Green tea extract attenuates muscle loss and improves muscle function during disuse, but fails to improve muscle recovery following unloading in aged rats

Abstract

In this study we tested the hypothesis that green tea extract (GTE) would improve muscle recovery after reloading following disuse. Aged (32 mo) Fischer 344 Brown Norway rats were randomly assigned to receive either 14 days of hindlimb suspension (HLS) or 14 days of HLS followed by normal ambulatory function for 14 days (recovery). Additional animals served as cage controls. The rats were given GTE (50 mg/kg body wt) or water (vehicle) by gavage 7 days before and throughout the experimental periods. Compared with vehicle treatment, GTE significantly attenuated the loss of hindlimb plantaris muscle mass (-24.8% vs. -10.7%, P < 0.05) and tetanic force (-43.7% vs. -25.9%, P <0.05) during HLS. Although GTE failed to further improve recovery of muscle function or mass compared with vehicle treatment, animals given green tea via gavage maintained the lower losses of muscle mass that were found during HLS (-25.2% vs. -16.0%, P < 0.05) and force (-45.7 vs. -34.4%, P < 0.05) after the reloading periods. In addition, compared with vehicle treatment, GTE attenuated muscle fiber cross-sectional area loss in both plantaris (-39.9% vs. -23.9%, P < 0.05) and soleus (-37.2% vs. -17.6%) muscles after HLS. This green tea-induced difference was not transient but was maintained over the reloading period for plantaris (-45.6% vs. -21.5%, P <0.05) and soleus muscle fiber cross-sectional area (-38.7% vs. -10.9%, P <0.05). GTE increased satellite cell proliferation and differentiation in plantaris and soleus muscles during recovery from HLS compared with vehicle-treated muscles and decreased oxidative stress and abundance of the Bcl-2-associated X protein (Bax), yet this did not further improve muscle recovery in reloaded muscles. These data suggest that muscle recovery following disuse in aging is complex. Although satellite cell proliferation and differentiation are critical for muscle repair to occur, green tea-induced changes in satellite cell number is by itself insufficient to improve muscle recovery following a period of atrophy in old rats.

Dietary resveratrol confers apoptotic resistance to oxidative stress in myoblasts

“…Immunodetection was performed using established methods as described previously [3,15]. Protein concentrations of samples were determined by the Lowry method, and the purity of each fraction was confirmed as reported previously [62].…”

Mitochondria Initiate and Regulate Sarcopenia

“…Apoptosis signaling has been reported in muscle and neuronal cells of aged rodents (4, 7, 26, 34, 47, 77, 88, 130), and humans (44, 145). Aging-associated muscle denervation may also contribute to increased mPTP opening, that in turn induces apoptosis and muscle loss (76, 133).…”

“…We know that exercise downregulates apoptosis and upregulates mitophagy (4, 52, 128, 146). Nevertheless, future studies should explore the mechanisms by which exercise activates mitophagic, and attenuates apoptotic, and necrotic signaling pathways in muscle cells and motor neurons of older individuals (4, 47).…”

“…Nevertheless, future studies should explore the mechanisms by which exercise activates mitophagic, and attenuates apoptotic, and necrotic signaling pathways in muscle cells and motor neurons of older individuals (4, 47). We recognize that increased apoptosis and reduced mitophagy have not been identified as an aging-related condition in every study, but in our view, there is sufficient data to suggest that this is probably an underlying process for most cells in aging.…”

“…It will also be important to find out if it is possible to reverse the process responsible for regional disassembly in the absence of mitochondrial biogenesis, and then to focus on molecular events and targets in muscle and motor neurons that are upstream of this point. In the quest to attenuate sarcopenia, it will also be important to understand the limit for mitochondrial health to impact satellite cell function for repairing and replacing sections of fibers or whole fibers, as satellite cells are affected adversely by aging, mitochondrial damage and death signaling (4, 6, 7, 144). …”