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The Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 11 4075-4078
Copyright © 1998 by The Endocrine Society

Original Studies

Ineffective Cardiorespiratory Function in Hyperthyroidism1

George J. Kahaly, Jana Nieswandt, Stefan Wagner, Jens Schlegel, Susanne Mohr-Kahaly and Gerhard Hommel

Departments of Endocrinology/Metabolism, Cardiology (S.W., S.M.K.), Respiratory Medicine (J.S.), and Medical Statistics (G.H.), Gutenberg University Hospital, 55101 Mainz, Germany

Address correspondence and requests for reprints to: Prof. George J. Kahaly, M.D., University Hospital, Bldg. 303, 55101 Mainz, Germany.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
Dyspnea on exertion is a common complaint in hyperthyroidism, and this thyroid dysfunction has been implicated as a primary cause of impaired effort tolerance. Using spirometry and spiroergometry, 42 patients with untreated hyperthyroidism were examined, and the condition was controlled 7 days later under propranolol monotherapy, as well as after 6 months in euthyroidism.

While hyperthyroid, reduced forced vital capacity and tidal volume at the anaerobic threshold (AT) were observed in comparison to euthyroidism. Decreased oxygen (O2) pulse at AT (7 ± 0.4 vs. 9.1 ± 0.4 mL/beat, P = 0.0012) and at maximal exercise was noted in hyperthyroidism and was enhanced under propranolol (8.9 ± 0.4 mL/beat, P = 0.0001). During exercise, the increment of minute ventilation (16.1 ± 0.7 vs. 20.2 ± 1.0 L/min, P = 0.0015), O2 uptake (9 ± 0.5 vs. 11.4 ± 0.5 mL/min/kg, P = 0.0022), O2 pulse (4.0 ± 0.3 vs. 5.6 ± 0.3 mL/beat, P = 0.0001), and heart rate (53 ± 2 vs. 65 ± 3 beat/min, P = 0.0004) was markedly lower in hyper- vs. euthyroidism. Work rate at AT and at maximum was reduced in hyper- vs. euthyroidism (107.4 ± 3 vs. 141.1 ± 4 watt, P = 0.0001). Negative correlations between free T3 and O2 pulse at AT (r = -0.59, P = 0.0005), delta O2 uptake (r = -0.54, P = 0.0007), delta minute ventilation (r = -0.48, P = 0.0007), and maximal work rate (r = -0.62, P = 0.0001) were noted.

In hyperthyroidism, analysis of respiratory gas exchange showed low efficiency of cardiopulmonary function, respiratory muscle weakness, and impaired exercise capacity, which were reversible in euthyroidism.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
DYSPNEA on exertion is a common complaint in patients with hyperthyroidism, but the causes of this symptom remain unclear and may vary from one patient to another (1, 2, 3, 4, 5). Proposed explanations include respiratory muscle weakness, increased ventilatory drive to breathe, increased airway resistance, diminished lung compliance, and high-output left heart failure causing an engorged pulmonary capillary bed (5, 6, 7). The enhanced metabolic rate stresses the lungs, necessitating a more rapid net rate of gas exchange to accommodate the increased oxygen (O2) consumption and carbon dioxide (CO2) production. Exertion further challenges cardiorespiratory function. Healthy persons can easily accomplish this, but hyperthyroid patients may not be able to meet the additional demand for increased gas exchange.

Based on the linear relationship between cardiac output and O2 uptake, direct breath-to-breath gas exchange measurements during exercise (spiroergometry) allow accurate determinations of cardiovascular and lung function, as well as distinction between cardiorespiratory causes for impaired exercise capacity (8). The advantage of gas exchange analysis is the objective determination of maximal O2 uptake and ventilatory anaerobic threshold (AT, the reflection point at which there is a disproportionate increase in CO2 production, compared with O2 uptake). Exercise duration or maximal O2 uptake as the index of work capacity have been used. This may be limited by symptoms or patient motivation and is, therefore, not entirely objective. Anaerobic threshold obtained by respiratory gas analysis on a ramp-loading cycle ergometer seems to be a more objective measure of exercise capacity.

Thus, to objectively analyze possible alterations of cardiorespiratory function and work capacity in hyperthyroidism, we performed spirometry and spiroergometry in a large group of hyperthyroid patients before and during propranolol monotherapy and in euthyroidism, allowing each patient to serve as his or her own control subject.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Forty-two consecutive outpatients (32 female) age 42 ± 2 yr, range 29–59 years, with untreated hyperthyroidism (32 with Graves’ disease, 10 with toxic goiter) were eligible for this prospective study. We selected hyperthyroid subjects with no history of arrhythmia, valvular or coronary heart disease, neuromuscular, or pulmonary disease that could contribute to their exercise intolerance. Diagnosis of hyperthyroidism was based on increased free T3 (17.33 ± 1.4 pg/mL) and free T4 (4.1 ± 0.3 ng/dL) levels, as well as a suppressed TSH (0.03 ± 0.009 mU/L). In 14 patients (33%) with a free T3 of more than 20 pg/mL, symptoms (palpitations, dyspnea, fatigue) and signs (sinus tachycardia, weight loss) of hyperthyroidism were more frequent and marked. Clinical and biochemical data were registered before and after therapy for hyperthyroidism. Serum free T3 (range 3–6 pg/mL), free T4 (0.8–2 ng/dL), and TSH (0.23–4 mU/L) were measured using commercially available kits (Boehringer, Mannheim, Germany). All patients were then treated with propranolol (ICI-Zeneca, Heidelberg, Germany) (120 mg/day) for one week, then additionally received methimazole (Henning, Berlin, Germany) (20 mg/day), and propranolol was gradually reduced. Patients performed the identical exercise protocol in hyper- and euthyroidism states (free T3 4.4 ± 0.1 pg/mL; free T4 1 ± 0.06 ng/dL; TSH 2.5 ± 0.9 mU/L) and were free of cardiovascular medication. The reported investigations were approved by the responsible ethic committee, and informed consent was obtained from all patients to perform the required tests.

Spirometry

Spirometry was performed with the subject in a seated position with a calibrated pneumotachograph (Medical Graphics Corporation MGC, St. Paul, MN). All volumes were corrected to body temperature pressure saturated (BTPS) and expressed as the percentage of predicted values (9). Sufficient compliance of the patients during breathing maneuvers was fulfilled. Maximal values of three reproducible measurements were considered. The parameters of vital capacity, forced vital capacity (FVC), inspiratory capacity, and 1-second capacity (FEV1) were measured, and the ratio FEV1/FVC was calculated.

Spiroergometry

Spiroergometry was performed on an electromagnetically braked cycle ergometer (Ergometrics 900L, Ergoline; Bitz, Germany) with the patient in a semisupine position using a ramp protocol with a continuous increase of work rate by 20 watt/min. With a computerized system (CPX, MGC Corporation; St. Paul, MN), respiratory gas exchange was analyzed. A zirconium fuel cell and the infra red absorption measured O2 and CO2 concentrations, respectively. A pneumotach airflow sensing device was used to monitor tidal volume and respiratory rate. Continuous gas exchange analysis via breath-to-breath sampling allowed the determination of the AT, using computerized regression analysis of the slopes of the CO2 production vs. O2 uptake plot. Airflow measurements were displayed on-line using an 8-sec moving average together with heart rate recorded from simultaneous 12-lead ECG monitoring. The following parameters were measured: heart rate (bpm), blood pressure (mm Hg), work rate (watt), O2 uptake (mL/min), CO2 output (mL/min), respiratory rate (breaths/min), and tidal volume (mL). We calculated pressure rate product (mm Hg x bpm), O2 pulse (O2 uptake/heart rate, mL/beat), minute ventilation (respiratory rate x tidal volume, L/min), ratio delta ({Delta}) O2 uptake/{Delta} work rate (mL/min/watt) according to Wasserman (8).

Statistics

Results are presented as mean value ± SE. Data were analyzed with the statistical software (SAS) (10). Comparison of group mean values between hyper- and euthyroid subjects was made using two-tailed Wilcoxon tests and chi-square tests, as appropriate. The Bonferroni correction for multiple testing was used to test the differing responses between hyper- and euthyroid subjects. Where needed, correlation coefficients were generated with the Pearson bivariate correlation test. Statistical significance was accepted at the 95% confidence level (P < 0.05).


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
In patients with hyperthyroidism, both forced vital capacity and 1-second capacity were reduced (Table 1Go), and in comparison with euthyroidism, increased respiratory rate and decreased tidal volume at the AT were observed. In hyperthyroidism, mean resting O2 uptake was higher than for euthyroidism, whereas during exercise, the increment of minute ventilation, O2 uptake, and O2 pulse was deeply lower in hyper- vs. euthyroidism. Markedly decreased O2 pulse at AT and maximal exercise was observed in hyperthyroidism, and was enhanced under Propranolol monotherapy.


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  		Table 1. Spirometry (data as percentage of normal values, according to ref. 9) and spiroergometry in 42 patients with untreated hyperthyroidism (H), after one week of monotherapy with propranolol (P) 120 mg/day, and 6 months later in euthyroidism (E)

 
Work rate at AT (70 ± 5 vs. 89 ± 5 watt, P = 0.0019) and at maximum (107.4 ± 3 vs. 141.1 ± 4 watt, P = 0.0001) was reduced in hyperthyroidism, but augmented during Propranolol therapy at AT and maximal exercise (77 ± 3 and 115 ± 5 watt, respectively). In patients with hyperthyroidism, heart rate at rest was higher than in euthyroidism and showed a lower increase between rest and maximum compared with euthyroid patients (53 ± 2 vs. 65 ± 3 bpm, P = 0.0004). At rest, the pressure rate product (systolic blood pressure x heart rate) was strongly enhanced in hyper- in contrast to euthyroidism (87 ± 6.6 vs. 73 ± 4.2 mm Hg x bpm, P = 0.0001) and after ß-blockade (56 ± 5, P = 0.0001).

In patients with severe hyperthyroidism and a free T3 of more than 20 pg/mL, the vital capacity, the O2 pulse at AT and at maximum, as well as the work rate at maximal exercise were markedly lower compared with patients with a free T3 of less than 20 pg/mL (Table 2Go). Negative correlations between free T3 and O2 pulse at AT (r = -0.59, P = 0.0005), {Delta} O2 uptake from rest to AT (r = -0.54, P = 0.0007), {Delta} minute ventilation (r = -0.48, P = 0.0007), maximal work rate (r = -0.62, P = 0.0001), and maximal pressure rate product (r = -0.38, P = 0.0013) were noted.


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  		Table 2. Relationship between severity of thyroid dysfunction and cardiorespiratory parameters in 42 patients with untreated hyperthyroidism

 

   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
In a large group of hyperthyroid patients, this study showed marked changes in cardiorespiratory function that were related to severity of thyroid dysfunction. In concordance with a previous study (6), the spirometry parameters were significantly decreased in hyperthyroidism, but were reversible in euthyroidism. Another paper also showed these results in hyperthyroidism, but a control investigation in euthyroidism was not performed (7). Respiratory muscle weakness (3, 11) or induced by hyperthyroidism myopathy (12) are likely explanations for these findings: global respiratory muscle strength, assessed by measuring mouth pressure during maximal static inspiratory and expiratory efforts, was markedly reduced in untreated hyperthyroid patients and was increased again after therapy (11). A possible limitation in study design is that objective data with respect to respiratory muscle function in hyperthyroidism is derived from the experience of others and not drawn from our patients.

Spiroergometry revealed alterations of breathing patterns at rest and at the ventilatory AT. The enhanced respiratory rate and the lower tidal volume in hyperthyroidism may lead to an increased ventilation of the dead space. Furthermore, insufficient increase in ventilation was noted up to the AT. Currently, the AT is used as an index of exercise capacity, being low in unfit subjects. In our patients, reduced work capacity in hyperthyroidism may be caused by the impaired increase of O2 uptake from rest to maximum due to the enhanced resting O2 uptake. Thus, inefficiently rapid and shallow breathing patterns, as well as the lacking response of O2 uptake, reduced effort tolerance. Low efficiency of O2 utilization during exercise in hyperthyroidism was also reported (13, 14). O2 uptake as a measure of total body work rate, and {Delta} work rate/{Delta} O2 uptake (index of work efficiency) were significantly higher than in euthyroidism at every watt step during ramp-loading exercise.

In this study, O2 pulse, a parameter for effective cardiorespiratory function was markedly decreased in hyper- vs. euthyroidism. Although, (and as expected) heart rate was enhanced in hyperthyroidism, O2 uptake at AT did not significantly change, suggesting an ineffective cardiorespiratory work. Heart rate also did not increase sufficiently during exercise as a sign of impaired effort tolerance. The present results are consistent with an already described depression of the efferent activity of the vagal component of the autonomic nervous system during exercise in hyperthyroidism (15, 16). Furthermore, although the pressure rate product was significantly higher in hyper- vs. euthyroidism, work rate was markedly lower in patients with hyperthyroidism. This product is an index of cardiac work that correlates with myocardial O2 consumption (17). In concordance with a previous paper (13), our results of this product demonstrated low efficiency of cardiovascular function.

In patients with a free T3 of more than 20 pg/mL, the cardiorespiratory parameters were markedly decreased and may be explained by the impaired response of O2 uptake and heart rate to incremental exercise. Regarding possible metabolic causes of reduced work efficiency, hyperthyroidism increases fast myosin (18) and fast-twitch fibers in skeletal muscle (19), which are less economic in O2 utilization during contraction than slow-twitch muscle (20). Reduced exercise efficiency may also be induced by excessive heat production in hyperthyroidism (21). Effort tolerance was also impaired in short-duration experimental hyperthyroidism, because of decreased skeletal muscle mass and oxidative capacity related to accelerated protein catabolism (22). Thyroid hormones affect mitochondria mass and enzyme activities (23), and clinical symptoms of exercise intolerance in hyperthyroidism may be due to decreased rather than increased muscle oxidative capacity (24). Because elevated skeletal muscle blood flow during exercise was reported in hyperthyroid rats (25), cardiovascular dysfunction cannot explain exercise limitation.

Action of thyroid hormones in the respiratory centers may be mediated by adrenergic receptor stimuli that can be blocked by ß-antagonists (26). In hyperthyroidism, an inappropriate increase in respiratory central drive was observed that correlated with T3 and was normalized by ß-blockade (7). This effect is quite plausible as there is a high cardiac sensitivity to ß-adrenergic stimulation in hyperthyroidism (27). Furthermore, in contrast to the effects of ß-blockade in controls, Propranolol partially improved muscle weakness in hyperthyroid patients (12) and reversed T4-induced cardiac hypertrophy in animals and humans (28, 29). Although older patients with hyperthyroidism may lack an appropriate peripheral circulatory response, Propranolol slightly enhanced work capacity in our study. With respect to O2 pulse, Propranolol also reduced the intensity of heart rate response to exercise. Thus, ß-blockade led to economical work and higher effectivity of cardiorespiratory function. This may explain clinical amelioration of symptoms in hyperthyroid patients during Propranolol monotherapy (30).

In conclusion, analysis of respiratory gas exchange showed low efficiency of cardiopulmonary function, respiratory muscle weakness, and impaired work capacity in hyperthyroidism, which were reversible in euthyroidism. Thyroid hormones may affect regulatory mechanisms of adaptation to incremental effort. In hyperthyroidism, already at rest, cardiorespiratory capacity is maximally increased, leading to a limited functional reserve, which may explain the inadequate response of ventilation and circulation to incremental work.


   Footnotes
 
1 This work was presented in part at the 69th Annual Meeting of the American Thyroid Association, San Diego, California, November 13–17, 1996. Back

Received March 10, 1998.

Revised June 12, 1998.

Revised August 3, 1998.

Accepted August 10, 1998.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

  1. Ladenson PW. 1996 The heart and thyroid disease. Mt. Sinai J Med. 63:118–125.
  2. Klein I, Ojamaa K. 1994 Thyroid hormone and the cardiovascular system: from theory to practice. J Clin Endocrinol Metab. 78:1026–1028.[CrossRef][Medline]
  3. Dillmann WH. 1996 Thyroid hormones and the heart: basic mechanistic and clinical issues. Thyroid today. 19:1–11.
  4. Klein I, Levey GS. 1996 The cardiovascular system in thyrotoxicosis. In: Braverman LE, Utiger RD, eds. Werner and Ingbar’s the thyroid, 7th ed. Philadelphia: Lippincott-Raven; 607–615.
  5. Ingbar DH. 1996 The respiratory system in thyrotoxicosis. In: Braverman LE, Utiger RD, eds. Werner and Ingbar’s the thyroid, 7th ed. Philadelphia: Lippincott-Raven; 616–627.
  6. Kendrick AH, O’Reilly JF, Laszlo G. 1988 Lung function and exercise performance in hyperthyroidism before and after treatment. Q J Med. 256:615–627.
  7. Small D, Gibbons W, Levy RD, et al. 1992 Exertional dyspnea and ventilation in hyperthyroidism. Chest. 101:1268–1273.[Abstract/Free Full Text]
  8. Wassermann K. 1997 Diagnosing cardiovascular and lung pathophysiology from exercise gas exchange. Chest. 112:1091–1101.[Free Full Text]
  9. Knudson RJ, Slatin RC, Lebowitz MD, Burrows B. 1976 The maximal expiratory flow-volume curve. Normal standards, variability and effects of age. Am Rev Resp Dis. 113:587–600.[Medline]
  10. SAS Institute Inc. Cary, NC. 1991 SAS/STAT User’s Guide, Version 6.10.
  11. Siafakas NM, Milona I, Salesiotou V, et al. 1992 Respiratory muscle strength in hyperthyroidism before and after treatment. Am Rev Respir Dis. 146:1025–1029.[Medline]
  12. Olson BR, Klein I, Benner R, Burdett R, Trzepacz P, Levey GS. 1991 Hyperthyroid myopathy and the response to treatment. Thyroid. 1:137–141.[Medline]
  13. Kimura H, Kawagoe Y, Kaneko N, Fessler HE, Hosoda S. 1996 Low efficiency of oxygen utilization during exercise in hyperthyroidism. Chest. 110:1264–1270.[Abstract/Free Full Text]
  14. Massey DG, Becklake MR, McKenzie JM, Bates DV. 1967 Circulatory and ventilatory response to exercise in thyrotoxicosis. N Engl J Med. 276:1104–1112.
  15. Kollai B, Kollai M. 1988 Reduced cardiac vagal excitability in hyperthyroidism. Brain Res Bull. 20:785–790.[CrossRef][Medline]
  16. Kahaly G, Hellerman J, Mohr-Kahaly S, Treese N. 1996 Impaired cardiopulmonary exercise capacity in hyperthyroidism. Chest. 109:57–61.[Abstract/Free Full Text]
  17. Nelson RR, Gobel FL, Jorgensen CR, et al. 1974 Hemodynamic predictors of myocardial oxygen consumption during static and dynamic exercise. Circulation. 50:1179–1189.[Abstract/Free Full Text]
  18. Ianuzzo CD, Patel P, Chen V. 1977 Thyroidal trophic influence on skeletal muscle myosin. Nature. 270:74–76.[CrossRef][Medline]
  19. Caiozzo VJ, Herrick RE, Baldwin KM. 1991 Influence of hyperthyroidism on maximal shortening velocity and myosin isoform distribution in skeletal muscles. Am J Physiol. 261:C285–295.
  20. Crow MT, Kushmerik MJ. 1982 Chemical energetics of slow- and fast-twitch muscles of the mouse. J Gen Physiol. 79:147–166.[Abstract/Free Full Text]
  21. Nazar K, Chwalbinska-Moneta J, Machalla J. 1978 Metabolic and body temperature changes during exercise in hyperthyroid patients. Clin Sci. 54:323–327.
  22. Martin WH, Spina RJ, Korte E, et al. 1991 Mechanisms of impaired exercise capacity in short duration experimental hyperthyroidism. J Clin Invest. 88:2047–2053.
  23. Winder WW, Holloszy JO. 1977 Response of mitochondria of different types of muscle to thyrotoxicosis. Am J Physiol. 232:C180–184.
  24. Sestoft L, Saltin B. 1985 Working capacity and mitochondrial enzyme activities in muscle of hyperthyroid patients before and after 3 months of treatment. Biochem Soc Trans. 13:733–734.
  25. McAllister RM, Sansone JC, Laughlin JR. 1995 Effect of hyperthyroidism on muscle blood flow during exercise in rats. Am J Physiol. 268:H330–335.
  26. Zwillich CW, Matthay M, Potts DE, et al. 1978 Thyrotoxicosis: comparison of effects of thyroid ablation and beta adrenergic blockage on metabolic rate and ventilatory control. J Clin Endocrinol Metab. 46:496–502.
  27. Martin WH, Spina RJ, Korte E. 1992 Effect of hyperthyroidism of short duration on cardiac sensitivity to beta-adrenergic stimulation. J Am Coll Cardiol. 19:1185–1191.[Abstract]
  28. Klein I. 1988 Thyroxin-induced cardiac hypertrophy: time course of development and inhibition by propranolol. Endocrinology. 123:203–206.[Abstract/Free Full Text]
  29. Biondi B, Fazio S, Carella C, et al. 1994 Control of adrenergic overactivity by beta-blockade improves quality of life in patients on long-term suppressive therapy with levothyroxine. J Clin Endocrinol Metab. 78:1028–1033.[Abstract]
  30. Ventrella S, Klein I. 1994 Beta-adrenergic receptor blocking drugs in the management of hyperthyroidism. Endocrinologist. 4:391–397.



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