Speed- and Circuit-Based High-Intensity Interval Training on Recovery Oxygen Consumption

International Journal of Exercise Science 10(7): 942-953, 2017. Due to the current obesity epidemic in the United States, there is growing interest in efficient, effective ways to increase energy expenditure and weight loss. Research has shown that high-intensity exercise elicits a higher Excess Post-Exercise Oxygen Consumption (EPOC) throughout the day compared to steady-state exercise. Currently, there is no single research study that examines the differences in Recovery Oxygen Consumption (ROC) resulting from high-intensity interval training (HIIT) modalities. The purpose of this study is to review the impact of circuit training (CT) and speed interval training (SIT), on ROC in both regular exercising and sedentary populations. A total of 26 participants were recruited from the UW-Eau Claire campus and divided into regularly exercising and sedentary groups, according to self-reported exercise participation status. Oxygen consumption was measured during and after two HIIT sessions and was used to estimate caloric expenditure. There was no significant difference in caloric expenditure during and after exercise among individuals who regularly exercise and individuals who are sedentary. There was also no significant difference in ROC between regular exercisers and sedentary or between SIT and CT. However, there was a significantly higher caloric expenditure in SIT vs. CT regardless of exercise status. It is recommended that individuals engage in SIT vs. CT when the goal is to maximize overall caloric expenditure. With respect to ROC, individuals can choose either modalities of HIIT to achieve similar effects on increased oxygen consumption post-exercise

Speed- and Circuit-Based High-Intensity Interval Training on Excess Post-Exercise Oxygen Consumption

Color poster with text, images, and tables.Due to the current obesity epidemic in the United States, there is growing interest in efficient, effective ways to increase energy expenditure and weight loss. Research has shown that high-intensity exercise elicits a higher Excess Post-Exercise Oxygen Consumption (EPOC) throughout the day compared to steady-state exercise. Currently, there is no research study that examines the differences in EPOC resulting from high-intensity interval training (HIIT) modalities. The purpose of this study is to review the impact of circuit training (CT) and speed interval training (SIT), on EPOC in both regular exercising and sedentary populations. Methods: Twenty-four participants were recruited from the UW-Eau Claire campus. They were divided into regularly exercising and sedentary groups, according to self-reported physical activity levels. Oxygen consumption was measured during and after two HIIT sessions, which was used to estimate caloric expenditure. There was no significant difference in caloric expenditure among the individuals who regularly exercise and the individuals who are sedentary. There was also no significant difference in EPOC between sedentary individuals and those who regularly exercise or between SIT and CT. However, there was a significantly higher caloric expenditure from SIT compared CT in both groups. Conclusion: Individuals do not need to complete one modality of HIIT (SIT or CT) over the other to have a greater influence on EPOC.University of Wisconsin--Eau Claire Office of Research and Sponsored Program

Effects of MAPK inhibitors on FLUA-induced CK/CHK from RAW 264.7 cells at short time points.

<p>Supernatants from cells treated with the indicated inhibitors as described in Methods then exposed to FLUA were collected 3 or 6 h after exposure, along with those from mock infected controls. They were assayed for selected CK/CHK by multiplexed fluid phased antibody based analysis. Cytokine concentrations were calculated based on known concentration standards run at the same time. Data shown are the mean ± SEM, n = 3 independent experiments. FO–FLUA only; JEI–both JNK and ERK Inhibition; JI–JNK inhibition; EI–ERK inhibition.</p

Early Activation of MAP Kinases by Influenza A Virus X-31 in Murine Macrophage Cell Lines

<div><p>Early molecular responses to Influenza A (FLUA) virus strain A/X-31 H3N2 in macrophages were explored using J774.A1 and RAW 264.7 murine cell lines. NF-kappa B (NFκB) was reported to be central to FLUA host-response in other cell types. Our data showed that FLUA activation of the classical NFκB dependent pathway in these macrophages was minimal. Regulator proteins, IkappaB-alpha and –beta (IκBα, IκBβ), showed limited degradation peaking at 2 h post FLUA exposure and p65 was not observed to translocate from the cytoplasm to the nucleus. Additionally, the non-canonical NFκB pathway was not activated in response to FLUA. The cells did display early increases in TNFα and other inflammatory cytokine and chemokine production. Mitogen activated phosphokinase (MAPK) signaling pathways are also reported to control production of inflammatory cytokines in response to FLUA. The activation of the MAPKs, cJun kinases 1 and 2 (JNK 1/2), extracellular regulated kinases 1 and 2 (ERK 1/2), and p38 were investigated in both cell lines between 0.25 and 3 h post-infection. Each of these kinases showed increased phosphorylation post FLUA exposure. JNK phosphorylation occurred early while p38 phosphorylation appeared later. Phosphorylation of ERK 1/2 occurred earlier in J774.A1 cells compared to RAW 264.7 cells. Inhibition of MAPK activation resulted in decreased production of most FLUA responsive cytokines and chemokines in these cells. The results suggest that in these monocytic cells the MAPK pathways are important in the early response to FLUA.</p></div

Effects of MAPK inhibitors on FLUA-induced CK/CHK from cell lines at 24 h.

<p>Supernatants from cells pre-treated with the indicated inhibitors as described in Methods then exposed to FLUA were collected 24 h after exposure, along with those from mock infected controls. They were assayed for selected CK/CHK by multiplexed fluid phased antibody based analysis. Cytokine concentrations were calculated based on known concentration standards run at the same time. Data shown are the mean ± SEM, n = 3 independent experiments. FO–FLUA only; JEI–both JNK and ERK Inhibition; JI–JNK inhibition; EI–ERK inhibition.</p

Effects of MAPK inhibitors on FLUA-induced CK/CHKs from J774.A1 cells at short time points.

<p>Supernatants from cells pre-treated with the indicated inhibitors for 1 h then exposed to FLUA were collected 3 or 6 h after exposure, along with those from mock infected controls. They were assayed for selected CK/CHK by multiplexed fluid phased antibody based analysis. Cytokine concentrations were calculated based on known concentration standards run at the same time. Data shown are the mean ± SEM, n = 3 independent experiments. FO–FLUA only; JEI–both JNK and ERK inhibition; JI–JNK inhibition; EI–ERK inhibition.</p

MAPKs are rapidly phosphorylated following FLUA infection.

<p><b>A.</b> J774.A1 and RAW 264.7 cells rapidly phosphorylate JNK 1/2 in response to X-31 exposure. In both cell lines maximal response was reached by 15 minutes post virus exposure. Control and LPS treated (1 µg/ml for 15 minutes) cells were mock infected. Representative Western blots and densitometry graphs from the Western blots (data are mean ± SEM, n = 5 independent experiments). <b>B.</b> J774.A1 and RAW 264.7 cells rapidly phosphorylate ERK 1/2 in response to X-31 exposure. In J774.A1 cells maximal response was reached by 30 minutes. RAW 264.7 cells had a lower maximal expression that was reached by 1 h. Control and LPS treated (1 µg/ml for 15 minutes) cells were mock infected. Representative Western blots and densitometry graphs from the Western blots (data are mean ± SEM, n = 4 independent experiments). <b>C.</b> J774.A1 and RAW 264.7 cells phosphorylate p38 in response to X-31 exposure. In both cell lines maximal response was reached by 3 h, a noticeable delay compared to the JNK1/2 and ERK1/2 activations. The antibody used recognizes α, β and γ p38 isoforms. Control and LPS treated (1 µg/ml for 15 minutes) cells were mock infected. Representative western blots and densitometry graphs from the western blots (data are mean ± SEM, n = 5 independent experiments).</p

Proinflammatory cytokines are induced by X-31 exposure at early time points post exposure.

<p><b>A.</b> Supernatants from cells 3 h or 6 h after exposure to X-31, along with those from mock infected controls, were assayed for CK/CHK by multiplexed fluid phased antibody based analysis. Cytokine concentrations were calculated based on known concentration standards run at the same time. Data shown are the mean ± SEM, n = 5 independent experiments. <b>B.</b> Production kinetics of selected CK/CHK induced by FLUA. The charts illustrate commonalities and differences. TNFα and IL6 showed a lag of 3–6 h whereas MIP1α and IP10 were maximal by 3 h. The RANTES and MCP1 responses were intermediate. RAW 264.7 cells responded faster and to higher levels than J774.A1 cells especially at 3 and 6 h pi. Means ± SEM, n = 3 independent experiments.</p

NFkB is not activated by FLUA at early time-points.

<p><b>A.</b> In J774.A1 cells IκBα levels were reduced at 2 h while IκBβ levels showed a gradual decline across the time points (but approximated control levels at 2 h). In RAW 264.7 cells, IκBα stayed near or above control levels while IκBβ levels showed a mild decline. Representative Western blots of cell lysates collected at the indicated time points post exposure to X-31 FLUA. Control and LPS treated (1 µg/ml for 15 minutes) cells were mock infected. <b>B.</b> Densitometry graphs from the Western blots. Data are normalized to actin, background is subtracted and protein levels are expressed as percentage of the mock infected control. Means are shown ± SEM, n = 3 to 6 independent experiments depending on time point. <b>C.</b> Nuclear localization of NFκB subunit p65 is not increased by X-31 infection of J774.A1 cells. Cells were infected or mock infected for the indicated periods, fixed, permeabilized and stained with anti-p65 antibody. LPS cells received 1 µg/ml LPS 30 minutes before fixation. LPS did increase NFκB nuclear localization as indicated by immunofluorescence. LPS activation was not blocked by prior X-31 exposure. 60X scale fields are shown with 255X digitally zoomed insets.</p

The non-canonical NFκB pathway is not activated by X-31 exposure.

<p>The percent of the total p52 and p100 protein in the activated p52 form did not change from that in the control mock infected cells. The expression of RelB, the partner of p52, was also unchanged. <b>A.</b> Representative Western blots. <b>B.</b> Densitometry graphs from the Western blots. Means are shown ± SEM, n = 4 to 7 independent experiments depending on time point.</p