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Polycystic ovary syndrome (PCOS) predisposes women to cardiovascular diseases. Blood pressure (BP) responses to the cold pressor test (CPT) predict future cardiovascular risk but have yet to be characterized in PCOS. Therefore, we compared BP responses to the CPT between females with PCOS [ n = 10; age: 22 ± 3 yr, body mass index (BMI): 23.9 ± 3 kg/m 2 ] and healthy controls (CTRL; n = 10; age: 22 ± 2 yr, BMI: 22.1 ± 2 kg/m 2 ). BP (finger photoplethysmography calibrated to manual sphygmomanometry-derived values), femoral blood flow (duplex ultrasound), and vascular resistance [FVR; mean arterial pressure (MAP)/blood flow] were measured continuously at baseline and across a 3-min hand CPT. Venous blood samples were used to quantify the free androgen index (FAI; total testosterone/sex hormone binding globulin × 100). Baseline MAP was not different between PCOS and CTRL (87 ± 7 vs. 82 ± 11 mmHg, respectively; P = 0.25), nor was systolic BP (SBP; 109 ± 9 vs. 106 ± 7 mmHg; P = 0.42). Across the CPT, MAP and SBP were higher in PCOS than CTRL (main effects of group, both P < 0.05). Peak CPT induced increases in MAP (+12 ± 5 vs. +7 ± 4 mmHg; P = 0.04) and corresponding changes in SBP (+13 ± 7 vs. +7 ± 3 mmHg; P = 0.04) and FVR (+0.17 ± 0.08 vs. +0.02 ± 0.13 mmHg/mL/min; P = 0.01) were larger in PCOS than CTRL. Within-group regressions indicated that FAI was positively associated with relative increases in peak MAP ( R 2 < 0.01) and corresponding changes in FVR ( P < 0.01) and corresponding changes in FVR ( R 2 = 0.83, P < 0.01) in females with PCOS but not in CTRL (MAP: R 2 = 0.41). Young, lean females with PCOS demonstrate exaggerated BP and vascular responses to the CPT that may be indicative of elevated cardiovascular risk mediated in part by the detrimental effects of elevated androgens. P Young, lean, and otherwise healthy females with polycystic ovary syndrome (PCOS) demonstrated exaggerated blood pressure responses to the cold pressor test (CPT) relative to controls. CPT responses were associated with bioavailable androgens, suggesting that hyperandrogenism contributes to exaggerated responses to the CPT in PCOS. Given associations between CPT responsiveness and the subsequent development of hypertension, these findings add to mounting evidence for increased cardiovascular risk even in lean females with PCOS.R 2 = 0.12, P = 0.41). Young, lean females with PCOS demonstrate exaggerated BP and vascular responses to the CPT that may be indicative of elevated cardiovascular risk mediated in part by the detrimental effects of elevated androgens. NEW & NOTEWORTHY Young, lean, and otherwise healthy females with polycystic ovary syndrome (PCOS) demonstrated exaggerated blood pressure responses to the cold pressor test (CPT) relative to controls. CPT responses were associated with bioavailable androgens, suggesting that hyperandrogenism contributes to exaggerated responses to the CPT in PCOS. Given associations between CPT responsiveness and the subsequent development of hypertension, these findings add to mounting evidence for increased cardiovascular risk even in lean females with PCOS.

Lactate has diverse roles in biology and has been implicated in the control of energy intake. A variety of methods (i.e., exercise, ingestion, and infusion) have been used to study its effects on different metabolic outcomes and the original intent of this project was to explore the effect of oral sodium lactate (Na-Lactate) ingestion on appetite regulation. During piloting, we were unable to show that Na-Lactate could increase blood lactate concentrations; thus, the purpose of this brief report is to highlight that oral Na-Lactate ingestion is not an effective method to study lactate metabolism. Five male participants (26 ± 3 yr, 82.4 ± 3.8 kg, 25.4 ± 1.6 kg·m -2 ) completed 15 experimental sessions where Na-Lactate solutions were consumed with the assessment of blood lactate preingestion, 30-min, 45-min, and 60-min postingestion. Oral Na-Lactate ingestion did not increase blood lactate concentrations (Pre: 0.9 ± 0.2; 30 min: 1.2 ± 0.7; 45 min: 1.0 ± 0.5; 60 min: 0.9 ± 0.4 mmol·L -1 ). In addition, there were moderate-to-severe gastrointestinal (GI) side effects (e.g., vomiting and diarrhea) following ingestion. Altogether, our data suggest that oral ingestion of Na-Lactate is not an effective method for studying lactate's role in metabolism as it did not increase blood lactate concentrations and was accompanied by problematic GI side effects. NEW & NOTEWORTHY Lactate has diverse roles in physiology, and a variety of methods have been used to explore its effects on metabolism. Here, we explored whether oral sodium lactate (Na-Lactate) ingestion could increase blood lactate concentrations. Oral Na-Lactate ingestion using a variety of dosing protocols did not increase blood lactate concentrations and was coupled with gastrointestinal issues. These results demonstrate that oral ingestion of Na-Lactate is not an effective method for studying lactate's role in metabolism.

The potential mechanisms involved in lactate's role in exercise-induced appetite suppression require further examination. We used sodium bicarbonate (NaHCO 3 ) supplementation in a double-blind, placebo-controlled, randomized crossover design to explore lactate's role on neuropeptide Y (NPY), agouti-related peptide (AgRP), and alpha-melanocyte-stimulating hormone (α-MSH) concentrations. Twelve adults (7 males; 24.2 ± 3.4 kg·m -2 ; 42.18 ± 8.56 mL·kg -1 ·min -1 ) completed two identical high-intensity interval training sessions following ingestion of NaHCO 3 (BICARB) or sodium chloride (PLACEBO) pre-exercise. Blood lactate, acylated ghrelin, NPY, AgRP, α-MSH, and appetite perceptions were measured pre-exercise, 0-, 30-, 60-, and 90-min postexercise. Free-living energy intake (electronic food diaries) was measured the day before, of, and after each experimental session. In BICARB, blood lactate was greater postexercise ( P < 0.002, d > 0.70), though acylated ghrelin was similar ( P = 0.075, [Formula: see text] = 0.206) at all time points postexercise ( P > 0.034, d < 0.22). NPY ( P = 0.006, [Formula: see text] > 0.509) and AgRP ( P < 0.001, [Formula: see text] > 0.488) had main effects of time increasing following exercise and returning to baseline, with no differences between sessions (NPY: P = 0.0.192, [Formula: see text] = 0.149; AgRP: P = 0.422, [Formula: see text] = 0.060). α-MSH had no main effect of time ( P = 0.573, [Formula: see text] = 0.063) or session ( P = 0.269, [Formula: see text] = 0.110). Appetite perceptions were similar during BICARB and PLACEBO ( P = 0.007, d = 0.28), increasing in both sessions postexercise ( P < 0.088, d > 0.57). Energy intake had a main effect of day ( P = 0.025, [Formula: see text] = 0.825), where the experimental session day was greater than the day before ( P = 0.010, d = 0.59) with no other differences between days ( P > 0.260, d < 0.38). The lower accumulation of lactate than our previous work did not generate exercise-induced appetite suppression as there were no differences in acylated ghrelin, appetite perceptions, or peripheral concentrations of neuropeptides. NEW & NOTEWORTHY Current evidence supports lactate's role in exercise-induced appetite suppression. Here, we demonstrate a smaller degree of lactate accumulation with sodium bicarbonate ingestion and HIIT than our previous work and no subsequent suppression of acylated ghrelin concentrations, subjective appetite perceptions, or peripheral concentrations of neuropeptides. These results suggest either changes in central appetite-regulating neuropeptides are not reflected peripherally or the smaller magnitude of lactate accumulation did not generate exercise-induced appetite suppression as seen previously.

A step-transition in external work rate (WR) increases pulmonary O 2 uptake (V̇o 2p ) in a monoexponential fashion. Although the rate of this increase, quantified by the time constant (τ), has frequently been shown to be similar between multiple different WR amplitudes (ΔWR), the adjustment of O 2 delivery to the muscle (via blood flow; BF), a potential regulator of V̇o 2p kinetics, has not been extensively studied. To investigate the role of BF on V̇o 2p kinetics, 10 participants performed step-transitions on a knee-extension ergometer from a common baseline WR (3 W) to: 24, 33, 45, 54, and 66 W. Each transition lasted 8 min and was repeated four to six times. Volume turbinometry and mass spectrometry, Doppler ultrasound, and near-infrared spectroscopy were used to measure V̇o 2p , BF, and muscle deoxygenation (deoxy[Hb + Mb]), respectively. Similar transitions were ensemble-averaged, and phase II V̇o 2p , BF, and deoxy[Hb + Mb] were fit with a monoexponential nonlinear least squares regression equation. With increasing ΔWR, τV̇o 2p became larger at the higher ΔWRs ( P < 0.05), while τBF did not change significantly, and the mean response time (MRT) of deoxy[Hb + Mb] became smaller. These findings that V̇o 2p kinetics become slower with increasing ΔWR, while BF kinetics are not influenced by ΔWR, suggest that O 2 delivery could not limit V̇o 2p in this situation. However, the speeding of deoxy[Hb + Mb] kinetics with increasing ΔWR does imply that the O 2 delivery-to-O 2 utilization of the microvasculature decreases at higher ΔWRs. This suggests that the contribution of O 2 delivery and O 2 extraction to V̇O 2 in the muscle changes with increasing ΔWR. NEW & NOTEWORTHY A step increase in work rate produces a monoexponential increase in V̇o 2p and blood flow to a new steady-state. We found that step transitions from a common metabolic baseline to increasing work rate amplitudes produced a slowing of V̇o 2p kinetics, no change in blood flow kinetics, and a speeding of muscle deoxygenation kinetics. As work rate amplitude increased, the ratio of blood flow to V̇o 2p became smaller, while the amplitude of muscle deoxygenation became greater. The gain in vascular conductance became smaller, while kinetics tended to become slower at higher work rate amplitudes.

Exercise in young adults (18-25 yr) suppresses appetite in a dose-response relationship with exercise intensity. Although several mechanisms have been proposed to explain this response, lactate is the most well established. To date, no study has investigated this specifically in middle-aged adults where the appetite response to a meal is different. To explore the effects of submaximal, near maximal, and supramaximal intensity exercise on appetite regulation in middle-aged adults. Nine participants (age: 45 ± 10 yr) completed four experimental sessions: 1 ) no-exercise control (CTRL); 2 ) moderate-intensity continuous training [MICT; 30 min, 65% maximal oxygen consumption (V̇o 2max )]; 3 ) high-intensity interval training (HIIT; 10 × 1 min efforts, 90% heart rate maximum, 1 min recovery); and 4 ) sprint interval training (SIT; 8 × 15 s "all-out" efforts, 2 min recovery). Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), active peptide tyrosine tyrosine (PYY), lactate, and subjective appetite perceptions were measured pre-exercise, 0-, 30-, and 90-min postexercise. Energy intake was recorded the day before and day of each session. Acylated ghrelin was suppressed ( P < 0.001, [Formula: see text] = 0.474) by HIIT (0-min and 30-min postexercise; P < 0.091, d > 1.84) and SIT (0-min, 30-min, and 90-min postexercise; P < 0.037, d > 1.72) compared with CTRL, and SIT suppressed concentrations compared with MICT (0-min and 30-min postexercise; P < 0.91, d > 1.19). There were no effects of exercise on active PYY, active GLP-1, appetite perceptions, or free-living energy intake ( P > 0.126, [Formula: see text] < 0.200). Intense interval exercise that generates lactate accumulation suppresses acylated ghrelin with little effect on anorexigenic hormones, overall appetite, or free-living energy intake. NEW & NOTEWORTHY We explored the effects of submaximal, near maximal, and supramaximal intensity exercise on appetite regulation in middle-aged adults. Our data support the intensity-dependent effect of exercise on acylated ghrelin suppression that is closely related to lactate accumulation, though there appears to be little effect on anorexigenic hormones [active peptide tyrosine tyrosine (PYY), active glucagon-like peptide-1 (GLP-1)], overall appetite, or free-living energy intake. These data support previous results in younger adults where lactate was implicated in the exercise-induced suppression of acylated ghrelin.

Polycystic ovary syndrome (PCOS) is associated with endothelial dysfunction; whether this is attributable to comorbid hyperandrogenism and/or obesity remains to be established. Therefore, we 1 ) compared endothelial function between lean and overweight/obese (OW/OB) women with and without androgen excess (AE)-PCOS and 2 ) examined androgens as potential modulators of endothelial function in these women. The flow-mediated dilation (FMD) test was applied in 14 women with AE-PCOS (lean: n = 7; OW/OB: n = 7) and 14 controls (CTRL; lean: n = 7, OW/OB: n = 7) at baseline (BSL) and following 7 days of ethinyl estradiol supplementation (EE; 30 µg/day) to assess the effect of a vasodilatory therapeutic on endothelial function; at each time point we assessed peak increases in diameter during reactive hyperemia (%FMD), shear rate, and low flow-mediated constriction (%LFMC). BSL %FMD was attenuated in lean AE-PCOS versus both lean CTRL (5.2 ± 1.5 vs. 10.3 ± 2.6%, P < 0.01) and OW/OB AE-PCOS (5.2 ± 1.5 vs. 6.6 ± 0.9%, P = 0.048). A negative correlation between BSL %FMD and free testosterone was observed in lean AE-PCOS only ( R 2 = 0.68, P = 0.02). EE increased %FMD in both OW/OB groups (CTRL: 7.6 ± 0.6 vs. 10.4 ± 2.5%, AE-PCOS: 6.6 ± 0.9 vs. 9.6 ± 1.7%, P = 0.99), and reduced %FMD in lean CTRL (10.3 ± 2.6 vs. 7.6 ± 1.2%, P = 0.03). Collectively, these data indicate that lean women with AE-PCOS exhibit more severe endothelial dysfunction than their OW/OB counterparts. Furthermore, endothelial dysfunction appears to be mediated by circulating androgens in lean but not in OW/OB AE-PCOS, suggesting a difference in the endothelial pathophysiology of AE-PCOS between these phenotypes. P = 0.03). Collectively, these data indicate that lean women with AE-PCOS exhibit more severe endothelial dysfunction than their OW/OB counterparts. Furthermore, endothelial dysfunction appears to be mediated by circulating androgens in lean but not in OW/OB AE-PCOS, suggesting a difference in the endothelial pathophysiology of AE-PCOS between these phenotypes. NEW & NOTEWORTHY We present evidence for marked endothelial dysfunction in lean women with androgen excess polycystic ovary syndrome (AE-PCOS) that is 1 ) impaired relative to overweight/obese women with AE-PCOS, and 2 ) unchanged following short-term ethinyl estradiol supplementation. These data indicate an important direct effect of androgens on the vascular system in women with AE-PCOS. Our data also suggest that the relationship between androgens and vascular health differs between phenotypes of AE-PCOS.3 ) unchanged following short-term ethinyl estradiol supplementation. These data indicate an important direct effect of androgens on the vascular system in women with AE-PCOS. Our data also suggest that the relationship between androgens and vascular health differs between phenotypes of AE-PCOS.

This study examined the effect of changes in end-inspiratory lung volume (EILV) and breathing pattern on neural activation of the crural diaphragm (EMG DIA ) and of the sternocleidomastoid (EMG SCM ), scalene (EMG SCA ), and external intercostal muscles (EMG INT ) at constant ventilation (V̇ E ). Twelve healthy adults performed a series of 30-s breathing trials at a constant V̇ E corresponding to 15% of their maximum voluntary ventilation while 1 ) altering EILV at a constant breathing pattern and 2 ) altering breathing pattern at a constant EILV. Using a real-time visual display of each participant's spirogram, EILV was voluntarily targeted at 65% (EILV 65% ), 75% (EILV 75% ), 85% (EILV 85% ), and 95% (EILV 95% ) of each participant's inspired vital capacity, whereas breathing frequency ( f ) was targeted at 15, 35, and 50 breaths/min using a metronome. The tidal volume needed for a participant to maintain V̇ R ) was targeted at 15, 35, and 50 breaths/min using a metronome. The tidal volume needed for a participant to maintain V̇ E constant across trials was achieved via changes in end-expiratory lung volume. A multipair esophageal electrode catheter was used to record EMG DIA , whereas surface electrodes were used to record EMG SCM , and EMG SCA , and EMG INT . On average, EMG DIA , EMG SCM , and EMG SCA increased as a function of increasing EILV at constant V̇ INT , independent of changes in breathing pattern. The magnitudes of these increases were particularly notable in the transition from EILV E , independent of changes in breathing pattern. The magnitudes of these increases were particularly notable in the transition from EILV 85% to EILV 95% and EMG SCM In healthy adults, as EILV increases toward total lung capacity, progressive compensatory increases in neural activation of the diaphragm and extra-diaphragmatic inspiratory muscles are needed to support V̇ SCA. , independent of changes in breathing pattern. E We examined the effect of changes in end-inspiratory lung volume (EILV) and breathing pattern on neural activation of the inspiratory muscles in healthy adults. We found that, at a constant ventilation, neural activation of the crural diaphragm and of the extra-diaphragmatic inspiratory muscles (sternocleidomastoid, scalene, and seventh external intercostals) increased as a function of increasing EILV, independent of changes in breathing pattern. Our results point to a critical mechanistic role of EILV in determining the level of central inspiratory neural drive needed to support ventilation.NEW & NOTEWORTHY We examined the effect of changes in end-inspiratory lung volume (EILV) and breathing pattern on neural activation of the inspiratory muscles in healthy adults. We found that, at a constant ventilation, neural activation of the crural diaphragm and of the extra-diaphragmatic inspiratory muscles (sternocleidomastoid, scalene, and seventh external intercostals) increased as a function of increasing EILV, independent of changes in breathing pattern. Our results point to a critical mechanistic role of EILV in determining the level of central inspiratory neural drive needed to support ventilation.

High-intensity exercise inhibits appetite, in part, via alterations in the peripheral concentrations of the appetite-regulating hormones acylated ghrelin, active glucagon-like peptide-1 (GLP-1), and active peptide tyrosine-tyrosine (PYY). Given lactate may mediate these effects, we used sodium bicarbonate (NaHCO 3 ) supplementation in a double-blind, placebo-controlled, crossover design to investigate lactate's purported role in exercise-induced appetite suppression. Eleven males completed two identical high-intensity interval training sessions (10 × 1 min cycling bouts at ~90% heart rate maximum interspersed with 1-min recovery), where they ingested either NaHCO 3 (BICARB) or sodium chloride (NaCl) as a placebo (PLACEBO) preexercise. Blood lactate, acylated ghrelin, GLP-1, and PYY concentrations, as well as overall appetite were assessed preexercise and 0, 30, 60, and 90 min postexercise. Blood lactate was greater immediately ( P < 0.001) and 30 min postexercise ( P = 0.049) in the BICARB session with an increased ( P = 0.009) area under the curve (AUC). The BICARB session had lower acylated ghrelin at 60 ( P = 0.014) and 90 min postexercise ( P = 0.016), with a decreased AUC ( P = 0.039). The BICARB session had increased PYY ( P = 0.034) with an increased AUC ( P = 0.031). The BICARB session also tended ( P = 0.060) to have increased GLP-1 at 30 ( P = 0.003) and 60 min postexercise ( P < 0.001), with an increased AUC ( P = 0.030). The BICARB session tended ( P = 0.059) to reduce overall appetite, although there was no difference in AUC ( P = 0.149). These findings support a potential role for lactate in the high-intensity exercise-induced appetite-suppression. NEW & NOTEWORTHY We used sodium bicarbonate to increase lactate accumulation or sodium chloride as a placebo. Our findings further implicate lactate as a mediator of exercise-induced appetite suppression, given exercise-induced increases in lactate during the sodium bicarbonate session altered peripheral concentrations of appetite-regulating hormones, culminating in a reduction of appetite. This supports a lactate-dependent mechanism of appetite suppression following high-intensity exercise and highlights the potential of using lactate as a means of inducing a caloric deficit.

Slow breathing (SLOWB) is recommended for use as an adjuvant treatment for hypertension. However, the extent to which blood pressure (BP) responses to SLOWB differ between men and women are not well-established. Therefore, we tested the hypothesis that an acute bout of SLOWB would induce larger decreases in BP in males than in females, given that males typically have higher resting BP. We also examined autonomic contributors to reduced BP during SLOWB; that is, muscle sympathetic nerve activity and spontaneous cardiovagal (sequence method) and vascular sympathetic baroreflex sensitivity. We tested normotensive females ( n = 10, age: 22 ± 2 y, body mass index: 22 ± 2 kg/m 2 ) and males ( n = 12, age: 23 ± 3 y, body mass index: 26 ± 4 kg/m 2 ). Subjects were tested at baseline and during the last 5 min of a 15-min RESPeRATE-guided SLOWB session. Overall, SLOWB reduced systolic BP by 3.2 ± 0.8 mmHg (main effect, P < 0.01). Females had lower systolic BP (main effect, P = 0.02); we observed no interaction between sex and SLOWB. SLOWB also reduced muscle sympathetic nerve activity burst incidence by -5.0 ± 1.4 bursts/100 heartbeats (main effect, P < 0.01). Although females tended to have lower burst incidence (main effect, P = 0.1), there was no interaction between sex and SLOWB. Cardiovagal baroreflex sensitivity improved during SLOWB (21.0 vs. 36.0 ms/mmHg, P = 0.03) with no effect of sex. Despite lower overall BP in females, our data support a lack of basement effect on SLOWB-induced reductions in BP, as SLOWB was equally effective in reducing BP in males and females. Our findings support the efficacy of the RESPeRATE device for reducing BP in both sexes, even in young, normotensive individuals. NEW & NOTEWORTHY We provide support for the effectiveness of device-guided slow breathing for blood pressure reduction in young normotensive women and men. Despite having lower baseline blood pressure and sympathetic nerve activity, women experienced equivalent reductions in both measures in response to RESPeRATE-guided slow breathing as men. Thus, slow breathing appears to be effective in young healthy normotensive individuals of both sexes and may be an ideal preventative therapy against future hypertension.

High-intensity exercise suppresses appetite partly through changes in peripheral appetite-regulating hormones. Lactate and IL-6 mediate the release of these hormones in animal/cell models and may provide a mechanistic link between exercise intensity and appetite regulation. The current study examined changes in appetite-regulating hormones, lactate, and IL-6 after different intensities of running. Eight males completed four experimental sessions: 1 ) moderate-intensity continuous training (MICT; 65% V̇o 2max ); 2 ) vigorous-intensity continuous training (VICT; 85% V̇o 2max ); 3 ) sprint interval training (SIT; repeated "all-out" sprints); and 4 ) Control (CTRL; no exercise). Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), total peptide YY (PYY), lactate, IL-6, and appetite perceptions were measured pre-, immediately postexercise, 30 min postexercise, and 90 min postexercise. Energy intake was recorded over 3 days. VICT and SIT suppressed ghrelin ( P < 0.001), although SIT elicited a greater ( P = 0.016 vs. MICT) and more prolonged ( P < 0.001 vs. all sessions) response. GLP-1 increased immediately after MICT ( P < 0.001) and 30 min after VICT ( P < 0.001) and SIT ( P < 0.002), while VICT elicited a greater postexercise increase in PYY vs. MICT ( P = 0.027). Postexercise changes in blood lactate and IL-6 correlated with the area under the curve values for ghrelin ( r  = -0.60, P < 0.001) and GLP-1 ( r  = 0.42, P = 0.017), respectively. Appetite was suppressed after exercise ( P < 0.001), although more so after VICT ( P < 0.027) and SIT ( P < 0.001) vs. MICT, and energy intake was reduced on the day after VICT ( P < 0.017 vs. MICT and CTRL) and SIT ( P = 0.049 vs. MICT). These findings support an intensity-dependent paradigm for appetite regulation following exercise and highlight the potential involvement of lactate and IL-6. NEW & NOTEWORTHY This study examines the involvement of two potential mechanisms (lactate and IL-6) that may explain the intensity-dependent effects of acute exercise on appetite-related parameters. Our findings support a clear intensity-dependent paradigm for appetite regulation following exercise, as highlighted by the change in acylated ghrelin and the suppression of appetite and energy intake after vigorous exercise (continuous and intermittent). Further, our findings extend previous work in animal/cell models by providing evidence for the potential role of lactate and IL-6 in mediating changes in appetite-related parameters following exercise in humans., (Copyright © 2017 the American Physiological Society.)

Our group has shown a greater number of functioning motor units (MU) in a cohort of highly active older (∼65 yr) masters runners relative to age-matched controls. Because of the precipitous loss in the number of functioning MUs in the eighth and ninth decades of life it is unknown whether older world class octogenarian masters athletes (MA) would also have greater numbers of functioning MUs compared with age-matched controls. We measured MU numbers and neuromuscular transmission stability in the tibialis anterior of world champion MAs (∼80 yr) and compared the values with healthy age-matched controls (∼80 yr). Decomposition-enhanced spike-triggered averaging was used to collect surface and intramuscular electromyography signals during dorsiflexion at ∼25% of maximum voluntary isometric contraction. Near fiber (NF) MU potential analysis was used to assess neuromuscular transmission stability. For the MAs compared with age-matched controls, the amount of excitable muscle mass (compound muscle action potential) was 14% greater (P < 0.05), there was a trend (P = 0.07) toward a 27% smaller surface-detected MU potential representative of less collateral reinnervation, and 28% more functioning MUs (P < 0.05). Additionally, the MAs had greater MU neuromuscular stability than the controls, as indicated by lower NF jitter and jiggle values (P < 0.05). These results demonstrate that high-performing octogenarians better maintain neuromuscular stability of the MU and mitigate the loss of MUs associated with aging well into the later decades of life during which time the loss of muscle mass and strength becomes functionally relevant. Future studies may identify the concomitant roles genetics and exercise play in neuroprotection., (Copyright © 2016 the American Physiological Society.)

Understanding sex differences in the qualitative dimensions of exertional dyspnea may provide insight into why women are more affected by this symptom than men. This study explored the evolution of the qualitative dimensions of dyspnea in 70 healthy, young, physically active adults (35 M and 35 F). Participants rated the intensity of their breathing discomfort (Borg 0-10 scale) and selected phrases that best described their breathing from a standardized list (work/effort, unsatisfied inspiration, and unsatisfied expiration) throughout each stage of a symptom-limited incremental-cycle exercise test. Following exercise, participants selected phrases that described their breathing at maximal exercise from a list of 15 standardized phrases. Intensity of breathing discomfort was significantly higher in women for a given ventilation, but differences disappeared when ventilation was expressed as a percentage of maximum voluntary ventilation. The dominant qualitative descriptor in both sexes throughout exercise was increased work/effort of breathing. At peak exercise, women were significantly more likely to select the following phrases: "my breathing feels shallow," "I cannot get enough air in," "I cannot take a deep breath in," and "my breath does not go in all the way." Women adopted a more rapid and shallow breathing pattern and had significantly higher end-inspiratory lung volumes relative to total lung capacity throughout exercise relative to men. These findings suggest that men and women do not differ in their perceived quality of dyspnea during submaximal exercise, but subjective differences appear at maximal exercise and may be related, at least in part, to underlying sex differences in breathing patterns and operating lung volumes during exercise., (Copyright © 2015 the American Physiological Society.)

We tested the hypothesis that neuromechanical uncoupling of the respiratory system forms the mechanistic basis of dyspnea during exercise in the setting of "abnormal" restrictive constraints on ventilation (VE). To this end, we examined the effect of chest wall strapping (CWS) sufficient to mimic a "mild" restrictive lung deficit on the interrelationships between VE, breathing pattern, dynamic operating lung volumes, esophageal electrode-balloon catheter-derived measures of the diaphragm electromyogram (EMGdi) and the transdiaphragmatic pressure time product (PTPdi), and sensory intensity and unpleasantness ratings of dyspnea during exercise. Twenty healthy men aged 25.7 ± 1.1 years (means ± SE) completed symptom-limited incremental cycle exercise tests under two randomized conditions: unrestricted control and CWS to reduce vital capacity (VC) by 21.6 ± 0.5%. Compared with control, exercise with CWS was associated with 1) an exaggerated EMGdi and PTPdi response; 2) no change in the relationship between EMGdi and each of tidal volume (expressed as a percentage of VC), inspiratory reserve volume, and PTPdi, thus indicating relative preservation of neuromechanical coupling; 3) increased sensory intensity and unpleasantness ratings of dyspnea; and 4) no change in the relationship between increasing EMGdi and each of the intensity and unpleasantness of dyspnea. In conclusion, the increased intensity and unpleasantness of dyspnea during exercise with CWS could not be readily explained by increased neuromechanical uncoupling but likely reflected the awareness of increased neural respiratory drive (EMGdi) needed to achieve any given VE during exercise in the setting of "abnormal" restrictive constraints on tidal volume expansion.

The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17beta-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater (P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats (P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower (P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater (P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower (P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower (P < 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content (P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.

The purpose of this study was to use the meta-analytic approach to examine the effects of exercise on bone mineral density (BMD) in men. A total of 26 effect sizes (ES) representing 225 subjects from 8 studies met the criteria for inclusion. When BMD sites assessed were specific to the sites loaded during exercise, increases of approximately 2.6% (2.1% in the exercisers and -0.5% in the controls) were found. These results were statistically significant (ES = 0.213, 95% bootstrap confidence interval = 0.007-0.452). Statistically significant ES changes were found for older (>31 yr) but not younger (<31 yr) adults, with differences between groups statistically significant (P = 0.04). Statistically significant changes were also observed at the femur, lumbar, and os calcis sites. The results of this study suggest that site-specific exercise may help improve and maintain BMD at the femur, lumbar, and os calcis sites in older men. However, the biological importance of the small changes observed for most outcomes, quality of studies, and limited data pool prevent us from forming any firm conclusion regarding the use of exercise for maintaining and/or improving BMD in men. Clearly, a need exists for additional studies.