Bee products probably reduced ROS production via regulation of the activity of mitochondrial enzymes. Royal jelly increased the maximal activity of citrate synthase (CS) and β-hydroxyacyl coenzyme A dehydrogenase (β-HAD) in the soleus muscle of rats on endurance training [106]. Bee pollen restored mitochondrial complex-I, -II, -III, and -IV enzyme activity to normal, increased SOD and glutathione, and reduced MDA, NO, and total protein content in the gastrocnemius muscle of rats on exhaustive exercise [90]. It also increased the activity of CS and complex IV in malnourished old rats via a mechanism that involved activation of mTOR [36]. mTOR is a major signaling pathway that regulates various signaling cascades involved in metabolism and autophagy such nuclear respiratory factor 2 (NRF2) [2]. Therefore, it is possible that the antioxidant activity demonstrated by bee products, particularly that expressed in the mitochondria, is associated with their metabolic and hypoglycemic activities. For instance, 10-HDA increased expression of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in skeletal muscle of diabetic mice [112,119]. Similarly, aged mice treated with amino acids similar to those found in royal jelly demonstrated improved size of muscle fiber by increasing PGC-1α mRNA levels. PGC-1α functions as a key regulator of sirtuin 1, which limits ROS production through stimulation of mitochondrial biogenesis and ROS defense system, thus protecting metabolically active tissues against oxidative damage [120]. Mechanistically, when PGC-1α gets activated, it interacts with other bioactive molecules such as muscle-specific transcription factors to stimulate the expression of genes that induce mitochondrial oxidative metabolism in brown fat and fiber-type switching in skeletal muscle [121].