A Study of Changes of Physical Functions According to Changes in Cognitive Functions in Community-Dwelling Elderly People Who Participated in an Exercise Program.

Although it is known that physical function differs depending on the state of cognitive function, there are no studies that consider changes in cognitive functions when evaluating physical functions of participants before and after an exercise program. In this study, it was observed changes in cognitive function and physical functions of elderly people who participated in a community-based exercise program for 6 months, and examined changes in physical functions that took into account changes in cognitive functions. Forty-nine participants, whose cognitive and physical functions were both measured before and after the exercise program, were included in the analysis. The Japanese version of the Montreal Cognitive Assessment (MoCA-J) was used to assess participants' cognitive function and to determine whether they had mild cognitive impairment (MCI). To assess physical functions, a battery of physical tests was completed. Participants were classified into four groups (before/after; non-MCI/non-MCI, MCI/MCI, non-MCI/MCI, and MCI/non-MCI) according to the changes in cognitive functions after six months. There was no significant difference in the physical functions of the four groups before the start of the program. When changes in physical functions were examined in each group, some changes in physical functions were observed in the groups other than the non-MCI/MCI group. However, there was no significant difference in the physical functions between the four groups after the program. It was suggested that changes in physical functions of elderly people who participated in a community-based exercise program over a 6-month period were not different due to changes in cognitive functions.

Brain and muscle adaptation to high-fat diets and exercise: Metabolic transporters, enzymes and substrates in the rat cortex and muscle.

There is evidence suggesting that the effects of diet and physical activity on physical and mental well-being are the result of altered metabolic profiles. Though the central and peripheral systems work in tandem, the interactions between peripheral and central changes that lead to these altered states of well-being remains elusive. We measured changes in the metabolic profile of brain (cortex) and muscle (soleus and plantaris) tissue in rats following 5-weeks of treadmill exercise and/or a high-fat diet to evaluate peripheral and central interactions as well as identify any common adaptive mechanisms. To characterize changes in metabolic profiles, we measured relative changes in key metabolic enzymes (COX IV, hexokinase, LDHB, PFK), substrates (BHB, FFA, glucose, lactate, insulin, glycogen, BDNF) and transporters (MCT1, MCT2, MCT4, GLUT1, GLUT3). In the cortex, there was an increase in MCT1 and a decrease in glycogen following the high-fat diet, suggesting an increased reliance on monocarboxylates. Muscle changes were dependent muscle type. Within the plantaris, a high-fat diet increased the oxidative capacity of the muscle likely supported by increased glycolysis, whereas exercise increased the oxidative capacity of the muscle likely supported via increased glycogen synthesis. There was no effect of diet on soleus measurements, but exercise increased its oxidative capacity likely fueled by endogenous and exogenous monocarboxylates. For both the plantaris and soleus, combining exercise training and high-fat diet mediated results, resulting in a middling effect. Together, these results indicate the variable adaptions of two main metabolic pathways: glycolysis and oxidative phosphorylation. The results also suggest a dynamic relationship between the brain and body.

Acute exercise increases brain region-specific expression of MCT1, MCT2, MCT4, GLUT1, and COX IV proteins.

The brain is capable of oxidizing lactate and ketone bodies through monocarboxylate transporters (MCTs). We examined the protein expression of MCT1, MCT2, MCT4, glucose transporter 1 (GLUT1), and cytochrome-c oxidase subunit IV (COX IV) in the rat brain within 24 h after a single exercise session. Brain samples were obtained from sedentary controls and treadmill-exercised rats (20 m/min, 8% grade). Acute exercise resulted in an increase in lactate in the cortex, hippocampus, and hypothalamus, but not the brainstem, and an increase in ß-hydroxybutyrate in the cortex alone. After a 2-h exercise session MCT1 increased in the cortex and hippocampus 5 h postexercise, and the effect lasted in the cortex for 24 h postexercise. MCT2 increased in the cortex and hypothalamus 5-24 h postexercise, whereas MCT2 increased in the hippocampus immediately after exercise, and remained elevated for 10 h postexercise. Regional upregulation of MCT2 after exercise was associated with increases in brain-derived neurotrophic factor and tyrosine-related kinase B proteins, but not insulin-like growth factor 1. MCT4 increased 5-10 h postexercise only in the hypothalamus, and was associated with increased hypoxia-inducible factor-1α expression. However, none of the MCT isoforms in the brainstem was affected by exercise. Whereas GLUT 1 in the cortex increased only at 18 h postexercise, COX IV in the hippocampus increased 10 h after exercise and remained elevated for 24 h postexercise. These results suggest that acute prolonged exercise induces the brain region-specific upregulation of MCT1, MCT2, MCT4, GLUT1, and COX IV proteins.

Possible involvement of AMPK in acute exercise-induced expression of monocarboxylate transporters MCT1 and MCT4 mRNA in fast-twitch skeletal muscle.

OBJECTIVE: The regulatory mechanisms responsible for acute exercise-induced expression of monocarboxylate transporters MCT1 and MCT4 mRNA in skeletal muscle remain unclear. 5'-adenosine-activated protein kinase (AMPK) is a key signaling molecule that regulates gene expression at the mRNA level. We examined whether AMPK activation is involved in acute exercise-induced expression of MCT1 and MCT4 mRNA in fast-twitch muscle. MATERIALS/METHODS: Male Sprague-Dawley rats were subjected to an acute bout of either 5min high-intensity intermittent swimming (HIS) or 6-h low-intensity prolonged swimming (LIS). The effects of acute exercise on the phosphorylation of AMPK (p-AMPK), calcium/calmodulin pendent kinase II (p-CaMKII), p38 mitogen-activated protein kinase (p-p38MAPK), and MCTs mRNA were analyzed in vivo. To observe the direct effects of AMPK activation on MCTs mRNA, the effects of 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR), caffeine, and dantrolene were analyzed in vitro using an isolated muscle incubation model. RESULTS: The p-AMPK increased in response to both HIS and LIS, although the p-CaMKII and p-p38MAPK were increased only following HIS. Irrespective of exercise intensity, MCT1 and MCT4 mRNA was also transiently upregulated by both HIS and LIS. Direct exposure of the epitrochlearis muscle to 0.5mmol/L AICAR or 1mmol/L caffeine, which activated p-AMPK increased both MCT1 and MCT4 mRNA levels. When pAMPK was inhibited by dantrolene, neither MCT1 nor MCT4 mRNA was increased. CONCLUSION: These results suggest that acute exercise-induced increases in MCT1 and MCT4 mRNA expression may be possibly mediated by AMPK activation, at least in part in fast-twitch muscle.