Journal of Applied Physiology (J APPL PHYSIOL)

Publisher: American Physiological Society (1887- ), American Physiological Society

Journal description

The Journal of Applied Physiology publishes original papers that deal with diverse areas of research in applied physiology, especially those emphasizing adaptive and integrative mechanisms. Adaptive physiology includes 1) inherent adaptations such as those related to development, aging, and pathophysiological conditions and 2) adaptations to the external environment such as those occurring with exercise, microgravity, hypoxia, hypo- and hyperbaria, and hypo- and hyperthermic conditions. Integrative physiology includes 1) horizontal integration across organ systems and 2) vertical integration from molecule to cell to organ. In all areas of applied physiology, the use of cutting-edge techniques including molecular and cellular biology is strongly encouraged.

Current impact factor: 3.06

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.056
2013 Impact Factor 3.434
2012 Impact Factor 3.484
2011 Impact Factor 3.753
2010 Impact Factor 4.232
2009 Impact Factor 3.732
2008 Impact Factor 3.658
2007 Impact Factor 3.632
2006 Impact Factor 3.178
2005 Impact Factor 3.037
2004 Impact Factor 2.824
2003 Impact Factor 3.027
2002 Impact Factor 2.72
2001 Impact Factor 2.581
2000 Impact Factor 2.297
1999 Impact Factor 2.081
1998 Impact Factor 2.122
1997 Impact Factor 1.77
1996 Impact Factor 2.05
1995 Impact Factor 1.947
1994 Impact Factor 1.852
1993 Impact Factor 1.799
1992 Impact Factor 1.959

Impact factor over time

Impact factor

Additional details

5-year impact 3.77
Cited half-life >10.0
Immediacy index 0.69
Eigenfactor 0.04
Article influence 1.15
Website Journal of Applied Physiology website
Other titles Journal of applied physiology (Bethesda, Md.: 1985), Journal of applied physiology
ISSN 8750-7587
OCLC 11603017
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

American Physiological Society

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • Author's Pre-print on pre-print servers
    • NIH, Wellcome Trust, HHMI, MRC and BBSRC authors will on their behalf have the Publisher's version/PDF deposited in PubMed Central for release 12 months after publication
    • Publisher's version/PDF cannot be used
    • May link to publisher version with DOI
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: High rate of muscular oxygen utilization facilitates the development of hypoxemia during exercise at altitude. Because endurance training stimulates oxygen extraction capacity, we investigated whether endurance athletes are at higher risk to developing hypoxemia and thereby acute mountain sickness (AMS) symptoms during exercise at simulated high altitude. Elite athletes (ATL, n=8) and fit controls (CON, n=7) cycled for 20 min @100 Watt (EX100w) as well as performed an incremental VO2max test (EXMAX) in normobaric hypoxia (0.107 FIO2) or normoxia (0.209 FIO2). Cardiorespiratory responses, arterial PO2 (PaO2), and oxygenation status in m. vastus lateralis (TOIM) and frontal cortex (TOIC) by near-infrared spectroscopy, were measured. Muscle O2-uptake rate was estimated from Δ[O2Hb] during a 10-min arterial occlusion in m. gastrocnemius. VO2max in normoxia was 70±2 ml.min(-1).kg(-1) in ATL versus 43±2 in CON, and in hypoxia decreased more in ATL (- 41%) than in CON (-25%, p<0.05). Both in normoxia at PaO2 of ~95 mmHg, and in hypoxia at PaO2 of ~35 mmHg, muscle O2-uptake was 2-fold higher in ATL than in CON (0.12 vs. 0.06 ml.min(-1).100g(-1); p<0.05). During EX100W in hypoxia PaO2 dropped to lower (p<0.05) values in ATL (27.6±0.7 mmHg) than in CON (33.5±1.0 mmHg). During EXMAX, but not during EX100W, TOIM was ~15% lower in ATL than in CON (p<0.05). TOIC was similar between the groups at any time. This study shows that maintenance of high muscular oxygen extraction rate at very low circulating PaO2 stimulates the development of hypoxemia during submaximal exercise in hypoxia in endurance-trained individuals. This effect may predispose to premature development of AMS symptoms during exercise at altitude.
    Journal of Applied Physiology 11/2015; DOI:10.1152/japplphysiol.00210.2015

  • Journal of Applied Physiology 11/2015; 119(10):1243-1243. DOI:10.1152/japplphysiol.00711.2015
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    ABSTRACT: Background: In many diseases across a range of pathologies (e.g. cardiopulmonary, neuromuscular, cancer), chronic dyspnea, particularly on exertion, is a major debilitating symptom often associated with clinical anxiety/depression. This study aims to explore the interaction between mood state and exertional dyspnea in a healthy population. Methodology: Following familiarization, 20 healthy subjects (27-54 years) performed six 5-min treadmill tests on 3 separate days. On each day subjects viewed randomly-assigned images designed to induce positive, negative or neutral mood states (International Affective Picture System-IAPS). For each condition, at minute intervals, subjects rated dyspnea (sensory and affective domains) in the first test and mood (valence and arousal domains), in the second test. Oxygen uptake (V̇O2, L/min), carbon dioxide production (V̇CO2, L/min), ventilation (V̇E, L/min), respiratory frequency (fR, beats/min) and heart rate (HR, bpm), were measured throughout the exercise. Results: V̇O2, V̇CO2, V̇E, HR and fR were not statistically significantly different among the three mood states (p>0.05). Mood valence was significantly higher with parallel viewing of positive (last 2-min mean ± SEM = 6.9±0.2) compared to negative pictures (2.4±0.2; p<0.001). Both sensory and affective domains of dyspnea were significantly higher during negative (sensory: 5.6±0.3; affective: 3.3±0.5) compared to positive mood (sensory: 4.4±0.4, p<0.001); affective: 2.1±0.4, p=0.002). Conclusion: These findings suggest that positive mood alleviates both the sensory and affective domains of exertional dyspnea in healthy subjects. Thus the treatment of anxiety/depression in dyspenic populations could be a worthwhile therapeutic strategy in increasing symptom-limited exercise tolerance thereby contributing to improved quality of life.
    Journal of Applied Physiology 11/2015; DOI:10.1152/japplphysiol.00122.2015
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    ABSTRACT: Oxygen uptake (V̇O2) kinetics have been shown to be governed by a nonlinear control system across a range of work rates. However, the linearity of the V̇O2 response to ramp incremental exercise would appear to be the result of a linear control system. This apparent contradiction could represent a balancing of changing V̇O2 kinetics parameter values across a range of work rates. To test this, six healthy men completed bouts of ramp incremental exercise at 15, 30, and 60 W∙min(-1) (15R, 30R, 60R, respectively) and four bouts of an extended-step incremental exercise. V̇O2 parameter values were derived from the step exercise using two mono-exponential models: one starting at time zero and encompassing the entire stage (MONO), the other truncated to the first five minutes and allowing a time delay (5TD). The resulting parameter values were applied to an integrative model to estimate the ramp responses. As work rate increased, gain values increased (p<0.001 for MONO and 5TD), as did mean response time (or time constant) values (MONO: p<0.001; 5TD: p=0.003). Up to V̇O2MAX, the gains of the estimated ramp responses from both models were not different from the gains of the actual observed V̇O2 responses for 15R and 30R (15R: 11.3±1.2, 11.7±0.7, 10.9±0.3; 30R: 10.5±0.8, 11.0±0.5, 10.7±0.3 ml O2∙min(-1)∙W(-1), for actual, MONO, 5TD, respectively) but were significantly greater for 60R (8.7±1.0, 9.9±0.4, 10.3±0.3 ml O2∙min(-1)∙W(-1) for actual, MONO, 5TD, respectively). Up to 80%V̇O2MAX gain values were not significantly different for any ramp rate (p>0.05 for all). We conclude that the apparently linearity of the V̇O2 response to ramp incremental exercise is consequent to a balancing of increasing time constant and gain parameter values.
    Journal of Applied Physiology 11/2015; DOI:10.1152/japplphysiol.00507.2015
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    ABSTRACT: Bedridden patients in intensive care unit or after surgery intervention commonly develop skeletal muscle weakness. The latter is promoted by a variety of prolonged hospitalization-associated conditions. Muscle disuse is the most ubiquitous, and contributes to rapid skeletal muscle atrophy and progressive functional strength reduction. Disuse causes a reduction in fatty acid oxidation leading to their accumulation in skeletal muscle. We hypothesized that muscle fatty acids accumulation could stimulate ceramide synthesis and promote skeletal muscle weakness. Therefore, the present study was designed to determine the effects of sphingolipid metabolism on skeletal muscle atrophy induced by 7 days of disuse. For this purpose, male Wistar rats were treated with myriocin, an inhibitor of de novo synthesis of ceramides and subjected to hindlimb unloading (HU) for 7 days. Soleus muscles were assayed for fiber diameter, ceramide levels, protein degradation and apoptosis signaling. Serum and liver were removed to evaluate the potential hepatoxicity of myriocin treatment. We found that HU increases content of saturated C16:0 and C18:0 ceramides and decreases soleus muscle weight and fiber diameter. HU increased the level of polyubiquitinated proteins and induced apoptosis in skeletal muscle. Despite a prevention of C16:0 and C18:0 muscle accumulation, myriocin treatment did not prevent skeletal muscle atrophy and concomitant induction of apoptosis and proteolysis. Moreover, myriocin treatment increased serum transaminases and induced hepatocyte necrosis. These data highlight that inhibit de novo synthesis of ceramides during immobilization is not an efficient strategy to prevent skeletal muscle atrophy, and exerts adverse effects like hepatotoxicity.
    Journal of Applied Physiology 11/2015; DOI:10.1152/japplphysiol.00720.2015
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    ABSTRACT: Diabetic patients have an increased risk of foot ulcers, and glycation of collagen may increase tissue stiffness. We hypothesized that the level of glycemic control (glycation) may affect Achilles tendon stiffness, which can influence gait pattern. We therefore investigated the relationship between collagen glycation, Achilles tendon stiffness parameters and plantar pressure in poorly (n = 22) and well (n = 22) controlled diabetic patients, including healthy age matched (45-70 yrs) controls (n = 11). There were no differences in any of outcome parameters (collagen cross-linking or tendon stiffness) between patients with well-controlled and poorly controlled diabetes. The overall effect of diabetes was explored by collapsing the diabetes groups (DB) compared to the controls. Skin collagen cross-linking lysylpyridinoline (LP), hydroxylysylpyridinoline (HP), (136%, 80%, P < 0.01) and pentosidine concentrations (55%, P < 0.05) were markedly greater in DB. Furthermore, Achilles tendon material stiffness was higher in DB (54%, P < 0.01). Notably, DB also demonstrated higher forefoot/ rearfoot peak plantar pressure (PPP)-ratio (33%, P < 0.01). Overall, Achilles tendon material stiffness and skin connective tissue cross-linking were greater in diabetic patients compared to controls. The higher foot pressure indicates that material stiffness of tendon and other tissue (e.g skin and joint capsule) may influence on foot gait. The difference in foot pressure distribution may contribute to the development of foot ulcers in diabetic patients.
    Journal of Applied Physiology 11/2015; DOI:10.1152/japplphysiol.00547.2015
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    ABSTRACT: Sulforaphane (SFN), an activator of NF-E2-related factor 2 (Nrf2), has been found to have anti-fibrotic effect on liver and lung. However, its effects on dystrophic muscle fibrosis remain unknown. This work was undertaken to evaluate the effects of SFN-mediated activation of Nrf2 on dystrophic muscle fibrosis. 3-month-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 3 months. The experimental results demonstrated that SFN remarkably attenuated skeletal and cardiac muscle fibrosis as indicated by reduced Sirius red staining and immuno-staining of ECM. Moreover, SFN significantly inhibited TGF-β/Smad signaling pathway and ameliorated pro-fibrogenic gene and protein expression, such as α-SMA, fibronectin, collagen I, PAI-1 and TIMP-1 in Nrf2 dependent manner. Further, SFN significantly decreased the expression of inflammatory-cytokines CD45, TNF-α and IL-6 in mdx mice. In conclusion, these results show that SFN can attenuate dystrophic muscle fibrosis by Nrf2-mediated inhibition of TGF-β/Smad signaling pathway, which indicate Nrf2 may represent a new target for dystrophic muscle fibrosis.
    Journal of Applied Physiology 10/2015; DOI:10.1152/japplphysiol.00721.2015
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    ABSTRACT: It is known that repeated bouts of high-intensity interval training (Hiit) lead to enhanced levels of glycolysis, glycogenesis, and lactate transport proteins in skeletal muscle; however, little is known about the molecular mechanisms underlying these adaptations. To decipher the mechanism leading to improved skeletal muscle glycolytic capacity associated with Hiit, we examined the role of hypoxia-inducible factor-1α (Hif-1α), the major transcription factor regulating the expression of genes related to anaerobic metabolism, in the adaptation to Hiit. First, we induced Hif-1α accumulation using ethyl 3, 4-dihydroxybenzoate (EDHB) to assess the potential role of Hif-1α in skeletal muscle. Treatment with EDHB significantly increased the protein levels of Hif-1α, accompanied by elevated expression of genes related to glycolysis, glycogenesis, and lactate transport. Daily administration of EDHB for 1 week resulted in elevated glycolytic enzyme activity. Second, we examined whether a single bout of Hiit could induce Hif-1α protein accumulation and subsequent increase in the expression of genes related to anaerobic metabolism in skeletal muscle. We observed that the protein levels of Hif-1α and expression of the target genes were elevated 3 h after an acute bout of Hiit. Last, we examined the effects of long-term Hiit. We found that long-term Hiit increased the basal levels of Hif-1α as well as the glycolytic capacity. Our results suggest that Hif-1α is a key regulator in the metabolic adaptation to high-intensity training.
    Journal of Applied Physiology 10/2015; DOI:10.1152/japplphysiol.00499.2015
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    ABSTRACT: Suppressing sex hormones in women for 1 week reduces resting energy expenditure (REE). The effects of more chronic suppression on REE and other components of total energy expenditure (TEE), and whether this is specifically due to loss of estradiol (E2), are not known. We compared the effects of 5 months of sex hormone suppression (gonadotropin releasing hormone agonist therapy, GnRHAG) with placebo (GnRHAG+PL) or (GnRHAG+E2) add-back therapy on REE and the components of TEE. Premenopausal women received GnRHAG (leuprolide acetate 3.75 mg/mo) and were randomized to receive transdermal therapy that was either (E2) (0.075 mg/d; n=24; mean±SD, aged=37±8 yr, BMI=27.3±6.2 kg/m(2)) or placebo (n=21; aged=34±9 yr, BMI=26.8±6.2 kg/m2). REE was measured using a metabolic cart, and TEE, sleep EE (SEE), exercise EE (ExEE, 2 x 30 min bench stepping), non-Ex EE (NExEE), and the thermic effect of feeding (TEF) were measured using whole-room indirect calorimetry. REE decreased in GnRHAG+PL [mean (95% CI), -54 (-98, -15) kcal/d], but not GnRHAG+E2 [+6 (-33, +45) kcal/d)] (difference in between-group changes, P<0.05). TEE decreased in GnRHAG+PL [-128 (-214, -41) kcal/d] and GnRHAGAG+E2[-96 (-159, -32) kcal/d], with no significant difference in between-group changes (P=0.55). SEE decreased similarly in both GnRHAG+PL [-0.07 (-0.12, -0.03) kcal/min)] and GnRHAG+E2 [-0.07 (-0.12, -0.02) kcal/min)]. ExEE decreased in GnRHAG+PL [-0.46 (-0.79, -0.13) kcal/min)], but not GnRHAG+E2 [-0.30 (-0.65, +0.06) kcal/min]. There were no changes in TEF or NExEE in either group. In summary, chronic pharmacologic suppression of sex hormones reduced REE and this was prevented by E2 therapy. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 09/2015; 119(9):jap.00473.2015. DOI:10.1152/japplphysiol.00473.2015
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    ABSTRACT: In the last few years, genetic and functional studies have provided important insight on the pathophysiology of excessive erythrocytosis (EE), the main sign of Chronic Mountain Sickness (CMS). The recent finding of the association of the CMS phenotype with a single-nucleotide polymorphism (SNP) in the SENP1 gene, and its differential expression pattern in CMS and non-CMS Andean highlanders, has triggered large interest in the high-altitude field because of the potential role of its gene-product in the control of erythropoiesis. The SENP1 gene encodes for a protease that regulates the function of hypoxia-relevant transcription factors such as HIF and GATA, and thus might have an erythropoietic regulatory role in CMS through the modulation of the expression of Epo or Epo receptors. The different physiological patterns in the Epo-EpoR system found among Andeans, even within CMS highlanders, together with their different degrees of erythropoietic response, might indicate specific underlying genetic backgrounds, which in turn might reflect different levels of adaptation to lifelong high-altitude hypoxia. This mini-review discusses recent genetic findings potentially underlying EE and CMS, and their possible physiological mechanisms in Andean highlanders. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 08/2015; DOI:10.1152/japplphysiol.00271.2015
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    ABSTRACT: Acute hypoxia increases cerebral blood flow (CBF) and ventilation (VE). It is unknown if these responses are impacted with normal aging, or in patients with enhanced oxidative stress, such as chronic obstructive pulmonary disease (COPD). The purpose of the study was to 1) investigate the effects of aging and COPD on the cerebrovascular and ventilatory responses to acute hypoxia, and 2) to assess the effect of vitamin C on these responses during hypoxia. In 12 Younger, 14 Older, and 12 COPD, we measured peak cerebral blood flow velocity (VP; index of CBF), and VE during two 5-min periods of acute isocapnic-hypoxia, under conditions of: 1) saline-sham; and 2) intravenous vitamin C. Antioxidants (vitamin C, superoxide dismutase [SOD], glutathione peroxidase, and catalase), oxidative stress (malondialdehyde [MDA] and advanced protein oxidation product) and nitric oxide metabolism end-products (NOx) were measured in plasma. Following the administration of vitamin C, Vitamin C, SOD, catalase, and MDA increased, while NOx decreased. VP and VE sensitivity to hypoxia were reduced in Older by ~60% (P < 0.02). COPD patients exhibited similar VP and VE responses to Older (P > 0.05). Vitamin C did not have an effect on the hypoxic VE response, but selectively decreased the VP sensitivity in Younger only. These findings suggest a reduced integrative reflex (i.e., cerebrovascular and ventilatory) during acute hypoxemia in healthy older adults. Vitamin C does not appear to have a large influence on the cerebrovascular or ventilatory responses during acute hypoxia. Copyright © 2015, Journal of Applied Physiology.
    Journal of Applied Physiology 06/2015; 119(4). DOI:10.1152/japplphysiol.00389.2015
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    ABSTRACT: In humans, enhanced joint range of motion is observed after static stretch training and results either from an increased stretch tolerance or from a change in the biomechanical properties of the muscle-tendon unit. We investigated the effects of an intermittent stretch training on muscle biomechanical and structural variables. The left plantarflexors muscles of seven anesthetized New Zealand (NZ) White rabbits were passively and statically stretched three times a week for 4 wk, while the corresponding right muscles were used as nonstretched contralateral controls. Before and after the stretching protocol, passive torque produced by the left plantarflexor muscles as a function of the ankle angle was measured. The left and right plantarflexor muscles were harvested from dead rabbits and used to quantify possible changes in muscle structure. Significant mass and serial sarcomere number increases were observed in the stretched soleus but not in the plantaris or medial gastrocnemius. This difference in adaptation between the plantarflexors is thought to be the result of their different fiber type composition and pennation angles. Neither titin isoform nor collagen amount was modified in the stretched compared with the control soleus muscle. Passive torque developed during ankle dorsiflexion was not modified after the stretch training on average, but was decreased in five of the seven experimental rabbits. Thus, an intermittent stretching program similar to those used in humans can produce a change in the muscle structure of NZ White rabbits, which was associated in some rabbits with a change in the biomechanical properties of the muscle-tendon unit. Copyright © 2015 the American Physiological Society.
    Journal of Applied Physiology 06/2015; 118(12):jap.00515.2014. DOI:10.1152/japplphysiol.00515.2014
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    ABSTRACT: Recent studies demonstrate that high dietary sodium (HS) impairs endothelial function in those with salt-resistant (SR) blood pressure (BP). The effect of HS on endothelial function in those with salt-sensitive (SS) BP is not currently known. We hypothesized that HS would impair brachial artery flow-mediated dilation (FMD) to a greater extent in SS compared with SR adults. Ten SR (age 42 ± 5 yr, 5 men, 5 women) and 10 SS (age 39 ± 5 yr, 5 men, 5 women) healthy, normotensive participants were enrolled in a controlled feeding study consisting of a run-in diet followed by a 7-day low dietary sodium (LS) (20 mmol/day) and a 7-day HS (300 mmol/day) diet in random order. Brachial artery FMD and 24-h BP were assessed on the last day of each diet. SS BP was individually assessed and defined as a change in 24-h mean arterial pressure (MAP) of >5 mmHg between the LS and HS diets (ΔMAP: SR -0.6 ± 1.2, SS 7.7 ± 0.4 mmHg). Brachial artery FMD was lower in both SS and SR individuals during the HS diet (P < 0.001), and did not differ between groups (P > 0.05) (FMD: SR LS 10.6 ± 1.3%, SR HS 7.2 ± 1.5%, SS LS 12.5 ± 1.7%, SS HS 7.8 ± 1.4%). These data indicate that an HS diet impairs brachial artery FMD to a similar extent in adults with SS BP and SR BP. Copyright © 2015 the American Physiological Society.
    Journal of Applied Physiology 06/2015; 118(12):jap.00023.2015. DOI:10.1152/japplphysiol.00023.2015