Robert H Fitts
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Explore the profile of Robert H Fitts including associated specialties, affiliations and a list of published articles.
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26
Citations
722
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Recent Articles
1.
Sundberg C, Teigen L, Hunter S, Fitts R
J Physiol
. 2024 Nov;
603(1):187-209.
PMID: 39545875
The cellular causes of the age-related loss in power output and increased fatigability are unresolved. We previously observed that the depressive effects of hydrogen (H) (pH 6.2) and inorganic phosphate...
2.
Fitts R, Wang X, Kwok W, Camara A
Int J Sports Med
. 2024 Apr;
45(11):791-803.
PMID: 38648799
Cardiovascular disease is a leading cause of morbidity and mortality, and exercise-training (TRN) is known to reduce risk factors and protect the heart from ischemia and reperfusion injury. Though the...
3.
Thareja S, Anfinson M, Cavanaugh M, Kim M, Lamberton P, Radandt J, et al.
Am J Physiol Heart Circ Physiol
. 2023 May;
325(1):H149-H162.
PMID: 37204873
Patients with two congenital heart diseases (CHDs), Ebstein's anomaly (EA) and left ventricular noncompaction (LVNC), suffer higher morbidity than either CHD alone. The genetic etiology and pathogenesis of combined EA/LVNC...
4.
Anfinson M, Fitts R, Lough J, James J, Simpson P, Handler S, et al.
J Cardiovasc Dev Dis
. 2022 May;
9(5).
PMID: 35621855
Hypoplastic left heart syndrome (HLHS) is a severe congenital heart disease (CHD) with complex genetic inheritance. HLHS segregates with other left ventricular outflow tract (LVOT) malformations in families, and can...
5.
Kim M, Fleres B, Lovett J, Anfinson M, Samudrala S, Kelly L, et al.
Front Cell Dev Biol
. 2020 Jul;
8:440.
PMID: 32656206
Hypoplastic left heart syndrome (HLHS) is a clinically and anatomically severe form of congenital heart disease; however, its etiology remains largely unknown. We previously demonstrated that genetic variants in the...
6.
Teigen L, Sundberg C, Kelly L, Hunter S, Fitts R
Am J Physiol Cell Physiol
. 2020 Apr;
318(6):C1238-C1251.
PMID: 32348175
Age-induced declines in skeletal muscle contractile function have been attributed to multiple cellular factors, including lower peak force (P), decreased Ca sensitivity, and reduced shortening velocity (V). However, changes in...
7.
Wang X, Fitts R
J Appl Physiol (1985)
. 2020 Apr;
128(5):1177-1185.
PMID: 32240024
Exercise training is known to prolong the ventricular cardiomyocyte action potential duration (APD), increasing Ca influx and contractility. The prolonged APD is caused, in part, by a decreased responsiveness to...
8.
Sundberg C, Fitts R
Curr Opin Physiol
. 2019 Jul;
10:118-127.
PMID: 31342000
Energetic demand from high-intensity exercise can easily exceed ATP synthesis rates of mitochondria leading to a reliance on anaerobic metabolism. The reliance on anaerobic metabolism results in the accumulation of...
9.
Sundberg C, Prost R, Fitts R, Hunter S
J Physiol
. 2019 Apr;
597(19):4943-4957.
PMID: 31018011
Key Points: The mechanisms for the age-related increase in fatigability during dynamic exercise remain elusive. We tested whether age-related impairments in muscle oxidative capacity would result in a greater accumulation...
10.
Wang X, Fitts R
Am J Physiol Heart Circ Physiol
. 2018 Aug;
315(4):H885-H896.
PMID: 30074836
Exercise training is known to protect the heart from ischemia and improve function during exercise by reducing cardiomyocyte action potential duration (APD) and increasing contractility. The cellular mechanisms involve β-adrenergic...