Exercise capacity and cardiac function in trained and untrained thyroid-deficient rats

Area of Science:

• Exercise physiology
• Endocrinology
• Cardiovascular science

Background:

• Thyroid hormones are crucial for regulating metabolism and cardiac function.
• Thyroid deficiency (TD) is known to impair oxidative capacity and cardiac performance.
• The potential for exercise to reverse these impairments requires further investigation.

Purpose of the Study:

• To determine if physical training can reverse impairments in skeletal muscle oxidative capacity, cardiac function, and maximal oxygen consumption (VO2 max) in thyroid-deficient rats.
• To investigate the effects of an 8-week running program on these physiological parameters in TD female rats.

Main Methods:

• Thyroid deficiency was induced in female rats.
• One group of TD rats underwent an 8-week physical training program (running).
• Measurements included VO2 max, skeletal muscle homogenate respiratory capacity, cardiac myosin ATPase activity, and in situ ventricular contractility (dP/dt max).

Main Results:

• Thyroid deficiency significantly reduced VO2 max, skeletal muscle oxidative capacity, cardiac myosin ATPase, and ventricular dP/dt max compared to normal controls.
• Physical training normalized VO2 max and skeletal muscle oxidative capacity in TD rats.
• Cardiac myosin ATPase, Ca2+ regulation, and ventricular contractility were not improved by training in TD rats.
• The heart weight-to-body weight ratio was highest in the trained TD group.

Conclusions:

• Physical training can effectively restore maximal oxygen utilization and skeletal muscle oxidative capacity in thyroid deficiency.
• However, training does not reverse the intrinsic impairments in cardiac contractile function caused by thyroid deficiency.
• The adaptive cardiac remodeling (increased heart weight-to-body weight ratio) suggests a compensatory response to training in the hypothyroid state.