at the end of a three-hour interval after ingestion of glycerin will produce a large proportion of false-negative responses, as evidenced by a 39 per cent negative response rate three hours after ingestion of glycerin.

The purpose of this investigation was to determine whether the ventilatory gas exchange threshold (Tvent) changes significantly during the first 1-3 weeks of endurance training. Six men were studied during 3 weeks of training, which consisted of pedaling on a cycle ergometer 6 d X wk 30 min per session at 70% of pretraining VO2max. At the end of each week, VO2max, Tvent, and maximal and submaximal heart rates were determined during an incremental exercise test on the cycle ergometer. Constant-load submaximal exercise blood lactate concentrations were determined during training sessions on Monday, Wednesday, and Friday of each week of training. Tvent did not change significantly during the 3 weeks of training (+ 0.091 X min-1; P greater than 0.05). In contrast, significant changes occurred in all other training indexes measured. VO2max increased by 0.36 1 X min-1 (P less than 0.05) after just 2 weeks of training and did not change further after 3 weeks. Significant reductions (40-45%; P less than 0.05) in blood lactate levels during training sessions occurred by the middle of the 2nd week of training. Decreases in maximal (approximately 11 bt X min-1) and submaximal (approximately 14 bt X min-1) exercise heart rates after 1 week of training were significant (P less than 0.05). The results demonstrate that changes in Tvent lag behind alterations in several other cardiovascular and metabolic parameters in response to endurance training.(ABSTRACT TRUNCATED AT 250 WORDS)

We determined the time course of adaptation in blood lactate concentration ([La]) during constant-load exercise in response to training. Thirteen healthy subjects (11 males, 2 females) exercised on a cycle ergometer for 30 min/day at a work rate calculated to elicit 70% of pre-training VO2max, 6 days/week for 3 weeks. VO2max and blood [La] during constant-load exercise (training work rate) were determined at the end of each week of training. Training increased VO2max 8.5% (from 48.2 +/- 1.5 ml.kg-1.min-1 pre-training to 52.3 +/- 1.4 ml.kg-1.min-1 post-training, P less than 0.01) and decreased constant-load blood [La] 53% (from 7.8 +/- 0.6 mM pre-training to 3.7 +/- 0.3 mM post-training, P less than 0.01). The training-induced reduction in exercise blood [La] was well fit to an exponential (5.5e (-t/2.2) + 2.3, r = 0.99) with a half-time of 10.7 days. However, this was not the case for the time course of VO2max adaptation. The absolute decrease in blood [La] was correlated with the initial blood [La] (r = 0.88, P less than 0.01), but changes in VO2max were not significantly correlated with initial blood [La] (r = -0.14) nor with changes in blood [La] (r = -0.02). We conclude that (1) blood [La] response to constant-load exercise decreases rapidly and exponentially with training, with a t1/2 of 10.7 days, (2) the magnitude of training adaptation is positively related to the initial blood [La], and (3) the time course and extent of the training-induced adaptations of blood [La] and VO2max appear to be independent of one another.

Sarcomere length is practically never considered when fiber size and dependent variables are compared between muscles or experimental conditions. Because of the direct dependence of fiber cross-sectional area on muscle shortening, it is imperative to normalize measurements of fiber size, and related variables (e.g. capillary number/mm2 of fiber) to sarcomere length. We examined the relationship between fiber cross-sectional area and sarcomere length in muscles of animals chronically exposed to high altitude (deer mice, Peromyscus maniculatus, native to 3800 m, and rats, Sprague-Dawley, kept at the same altitude for 5 months) compared to sea-level controls. We found no difference in fiber cross-sectional area, normalized to sarcomere length, between high altitude and control animals in either species. It has been demonstrated that sarcomere length can vary by as much as 30-44% and 43-76% in biopsy and perfusion-fixed muscles, respectively. Therefore, identifying relatively small changes in fiber size in response to a given experimental condition in such material without normalizing for sarcomere length is difficult if not impossible. Furthermore, if the conditions of the investigation induce differences in sarcomere length between experimental and control animals, artifactual changes in fiber cross-sectional area will be produced.

We tested the hypothesis that the lactate threshold (Tlac) during incremental exercise could be increased significantly during the first 3 wk of endurance training without any concomitant change in the ventilatory threshold (Tvent). Tvent is defined as O2 uptake (VO2) at which ventilatory equivalent for O2 [expired ventilation per VO2 (VE/VO2)] increased without a simultaneous increase in the ventilatory equivalent for CO2 (VE/VCO2). Weekly measurements of ventilatory gas exchange and blood lactate responses during incremental and steady-rate exercise were performed on six subjects (4 male; 2 female) who exercised 6 days/wk, 30 min/session at 70-80% of pretraining VO2max for 3 wk. Pretraining Tlac and Tvent were not significantly different. After 3 wk of training, significant increases (P less than 0.05) occurred for mean (+/- SE) VO2max (392 +/- 103 ml/min) and Tlac (482 +/- 135 ml/min). Tvent did not change during the 3 wk of training, despite significant (P less than 0.05) reductions in VE responses to both incremental and steady-rate exercise. Thus ventilatory adaptations to exercise during the first 3 wk of exercise training were not accompanied by a detectable alteration in the ventilatory "threshold" during a 1-min incremental exercise protocol. The mean absolute difference between pairs of Tlac and Tvent posttraining was 499 ml/min. Despite the significant training-induced dissociation between Tlac and Tvent a high correlation between the two parameters was obtained posttraining (r = 0.86, P less than 0.05). These results indicate a coincidental rather than causal relationship.(ABSTRACT TRUNCATED AT 250 WORDS)

Patients with vertigo may be best evaluated when the physician has the various entities that may be responsible clearly in mind. Those diseases listed in group II are more familiar to the primary care physician than those listed in group I, which belong more in the realm of neuro-otology than in general medicine and neurology. The proper use of history, physical findings, and laboratory evaluations will allow the clinician to classify the patient's problem and to initiate treatment and consider appropriate referral when indicated.

Hyperinsulinism, impaired glucose tolerance, and hypertriglyceridemia may be risk factors for atherosclerotic heart disease and have also been described in patients with vertigo, whose symptoms and findings responded to appropriate dietary therapy. We studied 100 patients in an otolaryngology practice to determine the role of these abnormalities in identifying patients suitable for dietary therapy and to assess the efficacy of dietary therapy in the treatment of vertigo in such selected patients. The determination of hyperinsulinism and hypertriglyceridemia were of value as supplements to the traditional glucose tolerance test in detecting reversible metabolic vertigo. Reactive hypoglycemia was found in only four patients and thus appears overdiagnosed as a cause of vertigo. Insulin resistance appears to be the basic abnormality in this syndrome, which, in our series, occurred predominantly in overweight patients.

Vertigo or disequilibrium occurring in patients after concussive and nonconcussive head trauma may be due to a pathologic perilymphatic fistula from the inner ear through the oval and round window areas of the middle ear. Of 33 patients who had successful grafting of the fistulous area at middle ear exploration, 32 had resolution of vertigo, and 12 of 23 who had an associated hearing loss had improved hearing. Perilymphatic fistulas associated with vertigo and hearing loss after head trauma can be diagnosed with great certainty and are surgically curable in the great majority of cases. Patients with post-concussive syndrome, whose symptoms include vertigo or disequilibrium, should have a thorough otologic evaluation for the possibility of a perilymphatic fistula.

The purpose of this study was to evaluate the effects of continuous and interval training on changes in lactate and ventilatory thresholds during incremental exercise. Seventeen males were assigned to one of three training groups: group 1:55 min continuous exercise at approximately 50% maximum O2 consumption (VO2max); group 2: 35 min continuous exercise at approximately 70% VO2max; and group 3: 10 X 2-min intervals at approximately 105% VO2max interspersed with rest intervals of 2 min. All of the subjects were tested and trained on a cycle ergometer 3 day/wk for 8 wk. Lactate threshold (LT) and ventilatory threshold (VT) (in addition to maximal exercise measures) were determined using a standard incremental exercise test before and after 4 and 8 wk of training. VO2max increased significantly in all groups with no statistically significant differences between the groups. Increases (+/- SE) in LT (ml O2 X min-1) for group 1 (569 +/- 158), group 2 (584 +/- 125), and group 3 (533 +/- 88) were significant (P less than 0.05) and of the same magnitude. VT also increased significantly (P less than 0.05) in each group. However, the increase in VT (ml O2 X min-1) for group 3 (699 +/- 85) was significantly greater (P less than 0.05) than the increases in VT for group 1 (224 +/- 52) and group 2 (404 +/- 85). For group 1, the posttraining increase in LT was significantly greater than the increase in VT (P less than 0.05). We conclude that both continuous and interval training were equally effective in augmenting LT, but interval training was more effective in elevating VT.(ABSTRACT TRUNCATED AT 250 WORDS)