The hypothalamus plays a key role in the central control of energy balance and glucose homeostasis (; ). In particular, the ventral medial nucleus of the hypothalamus (VMH) and the orphan nuclear receptor, steroidogenic factor-1 (SF-1; official gene name Nr5a1) are critical for the regulation of metabolism (; ; ). Within the brain, SF-1 is expressed within the VMH and several studies have demonstrated that SF-1-expressing neurons (SF-1 neurons), and SF-1 itself, are required for adaptive responses to metabolic challenges that occur with high-fat diet (HFD) feeding (). VMH-specific deletions of SF-1 and other genes such as Sirt1, Slc17a6, and Esr1 blunt the adaptive thermogenic response to HFD (; ; ; ). Interestingly, these deletions had modest effects in chow-fed mice (). These data suggest that SF-1 in the VMH may regulate a transcriptional program required for responding to metabolic challenges such as HFD-feeding. Exercise is a robust metabolic challenge. We therefore postulated that SF-1 expression in the VMH may also be essential for mediating the beneficial effects of exercise on metabolism. To test our hypothesis, we produced mice with VMH-specific deletions of SF-1 and assessed several metabolic parameters following exercise training.
Exercise has numerous beneficial metabolic effects. The central nervous system (CNS) is critical for regulating energy balance and coordinating whole body metabolism. However, a role for the CNS in the regulation of metabolism in the context of the exercise remains less clear. Here, using genetically engineered mice we assessed the requirement of steroidogenic factor-1 (SF-1) expression in neurons of the ventromedial hypothalamic nucleus (VMH) in mediating the beneficial effects of exercise on metabolism. We found that VMH-specific deletion of SF-1 blunts (a) the reductions in fat mass, (b) improvements in glycemia, and (c) increases in energy expenditure that are associated with exercise training. Unexpectedly, we found that SF-1 deletion in the VMH attenuates metabolic responses of skeletal muscle to exercise, including induction of PGC-1α expression. Collectively, this evidence suggests that SF-1 expression in VMH neurons is required for the beneficial effects of exercise on metabolism.
Here’s the good news. Exercise increases metabolic flexibility in people who are overweight or obese by restoring the ability to burn fat as fuel, assuming you exercise consistently. That’s partially because exercise improves insulin sensitivity. Insulin can be a factor when your body tries to switch energy systems to be more adaptable. When your insulin level is high, your body has a hard time using fat as fuel.
It is true that people burn more calories during aerobics than . However, weight training increases post-exercise metabolism better than aerobics. Also, unlike aerobics, weight training has no effect on the amount of physical activity that people do after the workout. People compensate for aerobic workouts by doing less activity during the rest of the day. Weight training has no effect on 24-hour physical activity.