Hypothyroidism and exercise fatigue

6 Ways Exercise Can Help You Manage Hypothyroidism

Alamy

Sign up for more FREE Everyday Health newsletters.

Living with hypothyroidism can sometimes feel like a vicious cycle: The condition can cause symptoms like fatigue, achy joints, and weight gain. Weight gain can lead to achy joints and fatigue. And fatigue and achy joints can make exercise a chore. What’s more, as anyone with hypothyroidism knows, you may experience times when you feel that you don’t have the energy to move. Yet because it can help manage symptoms — including fatigue, weight gain, and joint stiffness — regular exercise plays a vital role in your hypothyroidism management plan.

While physical therapists say there’s no one regimen that’s perfect for everyone, they all agree that getting regular exercise — even at the most moderate levels — is important for anyone with hypothyroidism. Not only does regular exercise help with symptom management but it can also boost your metabolism.

The good news: You don’t have to run a marathon to reap the benefits of exercise. Ann Wendel, a physical therapist and certified athletic trainer, and the owner of Prana Physical Therapy in Alexandria, Virginia, encourages patients with hypothyroidism to start slowly, with stretching and weight-bearing exercises, and then increase their activity level as their tolerance grows.

It’s important, however, to avoid the temptation to push yourself. Too often, Wendel says, she sees patients who trigger exhaustion in an effort to lose the weight brought on by hypothyroidism. “You can’t push through that kind of fatigue,” she says. “You have to very gradually increase what your body is able to tolerate.” In place of running, or other high-impact aerobic exercises that would normally lead to weight loss, Wendel recommends that you begin with low-impact exercises — such as swimming and walking — as well as weight-bearing exercises.

Courteney Bealko, a physical therapist certified in mechanical diagnostic therapy and the owner of Active Physical Therapy in Seattle, knows a thing or two about using exercise to manage hypothyroidism. Not only does she counsel people with the condition but she’s been her own test subject: Bealko was diagnosed with Hashimoto’s disease, an autoimmune disease that is the most common cause of hypothyroidism in the United States, at age 14. Through the years, she says, daily exercise helped boost her metabolism and eventually enabled her to lower her dosage of hypothyroidism medication. The more she exercises, the less fatigued she feels.

Bealko urges those with hypothyroidism to exercise five to seven days a week whenever possible — and she emphasizes that exercise doesn’t have to be the high-intensity variety. Walking, using an exercise bike, or swimming is sufficient.

“Keeping exercise levels up is generally going to help with any muscle weakness that may have set in, and with general fatigue,” says Bealko. “Just getting the heart rate up — and it only has to be 50 percent of max heart rate — helps, because one of the side effects of hypothyroidism is depression, and exercise can help with depression.” In addition, says Bealko, lower-impact exercise, such as weight training and yoga, also builds muscle, which actually aids in weight maintenance.

When you have hypothyroidism, regular exercise can help you:

Lose weight. Often, one of the first symptoms people with hypothyroidism notice is weight gain. While simply taking the right dosage of medication for hypothyroidism can help relieve other symptoms of the condition, it won’t lead to instant weight loss. So losing weight becomes essential to many, both to help boost self-esteem and to reduce any added stress on joints. Physical therapists encourage low-impact cardiovascular exercises, such as cycling, elliptical training, swimming, and walking. As you build up your fitness level, talk to your doctor about moving on to more intense cardio workouts — such as running — if desired.

Maintain a healthy weight. While cardio exercises may help people shed pounds, activities like weight lifting and strength training help keep the weight off. That’s because muscle requires more energy to maintain than soft tissue or fat — you burn more calories by building and maintaining muscle than maintaining fat — so it can help to add a weight-training program to your routine. While weight lifting helps you ward off weight gain, it can also help boost your metabolism and improve overall strength.

Decrease joint pain. When you’re first getting started with an exercise routine, choose gentle stretching or gentle yoga, especially if you experience joint pain. Swimming and even walking in a pool are also excellent options, as the water reduces stress and pressure on joints.

Relieve depression. Depression often accompanies hypothyroidism. The good news, though, is that aerobic exercises such as biking, walking, elliptical training, and swimming can help elevate metabolism, improve energy, and relieve depression.

Boost energy. Walk, bike, swim, skip down the road — whatever you do, the most important thing is to move. Results of a small study published in March 2017 in Physiology & Behavior even showed that young women who experienced sleep deprivation were more energized by a 10-minute stair climb than by 50 milligrams of caffeine.

Increase muscle mass. In addition to building strength, increasing muscle mass can also help improve balance and stability. Try using weight machines, free weights, and even body-weight exercises to help increase muscle mass. Pilates and more intense types of yoga, such as Ashtanga, Bikram, and Vinyasa, also work well. An added benefit is that muscle helps ward off osteoporosis, a common concern of women — who have the highest incidence of hypothyroidism.

Yoga For Thyroid: 6 Poses to Help You Lead a Better Life

Thyroid disease is a medical condition which affects the function of thyroid gland. There are mainly two types of thyroid – Hypothyroidism caused by not having enough thyroid hormones and Hyperthyroidism caused by having too much thyroid hormones. Some of the most common symptoms of thyroid include fatigue, low energy, weight gain or loss, inability to tolerate the cold, slow or very fast heart rate, dry skin and constipation or diarrhea depending on what kind of thyroid it is. In both hypothyroidism and hyperthyroidism, there may be swelling of a part of the neck, which is also known as goiter. It’s best to consult a doctor and discuss the way forward but know that yoga and meditation can help in relieving a lot of issues associated with thyroid. A stressful lifestyle can be a major contributor to thyroid but it can be managed by indulging in peaceful yoga sessions every morning. According to Dr. Pushpa Saini, Yoga and Meditation Expert, “Thyroid can be curbed by practicing Ujjai Pranayam. You should also take care of your diet and avoid unhealthy eating when suffering from thyroid.Drinking a concoction of coriander seeds soaked in water is a good remedy for managing thyroid.”You should consult a physician before you start practicing yoga as it is important to check which kind of thyroid you are suffering from. Although these yoga asanas are good for both hypo and hyperthyroid, they can only help in coping with the system better and do not form a substitute for medication and have been suggested by Dr. Saini.

Try Yoga For Thyroid And Lead A Better Life

1. Sarvangasana (Shoulder Stand Pose)
It helps in stimulating thyroid glands and controls thyroxin. In this particular pose, the blood flows from the legs to the head region due to the inverted pose which helps in mitigating thyroid.
(How to do Sarvangasana (The Shoulder Stand): Steps and Benefits)
Yoga for Thyroid: Shoulder Stand Pose
2. Halasana (Plough Pose)
This exercise gives compression to the neck thereby, stimulating the abdominal and thyroid glands. It also calms the brain and reduces stress and fatigue.The pose resembles to the Indian plough, hence it is called Halasana.
(Halasana, the Miracle Pose that Helps Reduce Blood Pressure)Yoga for Thyroid: Plough Pose
3. Matsyasana (Fish Pose)
This pose takes the form of a fish and therefore, it is called the Matsyasana. It stretches your neck hence stimulating the thyroid glands. This asana provides gentle healing suited to the needs of thyroid patients, lowers stress levels and reduces the stiffness of muscles and joints. It helps in relaxing the body and preventing mood swings and depression which thyroid might cause.
(Matsyasana, The Fish Pose: An Incredible Yoga Posture for Your Back Issues)
Yoga for Thyroid: Fish Pose
4. Setubandhasana (Bridge Pose)
If you are able to perform the bridge pose successfully, you will be able to stretch your neck to quite and extent and activate the thyroid glands. It helps in calming the brain, reducing anxiety and improving the digestion system.
(How to do the Bridge Pose: Steps and Benefits of Setu Bandhasana)Yoga for Thyroid: Bridge Pose
5. Bhujangasana (Cobra Pose)
During this pose, there is a lot of compressing and stretching which helps in regulating the thyroid glands. This pose helps in improving blood circulation and the flexibility of upper and middle back, strengthens the entire back and shoulders, tones the abdomen, expands the chest and reduces stress and fatigue.
(How to Do Bhujangasana (The Cobra Pose): Steps and Benefits)Yoga for Thyroid: Cobra Pose
6. Sirshasana (Headstand Pose)
It is one of the finest yoga postures as it helps in managing acts directly on the thyroid glands. It aids in balancing the metabolic functions and brings wakefulness and alertness in body.
(Why the Headstand is Known as the King of All Yoga Poses)
Yoga for Thyroid: Headstand Pose
Disclaimer:
CommentsThe opinions expressed within this article are the personal opinions of the author. NDTV is not responsible for the accuracy, completeness, suitability, or validity of any information on this article. All information is provided on an as-is basis. The information, facts or opinions appearing in the article do not reflect the views of NDTV and NDTV does not assume any responsibility or liability for the same.

Muscle Metabolism and Exercise Tolerance in Subclinical Hypothyroidism: A Controlled Trial of Levothyroxine

Abstract

Background: Neuromuscular symptoms and impaired muscle energy metabolism have been described in subclinical hypothyroidism (sHT).

Aim: The aim of the study was to evaluate the energy and substrate response to exercise in sHT patients using a standardized protocol and to test the effect of l-T4 replacement in a double-blind, randomized, placebo-controlled fashion.

Patients and Methods: We studied 23 sHT patients and 10 matched euthyroid controls. Oxygen uptake (VO2), carbon dioxide output, and heart rate were measured during incremental step-up exercise. Blood glucose, lactate, pyruvate, free fatty acid, glycerol, and β-hydroxybutyrate concentrations were measured at rest, every 2 min during exercise, and during 20 min of recovery. The exercise protocol was repeated after 6 months of placebo or l-T4-restored euthyroidism.

Results: Maximal power output (P = 0.02) and VO2 max (P = 0.04) were reduced in sHT, and, with increasing workload, patients achieved higher heart rates (P < 0.03) at VO2 values equivalent to those of controls. The respiratory quotient increments were significantly higher in patients than controls (P < 0.04). Blood lactate and pyruvate and their ratio rose with a steeper slope (P < 0.0001, P < 0.001, and P < 0.01, respectively) in patients than controls. Resting plasma free fatty acid and blood glycerol levels were significantly higher in patients than controls (P < 0.0003 and P < 0.003, respectively) throughout baseline, exercise, and recovery. l-T4 replacement, while improving neuromuscular symptoms, did not produce significant changes in the energy or substrate response to exercise.

Conclusions: The response to exercise is altered both in terms of tolerance and pattern of substrate utilization in sHT patients. Restoring stable euthyroidism does not correct this defect over a 1-yr period.

SKELETAL MUSCLE IS a target organ for thyroid hormones (1), and neuromuscular deficits are well-established findings in hypothyroidism (2). Biochemical abnormalities such as glycogen accumulation and decreased activity of enzymes involved in energy production have been described in hypothyroid type I muscle fibers (3–5). The presence of T3 receptors on the mitochondrial membrane in skeletal muscle suggests a direct effect of thyroid hormones on oxidative metabolism (6). A degree of mitochondrial impairment in hypothyroidism is suggested by the reduced activity of key mitochondrial enzymes and electron transport chain cytochrome complexes (7–9). In two studies using phosphorus nuclear magnetic resonance (1, 10), the rapid decline in energy reserves of exercising hypothyroid muscle was attributed to reduced mitochondrial activity. Another study using the same technique, however, proposed a defect in glycogen breakdown as the mechanism (11). Thus, the metabolic consequences of hypothyroidism in skeletal muscle are still controversial.

Subclinical hypothyroidism (sHT) is defined by an isolated elevation in circulating TSH levels in the face of normal free thyroid hormone concentrations (12). Several studies have reported that sHT may be associated with metabolic, cardiovascular, and neuromuscular features similar to those observed in frank hypothyroidism (13–15). Previous work from our laboratory has documented an impairment of muscle energy metabolism in sHT patients during incremental, submaximal exercise leading to an excessive lactate production; a defective mitochondrial function was postulated as the pathogenic factor (16).

The aim of the present study was to measure the energy and metabolic response to a standardized bout of physical exercise in patients with sHT and the effect on this response of 12 months of levothyroxine (l-T4) replacement in a double-blind, randomized, placebo-controlled fashion.

Patients and Methods

Patients

Twenty-three sHT patients, recruited from the outpatient clinic, participated in the study (Table 1). All patients were characterized by elevated serum TSH levels (>3.6 mIU/liter) and free thyroid hormone (FT4 and FT3) levels within the normal range. All patients suffered from Hashimoto’s thyroiditis and had positive antithyroid peroxidase (TPOAb) and antithyroglobulin (TgAb) autoantibody titers. The control group included 10 healthy subjects, matched to the patients for sex, age, body mass index (BMI), and body composition, who were recruited among hospital staff and relatives of patients. Before entry into the study, a blood sample for TSH, FT4, FT3, TgAb, and TPOAb determination and routine laboratory chemistry was taken at 0800 h after an overnight fast. Neurological, cardiovascular, respiratory, and other systemic diseases were excluded in patients and controls by a complete clinical work-up; no study subject assumed any drugs. Neither patients nor controls were physically trained in the sense of participating in structured training programs or agonistic activities. An expert physician, who was not aware of their hormonal status, administered a simple questionnaire on neuromuscular symptoms to all study subjects. The questionnaire asked whether any of four symptoms (paresthesias, muscle cramps, fatigue, and muscle weakness) had occurred at least once over the previous 30 d.

TABLE 1.

Baseline anthropometric, hormonal, metabolic, and respiratory parameters

F, Female; FM, fat mass; HR, heart rate; LBM, lean body mass; M, male.

a

P < 0.001 vs. controls.

TABLE 1.

Baseline anthropometric, hormonal, metabolic, and respiratory parameters

F, Female; FM, fat mass; HR, heart rate; LBM, lean body mass; M, male.

a

P < 0.001 vs. controls.

The Institutional Ethics Committee approved the study protocol, and all study subjects gave their signed informed consent.

Exercise protocol

The day before the exercise test, a 2-h, 75-g oral glucose tolerance test (OGTT) was performed in all study subjects for the determination of plasma glucose and insulin concentrations. An entry criterion for both sHT patients and controls was that they had normal glucose tolerance (i.e. a fasting plasma glucose <7 mmol/liter and a 2-h glucose level <7.8 mmol/liter). For the exercise test, subjects were instructed to avoid physical exertion during the 48 h preceding the test session and to arrive at the research center in a rested and fully hydrated state. The test was performed at 0800 h after an overnight fast, in a quiet, air-conditioned room (22–24 C), with the subjects wearing lightweight running clothes and running shoes. The test took place at the same time of day to minimize the effect of circadian rhythms. Before the exercise session, subjects had an indwelling venous catheter placed in the antecubital vein and were accustomed to the procedure by 3 min of low-intensity exercise, after which they sat quietly for 20 min. The test was performed on a bicycle ergometer (2400 Siemens) with subjects breathing through a mouthpiece with a one-way valve for exhaled gas collection. Seat and handlebar positions on the bicycle were adjusted to each subject’s comfort and maintained in that position for the subsequent exercise test. The exercise protocol consisted of 4 min of unloaded cycling followed by step increments of workload of 10 W·min−1 in women and 15 W·min−1 in men every 2 min. Both patients and controls were instructed to maintain a pedaling rate of 70 rpm. Subjects were given verbal encouragement throughout the test, which was interrupted when subjects could no longer maintain the desired pedaling rate and/or felt exhausted. Breath-to-breath oxygen uptake (VO2), carbon dioxide output, and minute ventilation were measured with the use of a computer-based system (Metabolic Measurement Cart/System 2900n; Sensor Medics, Yorba Linda, CA), and averaged over 60-sec intervals. VO2 and carbon dioxide output were normalized to the subject’s lean body mass, and expressed as ml·min−1·kg−1. Before each exercise test, the O2 and CO2 analyzers were calibrated using gaseous standards of known concentration with an error of 0.01%. The flow sensor was calibrated by flushing air from a 3-liter syringe at varying flows and frequencies.

Blood samples were obtained at rest (immediately after the warm-up), at the end of each step of the ramp, and every 2 min during recovery for the measurement of glucose, lactate, pyruvate, free fatty acids (FFA), glycerol, and β-hydroxybutyrate. The exercise protocol was repeated after 6 months of placebo therapy or 6 and 12 months of restored euthyroidism with l-T4 therapy. Patients were randomly assigned to receive either l-T4 (Eutirox; Bracco S.p.A., Milan, Italy) replacement therapy (n = 12), 25 μg twice daily, or two identical placebo tablets (n = 11) in a blinded manner. All patients returned after 3 months for repeat thyroid function tests. One of us (N.C.) had access to the treatment code and increased the l-T4 dose by 25 μg if the TSH level was still higher than 3.6 mIU/liter. Titration continued until euthyroidism was reached; the mean final replacement dose of l-T4 was 65 μg daily. Patients taking placebo completed an identical protocol, some of them being given additional placebo tablets to maintain the blindness of the study. Six months after the serum TSH level had become normal (in the l-T4-treated patients) or 6 months and 1 yr after the final dosage was assigned (in the placebo-treated patients), the patients were readmitted to the Clinical Research Center for repeat OGTT and complete exercise protocol. After completion of this second set of studies, the patient code was broken, and the patients on placebo were put on l-T4 therapy. The patients already on l-T4 therapy were maintained on it, and 11 of them returned 6 months later for repeat OGTT and exercise protocol.

Analytical measurements

Serum FT3 and FT4 levels were measured by specific RIA (Techno-Genetics Recordati, Milan, Italy). TSH was determined with an ultrasensitive immunoradiometric assay (IRMA) method (Cis Diagnostici, Tronzano Vercellese, Italy). TgAb were measured by a specific IRMA (TG-Ab IRMA; Biocode, Sclessin, Belgium); TPOAb were measured by a specific RIA (AB-TPO; Sorin Biomedica, Saluggia, Italy). Insulin was assayed by a specific RIA (LINCO Research, Inc., St. Charles, MO). Plasma glucose was measured on an automatic analyzer, Hitachi 717 (Boehringer Mannheim, Mannheim, Germany); plasma FFA were measured spectrophotometrically (Wako, Neuss, Germany). Whole-blood lactate, pyruvate, glycerol, and β-hydroxybutyrate levels were determined spectrophotometrically on an ERIS analyzer 6170 (Eppendorf Garatebau, Hamburg, Germany). For the latter assays, blood samples were collected into iced tubes containing 1 m perchloric acid for immediate deproteinization; the supernatant obtained from centrifugation was stored at −20 C and assayed within 30 d. Normal values in our laboratory are as follows: FT4, 6.8–20 pmol/liter; FT3, 4.3–8.6 pmol/liter; TSH, 0.30–3.6 mIU/liter; Tg-Ab, less than 50 IU/ml; and TPO-Ab, less than 10 IU/ml.

Statistical analysis

Data are expressed as the mean ± sem. Areas under time-concentration curves (AUC) were calculated by the trapezium rule. Group comparisons were performed using ANOVA for independent samples. ANOVA for repeated measures was used to test for group differences in the response to exercise.

Results

Baseline studies

At baseline, serum TSH levels were significantly higher in sHT patients than controls, whereas free thyroid hormone concentrations were not significantly different. Glucose tolerance and the insulin response to oral glucose (as the respective AUC) did not differ between the two groups. No differences were observed in resting VO2 rates or the respiratory quotient (RQ) (Table 1).

The response to exercise was significantly impaired in sHT patients. In terms of exercise tolerance, both maximal power output (79 ± 6 vs. 114 ± 17 W; P = 0.02) and maximal VO2 (38.0 ± 1.0 vs. 42.4 ± 2.1 ml·min−1·kg−1; P = 0.04) were lower in the patients. With increasing workload, patients achieved higher heart rates (P < 0.03 for the first five steps, completed by all patients) at equivalent VO2 rates as those of the controls. The RQ rose during exercise (P < 0.0001); this change was significantly greater in patients than controls (P < 0.04) (Fig. 1).

Fig. 1.

Time course of heart rate, VO2 (in ml·min−1·kg−1 of lean body mass), and RQ in patients with sHT and euthyroid control subjects. All sHT patients completed the fifth step (10 min), 19 completed the sixth, 13 completed the seventh, 11 completed the eighth, eight completed the ninth, five completed the 10th, and only one completed the 11th. During recovery, all study subjects are represented at equivalent times (ergo, the break in the time scale between stepped exercise and recovery).

Fig. 1.

Time course of heart rate, VO2 (in ml·min−1·kg−1 of lean body mass), and RQ in patients with sHT and euthyroid control subjects. All sHT patients completed the fifth step (10 min), 19 completed the sixth, 13 completed the seventh, 11 completed the eighth, eight completed the ninth, five completed the 10th, and only one completed the 11th. During recovery, all study subjects are represented at equivalent times (ergo, the break in the time scale between stepped exercise and recovery).

Plasma glucose concentrations remained stable in both groups, whereas plasma insulin levels decreased slightly, with no difference between groups during either stepped exercise or recovery (data not shown). Blood lactate and pyruvate concentrations rose quickly (P < 0.0001 for both) as did their ratio (P < 0.0001) to return toward baseline during recovery. For all three parameters, the exercise-related rise was steeper in patients than controls (P < 0.0001 for lactate; P < 0.01 for pyruvate; and P < 0.01 for their ratio) (Fig. 2), whereas none of them differed during recovery. In relation to oxygen consumption, blood lactate concentrations increased exponentially in both patients and controls (Fig. 3) but with significantly different slopes; increasing VO2 from 20–40 ml·min−1·kg−1 resulted in a double lactate increment in patients vs. controls (2.9 vs. 1.4 mmol/liter; P < 0.0001). Serum TSH levels were correlated inversely with both maximal power output (r = −0.55; P = 0.001) and maximal VO2 (r = −0.5; P = 0.02) and directly related to lactate production rate (expressed as AUC) (r = 0.43; P < 0.05).

Fig. 2.

Time course of blood lactate and pyruvate concentrations, and their ratio, in patients and controls during stepped exercise and recovery.

Fig. 2.

Time course of blood lactate and pyruvate concentrations, and their ratio, in patients and controls during stepped exercise and recovery.

Fig. 3.

Blood lactate concentrations in relation to VO2 (in ml·min−1·kg−1 of lean body mass).

Fig. 3.

Blood lactate concentrations in relation to VO2 (in ml·min−1·kg−1 of lean body mass).

Fatty substrates presented different patterns in patients and controls. In the latter, stepped exercise was associated with a significant (P < 0.0001) decline in circulating FFA, a rise in blood glycerol (P = 0.02), and stable β-hydroxybutyrate levels; during recovery, FFA were stable, whereas glycerol decreased and β-hydroxybutyrate increased (P < 0.0001 for both). In patients, starting levels of all three substrates were significantly elevated (P = 0.0003, P = 0.003, and P = 0.06 for FFA, glycerol; and β-hydroxybutyrate, respectively); their changes during exercise and recovery were similar to those of controls, with the exception of β-hydroxybutyrate levels, which tended to decline during exercise (P = 0.08) (Fig. 4).

Fig. 4.

Time course of plasma FFA, blood glycerol, and β-hydroxybutyrate concentrations in patients and controls during stepped exercise and recovery.

Fig. 4.

Time course of plasma FFA, blood glycerol, and β-hydroxybutyrate concentrations in patients and controls during stepped exercise and recovery.

Follow-up studies

The baseline characteristics of the sHT patients randomized to placebo or l-T4 replacement therapy were similar. After 6 months of stable euthyroidism, serum TSH levels in l-T4-treated patients were normalized and no longer different from those of control subjects, whereas they were unchanged in placebo-treated patients (Table 2). However, in l-T4-treated patients, none of the measured parameters (glucose tolerance, insulin response to glucose, resting heart rate, resting and maximal VO2, and maximal power output) changed significantly, either with respect to baseline or in comparison with the corresponding changes observed in the placebo group. Likewise, changes in heart rate, VO2, and blood metabolites during exercise and recovery showed no significant differences between placebo and active treatment. The 11 patients maintained on active treatment until 1 yr failed to show any consistent change from the preceding treatment period or from baseline (Fig. 5).

Fig. 5.

Blood lactate, lactate/pyruvate ratio, and plasma FFA concentrations (expressed as AUC) in placebo- or l-T4-treated patients at baseline and follow-up. Note that placebo-treated patients were not restudied at 1 yr.

Fig. 5.

Blood lactate, lactate/pyruvate ratio, and plasma FFA concentrations (expressed as AUC) in placebo- or l-T4-treated patients at baseline and follow-up. Note that placebo-treated patients were not restudied at 1 yr.

TABLE 2.

Anthropometric, hormonal, metabolic, and respiratory parameters of sHT patients at baseline and after 6 months of treatment-induced stable euthyroidism or placebo therapy

F, Female; FM, fat mass; HR, heart rate; LBM, lean body mass; M, male.

a

P < 0.05;

b

P < 0.0001 vs. baseline or vs. placebo.

TABLE 2.

Anthropometric, hormonal, metabolic, and respiratory parameters of sHT patients at baseline and after 6 months of treatment-induced stable euthyroidism or placebo therapy

F, Female; FM, fat mass; HR, heart rate; LBM, lean body mass; M, male.

a

P < 0.05;

b

P < 0.0001 vs. baseline or vs. placebo.

Discussion

We have previously described elevated blood lactate levels in sHT patients during incremental, submaximal forearm exercise (16) and have postulated a defect in mitochondrial function as the pathogenetic mechanism. To confirm and extend these findings, in the present group of patients, we measured the energy and substrate response to exercise using a standardized protocol. It is important to emphasize that we selected sHT patients with rigorously normal glucose tolerance and matched them to euthyroid subjects with very similar anthropometric and clinical characteristics to rule out biases caused by differences in age, obesity, or glucose tolerance. In addition, we made an effort to also match patients and controls by reported physical activity, although the latter is known to be a relatively poor indicator of physical fitness.

Changes in cardiac function indices have been reported in sHT patients (17, 18). In a comprehensive study of exercise capacity, sHT was found to be associated with impairment of several exercise-related cardiopulmonary responses, resulting in some degree of exercise intolerance (19). In particular, cardiovascular function and work capacity was assessed by stress echocardiography and respiratory gas analysis on a ramp-loading cycle ergometer. Although the regression of heart rate on VO2 showed a reduced slope in comparison with controls, in sHT patients the oxygen pulse (VO2 per heart beat), an index of stroke volume, was significantly reduced either at the anaerobic threshold or at a maximal workload (19). Therefore, abnormal cardiovascular function contributed to the reduced work capacity in sHT patients.

In accord with these findings, in our sHT patients the response to exercise was impaired and was not corrected by l-T4 replacement to a significant extent over the period of time of the trial. With regard to the pattern of substrate use, in the euthyroid controls, stepped exercise was associated with the expected rise in circulating lactate and pyruvate concentrations and a moderate rise in their ratio. This result indicates that with increasing work rate the availability of glucose, from enhanced liver production as well as from glycogen stores, exceeded the ability of body tissues to oxidize it, resulting in lactate and pyruvate regurgitation into the bloodstream and a fall in intracellular pH. The observed increase in the RQ marks the preference given to carbohydrate over fat oxidation, which develops as the increasing workload mounts an oxygen debt. In line with these physiological responses is also the increase in lipolysis, signaled by the rising blood glycerol levels, activated by the adrenergic response to exercise. The fall in circulating FFA levels indicates that the increased energy demand is also met by fat oxidation, which is stimulated in excess of lipolysis (20, 21). In sHT patients, the increase in VO2 at each given level of work was very similar to that of controls, suggesting that work efficiency was normal at least up to their tolerance threshold. However, heart rate was higher than in controls at each level of VO2, indicating a reduced cellular oxygen extraction. The substrate response to exercise was fully compatible with their reduced ability to use oxygen. The exaggerated rise in blood lactate and pyruvate levels, and in their ratio, is the expected consequence of such impaired oxygen use (21).

The pattern of circulating fatty substrates differed from that of controls not so much in response to the exercise protocol but in the resting state. In sHT patients, FFA were higher throughout the protocol, and the higher blood glycerol levels suggested that this increase in circulating FFA was, at least in part, caused by enhanced lipolysis. The raised ketone levels indicated increased hepatic FFA oxidation; the greater rise in RQ indicates a relative inability to oxidize fat. In previous studies in animal models of hypothyroidism or in vitro systems, lipolysis has been found to be reduced (22). This notion, however, is not supported by studies in overtly hypothyroid humans, in whom rates of FFA turnover were normal (23), and has never been tested in sHT. Moreover, sHT is associated with increased levels of circulating catecholamines, possibly as a result of enhanced production (18, 24). An increased sympathetic activity may help explain the heart rate changes during exercise and the enhanced lipolysis observed in our patients. Lastly, if glucose use in fat cells were impaired, this would result in unrestrained lipolysis with the full set of metabolic consequences observed in our patients: increased delivery of FFA to the liver and increased hepatic FFA oxidation with enhanced ketone production. Indeed, in fat cells obtained from hypothyroid subjects, Pedersen et al. (25) found that both glucose transport and lipogenesis were impaired, to an extent that was conspicuously similar to that seen in adipocytes from hyperthyroid subjects. Furthermore, Matsuoka et al. (26) reported in vivo insulin resistance in a few patients with hypothyroidism, which was not reversed by normalization of thyroid function. Additional studies are needed to confirm this observation.

The possibility that a mitochondrial defect may contribute to the impaired oxygen use seen in sHT patients must be considered. A muscle mitochondrial defect (1, 10, 16), together with the known structural alterations of skeletal muscle, more pronounced in frank hypothyroidism (4, 11) but also present in sHT (20, 27), may underlie the muscular symptoms frequently reported by sHT patients. In turn, the neuromuscular deficit may account, at least in part, for the reduced physical fitness. In the present trial, successful l-T4 replacement therapy was associated with a clear improvement of the subjective symptoms but was insufficient, at least within 1 yr, to also normalize exercise tolerance and the metabolic response to exercise. It remains to be proven whether more prolonged euthyroidism may eventually restore fitness and adipose tissue insulin sensitivity.

Acknowledgements

We thank Sara Burchielli for her assistance.

This work was partly supported by grants from Ministero Istruzione, Università e Ricerca, Rome, and Bracco S.p.A., Milan, Italy.

Abbreviations:

  • AUC,

    Area under the curve;

  • BMI,

    body mass index;

  • FFA,

    free fatty acids;

  • FT4,

    free T4;

  • IRMA,

    immunoradiometric assay;

  • l-T4,

    levothyroxine;

  • OGTT,

    oral glucose tolerance test;

  • RQ,

    respiratory quotient;

  • sHT,

    subclinical hypothyroidism;

  • TgAb,

    antithyroglobulin antibody;

  • TPOAb,

    antithyroid peroxidase antibody;

  • VO2,

    oxygen uptake.

1 Argov Z , Renshaw PF , Boden B , Winkokur A , Bank WJ 1988 Effects of thyroid hormones on skeletal muscle bioenergetics. In vivo phosphorus-31 magnetic resonance spectroscopy study of humans and rats. J Clin Invest 81:1695–1701 2 Bastron JA 1984 Neuropathy in diseases of the thyroid and pituitary glands. In: Dyck PJ, Thomas PK, Lambert EH, Bunge RP, eds. Peripheral neuropathy. Philadelphia: Saunders; 1983–1846 3 Chu DTW , Shikama H , Khatra BS , Exton JH 1985 Effect of altered thyroid status on β-adrenergic actions of skeletal muscle glycogen metabolism. J Biol Chem 260:9994–10000 4 Khaleeli AA , Gohil K , McPhail G , Round JM , Edwards RH 1983 Muscle morphology and metabolism in hypothyroid myopathy: effect of treatment. J Clin Pathol 36:519–526 5 Leijendekker WJ , van Hardeveld C , Kassenaar AA 1985 Coupled diminished energy turnover and phosphorylase a formation in contracting hypothyroid rat muscle. Metabolism 34:437–441 6 Sterling K , Lazzarus JH , Milck PO , Sakurada T , Brenner MA 1978 Mitochondrial thyroid hormone receptor: localization and physiological significance. Science 201:1126–1129 7 Ianuzzo CD , Chen V , O’Brien P , Keens TG 1984 Effect of experimental dysthyroidism on the enzymatic character of the diaphragm. J Appl Physiol 56:117–121 8 Ianuzzo D , Patel P , Chen V , O’Brien P , Williams C 1977 Thyroidal trophic influence on skeletal muscle myosin. Nature 270:74–76 9 Janssen JV , Van Hardeveld C , Kassenaar AA 1978 Evidence of different response of red and white skeletal muscle of the rat in different thyroid states. Acta Endocrinol 87:768–775 10 Kaminsky P , Robin-Lherbier B , Brunotte F , Escanye JM , Walker P , Klein M , Robert J , Duc M 1992 Energetic metabolism in hypothyroid skeletal muscle, as studied by phosphorus magnetic resonance spectroscopy. J Clin Endocrinol Metab 74:124–129 11 Taylor DJ , Rajagopalan B , Radda GK 1992 Cellular energetics in hypothyroid muscle. Eur J Clin Invest 22:358–365 12 Ross DS 1996 Subclinical hypothyroidism. In: Braverman LE, Utiger RD, eds. Werner and Ingbar’s the thyroid. 7th ed. Philadelphia: Lippincott-Raven Press; 1010–1015 13 Cooper DS , Halpern R , Wood LC , Levin AA , Ridgway EC 1984 l-Thyroxine therapy in subclinical hypothyroidism. A double-blind, placebo-controlled trial. Ann Intern Med 101:18–24 14 Monzani F , Caraccio N , Del Guerra P , Casolaro A , Ferrannini E 1999 Neuromuscular symptoms and dysfunction in subclinical hypothyroid patients: beneficial effect of l-T4 replacement therapy. Clin Endocrinol 51:237–242 15 Monzani, F , Di Bello V , Caraccio C , Bertini A , Giorgi D , Giusti C , Ferrannini E 2001 Effect of levothyroxine on cardiac function and structure in subclinical hypothyroidism: a double blind, placebo-controlled study. J Clin Endocrinol Metab 86:1110–1115 16 Monzani F , Caraccio N , Siciliano G , Manca L , Murri L , Ferrannini E 1997 Clinical and biochemical features of muscle dysfunction in subclinical hypothyroidism. J Clin Endocrinol Metab 82:3315–3318 17 Biondi B , Palmieri EA , Lombardi G , Fazio S 2002 Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med 137:904–914 18 Faber J , Petersen L , Wiinberg N , Schifter S , Mehlsen J 2002 Hemodynamic changes after levothyroxine treatment in subclinical hypothyroidism. Thyroid 12:319–324 19 Kahaly GJ 2000 Cardiovascular and atherogenic aspects of subclinical hypothyroidism. Thyroid 10:665–679 20 Wasserman K , Whipp BJ , Davis JA 1981 Respiratory physiology of exercise: metabolism, gas exchange and ventilatory control. In: Widdicombe JG, ed. International review of physiology, respiratory physiology III. 23rd ed. Baltimore: University Park Press; 150–211 21 Wasserman K 1984 The anaerobic threshold measurement to evaluate exercise performance. Am Rev Respir Dis 129:S35–S40 22 Muller MJ , Seitz HJ 1984 Thyroid hormone action on intermediary metabolism. II. Lipid metabolism in hypo- and hyperthyroidism. Klin Wochenschr 62:49–55 23 Saunders J , Hall SE , Sonksen PH 1980 Glucose and free fatty acid turnover in thyrotoxicosis and hypothyroidism, before and after treatment. Clin Endocrinol (Oxf) 13:33–44 24 Fagius J , Westermark K , Karlsson A 1990 Baroreflex-governed sympathetic vasculature is increased in hypothyroidism. Clin Endocrinol 33:177–185 25 Pedersen O , Richelsen B , Bak J , Arnfred J , Weeke J , Schmitz O 1988 Characterization of the insulin resistance of glucose utilization in adipocytes from patients with hyper- and hypothyroidism. Acta Endocrinol 119:228–234 26 Matsuoka LY , Wortsman J , Gavin 3rd JR , Kupchella CE , Dietrich JG 1986 Acanthosis nigricans, hypothyroidism, and insulin resistance. Am J Med 81:58–62 27 Siciliano G , Monzani F , Manca ML , Tessa A , Caraccio N , Tozzi G , Piemonte F , Mancuso M , Santorelli FM , Ferrannini E , Murri L 2002 Human mitochondrial transcription factor A reduction and mitochondrial dysfunction in Hashimoto’s hypothyroid myopathy. Mol Med 8:326–333 Copyright © 2005 by The Endocrine Society

PMC

  • Ianuzzo D, Patel P, Chen V, O’Brien P, Williams C. Thyroidal trophic influence on skeletal muscle myosin. Nature. 1977 Nov 3;270(5632):74–76.
  • Gollnick PD, Ianuzzo CD. Hormonal deficiencies and the metabolic adaptations of rats to training. Am J Physiol. 1972 Aug;223(2):278–282.
  • Baldwin KM, Hooker AM, Herrick RE, Schrader LF. Respiratory capacity and glycogen depletion in thyroid-deficient muscle. J Appl Physiol Respir Environ Exerc Physiol. 1980 Jul;49(1):102–106.
  • van Hardeveld C, Kassenaar AA. Effects of experimental hypothyroidism on skeletal muscle metabolism in the rat. Acta Endocrinol (Copenh) 1978 Jan;87(1):114–124.
  • Janssen JW, van Hardeveld C, Kassenaar AA. Evidence for a different response of red and white skeletal muscle of the rat in different thyroid states. Acta Endocrinol (Copenh) 1978 Apr;87(4):768–775.
  • Terjung RL, Koerner JE. Biochemical adaptations in skeletal muscle of trained thyroidectomized rats. Am J Physiol. 1976 May;230(5):1194–1197.
  • Wiles CM, Young A, Jones DA, Edwards RH. Muscle relaxation rate, fibre-type composition and energy turnover in hyper- and hypo-thyroid patients. Clin Sci (Lond) 1979 Oct;57(4):375–384.
  • Wiles CM, Jones DA, Edwards RH. Fatigue in human metabolic myopathy. Ciba Found Symp. 1981;82:264–282.
  • Leijendekker WJ, van Hardeveld C, Kassenaar AA. The influence of the thyroid state on energy turnover during tetanic stimulation in the fast-twitch (mixed type) muscle of rats. Metabolism. 1983 Jun;32(6):615–621.
  • Leijendekker WJ, van Hardeveld C, Kassenaar AA. Coupled diminished energy turnover and phosphorylase a formation in contracting hypothyroid rat muscle. Metabolism. 1985 May;34(5):437–441.
  • Winder WW, Holloszy JO. Response of mitochondria of different types of skeletal muscle to thyrotoxicosis. Am J Physiol. 1977 May;232(5):C180–C184.
  • Ianuzzo CD, Chen V, O’Brien P, Keens TG. Effect of experimental dysthyroidism on the enzymatic character of the diaphragm. J Appl Physiol Respir Environ Exerc Physiol. 1984 Jan;56(1):117–121.
  • Kubista V, Kubistová J, Pette D. Thyroid hormone induced changes in the enzyme activity pattern of energy-supplying metabolism of fast (white), slow (red), and heart muscle of the rat. Eur J Biochem. 1971 Feb;18(4):553–560.
  • Winder WW, Baldwin KM, Terjung RL, Holloszy JO. Effects of thyroid hormone administration on skeletal muscle mitochondria. Am J Physiol. 1975 May;228(5):1341–1345.
  • Chance B, Eleff S, Leigh JS, Jr, Sokolow D, Sapega A. Mitochondrial regulation of phosphocreatine/inorganic phosphate ratios in exercising human muscle: a gated 31P NMR study. Proc Natl Acad Sci U S A. 1981 Nov;78(11):6714–6718.
  • Chance B, Leigh JS, Jr, Clark BJ, Maris J, Kent J, Nioka S, Smith D. Control of oxidative metabolism and oxygen delivery in human skeletal muscle: a steady-state analysis of the work/energy cost transfer function. Proc Natl Acad Sci U S A. 1985 Dec;82(24):8384–8388.
  • Fundarò A, Molinengo L, Cassone MC. The transition from a fixed ratio to a fixed interval schedule of reinforcement in hypo and hyperthyroid rats. Pharmacol Res Commun. 1985 May;17(5):463–470.
  • Argov Z, Maris J, Damico L, Koruda M, Roth Z, Leigh JS, Jr, Chance B. Continuous, graded steady-state muscle work in rats studied by in vivo 31P-NMR. J Appl Physiol (1985) 1987 Oct;63(4):1428–1433.
  • Argov Z, Bank WJ, Maris J, Peterson P, Chance B. Bioenergetic heterogeneity of human mitochondrial myopathies: phosphorus magnetic resonance spectroscopy study. Neurology. 1987 Feb;37(2):257–262.
  • Argov Z, Bank WJ, Maris J, Leigh JS, Jr, Chance B. Muscle energy metabolism in human phosphofructokinase deficiency as recorded by 31P nuclear magnetic resonance spectroscopy. Ann Neurol. 1987 Jul;22(1):46–51.
  • Taylor DJ, Bore PJ, Styles P, Gadian DG, Radda GK. Bioenergetics of intact human muscle. A 31P nuclear magnetic resonance study. Mol Biol Med. 1983 Jul;1(1):77–94.
  • Arnold DL, Matthews PM, Radda GK. Metabolic recovery after exercise and the assessment of mitochondrial function in vivo in human skeletal muscle by means of 31P NMR. Magn Reson Med. 1984 Sep;1(3):307–315.
  • Edwards RH, Dawson MJ, Wilkie DR, Gordon RE, Shaw D. Clinical use of nuclear magnetic resonance in the investigation of myopathy. Lancet. 1982 Mar 27;1(8274):725–731.
  • Chance B. Applications of 31P NMR to clinical biochemistry. Ann N Y Acad Sci. 1984;428:318–332.
  • Arnold DL, Taylor DJ, Radda GK. Investigation of human mitochondrial myopathies by phosphorus magnetic resonance spectroscopy. Ann Neurol. 1985 Aug;18(2):189–196.
  • Meyer RA, Brown TR, Kushmerick MJ. Phosphorus nuclear magnetic resonance of fast- and slow-twitch muscle. Am J Physiol. 1985 Mar;248(3 Pt 1):C279–C287.
  • McCully KK, Argov Z, Boden BP, Brown RL, Bank WJ, Chance B. Detection of muscle injury in humans with 31-P magnetic resonance spectroscopy. Muscle Nerve. 1988 Mar;11(3):212–216.
  • Eleff S, Kennaway NG, Buist NR, Darley-Usmar VM, Capaldi RA, Bank WJ, Chance B. 31P NMR study of improvement in oxidative phosphorylation by vitamins K3 and C in a patient with a defect in electron transport at complex III in skeletal muscle. Proc Natl Acad Sci U S A. 1984 Jun;81(11):3529–3533.
  • Argov Z, Bank WJ, Maris J, Eleff S, Kennaway NG, Olson RE, Chance B. Treatment of mitochondrial myopathy due to complex III deficiency with vitamins K3 and C: A 31P-NMR follow-up study. Ann Neurol. 1986 Jun;19(6):598–602.
  • Gray SD, Staub NC. Resistance to blood flow in leg muscles of dog during tetanic isometric contraction. Am J Physiol. 1967 Sep;213(3):677–682.
  • Gustafsson R, Tata JR, Lindberg O, Ernster L. The relationship between the structure and activity of rat skeletal muscle mitochondria after thyroidectomy and thyroid hormone treatment. J Cell Biol. 1965 Aug;26(2):555–578.
  • Everts ME, van Hardeveld C, Ter Keurs HE, Kassenaar AA. Force development and metabolism in skeletal muscle of euthyroid and hypothyroid rats. Acta Endocrinol (Copenh) 1981 Jun;97(2):221–225.
  • Baldwin KM, Ernst SB, Herrick RE, Hooker AM, Mullin WJ. Exercise capacity and cardiac function in trained and untrained thyroid-deficient rats. J Appl Physiol Respir Environ Exerc Physiol. 1980 Dec;49(6):1022–1026.

9 Exercises to Fight Hypothyroidism

By

Jennifer Larson Was this helpful? (55)

Exercise has several major specific benefits for people with hypothyroidism:

  • It helps you achieve and maintain a healthy weight. A very common side effect of hypothyroidism is weight gain. Many people with hypothyroidism also report feeling tired and sluggish, which makes them less inclined to be physically active. But a sedentary lifestyle also makes you more likely to pack on a few unwanted pounds. Exercise is the solution to that problem.

  • It can help improve your cardiovascular health. Getting regular exercise benefits your heart and your cardiovascular system. People with hypothyroidism need to watch their “bad” cholesterol levels, which can increase their risk of developing heart disease.

  • It improves your mood and energy levels. Remember the fatigue and sluggish feelings that are the unpleasant hallmarks of hypothyroidism? Exercise promotes the production of those feel-good chemicals known as endorphins. Endorphins are neurotransmitters, which means they transmit electrical signals through your body. They can reduce your perception of pain, modulate your appetite and even reduce some of the side effects of stress and anxiety. Ever heard of the “runner’s high”? That’s endorphins at work.

The Centers for Disease Control and Prevention recommend aiming for 150 minutes of moderately intense aerobic exercise or 75 minute of vigorous intensity aerobic exercise each week. Add to your list some strength-training to build and maintain muscle mass at least two days per week.

Lifestyle changes are a big part of treating hypothyroidism, and this group talks about the challenges.

Medical Reviewers: William C. Lloyd III

2019 Healthgrades Operating Company, Inc. The content on Healthgrades does not provide medical advice. Always consult a medical provider for diagnosis and treatment. All rights reserved. May not be reproduced or reprinted without permission from Healthgrades Operating Company, Inc. Use of this information is governed by the Healthgrades User Agreement.

Talk to your doctor and add some of these exercises to your workout routine.

    Aerobic Activities

  1. Walking. No matter how out-of-shape you may claim to be, you can start by walking short distances. Gradually increase your speed and distance over time as you’re able.

  2. Jogging or running. Feel like you’re ready to take things to the next level? Try increasing your pace to a jog. Use an app on your smartphone to help you track your speed and distance.

  3. Biking. Whether you prefer a stationary bike, a mountain bike, or a traditional two-wheeler with a bell, riding a bicycle is great cardiovascular exercise that can put less strain on your knees than jogging or running.

  4. Dancing. Recreation and community centers and dance studios offer a plethora of dance classes for adults. Pick your favorite style and get down!

  5. Swimming. Maybe you like the backstroke, or perhaps the good old-fashioned crawl. Whatever your favorite stroke is, don’t be afraid to get your hair wet. Jump in and swim a few laps, or use a kickboard to work on your legs.

  6. Pushing a lawnmower. Yes, maintaining your yard can help you maintain a healthy body, too. Of course, you do have to walk and push the lawnmower yourself for this to count as exercise—riding mowers are disqualified.

  7. Strength-Building Activities

  8. Lifting weights. Free weights or weight machines, you pick whatever works best for you. Before you try a new activity, check with a trainer to make sure you’re using proper form, so you can avoid injury. Do one set to start with, and work your way up to two or three sets per session.

  9. Using resistance bands. Resistance bands resemble long, heavy-duty rubber bands, and some even come with padded handles. The more you stretch them, the more resistance they offer. You can use them just about anywhere.

  10. Use your own body for resistance. These types of activity have a couple of big advantages—you don’t have to buy any special equipment, nor do you have to go anywhere to do them. You can do push-ups, sit-ups, abdominal crunches, and leg squats in your own home.

If you have a thyroid condition, it’s no secret that exercise and a healthy diet can help manage your symptoms and improve your overall health. But if you have an undiagnosed thyroid condition that is not being properly controlled, there are risks — even to “natural” supplements and exercise.

Cleveland Clinic is a non-profit academic medical center. Advertising on our site helps support our mission. We do not endorse non-Cleveland Clinic products or services. Policy

That’s why it’s so important to talk to your doctor about symptoms like fatigue, weight gain or loss, and trouble sleeping. These common symptoms can have many causes, including a thyroid disorder.

Exercising with either uncontrolled hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid) can be dangerous to your health as these conditions increase or depress people’s metabolism, respectively — speeding up or slowing down their heart rate.

Hyperthyroidism: revved up metabolism

For people with significant hyperthyroidism (commonly caused by the autoimmune disorder Graves’ disease), exercise can “overheat” the body in a dangerous way.

“For someone who has significant clinical hyperthyroidism, it’s as if they are already running a treadmill every day, even in their sleep,” says endocrinologist Christian Nasr, MD. “Excessive exercise can cause a patient to go into heart failure if their thyroid hormones are not under control.”

Hypothyroidism: sluggish metabolism

Patients with significant hypothyroidism (commonly caused by the autoimmune disorder Hashimoto’s disease) should also be cautious. Underactive thyroid causes the heart rate to slow, so a sudden return to exercise can be like a jolt to the heart.

“I advise my patients with hypothyroidism not to exercise for a few weeks until their condition is well-controlled with medications,” says Dr. Nasr.

A safe return to exercise

Once a person with a thyroid disorder returns to normal thyroid function with the use of medications, says Dr. Nasr, a return to exercise is safe and can help improve remaining symptoms.

People with hypothyroidism, for example, often experience fatigue and weight gain that doesn’t always abate with the use of thyroid medications. Exercise can help boost energy levels and control weight.

Be wary of ‘thyroid-friendly’ diets

There’s plenty of misinformation out there about foods and supplements that claim to ease the symptoms of thyroid disorders as well, and Dr. Nasr advises equal caution. For example:

  • Iodine deficiency is a leading cause of hypothyroidism worldwide, but the typical U.S. diet contains plenty of it, says Dr. Nasr. Americans should avoid iodine supplements or daily servings of high-iodine foods like kelp to keep their thyroid in balance.
  • Soy can be a healthy addition to anyone’s diet, “but the question is how much,” says Dr. Nasr. “When you eat a lot of it on a daily basis, it can precipitate hypothyroidism in a person with Hashimoto’s disease.” It may also affect the absorption of thyroid hormone.
  • Selenium is a trace element that limited studies have connected to reducing the inflammation found in those with Hashimoto’s disease and may possibly delay progression into hypothyroidism. Dr. Nasr tells such patients they could try 200 micrograms once or twice a day which can be done naturally by consuming 3-5 Brazil nuts.

When it comes to thyroid conditions, including symptoms and dietary questions, it’s critical to keep your doctor informed and vital to your health.

Hypothyroidism Exercise Plan

Hypothyroidism, or having an underactive thyroid, can cause many symptoms like fatigue, joint pain, heart palpitations, and depression. The condition also reduces overall metabolism, making those with hypothyroidism more prone to weight gain. Exercise can relieve many of the symptoms associated with hypothyroidism and can improve cardiovascular health and muscle mass.

Get Your Heart Pumping

If left untreated, having low levels of thyroid hormones can reduce cardiac fitness. Those with hypothyroidism are also at a greater risk of ventricular arrhythmias, or a rapid heart beat. In addition to medications, exercise also plays a key role in strengthening the cardiovascular system.

Regularly participating in activities like running, walking at a brisk pace, or playing a sport can improve cardiac health. The related mood-boosting benefits can also relieve other hypothyroidism symptoms including depression and fatigue.

Protect Your Joints

Those with hypothyroidism frequently experience muscle and joint pain. Low-impact activities that minimize stress on joints such as the knee, hip, or back may be easier to do as opposed to more strenuous activities. Some options include yoga, Pilates, walking, swimming, and biking.

Build Muscle

Because hypothyroidism lowers your body’s resting metabolic rate, people with this condition are more liable to gain weight and suffer secondary problems caused by obesity. Building muscle through strength training can counteract these effects.

Some research shows that obesity can reduce a person’s response to exercise. These individuals may find it harder to develop skeletal muscle proteins in response to exercise. The reasons for this are unclear, but it’s possible that underlying hormonal deficiencies, including hypothyroidism, may be to blame.

Be Athletic

Having hypothyroidism doesn’t mean you can’t participate in competitive sports or train for a race or marathon. But, a recent study of highly-trained male athletes found that it may be more difficult to do any kind of high-intensity exercises. Athletes may need to adapt their training plans to let their bodies recover from this effect.

Exercise isn’t a substitute for hormone therapy to treat hypothyroidism. Some studies even suggest that in spite of prescribed medication, those with hypothyroidism may experience greater discomfort during exercise. Still, when practiced safely, many forms of exercise offer specific benefits to individuals with hypothyroidism. Always discuss your exercise plan and goals with your doctor before starting a new routine or regimen.

Here’s How Hypothyroidism Affects Exercise—and How to Combat It

More than 20 million Americans struggle with thyroid disorders—and I just so happen to be one of them.

I have an autoimmune disease called Hashimoto’s, which causes my body to attack my thyroid gland. As a result, I also have hypothyroidism (doc talk for an under-active thyroid).

Before I was diagnosed a few years ago, being active was a given. I ran almost every day, hit the gym a few times a week, and went hiking every weekend.

But since my thyroid went wonky, staying active has become much more of an uphill battle. The symptoms that come standard with a hypothyroidism diagnosis—such as brain fog, weakness, muscle pain, and extreme fatigue—aren’t exactly a recipe for an active lifestyle.

Aaptiv have meditation classes to help with brain fog and fatigue. View them in the app today.

I’m going to be honest. There are days when my hypothyroidism definitely makes staying active a challenge.

But it certainly doesn’t make it impossible! There are ways to maintain an active lifestyle even when your thyroid symptoms leave you feeling totally exhausted and depleted.

Here’s what I’ve learned and what experts have to say about working out with hypothyroidism.

Understanding the Thyroid

Before we dive into how to stay active when your thyroid doesn’t want to cooperate, let’s quickly touch base on how the thyroid works.

“The thyroid is a gland that… two main hormones, triiodothyronine (T3) and thyroxine (T4)…which regulate your body’s energy use, along with many other important functions such as breathing, heart rate, central and peripheral nervous systems, body weight, muscle strength, menstrual cycles, body temperature, and cholesterol levels,” says Carolyn Dean, M.D., N.D., medical advisory board member, Nutritional Magnesium Organization.

When your thyroid doesn’t produce enough of those hormones, all those systems in your body can’t function properly.

You can end up feeling totally exhausted as a result. “The reason patients struggle with feeling tired and fatigued when dealing with thyroid disorders is that the thyroid plays a major role in metabolism, heart rate, and body temperature,” says Alissia Zenhausern, N.M.D., of NMD Wellness of Scottsdale.

“When your thyroid is under-active, it slows down your metabolism, heart rate, and ability to regulate your body temperature, which means your body must find other ways to self-regulate these pathways—making your body work harder and leading to you feeling more fatigued and tired.”

How to Stay Active in Spite of Your Hypothyroid Symptoms

Now we know how the thyroid works and why an underactive thyroid can make it harder to stay active. But enough about the problem!

Let’s talk about the solution and how to stay active in spite of those pesky hypothyroid symptoms.

Catch plenty of zzz’s.

Getting enough sleep is important for everyone—but especially for those with thyroid disorders. “ sleep is important to allow the adrenals to rest and recover. This is vital for the thyroid-adrenal conversation,” says Heidi Iratcabal, N.D., D.P.T., C.G.P., I.F.M.C.P., founding partner of Carpathia Collaborative.

“If the body is stressed and adrenals are pumping out cortisol, this will put more pressure on the thyroid.”

Too little sleep can also increase inflammation. This, if your hypothyroid comes courtesy of Hashimoto’s, will definitely make your symptoms worse.

“Research has shown that people who get about six or fewer hours of sleep a night have higher blood levels of inflammatory proteins than those who get more. So lack of sleep increases chronic inflammation and reduces overall health,” Dr. Dean says.

Cut back on the caffeine.

When you’re struggling with thyroid-related low energy, you may be tempted to down a Red Bull or a few cups of coffee to get yourself going (I know I’ve been there!). But caffeine can mess with the way your body absorbs thyroid medication and make your symptoms, including fatigue, worse.

“Caffeine has been shown to block the absorption of thyroid hormone replacement medications,” Dr. Zenhausern says. “If you inhibit absorption, the medication is not able to function properly, which will prevent you from improving your thyroid function.”

A little caffeine is OK, but if you want to have the energy to stay active, don’t go crazy. Stick to one cup of coffee a day.

Give your thyroid what it needs to function through diet…

You can’t cure your thyroid through diet, but you can definitely make some major improvements. By giving your body the foods it needs to support proper thyroid function, you can keep your symptoms in check and have more energy to stay active as a result.

“Diet has a huge impact on thyroid function and hormone production,” Dr. Iratcabal says. “The foods that provide the greatest amount of energy are healthy fats and proteins, such as olive oil, avocados and avocado oil, fatty fish, nuts, seeds, and pasture-raised animals.”

If you have Hashimoto’s, stay away from gluten. “Gluten can cause unnecessary inflammation and can worsen the symptoms of Hashimoto’s disease,” Dr. Zenhausern notes.

…and the right supplements.

“In my experience, most low thyroid conditions are caused by mineral deficiency,” Dr. Dean says.

“There are nine minerals necessary for the creation, conversion, activation, and transport of thyroid hormones: iodine, selenium, zinc, molybdenum, boron, copper, chromium, manganese, and magnesium.”

It’s possible to get some of these must-have minerals through your diet. “Brazil nuts, sardines, and salmon are rich sources of selenium, while sesame seeds, pumpkin seeds, and lentils are rich in zinc,” Dr. Iratcabal says.

However, the best way to get all the minerals you need to support your thyroid (and in the proper doses) is through supplements.

Incorporating the right supplements into your routine can help manage your hypothyroid symptoms. As a result, it’ll be easier to maintain an active lifestyle.

Keep your workouts short and sweet.

When I’m feeling super exhausted (thanks, lazy thyroid!), the thought of a long, strenuous workout could not be any less appealing.

Luckily, you don’t have to subject yourself to long, strenuous workouts in order to stay active. Keeping your workouts short and sweet can help you find the motivation to get up and go, even when you’re feeling depleted. Plus, exercise could be just what you need to boost your energy.

Try Aaptiv’s quick HIIT workouts (or other classes) to keep your workouts short, but impactful.

If you’re struggling to find the energy to work out, commit to five minutes. Chances are, once you’ve started, you’ll find the energy for a longer workout. But, if not, five minutes is better than zero minutes.

Dr. Iratcabal recommends high-intensity interval training to get the most bang for your buck. “ will activate the adrenals and the hippocampus to produce more acetylcholine (the ‘focus’ neurotransmitter) and dopamine (the ‘get-up-and-go’ neurotransmitter),” she says.

You can stay active.

I’ll be honest. Dealing with an underactive thyroid can be a drag, and I’ve had to make more of an effort to stay active since I was diagnosed with a thyroid disorder. But while dealing with an underactive thyroid can be a drag, it doesn’t have to keep you from living an active lifestyle!

(Side note: If you’re struggling with an underactive thyroid, it’s important to talk to a medical professional. Without the right treatment and medication, your hypothyroidism symptoms are pretty much guaranteed to get worse—so do yourself a favor and get to the doctor, stat.)

A New You In 30 Days. Introducing Aaptiv “Coach” – Click the image below to learn more.

What Type of Workout Should I Do?

If your condition is well controlled, you should be able to do the same physical activity as someone without a thyroid disorder, says John C. Morris, MD, professor of medicine and endocrinology at the Mayo Clinic College of Medicine.

But if you’re just starting an exercise plan or if you’re still dealing with symptoms, low-impact aerobic exercise and strengthening moves are best.

“Low-impact exercise doesn’t apply as much pressure,” says Norma Lopez, MD, an associate professor of endocrinology and metabolism at Loyola University Medical Center. “That’s key, since hypothyroidism can cause pain and swelling in your muscles and joints.”

Try these activities:

Walking: One of the easiest workouts to do. All you need is a pair of comfortable shoes. It gets your heart pumping and burns about 280 calories an hour.

Water aerobics: If you have swelling in your ankles or feet, some exercises may be painful. Water aerobics is a good option. The water holds you up and lowers the impact on your joints.

Yoga: This can stretch and strengthen your muscles. It also helps you focus on breathing. One study found that people with hypothyroidism had better lung strength after practicing yoga breathing for 6 months.

Tai chi: Described as “moving meditation,” this slow-motion form of martial arts is a proven stress-buster. Research shows it can help improve strength, balance, and mood.

Strength training: Whether you lift weights or use your body weight, building muscle helps you burn more calories — even when you’re sitting still. And that can help you shed extra pounds. Strong muscles also help ease pressure on your joints.

30 Oct Hypothyroidism – What is it & can being active help?

Posted at 09:14h in Weight Loss by Exercise Right

The term “underactive metabolism” is thrown around a lot, and is often blamed for difficulty losing weight. So, what does it actually mean? A slow or underactive metabolism is simply the result of hypothyroidism.

Hypothyroidism occurs when the thyroid gland fails to produce the necessary amount of the hormone thyroxine. This can be due to an iodine deficiency, autoimmune conditions such as Hashimoto’s, or many other reasons. The thyroid gland is found in your throat, and is made up of a left and a right half. The thyroid may be small, but it can have a big impact when it misfunctions!

How do I know if I have hypothyroidism?

Symptoms of hypothyroidism include, but are not limited to:

  • Unexplained weight gain, or difficulty losing weight
  • Fatigue or low energy levels
  • Depression
  • Issues with concentration
  • Hair loss
  • Always feeling cold, or increased sensitivity to cold environments
  • Aching muscles or feeling weak

If you think you may have undiagnosed hypothyroidism it’s important to see your GP. They will organise any required tests and assist in management.

How does exercise help with hypothyroidism?

Exercise has so many fantastic benefits to help manage hypothyroidism. When you exercise a rush of feel-good hormones are released. This helps to improve mood, alleviate feelings of depression, and increase your self-esteem. Regular exercise reduces feelings of fatigue and improves sleep quality, which results in increased energy levels. Incorporating resistance training in to your exercise program can reduce joint pain and stiffness and improve muscle strength. It also enable your muscles to burn more energy to repair and recover afterwards. This assists with weight management, as your body burns more energy both while you’re exercising and resting.

What type of exercise is best?

It’s important to do a mix of cardiovascular and strength training exercises. The Department of Health recommends adults do a minimum of 150 minutes per week of moderate to vigorous physical activity. This recommendation increases to 300 minutes per week for those looking to manage their weight. Some good activities to begin with include walking, swimming, and beginner gym classes.

Where to from here?

Contact your local Accredited Exercise Physiologist (AEP) to have an individualised exercise program designed specific to your needs. They will consider any other medical conditions or injuries you may have. See your GP prior to starting an exercise program if you’re currently inactive or have any pre-existing cardiac, respiratory or other major health conditions.

To find an AEP near you, .

A recent study published in Heart and Vessels provides further insight into the topic of aerobic exercise and its effect on subclinical hypothyroidism. This study compared patients with untreated subclinical hypothyroidism (n = 53, age 65 ± 12 years) with euthyroid patients (n = 55, age 64 ± 10 years). Exercise performance was measured by a ramp-cycle ergometer test. Arterial stiffness (cardio-ankle vascular index ) was measured at baseline and 5 minutes after exercise. Subjects’ blood samples were collected for serum thyroid-stimulating hormone (TSH) and free thyroxine measurements before and 5 minutes after exercise.
At the end of the study, the CAVI and serum TSH levels significantly decreased after exercise in the subclinical-hypothyroidism group (CAVI: 8.1 ± 1.6 vs. 8.5 ± 1.5, P <.001; TSH: 6.7 ± 1.4 vs. 7.6 ± 1.2 mIU/mL, P <.001) and euthyroid group (CAVI: 7.6 ± 1.0 vs. 8.3 ± 0.9, P <.001; TSH: 2.2 ± 1.1 vs. 2.4 ± 1.2 mIU/mL, P = .005). The changes in CAVI from baseline compared with those after exercise were lower, in absolute values, in the subclinical hypothyroidism group than in the euthyroid group (subclinical hypothyroidism group vs. euthyroid group; Delta-CAVI: –0.4 ± 0.6 vs. –0.7 ± 0.7, P = .012).
The changes in serum TSH from baseline to after exercise were higher, in absolute values, in the subclinical-hypothyroidism group than in the euthyroid group (subclinical hypothyroidism group vs. euthyroid group; Delta serum TSH: -1.3 ± 1.4 vs. –0.3 ± 0.5, P <.001). The changes in CAVI from baseline to after exercise were negatively correlated with changes in TSH (r = –0.32, P = .038) in the subclinical-hypothyroidism group.
The authors concluded that acute aerobic exercise decreased both arterial stiffness and serum TSH levels in patients with subclinical hypothyroidism and in euthyroid subjects. While the absolute change in arterial stiffness decreased, the absolute change in serum TSH levels increased in patients with subclinical hypothyroidism compared with euthyroid subjects. These findings suggest that subclinical hypothyroidism reduces CAVI during acute aerobic exercise. Further, changes in absolute levels of serum TSH in subclinical hypothyroidism may result in reduced CAVI improvement by acute aerobic exercise.

About the author

Leave a Reply

Your email address will not be published. Required fields are marked *