Recognizing the long-term sequelae of burns as a chronic medical condition.

As medicine continues to advance, many individuals are living longer with injuries previously considered life threatening. These individuals often face numerous long-term physical and psychological sequelae associated with their injury that persist through the course of their lives. Recently, other injury populations have begun to think of their condition as "chronic". Using data collected from the Burn Model System National Database, a framework for the reconsideration of burn injury as a chronic condition is proposed.

Thermoregulation during exercise in severely burned children.

INTRODUCTION: Severe burns result in skeletal muscle catabolism and weakness, which is worsened by prolonged physical inactivity. Exercise would be an ideal tool in the rehabilitation of burned children. However, it has been postulated that burned children may have an excessive rise in body temperature during exercise compared to non-burned children, partly due to the reduced area available for heat dissipation, thereby questioning the safety of exercise in burned children. METHODS: Children (n = 15) with >40% total body surface area (TBSA) burns and non-burned children (n = 13) successfully completed this study. All subjects completed 20 minutes of treadmill exercise at approximately 75% of their peak aerobic power. Tympanic temperature (Ttym), burned and unburned skin temperature were recorded pre-exercise, every 2 minutes during exercise and during recovery. RESULTS: Within burned children, significant differences between the temperature of unburned skin and burned skin, during later stages of sub-maximal exercise (minutes 12-20) were present. However, there were no significant differences between burned and non-burned children in Ttym or unburned skin temperature indicating that severely burned children do not demonstrate an impaired thermoregulatory response to 20 minutes of sub-maximal exercise at room temperatures. CONCLUSION: It is concluded that exercise at moderate intensities conducted at room temperature is safe in burned children with <75% TBSA burns.

Effects of a 12-wk resistance exercise program on skeletal muscle strength in children with burn injuries.

The posttraumatic response to burn injury leads to marked and prolonged skeletal muscle catabolism and weakness, which persist despite standard rehabilitation programs of occupational and physical therapy. We investigated whether a resistance exercise program would attenuate muscle loss and weakness that is typically found in children with thermal injury. We assessed the changes in leg muscle strength and lean body mass in severely burned children with >40% total body surface area burned. Patients were randomized to a 12-wk standard hospital rehabilitation program supplemented with an exercise training program (n = 19) or to a home-based rehabilitation program without exercise (n = 16). Leg muscle strength was assessed before and after the 12-wk rehabilitation or training program at an isokinetic speed of 150 degrees /s. Lean body mass was assessed using dual-energy X-ray absorptiometry. We found that the participation in a resistance exercise program results in a significant improvement in muscle strength, power, and lean body mass relative to a standard rehabilitation program without exercise.

Role of nitric oxide during hyperventilation-induced bronchoconstriction in the guinea pig.

Airway function is largely preserved during exercise or isocapnic hyperventilation in humans and guinea pigs despite likely changes in airway milieu during hyperpnea. It is only on cessation of a hyperpneic challenge that airway function deteriorates significantly. We tested the hypothesis that nitric oxide, a known bronchodilator that is produced in the lungs and bronchi, might be responsible for the relative bronchodilation observed during hyperventilation (HV) in guinea pigs. Three groups of anesthetized guinea pigs were given saline and three groups given 50 mg/kg N(G)-monomethyl-L-arginine (L-NMMA), a potent nitric oxide synthase inhibitor. Three isocapnic ventilation groups included normal ventilation [40 breaths/min, 6 ml/kg tidal volume (VT)], increased respiratory rate only (150 breaths/min, 6 ml/kg VT), and increased respiratory rate and increased volume (100 breaths/min, 8 ml/kg VT). L-NMMA reduced expired nitric oxide in all groups. Expired nitric oxide was slightly but significantly increased by HV in the saline groups. However, inhibition of nitric oxide production had no significant effect on rate of rise of respiratory system resistance (Rrs) during HV or on the larger rise in Rrs seen 6 min after HV. We conclude that nitric oxide synthase inhibition has no effect on changes in Rrs, either during or after HV in guinea pigs.

Airway function after cyclooxygenase inhibition during hyperpnea-induced bronchoconstriction in guinea pigs.

Airway function deteriorates significantly on cessation of exercise or isocapnic hyperventilation challenges but is largely preserved during the challenge in humans and guinea pigs. PGE(2), an endogenous bronchodilator, might be responsible for the preservation of lung function during hyperventilation (HV). We hypothesized that PGE(2) might have a protective effect during HV, partially explaining the minimal changes in respiratory system resistance (Rrs) usually seen during HV in humans and guinea pigs. Therefore, changes in Rrs were measured during and after HV in anesthetized, mechanically ventilated guinea pigs treated with flurbiprofen (FBN) or placebo. With HV, there was an initial bronchodilation that was unaffected by FBN. Rrs then increased with time during HV, an effect that was blocked by FBN. After HV, Rrs increased further in all groups, but the increase in Rrs was less in the FBN-treated groups. FBN treatment reduced the PGE(2) concentration slightly in lung lavage fluid compared with placebo. We found no enhancement or refractoriness of the Rrs response to repeat bouts of HV and no effect of FBN treatment on the response of Rrs to repeat HV. These results suggest that a constrictor PG is released during and possibly after HV and that the post-HV increase in Rrs is the sum of effects of the PG released during HV and a second constrictor mechanism operating after HV. We found no evidence for bronchodilator PG during or after HV in the guinea pig.

Enhanced inotropic response to dobutamine in strength-trained subjects with left ventricular hypertrophy.

To determine whether strength-trained individuals with physiological concentric left ventricular (LV) hypertrophy exhibit enhanced inotropic responses to catecholamines, we studied 11 bodybuilders, aged 33.0 +/- 2 (SE) yr old, and 10 sedentary healthy subjects, aged 31.3 +/- 2.4 yr old, at baseline and during infusion of incremental doses of dobutamine after atropine. The bodybuilders had larger LV mass, posterior wall and septal wall thicknesses, and wall thickness-to-radius ratio, assessed with two-dimensional echocardiography, than did the sedentary subjects. There was a significant correlation between LV mass and lean body mass irrespective of training status. Baseline LV fractional shortening was similar in the two groups. There was a greater inotropic response to dobutamine in the strength-trained individuals, as evidenced by a steeper slope of the fractional shortening-end-systolic wall stress relationship with a higher y-axis intercept and by a shallower end-systolic wall stress-end systolic diameter relationship without changes in end-diastolic diameter. The heart rate response to dobutamine was attenuated in the strength-trained athletes. There was a significant correlation (r = 0.604, P < 0.05) between the inotropic sensitivity to dobutamine and LV mass normalized for lean body mass in the bodybuilders. The data suggest that concentric LV physiological hypertrophy in the resistance-trained individuals is associated with enhanced inotropic but not chronotropic responses to catecholamines.

Airway obstruction during exercise and isocapnic hyperventilation in asthmatic subjects.

We compared pulmonary mechanics measured during long-term exercise (LTX = 20 min) with long-term isocapnic hyperventilation (LTIH = 20 min) in the same asthmatic individuals (n = 6). Peak expiratory flow (PEF) and forced expiratory volume in 1 s (FEV(1)) decreased during LTX (-19.7 and -22.0%, respectively) and during LTIH (-6.66 and 10. 9%, respectively). In contrast, inspiratory pulmonary resistance (RL(I)) was elevated during LTX (57.6%) but not during LTIH (9.62%). As expected, airway function deteriorated post-LTX and post-LTIH (FEV(1) = -30.2 and -21.2%; RL(I) = 111.8 and 86.5%, respectively). We conclude that the degree of airway obstruction observed during LTX is of a greater magnitude than that observed during LTIH. Both modes of hyperpnea induced similar levels of airway obstruction in the posthyperpnea period. However, the greater airway obstruction during LTX suggests that a different process may be responsible for the changes in airway function during and after the two modes of hyperpnea. This finding raises questions about the equivalency of LTIH and LTX in the study of airway function during exercise-induced asthma.

Airway obstruction during exercise in asthma.

Airway obstruction (AO) in exercise-induced asthma (EIA) is considered a postexercise phenomenon. However, many with EIA complain of respiratory distress during exercise. We evaluated AO in six asthmatic subjects during a short (SX = 6 min) and a long (LX = 20 min) exercise session. We measured peak expiratory flow (PEF) rate, forced expiratory volume in one second (FEV1), and forced expiratory flow at 50% of vital capacity (Vmax50) and calculated expiratory and inspiratory pulmonary resistance (RLe and RLi). Rated perceived exertion (RPE) was evaluated as a measure of dyspnea. All three indices of airflow significantly decreased following SX and LX, but RLi and RLe increased. During SX, PEF, FEV1, and Vmax50 did not decrease, but RLi decreased. During LX, PEF, FEV1, and Vmax50 decreased (20.0, 26.0, and 17.7%, respectively), whereas RLi and RLe significantly increased (74.0 and 53.0%). Rated perceived exertion correlated highly with RLi during exercise (r = 0.95). In summary, there was little or no AO during SX but a frank AO during LX in asthmatic subjects. We conclude that AO occurs during LX and that the manifestation of dyspnea is associated with AO during exercise, as well as in recovery.

Contribution of diaphragmatic power output to exercise-induced diaphragm fatigue.

In nine normal humans we compared the effects on diaphragm fatigue of whole body exercise to exhaustion (86-93% of maximal O2 uptake for 13.2 +/- 2.0 min) to voluntary increases in the tidal integral of transdiaphragmatic pressure (integral of Pdi) while at rest at the same magnitude and frequency and for the same duration as those during exercise. After the endurance exercise, we found a consistent and significant fall (-26 +/- 2.9%, range -19.2 to -41.0%) in the Pdi response to supramaximal bilateral phrenic nerve stimulation at all stimulation frequencies (1, 10, and 20 Hz). Integral of Pdi.fB (where fB is breathing frequency) achieved during exercise averaged 509 +/- 81.0 cmH2O/min (range 304.0-957.0 cmH2O/min). At rest, voluntary production of integral of Pdi.fB, which was < 550-600 cmH2O/min (approximately 4 times the resting eupenic integral of Pdi.fB or 60-70% of Pdi capacity), did not result in significant diaphragmatic fatigue, whereas sustained voluntary production of integral of Pdi.fB in excess of these threshold values usually did result in significant fatigue. Thus, with few exceptions (5 of 23 tests) the ventilatory requirements of whole body endurance exercise demanded a level of integral of Pdi.fB that, by itself, was not fatiguing. The rested first dorsal interosseous muscle showed no fatigue in response to supramaximal ulnar nerve stimulation after whole body exercise. We postulate that the effects of locomotor muscle activity, such as competition for blood flow distribution and/or extracellular fluid acidosis, in conjunction with a contracting diaphragm account for most of the exercise-induced diaphragm fatigue.

Hypoxic effects on exercise-induced diaphragmatic fatigue in normal healthy humans.

We examined the effects of hypoxia on exercise-induced diaphragmatic fatigue. Eleven subjects with a mean maximal O2 uptake of 52.4 +/- 0.7 ml.kg-1.min-1 completed one normoxic (arterial O2 saturation 96-94%) and one hypoxic (inspiratory O2 fraction = 0.15; arterial O2 saturation 83-77%) exercise test at 85% maximal O2 uptake to exhaustion on separate days. Supramaximal bilateral phrenic nerve stimulation (BPNS) was used to determine the pressure generation of the diaphragm pre- and postexercise at 1, 10, and 20 Hz. There was increased flow limitation during hypoxic vs. normoxic exercise. There was a decrease in hypoxic exercise time (normoxic 24.9 +/- 0.7 min vs. hypoxic 15.8 +/- 0.8 min; P < 0.05). After exercise the BPNS transdiaphragmatic pressure (Pdi) was significantly reduced at 1 and 10 Hz after both exercise tests. The BPNS Pdi was recovered to control values by 60 min postnormoxic exercise but was still reduced 90 min posthypoxic exercise. The mean percent fall in the stimulated BPNS Pdi was similar (normoxic -24.8 +/- 4.7%; hypoxic -18.8 +/- 3.0%) after both exercise conditions. Experiencing the same amount of diaphragm fatigue in a shorter time period in hypoxic exercise may have been due to 1) the increased expiratory flow limitation and diaphragmatic muscle work, 2) decreased O2 transport to the diaphragm, and/or 3) increased levels of circulating metabolites.

Exercise-induced diaphragmatic fatigue in healthy humans.

1. Twelve healthy subjects (33 +/- 3 years) with a variety of fitness levels (maximal oxygen uptake (VO2, max) = 61 +/- 4 ml kg-1 min-1, range 40-80), exercised at 95 and 85% VO2, max to exhaustion (mean time = 14 +/- 3 and 31 +/- 8 min, expired ventilation (VE) over final minute of exercise = 149 +/- 9 and 126 +/- 10 l min-1). 2. Bilateral transcutaneous supramaximal phrenic nerve stimulation (BPNS) was performed before and immediately after exercise at four lung volumes, and 400 ms tetanic stimulations were performed at 10 and 20 Hz. The coefficients of variation of repeated measurements for the twitch transdiaphragm pressures (Pdi) were +/- 7-10% and for compound muscle action potentials (M wave) +/- 10-15%. 3. Following exercise at 95% of VO2, max, group mean Pdi twitch values were reduced at all lung volumes (range -8 +/- 3 to -32 +/- 5%) and tetanically stimulated Pdi values were reduced at both 10 and 20 Hz (-21 +/- 3 and -13 +/- 2%, respectively) (P = 0.001-0.047). Following exercise at 85% VO2, max, stimulated Pdi values were reduced at all lung volumes and stimulating frequencies, but only significantly so with the twitch at functional residual capacity (-15 +/- 5%). Stimulated Pdi values recovered partially by 30 min post-exercise and almost completely by an average time of 70 min. 4. The fall in stimulated Pdi values post-exercise was significantly correlated with the percentage increase in diaphragmatic work (integral of Pdi min-1) from rest to end-exercise and the relative intensity of the exercise. 5. The integral of Pdi min-1 and the integral of Po min-1 (Po, esophageal pressure) rose together from rest through the fifth to tenth minute of exercise, after which integral of Pdi min-1 plateaued even though integral of Po min-1, VE and inspiratory flow rate all continued to rise substantially until exercise terminated. Thus, the relative contribution of the diaphragm to total respiratory motor output was progressively reduced with exercise duration. 6. We conclude that significant diaphragmatic fatigue is caused by the ventilatory requirements imposed by heavy endurance exercise in healthy persons with a variety of fitness levels. The magnitude of the fatigue and the likelihood of its occurrence increases as the relative intensity of the exercise exceeds 85% of VO2, max.