SEACSM 2021 ANNUAL MEETING ABSTRACTS
and cfPWV, and that change in bfPWV is very strongly associated with change in
cfPWV. The use of bfPWV, a more user-friendly method than cfPWV, can be used
interchangeably to assess arterial stiffness.
CLINICAL PREDICTORS OF VO
2
MAX RESPONSE TO ENDURANCE
TRAINING: HERITAGE FAMILY STUDY
Emanuel J. Ayala
1
, Jacob L. Barber
1
, Charles S. Schwartz
1
, Jeremy M. Robbins
2
,
Robert E. Gerszten
2
, Xuewen Wang
1
, James S. Skinner, FACSM
3
, Claude
Bouchard, FACSM
4
, Mark A. Sarzynski, FACSM
1
.
1
University of South Carolina,
Columbia, SC.
2
Beth Israel Deaconess Medical Center, Boston, MA.
3
Indiana
University, Bloomington, IN.
4
Pennington Biomedical Research Center, Baton
Rouge, LA.
Background: There is wide variation in the response of VO
2
max to exercise
training. However, the influence of baseline phenotypes on VO
2
max trainability
(ΔVO
2
max) is not well studied. Thus, the purpose of this study was to examine
the contribution of modifiable, biologically, and clinically relevant baseline traits
to absolute ΔVO
2
max (mL/min). Methods: Participants were 488 sedentary,
healthy adults between the ages of 17-65 (56% female, 33% Black) who
completed 20 weeks of standardized aerobic exercise training as part of the
HERITAGE Family Study. Phenotypes were measured at baseline and post-
training. Baseline resting and submaximal exercise (i.e., 50 Watts) measures of
cardiopulmonary (e.g., cardiac output, ventilation, blood pressure) and metabolic
traits (e.g., lactate, free fatty acids), as well as body composition traits (e.g.,
percent body fat, fat free mass) were entered into a forward selection regression
model predicting ΔVO
2
max with age, sex, and race forced into the model.
Results: A total of 34 traits were entered into the forward selection model, with
10 traits associated with ΔVO
2
max at p<0.05: fat free mass (partial r
2
= 2.9%);
percent body fat (partial r
2
= 1.7%); arteriovenous oxygen difference at 50W
(partial r
2
= 1.6%); stroke index at 50W (partial r
2
= 1.5%); visceral fat (partial
r
2
= 1.5%); ventilation at 50W (partial r
2
= 1.0%); concentration of hemoglobin
(partial r
2
= 1.6%), hematocrit (partial r
2
= 1.4%), and resting lactate (partial r
2
= 0.6%); and tidal volume at 50W (partial r
2
= 0.7%). This panel of 10 traits
explained approximately 14.5% of the variance in ΔVO
2
max. Conclusion: The
contribution of baseline measures of modifiable cardiopulmonary, metabolic, and
body composition traits to absolute ΔVO
2
max was minimal. The variance in
ΔVO
2
max explained in this study may be higher than normal due to the use of
predictor variables derived and tested in a single study cohort. There remains a
large portion of the variance in ΔVO
2
max that is not yet explained. Further
research is needed to identify other modifiable factors that may influence
VO
2
max trainability.
EFFECTS OF CLEAR, TINTED, AND MIRROR TINTED FOOTBALL HELMET
VISORS ON REACTION TIME AND TARGET-DETECTION
Rachel Miller
1
,
,2
, Anna Covington
1
, Rebecca Rogers
1
, Justin Moody
1
, Christopher
Ballmann
1
.
1
Samford University, Birmingham, AL.
2
University of West Alabama,
Livingston, AL.
BACKGROUND: We have previously shown that clear football helmet visors do
not impair peripheral vision reactive time (PRT). Currently, almost all
organizations and levels of competitive football allow clear visor use but ban the
wearing of dark tinted visors during gameplay. However, whether tinted visors
influence visuomotor ability is currently unknown. PURPOSE: The purpose of
this study was to examine the effects of clear, tinted, and mirror tinted helmet
visors on PRT and target detection in collegiate football players. METHODS:
Division 1 NCAA football players with normal/corrected to normal vision
participated. In a randomized manner, participants completed PRT tests for the
following conditions: Baseline/no helmet (BL), Helmet only (HO), Helmet + Clear
Visor (HCV), Helmet + Tinted (40% Visual Light Transmittance) Visor (HTV), and
Helmet + Mirror Tinted (28% Visual Light Transmittance) Visor (HMV). For each
condition, a 60 s PRT test was completed on a Dynavision D2 visuomotor board.
Subjective perception of how visors would affect field performance was assessed
with a 7-point Likert scale questionnaire. RESULTS: Independent of visors, all
helmet conditions resulted in significantly slower average PRT and lower target
hits compared to BL (p<0.05). HMV resulted in slower average PRT compared to
HO (p<0.001) and HCV (p=0.015). Target hits were lower with HMV versus HO
(p<0.001) and HCV (p=0.008). However, no differences existed between HTV or
HMV for PRT or target hits (p>0.05). Subjectively, participants believed that the
HTV and HMV would make their performance worse on the field compare to HCV
(p<0.05). CONCLUSIONS: Wearing a helmet regardless of visor type worsens
PRT and target detection. However, only the mirror tinted visor exacerbated
impairments in peripheral visuomotor ability. Since mirrored visors resulted in
poorer visuomotor ability beyond that of solely a helmet or clear visor, caution is
warranted in use of mirrored visors during competition for both performance and
safety concerns.
THE EFFECTS OF PREVIOUS AMENORRHEA ON VASCULAR FUNCTION
Katherine T. Williford, Emma Frye, Erin Bouldin, Denise Martz, Rebecca Kappus.
Appalachian State University, Boone, NC.
BACKGROUND: Young premenopausal women are susceptible to amenorrhea,
which contributes to negative vascular remodeling and endothelial dysfunction. It
is unknown whether these vascular changes are permanent or reversable when
regaining a consistent menstrual cycle. METHODS: This study examined
subclinical cardiovascular disease risk factors and the vascular function of 10
eumenorrheic women, and 6 previously amenorrhoeic women (mean age: 23 ± 2
years). The amenorrheic women ceased menses for an average of 11.5 ± 2
months and regained menus for a mean of 33 ± 30 months before testing.
Anthropometric measurements, physical activity, central (aortic) and peripheral
(brachial) blood pressures, carotid intima media thickness, carotid beta stiffness,
and brachial flow mediated dilation were analyzed using a one-way ANOVA.
When significance was detected a Bonferroni Post Hoc analysis was performed.
An ANCOVA was performed to control for variance and confounding factors.
RESULTS: Compared to the eumenorrheic group, the previously amenorrheic
females had significantly lower brachial systolic blood pressure (116 ± 7 mmHg
vs 106 ± 10 mmHg), mean arterial pressure (82 ± 5 mmHg vs 75 ± 6 mmHg),
aortic systolic blood pressure (100 ± 7 mmHg vs 89 ± 6 mmHg), aortic diastolic
blood pressure (67 ± 7 mmHg vs 59 ± 6 mmHg), aortic mean arterial pressure
(82 ± 6 mmHg vs 73 ± 4 mmHg), and higher weekly minutes of physical activity
(156 ± 71 mins vs 280 ± 30 mins). After controlling for physical activity using an
ANCOVA, group differences in SBP (p=0.03) and aortic MAP (p=0.05) remained
significant. There were no significant differences in carotid intima media
thickness, beta stiffness, and brachial flow mediated dilation. CONCLUSION:
There were no significant differences in vascular structure remodeling between
groups. The amenorrhoeic group displayed higher amounts of exercise, and
lower peripheral and central blood pressure. This suggests that there are no
long-term detrimental cardiovascular effects from previous amenorrhea and that
physical activity may play a role in lowering central and peripheral blood
pressure.
MUSCLE CONTRACTION BY HIGH-FREQUENCY ELECTRICAL STIMULATION
INDUCES HIPPO SIGNALING EFFECTOR YAP RESPONSE IN APC
MIN/+
MICE
Richard Thomas Yongue, Shuichi Sato, Emily Walker. University of Louisiana at
Lafayette, Lafayette, LA.
BACKGROUND: mTOR is an established anabolic signaling that controls the
tissue size and responds to resistance-type exercise, even under muscle-wasting
conditions. Hippo signaling effector YAP also plays a role in regulating skeletal
muscle size. However, whether YAP responds to such an external stimulus is
unknown. The purpose of this study was to determine whether muscle
contraction would trigger YAP response in mice with tumor burden. METHODS:
Male Apc
Min/+
(Min, n=6) mice and age-matched Wild-type (WT, n=6) mice were
used in this study. A single bout of high-frequency electric stimulations (HFES,
ten sets of six repetitions, ~18 min) was applied to both groups under
anesthesia. This intervention induced eccentric contraction on the left tibialis
anterior (TA) muscle. Right TA served as contra-lateral control. 30 min following
the HFES, both TA muscles were excised and snap-frozen in the liquid nitrogen
for further analysis. Total protein was extracted from the tissues, and routine
western blotting was conducted using approximately 60~100 µg of the total
protein. Muscle weight datum was analyzed by a Student’s t-test. Western blot
data were analyzed by a two-way ANOVA with repeated measures (genotype x
HFES). Post-hoc analyses were performed with the Bonferroni test when
appropriate. The coefficient of determination (r
2
) was used to examine whether a
linear regression model fits the plots. RESULTS: Min mice lost approximately
18.0% of body weight (BW) compared to their peak BW at the time of HFES.
Control TA muscle was smaller in Min mice than WT mice (52.6 mg±1.1 vs. 35.4
mg±1.2, respectively, p<0.01). These data confirmed that Min mice developed
cachexia. Densitometry analysis of Western blot data showed that HFES
increased the phosphorylation (p-) levels of p70S6K regardless of genotype
(p<0.01). However, the p-p70S6K response to HFES was higher in WT mice than
Min mice (2.5 folds vs. 1.5 folds, p<0.01). HFES upregulated pYAP levels
(p<0.01), but we observed a significant interaction between genotype and HFES
(p<0.05), indicative of altered responses to HFES. When the fold differences
were plotted, there was a significant inversed relationship between p-p70S6K
and p-YAP (r
2
=0.565, p<0.05). CONCLUSIONS: These results suggest that
muscle contraction by HFES evokes YAP activity, but the response is different
between healthy and cachectic mice.
SLEEP DURATION AND ARTERIAL STIFFNESS, A META ANALYSIS
Alex N. Pomeroy
1
, Patricia Pagan Lassalle
1
, Christopher E. Kline, FACSM
2
, Kevin
S. Heffernan
3
, Lee Stoner, FACSM
1
.
1
University of North Carolina at Chapel Hill,
Chapel Hill, NC.
2
University of Pittsburgh, Pittsburgh, PA.
3
Syracuse University,
Syracuse, NY.
BACKGROUND: Research has shown chronically short (<7 hours) and long (>9
hours) sleep duration may increase cardiovascular disease (CVD) risk relative to
recommended sleep duration (7-9 hours). However, the factors contributing to
CVD risk that also relate to sleep duration are less understood. One factor could
be arterial stiffness (AS), an indicator of CVD risk. This study sought to
consolidate the literature examining the association between sleep duration and
AS. Studies using pulse wave velocity (PWV), the “gold standard” for AS
measurement, were selected for analysis. METHODS: Electronic databases
(PubMed, SPORTDiscus) from inception to July 2020 were referenced. Initially,
464 studies were identified. After evaluation of study eligibility, data from 10
cross-sectional studies involving 83,032 participants (65% male) were extracted
for meta-analysis. Meta-analyses were completed on 3 sleep duration categories
(short, recommended, and long), including sub-group analysis for
cardiometabolic health status, sleep disorder status, PWV method, and age
category (<65 or 65+ y). Effect sizes were calculated as weighted mean
differences (WMD) using a random-effects model. Standardized mean differences
(SMD) were also calculated to determine effect size magnitude, with a SMD of
<0.2 as a small effect, 0.2-0.8 as moderate, and >0.8 as large. RESULTS: Short
sleep duration resulted in a small but significant increase in PWV (WMD=15.25
cm/s, 95% confidence intervals (CI): 9.02-21.48 cm/s, p<0.001, SMD=0.02).
Long sleep duration resulted in a large and positive increase in PWV
(WMD=33.83 cm/s, 95% CI: 19.87-47.80 cm/s, p<0.001, SMD=0.82). Older
age had a small moderating effect in short (WMD=16.8 cm/s, 95% CI: 10.3-23.2
cm/s, p<0.001, SMD=0.02) and a large moderating effect in long (WMD=16.7
cm/s, 95% CI: 10.3-23.2 cm/s, p<0.001, SMD= 0.95) sleep. Cardiometabolic