BACKGROUND: Patients with subclinical hypothyroidism (SCH) have lower exercise tolerance, but the impact on oxygen uptake (VO2) kinetics is unknown. This study evaluated VO2 kinetics during and after a constant load submaximal exercise in SCH. METHODS: The study included 19 women with SCH (thyrotropin (TSH)=6.87±2.88 μIU/mL, free thyroxine (fT4)=0.97±0.15 ng/dL) and 19 controls (TSH=2.29±0.86 μIU/mL, T4=0.99±0.11 ng/dL) aged between 20 and 55 years. Ergospirometry exercise testing was performed for six minutes with a constant load of 50 W, followed by six minutes of passive recovery. The VO2 kinetics was quantified by the mean response time (MRT), which is the exponential time constant and approximates the time needed to reach 63% of change in VO2 (ΔVO2). The O2 deficit-energy supplied by anaerobic metabolism at the onset of exercise-and O2 debit-extra energy demand during the recovery period-were calculated by the formula MRT×ΔVO2. Values are mean±standard deviation. RESULTS: In the rest-exercise transition, patients with SCH showed slower VO2 kinetics (MRT=47±8 sec vs. 40±6 sec, p=0.004) and a higher oxygen deficit (580±102 mL vs. 477±95 mL, p=0.003) than controls respectively. In the exercise-recovery transition, patients with SCH also showed slower VO2 kinetics (MRT=54±6 sec vs. 44±6 sec, p=0.001) and a higher oxygen debit (679±105 mL vs. 572±104 mL, p=0.003). The VO2 kinetics showed a significant correlation with TSH (p<0.05). CONCLUSIONS: This study demonstrates that women with SCH have the slowest VO2 kinetics in the onset and recovery of a constant-load submaximal exercise and highlights that this impairment is already manifest in the early stage of the disease.
BACKGROUND:Patients with subclinical hypothyroidism (SCH) have lower exercise tolerance, but the impact on oxygen uptake (VO2) kinetics is unknown. This study evaluated VO2 kinetics during and after a constant load submaximal exercise in SCH. METHODS: The study included 19 women with SCH (thyrotropin (TSH)=6.87±2.88 μIU/mL, free thyroxine (fT4)=0.97±0.15 ng/dL) and 19 controls (TSH=2.29±0.86 μIU/mL, T4=0.99±0.11 ng/dL) aged between 20 and 55 years. Ergospirometry exercise testing was performed for six minutes with a constant load of 50 W, followed by six minutes of passive recovery. The VO2 kinetics was quantified by the mean response time (MRT), which is the exponential time constant and approximates the time needed to reach 63% of change in VO2 (ΔVO2). The O2 deficit-energy supplied by anaerobic metabolism at the onset of exercise-and O2 debit-extra energy demand during the recovery period-were calculated by the formula MRT×ΔVO2. Values are mean±standard deviation. RESULTS: In the rest-exercise transition, patients with SCH showed slower VO2 kinetics (MRT=47±8 sec vs. 40±6 sec, p=0.004) and a higher oxygen deficit (580±102 mL vs. 477±95 mL, p=0.003) than controls respectively. In the exercise-recovery transition, patients with SCH also showed slower VO2 kinetics (MRT=54±6 sec vs. 44±6 sec, p=0.001) and a higher oxygen debit (679±105 mL vs. 572±104 mL, p=0.003). The VO2 kinetics showed a significant correlation with TSH (p<0.05). CONCLUSIONS: This study demonstrates that women with SCH have the slowest VO2 kinetics in the onset and recovery of a constant-load submaximal exercise and highlights that this impairment is already manifest in the early stage of the disease.
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