Respiratory muscle fatigue has been demonstrated in the laboratory as well as in pathological states, but whether it occurs in healthy individuals under physiological conditions is unknown. To determine whether fatigue of the respiratory muscles may develop with endurance exercise, we measured spirometry and respiratory muscle strength and endurance in four runners before and after completion of a marathon race (42.2 km). Strength was assessed by measuring maximal inspiratory (PImax) and expiratory (PEmax) pressures and transdiaphragmatic pressure during inspiratory capacity (PdiIC); endurance was determined by measuring maximal voluntary ventilation (MVV). After marathon running (mean time, 3 h 24 min) there was no change in forced vital capacity, inspiratory capacity, or flow rates from prerace values. Decreases were observed between pre- and postrace PImax (165.8 +/- 11.0 vs. 138.5 +/- 7.6 cmH2O; P less than 0.01) PEmax (240.0 +/- 20.4 vs. 173.0 +/- 22.6 cmH2O; P less than 0.05), PdiIC (78.8 +/- 11.6 vs. 63.3 +/- 7.0 cmH2O; P less than 0.10), and MVV (178 +/- 24.2 vs. 161.2 +/- 23.2 l/min; P less than 0.005). The decrements in respiratory muscle strength and endurance suggest the development of respiratory muscle fatigue after marathon running.
To evaluate the effects of exercise on net protein catabolism, the losses of urea in sweat and urine and urinary creatinine and 3-methylhistidine (3MH) excretion were determined in eight healthy subjects during cycle ergometer exercise performed at approximately 45% of VO2max for 90 min. The subjects ingested a meat-free diet for 5 days starting 3 days before and continuing for 1 day after the day of exercise. During exercise, total urea excretion (urine + sweat losses) increased 100% above pre- and postexercise values. Thirty percent of the total urea excretion during exercise was in the form of sweat losses. Total protein breakdown (as reflected by urea excretion), however, could account for less than 5% (21 +/- 4 kcal) of total calorie expenditure during the exercise (567 +/- 83 kcal). Urinary creatinine excretion increased by 50% during exercise. Urinary excretion of 3MH also tended to rise, but the ratio of urinary 3MH to creatinine showed no change in response to exercise. We conclude that 1) light to moderate exercise results in an increase in net protein catabolism and an increase in creatinine excretion; 2) sweat losses are an important route for urea excretion during exercise; 3) there is no evidence of a disproportionate increase in breakdown of myofibrillar contractile proteins; and 4) in spite of the increase in the rate of protein catabolism, protein is only a minor source of energy during light to moderate exercise.
We provided full-time ventilatory support in five patients with respiratory paralysis accompanying quadriplegia by continuous electrical pacing of both hemidiaphragms simultaneously for 11 to 33 months through the application to the phrenic nerves of a low-frequency stimulus. The strength and endurance of the diaphragm muscle increased with pacing. Biopsy specimens taken from two patients who had uninterrupted stimulation for 6 and 16 weeks showed changes suggestive of the development of fatigue-resistant muscle fibers. When we compared these results with those of our earlier experience with intermittent unilateral stimulation of the diaphragm in 17 patients with respiratory paralysis, we found that continuous bilateral pacing using low-frequency stimulation appeared to be superior because of more efficient ventilation of both lungs, fewer total coulombs required to effect the same ventilation, and absence of myopathic changes in the diaphragm muscle. For patients with respiratory paralysis and intact phrenic nerves, continuous simultaneous pacing of both hemidiaphragms with low-frequency stimulation and a slow respiratory rate is a satisfactory method of providing full-time ventilatory support.
Right and left ventricular pump performance was assessed at rest and during upright bicycle exercise in 30 patients with chronic obstructive pulmonary disease and in 25 normal control subjects. Right ventricular and left ventricular ejection fractions were ascertained noninvasively using first-pass quantitative radionuclide angiocardiography. The normal ventricular response to exercise was at least a 5% absolute increase in the ejection fraction of either ventricle. In patients the predominant cardiac abnormality involved performance of the right ventricle. Right ventricular ejection fraction was abnormal at rest in eight patients. Twenty-three patients demonstrated an abnormal right ventricular response to submaximal exercise. Airway obstruction and arterial hypoxemia were significantly more severe in patients with abnormal right ventricular exercise reserve than in those with normal reserve. Abnormal left ventricular performance was infrequent either at rest (four patients) or during exercise (six patients). Thus, this radionuclide technique allows noninvasive assessment of biventricular exercise reserve in chronic obstructive pulmonary disease.
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