scholarly journals Cerebral Vasomotor Reactivity during Hypo- and Hypercapnia in Sedentary Elderly and Masters Athletes

2013 ◽  
Vol 33 (8) ◽  
pp. 1190-1196 ◽  
Author(s):  
Yong-Sheng Zhu ◽  
Takashi Tarumi ◽  
Benjamin Y Tseng ◽  
Dean M Palmer ◽  
Benjamin D Levine ◽  
...  

Physical activity may influence cerebrovascular function. The objective of this study was to determine the impact of life-long aerobic exercise training on cerebral vasomotor reactivity (CVMR) to changes in end-tidal CO2 (EtCO2) in older adults. Eleven sedentary young (SY, 27 ± 5 years), 10 sedentary elderly (SE, 72 ± 4 years), and 11 Masters athletes (MA, 72 ± 6 years) underwent the measurements of cerebral blood flow velocity (CBFV), arterial blood pressure, and EtCO2 during hypocapnic hyperventilation and hypercapnic rebreathing. Baseline CBFV was lower in SE and MA than in SY while no difference was observed between SE and MA. During hypocapnia, CVMR was lower in SE and MA compared with SY (1.87 ± 0.42 and 1.47 ± 0.21 vs. 2.18 ± 0.28 CBFV%/mm Hg, P < 0.05) while being lowest in MA among all groups ( P < 0.05). In response to hypercapnia, SE and MA exhibited greater CVMR than SY (6.00 ± 0.94 and 6.67 ± 1.09 vs. 3.70 ± 1.08 CBFV1%/mm Hg, P < 0.05) while no difference was observed between SE and MA. A negative linear correlation between hypo- and hypercapnic CVMR ( R2 = 0.37, P < 0.001) was observed across all groups. Advanced age was associated with lower resting CBFV and lower hypocapnic but greater hypercapnic CVMR. However, life-long aerobic exercise training appears to have minimal effects on these age-related differences in cerebral hemodynamics.

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1916-P
Author(s):  
REBECCA L. SCALZO ◽  
GRAHAME F. EVANS ◽  
SARA E. HULL ◽  
LESLIE KNAUB ◽  
LORI A. WALKER ◽  
...  

Circulation ◽  
1999 ◽  
Vol 100 (10) ◽  
pp. 1085-1094 ◽  
Author(s):  
Polly A. Beere ◽  
Stuart D. Russell ◽  
Miriam C. Morey ◽  
Dalane W. Kitzman ◽  
Michael B. Higginbotham

2016 ◽  
Vol 173 (1-2) ◽  
pp. 116-117 ◽  
Author(s):  
Hilary F. Armstrong ◽  
Matthew N. Bartels ◽  
Orest Paslavski ◽  
Darnell Cain ◽  
Hannah A. Shoval ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 533-533
Author(s):  
Tyler Marx ◽  
Anastasiia Vasileva ◽  
Stephen Hutchison ◽  
Jennifer Stern

Abstract Aerobic exercise training is a potent intervention for the treatment and prevention of age-related disease, such as heart disease, obesity, and Type 2 Diabetes. Insulin resistance, a hallmark of Type 2 Diabetes, is reversed in response to aerobic exercise training. However, the effect of aerobic exercise training on glucagon sensitivity is unclear. Glucagon signaling at the liver promotes fatty acid oxidation, inhibits De novo lipogenesis, and activates AMP Kinase, a key mediator of healthy aging. Like humans, aging in mice age leads to a decline in physical and metabolic function. To understand the role of glucagon signaling in exercise-induced improvements in physical and metabolic function in the mouse, we implemented a 16-week aerobic exercise training protocol in young and aged mice. 16 weeks of exercise training initiated at 6 months of age increased markers of physical function (P&lt;0.01) and attenuated age-related weight gain (P&lt;0.05) and fat mass (P&lt;0.0001). Additionally, exercise training improved glucose clearance (P&lt;0.01), enhanced glucose-stimulated insulin secretion (P&lt;0.01) and decreased hepatic lipid accumulation (P&lt;0.05). Importantly, exercise training decreased hypoglycemia stimulated glucagon secretion (P&lt;0.01), with no effect on hepatic glucagon receptor mRNA expression or serum glucagon. Thus, we propose that aerobic exercise training enhances glucagon sensitivity at the liver, implicating glucagon as a potential mediator of exercise-induced improvements in aging. Studies initiating the same aerobic exercise training intervention at 18 months of age in the mouse are currently underway to establish the role of glucagon receptor signaling in exercise-induced improvements in aging.


2012 ◽  
Vol 18 (5) ◽  
pp. CR290-CR295 ◽  
Author(s):  
Nikolaos P.E. Kadoglou ◽  
Ioannis S. Vrabas ◽  
Alkistis Kapelouzou ◽  
Stilianos Lampropoulos ◽  
Nikolaos Sailer ◽  
...  

Cancers ◽  
2021 ◽  
Vol 14 (1) ◽  
pp. 28
Author(s):  
Marcelo G. Pereira ◽  
Vanessa A. Voltarelli ◽  
Gabriel C. Tobias ◽  
Lara de Souza ◽  
Gabriela S. Borges ◽  
...  

Cancer cachexia is a multifactorial and devastating syndrome characterized by severe skeletal muscle mass loss and dysfunction. As cachexia still has neither a cure nor an effective treatment, better understanding of skeletal muscle plasticity in the context of cancer is of great importance. Although aerobic exercise training (AET) has been shown as an important complementary therapy for chronic diseases and associated comorbidities, the impact of AET on skeletal muscle mass maintenance during cancer progression has not been well documented yet. Here, we show that previous AET induced a protective mechanism against tumor-induced muscle wasting by modulating the Akt/mTORC1 signaling and eukaryotic initiation factors, specifically eIF2-α. Thereafter, it was determined whether the in vivo Akt activation would induce a hypertrophic profile in cachectic muscles. As observed for the first time, Akt-induced hypertrophy was able and sufficient to either prevent or revert cancer cachexia by modulating both Akt/mTORC1 pathway and the eIF-2α activation, and induced a better muscle functionality. These findings provide evidence that skeletal muscle tissue still preserves hypertrophic potential to be stimulated by either AET or gene therapy to counteract cancer cachexia.


Author(s):  
Tsubasa Tomoto ◽  
Takashi Tarumi ◽  
Jason N. Chen ◽  
Linda S. Hynan ◽  
C. Munro Cullum ◽  
...  

The purpose of this study was to test the hypothesis that changes in cerebral vasomotor reactivity (CVMR) after one-year aerobic exercise training (AET) are associated with cognitive performances in individuals with amnestic mild cognitive impairment (MCI). Seventy sedentary patients with amnestic MCI were randomized to one-year moderate to vigorous intensity AET or stretching and toning (SAT) interventions. Cerebral blood flow velocity (CBFV) with transcranial Doppler, mean arterial pressure (MAP) with finapres plethysmograph, and EtCO2 with capnography were measured during hyperventilation (hypocapnia) and a modified rebreathing protocol (hypercapnia) to assess CVMR. Cerebrovascular conductance index (CVCi) was calculated by CBFV/MAP, and CVMR by ΔCBFV/ΔEtCO2 and ΔCVCi/ΔEtCO2. Episodic memory and executive function were assessed using standard neuropsychological tests (CVLT-II and D-KEFS). Cardiorespiratory fitness was assessed by peak oxygen uptake (VO2peak). A total of 37 patients (19 in SAT and 18 in AET) completed one-year interventions and CVMR assessments. AET improved VO2peak, increased hypocapnic CVMR, but decreased hypercapnic CVMR. AET effects on cognitive performance were minimal when compared with SAT. Across both groups, there was a negative correlation between changes in hypo- and hypercapnic CVMRs in CBFV% and CVCi% (r = -0.741, r = -0.725, p < 0.001). Attenuated hypercapnic CVMR, but not increased hypocapnic CVRM, was associated with improved cognitive test scores in the AET group. In conclusion, one-year AET increased hypocapnic CVMR and attenuated hypercapnic CVMR which is associated cognitive performance in patients with amnestic MCI.


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