Exercise-enhanced satellite cell proliferation and new myonuclear accretion in rat skeletal muscle.

The effects of increased functional loading on early cellular regenerative events after exercise-induced injury in adult skeletal muscle were examined with the use of in vivo labeling of replicating myofiber nuclei and immunocyto- and histochemical techniques. Satellite cell proliferation in the soleus (Sol) of nonexercised rats (0.4 +/- 0.2% of fibers) was unchanged after an initial bout of declined treadmill exercise but was elevated after two (1.0 +/- 0.2%, P < or = 0.01), but not four or seven, daily bouts of the same task. Myonuclei produced over the 7-day period comprised 0.9-1.9% of myonuclei in isolated fibers of Sol, tibialis anterior, and vastus intermedius of nonexercised rats. The accretion of new myonuclei was enhanced (P < or = 0.05) in Sol and vastus intermedius by the initial exercise followed by normal activity (to 3.1-3.4% of myonuclei) and more so by continued daily exercise (4.2-5.3%). Observed coincident with a lower incidence of histological fiber injury and unchanged fiber diameter and myonuclei per millimeter, the greater new myonuclear accretion induced by continued muscle loading may contribute to an enhanced fiber repair and regeneration after exercise-induced injury.

Oxygen uptake kinetics during exercise in chronic heart failure: influence of peripheral vascular reserve.

Exercise performance in chronic heart failure is severely impaired, due in part to a peripherally mediated limitation. In addition to impaired maximal exercise capacity, the O(2) uptake (VO(2)) response during submaximal exercise may be affected, with a greater reliance on anaerobiosis leading to early fatigue. However, the response of VO(2) kinetics to submaximal exercise in chronic heart failure has not been studied extensively; in particular, the relationship between oxygen utilization and the peripheral response to exercise has not been studied. The present investigation examined the time-constant (tau, corresponding to 63% of the total response fitted from exercise onset) of the VO(2) kinetics on-response to submaximal exercise and its relationship to maximal peripheral blood flow in patients with chronic heart failure, and compared responses with those in healthy sedentary subjects. Subjects were 10 patients with chronic heart failure (NYHA class II/III). The mean age was 50+/-12 years, with a mean resting left ventricular ejection fraction of 25+/-9%. Controls were 10 age-matched healthy subjects. VO(2(max)) was first determined for all subjects. Repeated transitions from rest to exercise were performed on a cycle ergometer while measuring breath-by-breath responses of VO(2) at a fixed work rate of 50% of VO(2(max)) (heart failure patients and healthy controls) and at a work rate equivalent to the average in heart failure patients (65 W; healthy controls only). On a separate occasion, post-maximal ischaemic exercise calf blood flow was measured (strain-gauge plethysmography). Whereas heart failure subjects displayed a significantly prolonged VO(2) kinetics response at a similar absolute workload (i.e. 65 W), as indicated by a longer tau value (42 s, compared with 22 s in controls; P<0.01), there was no difference in tau at a similar relative work rate [50% of VO(2(max))]. In addition, heart failure subjects demonstrated a lower maximal calf blood flow (P<0.05) than control subjects. These results indicate that patients with heart failure have a prolonged VO(2) kinetics on-response compared with healthy subjects at a similar absolute work rate (i.e. 65 W), but not at a similar relative work rate [50% of VO(2(max))]. Thus, despite a reduced maximal calf blood flow response associated with heart failure, it does not appear that this contributes to an impairment of the submaximal exercise response beyond that explained by a reduced maximal exercise capacity [VO(2(max))].

Dissociation of peak vascular conductance and V(O2) max among highly trained athletes.

Previously, a strong relationship has been found between whole body maximal aerobic power (VO(2 max)) and peak vascular conductance in the calf muscle (J. L. Reading, J. M. Goodman, M. J. Plyley, J. S. Floras, P. P. Liu, P. R. McLaughlin, and R. J. Shephard. J. Appl. Physiol. 74: 567-573, 1993; P. G. Snell, W. H. Martin, J. C. Buckley, and C. G. Blomqvist. J. Appl. Physiol. 62: 606-610, 1987), suggesting a matching between maximal exercise capacity and peripheral vasodilatory reserve across a broad range of aerobic power. In contrast, long-term training could alter this relationship because of the unique demands for muscle blood flow and cardiac output imposed by different types of training. In particular, the high local blood flows but relatively low cardiac output demand imposed by the type of resistance training used by bodybuilders may cause a relatively greater development in peripheral vascular reserve than in aerobic power. To examine this possibility, we studied the relationship between treadmill VO(2 max) and vascular conductance in the calf by using strain-gauge plethysmography after maximal ischemic plantar flexion exercise in 8 healthy sedentary subjects (HS) and 28 athletes. The athletes were further divided into three groups: 10 elite middle-distance runners (ER), 11 power athletes (PA), and 7 bodybuilders (BB). We found that both BB and ER deviate from the previously demonstrated relationship between VO(2 max) and vascular conductance. Specifically, for a given vascular conductance, BB had a lower VO(2 max), whereas ER had a higher VO(2 max) than did HS and PA. We conclude that the relationship between peak vascular conductance and aerobic power is altered in BB and ER because of training-specific effects on central vs. peripheral cardiovascular adaptation to local skeletal muscle metabolic demand.

Expression of developmental myosin and morphological characteristics in adult rat skeletal muscle following exercise-induced injury.

The extent and stability of the expression of developmental isoforms of myosin heavy chain (MHCd), and their association with cellular morphology, were determined in adult rat skeletal muscle fibres following injury induced by eccentrically-biased exercise. Adult female Wistar rats [274 (10) g] were either assigned as non-exercised controls or subjected to 30 min of treadmill exercise (grade, -16 degrees; speed, 15 m x min(-1)), and then sacrificed following 1, 2, 4, 7, or 12 days of recovery (n = 5-6 per group). Histologically and immunohistologically stained serial, transverse cryosections of the soleus (S), vastus intermedius (VI), and tibialis anterior (TA) muscles were examined using light microscopy and digital imaging. Fibres staining positively for MHCd (MHCd+) were seldom detected in the TA. In the VI and S, higher proportions of MHCd+ fibres (0.8% and 2.5%, respectively) were observed in rats at 4 and 7 days post-exercise, in comparison to all other groups combined (0.2%, 1.2%; P < or = 0.01). In S, MHCd+ fibres were observed less frequently by 12 days (0.7%) than at 7 days (2.6%) following exercise. The majority (85.1%) of the MHCd+ fibres had morphological characteristics indicative of either damage, degeneration, repair or regeneration. Most of the MHCd+ fibres also expressed adult slow, and/or fast myosin heavy chain. Quantitatively, the MHCd+ fibres were smaller (< 2500 microm2) and more angular than fibres not expressing MHCd. Thus, there was a transient increase in a small, but distinct population of MHCd+ fibres following unaccustomed, functional exercise in adult rat S and VI muscles. The observed close coupling of MHCd expression with morphological changes within muscle fibres suggests that these characteristics have a common, initial exercise-induced injury-related stimulus.

Central and peripheral adaptations after 12 weeks of exercise training in post-coronary artery bypass surgery patients.

PURPOSE: Training adaptations in patients with coronary artery disease (CAD) have been reported previously, but little is known about central and peripheral adaptations in those recovering from coronary artery bypass graft surgery (CABG). The purpose of this study was to examine the effects of 12 weeks of endurance exercise training on exercise performance and left ventricular and peripheral vascular reserve in a group of uncomplicated CABG patients. METHODS: Thirty-one patients were recruited and began training 8 to 10 weeks after uncomplicated CABG. Patients underwent progressive exercise training consisting of walking and jogging, at 75% to 80% maximal oxygen intake (VO2max). Measures of left ventricular function included ejection fraction (EF), ventricular volumes, and the pressure volume ratio, an index of contractility. Peak ischemic exercise calf blood flow and vascular conductance was determined using strain-gauge plethysmography. Maximal oxygen intake and submaximal blood lactate concentration also was determined. RESULTS: A significant improvement in VO2max (1497 +/- 60 mL/min versus 1691 +/- 71 mL/min) was observed after training. This change was accompanied by an increase in the EF during submaximal exercise (60 +/- 3% versus 63 +/- 2% at 40% VO2max; 61 +/- 3% versus 64 +/- 3% at 70% VO2max) (P < 0.05), and the change in EF from rest to exercise (delta EF). No changes were observed for ventricular volumes during exercise, although there was a trend for a higher stroke volume at 70% VO2max. A significant increase (18%) was observed for peak ischemic exercise calf blood flow and vascular conductance. In addition, submaximal blood lactate concentration was lower after training. CONCLUSIONS: These data indicate that exercise training for 12 weeks in patients recovering from CABG can elicit significant improvements in functional capacity that, for the most part, are secondary to peripheral adaptations, with limited support for improvement in left ventricular function.

The effect of lower body positive pressure on the cardiovascular response to exercise in sedentary and endurance-trained persons with paraplegia.

Exercise intolerance in persons with paraplegia (PARAS) is thought to be secondary to insufficient venous return and a subnormal cardiac output at a given oxygen uptake. However, these issues have not been resolved fully. This study utilized lower-body positive pressure (LBPP) as an intervention during arm crank exercise in PARAS in order to examine this issue. Endurance-trained (TP, n = 7) and untrained PARAS (UP, n = 10) with complete lesions between T6 and T12, and a control group consisting of sedentary able-bodied subjects (SAB, n = 10) were tested. UP and TP subjects demonstrated a diminished cardiac output (via CO2 rebreathing) during exercise compared to SAB subjects. Peak oxygen uptake (O2peak) remained unchanged for all groups following LBPP. LBPP resulted in a significant decrease in heart rate (HR) in UP and TP (P < 0.05), but not SAB subjects. LBPP produced an insignificant increase in cardiac output (Q) and stroke volume (SV). The significant decrease in HR in both PARA groups may indicate a modest hemodynamic benefit of LBPP at higher work rates where circulatory sufficiency may be most compromised. We conclude that PARAS possess a diminished cardiac output during exercise compared to the able-bodied, and LBPP fails to ameliorate significantly their exercise response irrespective of the conditioning level. These results support previous observations of a lower cardiac output during exercise in PARAS, but indicate that lower-limb blood pooling may not be a primary limitation to arm exercise in paraplegia.

Time course of changes in capillarization in hypertrophied rat plantaris muscle.

The time course of angiogenesis during hypertrophy of the rat plantaris muscle was studied by using a unilateral, synergistic ablation model. Animals (n = 6/group) were euthanized 2, 5, 7, 15, 21, and 30 days postmyectomy. Sections from both the hypertrophied and contralateral muscles were simultaneously stained for capillaries and muscle fiber type. Mean fiber cross-sectional area (FA) and various indexes of capillarity were determined by using a video analysis system. The capillary supply to individual fibers, assessed as the FA supplied per capillary contact, remained unchanged until day 21 (compared with day 2) and exhibited a significant increase at day 30. Analysis of the time course of capillary development on the basis of the number of capillary contacts per fiber, and of hypertrophy on the basis of FA, yielded half-lives of 10.1 and 11.2 days, respectively. It was concluded that angiogenesis during muscle overload is tightly coupled to the changes in FA, which could suggest that the two processes are initiated and/or driven by some common factor(s).

Resistance and aerobic training in older men: effects on VO2peak and the capillary supply to skeletal muscle.

Both aerobic training (AT) and resistance training (RT) may increase aerobic power (VO2peak) in the older population; however, the role of changes in the capillary supply in this response has not been evaluated. Twenty healthy men (age 65-74 yr) engaged in either 9 wk of lower body RT followed by 9 wk of AT on a cycle ergometer (RT-->AT group) or 18 wk of AT on a cycle ergometer (AT-->AT group). RT was performed three times per week and consisted of three sets of four exercises at 6-12 repetitions maximum. AT was performed three times per week for 30 min at 60-70% heart rate reserve. VO2peak was increased after both RT and AT (P < 0.05). Biopsies (vastus lateralis) revealed that the number of capillaries per fiber perimeter length was increased after both AT and RT (P < 0.05), paralleling the changes in VO2peak, whereas capillary density was increased only after AT (P < 0.01). These results, and the finding of a significant correlation between the change in capillary supply and VO2peak (r = 0.52), suggest the possibility that similar mechanisms may be involved in the increase of VO2peak after high-intensity RT and AT in the older population.

Skeletal muscle damage in the rat hindlimb following single or repeated daily bouts of downhill exercise.

This study was conducted to quantify and compare the extent of fibre degenerative and regenerative processes in different muscles of the rat hindlimb following single or repeated daily bouts of treadmill exercise. Wistar rats were used as non-exercised controls, or subjected to one, five, or ten (n = 8 per group), 30-minute daily bouts (-16 degrees, 12-15m.min-1) of downhill exercise. Soleus (S), vastus lateralis (VL), medial gastrocnemius (MG), plantaris (P), and tibialis anterior (TA) muscles were analyzed from transverse cryosections stained with either H&E for morphological alterations indicative of fibre degeneration or regeneration, or mATPase activity for determination of fibre type. Results showed that in all groups, the percentage of morphologically altered fibres (%AF) was greater in S (4-8%) than in MG, VL, P, or TA (1-2%). The %AF across all muscles was greater following only one, versus multiple exercise bouts, or versus no exercise. The proportions of AF of different histochemical types followed the same distribution as the fibre type in the muscle area examined. These direct assessments indicate that the extent of fibre degenerative and regenerative processes varies among the different muscles involved, and is greater following a single bout, compared to repeated daily bouts of exercise.

Quantitating the capillary supply and the response to resistance training in older men.

Resistance training (RT) has been shown to increase aerobic power in older humans. To determine the effects of RT on the capillary supply in this population, nine older men (65-74 y) engaged in 9 weeks RT of the lower body. Following RT, peak O2 uptake (V.O2,peak) increased by 7% (P<.01). Needle biopsies (vastus lateralis muscle) revealed significant increases (mean +/- SE) in fibre area (3,874 +/- 314 microm2 to 4,778 +/- 309 microm2), fibre perimeter (P, 262 +/- 11 microm to 296 +/- 11 microm), capillary contacts (3.7 +/- .2 to 4.3 +/- .3) and the individual capillary-to-fibre ratio (C:Fi, 1. 33 +/- .32 to 1.61 +/- .37, P<.005). To evaluate the potential for blood-tissue exchange, both fibre area-based and perimeter-based measures of the capillary supply were compared. While the area-based measures were maintained, C:Fi/P was increased, consistent with an increase in the size of the fibre-capillary interface and thus, an increased potential for oxygen flux following RT. Of the measurements of capillary supply, V.O2,peak correlated best with C:Fi/P (r = 0.69, P<.005). These results indicate a significant increase in the capillary supply relative to the perimeter, but not the cross-sectional area, of the muscle fibres following RT in older men, and that C:Fi/P is strongly correlated to the V.O2,peak in this population.

Endurance-trained and untrained skeletal muscle bioenergetics observed with magnetic resonance spectroscopy.

Resting and submaximal isometric exercise 31P magnetic resonance spectroscopy (MRS) was carried out on 7 endurance-trained males (26.0 +/- 3 yrs) and 7 sedentary males (27.0 +/- 4 yrs). Spectral analysis provided peak areas of phosphocreatine (PCr), inorganic phosphate (Pi), adenosine triphosphate (ATP), and the chemical shift of Pi relative to PCr. The ratio of PCr/Pi was moderately lower during rest (preexercise p = .13, postexercise p = .18), and significantly higher during exercise (p < .05) in the trained subjects. Intracellular pH patterns were the same for both groups; a transient alkalosis was observed at the onset of exercise with a return to resting levels after 2 min. Differences suggest improved ATP resynthesis rate in the trained subjects during exercise. Intracellular pH changes can be attributed to the utilization of hydrogen ions that accompany PCr hydrolysis during work. The findings are congruent with previous reports indicating a superior oxidative capacity in trained skeletal muscle.

Skeletal muscle form and function after 4 hr ischemia-hypothermia.

The purpose of this study was to examine the use of hypothermia to protect skeletal muscle from the effects of 4 hr of tourniquet ischemia. Muscle recovery was investigated at 6 weeks. Four hours of tourniquet ischemia was induced in two groups (n = 8 per group) of male, Wistar rats (344 +/- 15 g). In the ischemia-only group (IO), the ischemic leg was exposed to room temperature. In the ischemic-hypothermic group (IH), the ischemic leg was cooled to 5-8 degrees C throughout the ischemic period. The contralateral leg served as control. After 6 weeks, the isometric contractile function of the gastrocnemii of both the ischemic and nonischemic legs was determined. Following the functional assessment, the soleus and plantaris muscles were removed and weighed, and biopsies were taken for muscle fiber composition, mean fiber area, and myosin heavy chains (MHC) analysis. Differences between groups (P < 0.05) were determined using ANOVA. Muscle wet weight, tetanic forces, fiber area, fiber type, and MHC composition of IH group were the same as the control group. Yet, twitch tension and relaxation time were lower and longer in the IH group than control group. The tetanic force at 100 Hz of the IH group (12.62 +/- 0.73 N/g) was significantly greater than that of the IO group (2.12 +/- 0.84 N/g). The type 1 muscle fiber areas of plantaris in the IH (1.84 +/- 0.04 x 1000 microns 2) were significantly greater than those of the IO group (1.56 +/- 0.42 x 1000 microns 2).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of hypothermia on changes in isometric contractile function in skeletal muscle after tourniquet ischemia.

The effect of hypothermia on changes in contractile function of skeletal muscle observed after an episode of tourniquet ischemia has been investigated. Male Wistar rats were subjected to 2 hours of unilateral hypothermic (n = 33) or normothermic (n = 39) pneumatic tourniquet ischemia of a hind limb. Isometric contractile function was measured bilaterally from the gastrocnemius muscles after 1, 7, 14, 28, or 42 days of recovery. Compared to muscle subjected to normothermic ischemia, muscle that underwent hypothermic ischemia demonstrated more twitch tension at 1 day postischemia, higher maximum tetanic tension at all time periods, including 6 weeks after ischemia, and greater muscle weight at 6 weeks. Rat gastrocnemius muscle function is much better 1 day to 6 weeks after 2 hours of hypothermic ischemia than after 2 hours of normothermic ischemia. The results thus document the benefit of hypothermia during tourniquet ischemia in preventing or minimizing the changes in isometric contractile function observed after normothermic ischemia.

Vascular conductance and aerobic power in sedentary and active subjects and heart failure patients.

The relationship between peak aerobic power and a strain-gauge determination of local skeletal muscle vascular conductance 10-13 s after calf exercise to fatigue was examined in 21 middle-aged adults (age 38.1 +/- 2.5 yr): seven physically active men (A), seven sedentary men (S), and six men and one woman with compensated idiopathic heart failure (HF). The three subgroups were chosen as differing widely in peak O2 intake [48.2 +/- 1.2, 32.9 +/- 1.6, and 16.1 +/- 1.3 (SE) ml.kg-1 x min-1, respectively]. Calf vascular conductance showed a gradation with aerobic power: 64.8 +/- 3.8, 40.7 +/- 4.3, and 30.7 +/- 6.1 (SE) ml/min local flow per 10 liters of tissue per unit of blood pressure. There was a strong positive correlation between O2 intake and vascular conductance for the overall group (VO2 = 0.614 G + 3.5; r = 0.75, P < 0.001) and for the 14 normal subjects (VO2 = 0.377 G + 20.6; r = 0.74, P < 0.002). The mean conductance was smaller in HF (P < 0.001), with no significant slope in relation to O2 intake. There was no relationship between the resting cardiac ejection fraction [74.4 +/- 4.1% (SE) for A, 74.3 +/- 4.2% for S, and 25.8 +/- 5.2% for HF] and either peak aerobic power or calf vascular conductance. We conclude that peak aerobic power is strongly associated with local vascular conductance during peripherally limited exercise involving the calf muscles of one leg and that vascular conductance is particularly low in subjects with compensated idiopathic heart failure.

Repeated measurements of pulmonary function following spinal cord injury.

Twelve subjects (11 males, 1 female) with complete spinal cord lesion (level of lesion ranging from C4 to T10), with a mean age of 23.5 years participated in pulmonary function testing (PFT). Inspiratory and expiratory flow measurements were made at 2-month intervals from 25 to 351 days post injury. The values were interpolated and extrapolated to common dates to facilitate comparison. The effect of time on pulmonary function was determined by a repeated measures ANOVA. Forced expiratory volume in 1 second (FEV1.0) significantly increased during the course of the study (40%, p < 0.05), but increases in forced vital capacity (FVC) (32.5%) and maximal voluntary ventilation (MVV) (16%) were not statistically significant. Lesion level was found to be correlated (Spearman Product Moment Correlation) with pulmonary function if a single measure was made (r = 0.55 to 0.73), but emerged as a stronger predictor if the average of several repeated PFTs was correlated with lesion level (r = 0.74 to 0.84). In addition, lesion level was not correlated with the amount of improvement attained during the time period studied. We conclude that the time course of recovery of pulmonary function is variable between individuals with spinal cord injuries and can only be weakly predicted by knowledge of the initial value and the lesion level.

Design of a calf muscle ergometer for the study of local muscle blood flow.

A simple ergometer is described that allows highly reproducible plethysmographic measurements of blood flow to be made within 10 seconds of ceasing rhythmic quantitated exercise of the calf muscle. A power output of some 25 Watts is developed with a mechanical efficiency of some 20%. The device seems applicable to a variety of clinical assessments.

Evaluating the influence of sleep deprivation upon circadian rhythms of exercise metabolism.

Cardiorespiratory and gas exchange responses to a moderate, standardized treadmill walking task showed a weak circadian rhythm, with larger superimposed peaks attributable to feeding. However, both rhythms became progressively attenuated during a period of sleep deprivation. A method of exploring this phenomenon is illustrated by an analysis of data on walking heart rate, respiratory minute volume, oxygen intake, and rating of perceived exertion, collected on 11 young men at 3-hr intervals during 60 hours of sleep deprivation.

Impaired cardiopulmonary response to exercise in moderate hypertension.

OBJECTIVE: To identify the limiting factors of exercise performance in subjects with hypertension associated with left ventricular hypertrophy. The secondary objective was to establish relationship between peripheral function and exercise capacity. DESIGN: Cardiopulmonary exercise testing was conducted using two protocols: a graded exercise test to maximal effort established maximal exercise capacity, followed by a step-incremental test combining gas-exchange measures and radionuclide angiography. The exercise responses were compared within and between groups. SETTING: All hypertensive subjects were selected from the Toronto Tri-Hospital Hypertension Clinic. Normal subjects were recruited from the surrounding community. PATIENTS: Twelve patients with established hypertension and left ventricular hypertrophy (determined by echocardiography) were studied as a referred/volunteer sample. All had no evidence of coincident diseases and were unmedicated at time of testing. A volunteer sample of normal, healthy subjects acted as a control. INTERVENTIONS: Graded exercise to maximum and step-incremental (submaximal and steady-state) exercise was used to quantify cardiopulmonary function during exercise stress. MAIN OUTCOME MEASURES: These included (for exercise performance) maximal oxygen intake (VO2max), the ventilatory anaerobic threshold, total peripheral resistance and blood lactate. Cardiac function measures included ejection fraction and ventricular volumes. RESULTS: Cardiac function data obtained during exercise in hypertensive subjects included an increase in the pressure to volume ratio, but a blunted ejection fraction response at peak exercise (P less than 0.05). Although end-diastolic volume increased during exercise (P less than 0.05), values were lower during both levels of exercise compared with normal subjects. Mean +/- SD end-systolic volume increased from 39 +/- 22 at rest to 42 +/- 23 mL during peak exercise. Hypertensive subjects had a lower VO2 max (mean 27.4 +/- 4.8 mL/kg/min) compared with normals (40.0 +/- 8.5 mL/kg/min) and a lower ventilatory anaerobic threshold (14.4 +/- 2.9 versus 27.6 +/- 5.8 mL/kg/min, P less than 0.005). Furthermore, hypertensive patients had a significantly elevated total peripheral resistance at rest (2.5 +/- 1.0 versus 1.8 +/- 0.4 peripheral resistance units) and at peak exercise (1.6 +/- 0.7 versus 0.8 +/- 0.2, P less than 0.01) compared with normal subjects (P less than 0.05). A correlation coefficient of 0.92 was found between total peripheral resistance and VO2 max in hypertensive subjects (P less than 0.01). CONCLUSIONS: These data suggest that peripheral factors, specifically a failure to reduce significantly total peripheral resistance, limits exercise performance despite a maintenance of left ventricular function during exercise in patients with moderate hypertension. The use of cardiopulmonary exercise testing can help in identifying the underlying cause of exercise intolerance in this population and limited left ventricular reserve at peak exercise, and may offer a sensitive measure of therapeutic end-points.

Aerobic fitness and hormonal responses to prolonged sleep deprivation and sustained mental work.

This study examined the influence of aerobic fitness on the responses of selected hormones to the combined stressors of sleep deprivation (SD) and sustained mental work. Six aerobically high fit (HF) (VO2max greater than 50 ml.kg-1.min-1) and six average fit (AF) (VO2max less than 40 ml.kg-1.min-1) female subjects were subjected to a period of sleep loss of 60 h during which time they performed sustained mental tasks with no physical activity component. Venous blood samples were drawn every 12 h at 1330 hours and 0130 hours and plasmas analyzed for cortisol, growth hormone (hGH), prolactin, thyroxine (T4), triiodothyronine (T3), and reverse-triiodothyronine (rT3). For cortisol, both the HF and AF groups exhibited the normal high-daytime and low-nighttime pattern of secretion, with levels increasing significantly as the duration of SD increased. The normal elevations of hGH and prolactin levels during normal sleep were suppressed during SD. No significant fitness effects were found for cortisol, hGH, and prolactin responses. Plasma levels of T4, T3, and rT3 increased significantly during SD, with highly fit subjects exhibiting higher levels of these hormones than those of average fitness. We suggest that aerobic fitness may influence the peripheral metabolism of T4 during SD, but that aerobic fitness does not influence the regulation of the classical stress hormones during SD.

Left ventricular functional response to moderate and intense exercise.

The left ventricular (LV) volume and ejection fraction (EF) response to upright exercise was assessed on 15 normal subjects during cycle ergometry. Measures of cardiac function and gas exchange were made at rest, at 85% of the ventilatory anaerobic threshold (VAT; WL1), and at peak exercise (WL2). EF increased from rest (58 +/- 12%) during WL1 (66 +/- 10%), reaching significantly higher values at WL2 (69 +/- 8%; p less than .05). End-diastolic volume increased from rest during WL1 (136 +/- 36 ml vs. 118 +/- 32 ml; p less than .05), becoming significantly higher than rest during WL2 (141 +/- 41 ml). End-systolic volume was unchanged from rest (51 +/- 25 ml) during submaximal exercise (50 +/- 20 ml), but it decreased significantly during WL2 (44 +/- 21 ml; p less than .05). The systolic pressure/end-systolic volume ratio increased from 3.0 +/- 1.7 (rest) to 5.8 +/- 3.0 at WL2 (p less than .05). These results suggest that the Frank-Starling mechanism is operative throughout exercise, particularly during exercise below the VAT. LV performance after the VAT is further augmented by increased contractility with continued, yet diminished, utilization of the Frank-Starling mechanism.