Low nitrogen conditions accelerate flowering by modulating the phosphorylation state of FLOWERING BHLH 4 in Arabidopsis.

Nitrogen (N) is an essential nutrient that affects multiple plant developmental processes, including flowering. As flowering requires resources to develop sink tissues for reproduction, nutrient availability is tightly linked to this process. Low N levels accelerate floral transition; however, the molecular mechanisms underlying this response are not well understood. Here, we identify the FLOWERING BHLH 4 (FBH4) transcription factor as a key regulator of N-responsive flowering in Arabidopsis Low N-induced early flowering is compromised in fbh quadruple mutants. We found that FBH4 is a highly phosphorylated protein and that FBH4 phosphorylation levels decrease under low N conditions. In addition, decreased phosphorylation promotes FBH4 nuclear localization and transcriptional activation of the direct target CONSTANS (CO) and downstream florigen FLOWERING LOCUS T (FT) genes. Moreover, we demonstrate that the evolutionarily conserved cellular fuel sensor SNF1-RELATED KINASE 1 (SnRK1), whose kinase activity is down-regulated under low N conditions, directly phosphorylates FBH4. SnRK1 negatively regulates CO and FT transcript levels under high N conditions. Together, these results reveal a mechanism by which N levels may fine-tune FBH4 nuclear localization by adjusting the phosphorylation state to modulate flowering time. In addition to its role in flowering regulation, we also showed that FBH4 was involved in low N-induced up-regulation of nutrient recycling and remobilization-related gene expression. Thus, our findings provide insight into N-responsive growth phase transitions and optimization of plant fitness under nutrient-limited conditions.

Changes in blood volume and oxygenation level in a working muscle during a crank cycle.

PURPOSE: This study examined circulatory and metabolic changes in a working muscle during a crank cycle in a pedaling exercise with near-infrared spectroscopy (NIRS). METHODS: NIRS measurements sampled under stable metabolic and cadence conditions during incremental pedaling exercise were reordered according to the crank angles whose signals were obtained in eight male subjects. RESULTS: The reordered changes in muscle blood volume during a crank cycle demonstrated a pattern change that corresponded to changes in pedal force and electrical muscle activity for pedal thrust. The top and bottom peaks for muscle blood volume change at work intensities of 180 W and 220 W always preceded (88 +/- 32 and 92 +/- 23 ms, respectively) those for muscle oxygenation changes. Significant differences in the level of NIRS parameters (muscle blood volume and oxygenation level) among work intensities were noted with a common shape in curve changes related to pedal force. In addition, a temporary increase in muscle blood volume following a pedal thrust was detected at work intensities higher than moderate. This temporary increase in muscle blood volume might reflect muscle blood flow restriction caused by pedal thrusts. CONCLUSION: The results suggest that circulatory and metabolic conditions of a working muscle can be easily affected during pedaling exercise by work intensity. The present method, reordering of NIRS parameters against crank angle, serves as a useful measure in providing additional findings of circulatory dynamics and metabolic changes in a working muscle during pedaling exercise.

Cardiorespiratory responses to hypoxia and hypercapnia at rest in vocalists.

In order to clarify whether or not ventilatory and circulatory responses to hypoxia and hypercapnia at rest in male vocalists (n = 11) are identical to those of untrained subjects (n = 11), ventilatory responses to hypoxia (HVR) and hypercapnia (HCVR) were estimated as the slope of regression relating .VI to SaO(2) (Delta.VI/DeltaSaO(2)) or the slope factor (A) for the .VI-PETO(2) curve, and as the slope of regression relating .VI to PETCO(2) (Delta.VI/DeltaPETCO(2)), respectively. The respiratory frequency (f), tidal volume (VT), heart rate (HR), and blood pressure (BP) responses to hypoxia and hypercapnia were also estimated as the slope of the line calculated by linear regression related to SaO(2) and PETCO(2). Mean values of Delta.VI/DeltaSaO(2) and A as an index of hypoxic ventilatory response were lower in the vocalist group (0.39 +/- 0.25 l.min(-1).%(-1) and 76.8 +/- 55.7 l.min(-1).torr(-1)) than that in the control group (0.56 +/- 0.46 l.min(-1).%(-1) and 101.6 +/- 85.4 l.min(-1).torr(-1)), and there was no statistically significant difference. The Deltaf/DeltaSaO(2) was significantly (plt;0.05 ) lower in the vocalist group (-0.02 +/- 0.39 breaths.min(-1).%(-1)) than that in the control group (0.43 +/- 0.65 breaths.min(-1).%(-1)). In contrast, mean values of Delta.VI/DeltaPETCO(2) per body mass index were significantly (p<0.05) lower in the vocalist group (0.05 +/- 0.03 l.min(-1).torr(-1)) than those in the control group (0.10 +/- 0.06l.min(-1).torr(-1)). There were also significant differences in DeltaVT/DeltaPETCO(2) and Deltaf/DeltaPETCO(2) between the two groups (p<0.05). However, no significant differences in HR and BP responses to hypoxia and hypercapnia between the two groups were observed. These results suggest that the magnitude of ventilatory response, but not HR and BP, to hypoxia and hypercapnia at rest in vocalists is reduced by chronic vocal training, including breath control and elongation of phonation for long periods.

Cross education of muscular strength during unilateral resistance training and detraining.

The purpose of the present study was to examine the changes in maximum voluntary isometric contraction (MVC) in the contralateral untrained limb during unilateral resistance training and detraining, and to examine the factors inducing these changes by means of electrophysiological techniques. Nine healthy males trained their plantar flexor muscles unilaterally 4 day-s x week(-1) for 6 weeks using 3 sets of 10-12 repetitions at 70-75% of one-repetition maximum a day, and detrained for 6 weeks. Progressive unilateral resistance training significantly (P < 0.05) increased MVC, integrated electromyogram (iEMG), and voluntary activation in the trained and contralateral untrained limbs. The changes in MVC after training were significantly correlated with the changes in iEMG in both limbs. No significant changes occurred in MVC, voluntary activation, and iEMG in the contralateral limb after detraining. The changes in MVC after detraining did not correlate with the changes in voluntary activation or iEMG in either limb. Training and detraining did not alter twitch and tetanic peak torques in either limb. These results suggest that the mechanisms underlying cross education of muscular strength may be explained by central neural factors during training, but not solely so during detraining.

Enhanced chemosensitivity after intermittent hypoxic exposure does not affect exercise ventilation at sea level.

The purpose of the present study was to test the hypothesis that the ventilatory response to exercise at sea level may increase after intermittent hypoxic exposure for 1 week, accompanied by an increase in hypoxic or hypercapnic ventilatory chemosensitivity. One group of eight subjects (hypoxic group) were decompressed in a chamber to 432 torr (where 1 torr=1.0 mmHg, simulating an altitude of 4,500 m) over a period of 30 min and maintained at that pressure for 1 h daily for 7 days. Oxygen uptake and pulmonary ventilation (V(E)) were determined at 40%, 70%, and 100% of maximal oxygen uptake at sea level before (Pre) and after (Post) 1 week of daily exposures to hypoxia. The hypoxic ventilatory response (HVR) was determined using the isocapnic progressive hypoxic method as an index of ventilatory chemosensitivity to hypoxia, and the hypercapnic ventilatory response (HCVRSB) was measured by means of the single-breath carbon dioxide method as an index of peripheral ventilatory chemosensitivity to hypercapnia. The same parameters were measured in another group of six subjects (control group). In the hypoxic group, resting HVR increased significantly ( P<0.05) after intermittent hypoxia and HCVRSB increased at Post, but the change was not statistically significant ( P=0.07). In contrast, no changes in HVR and HCVRSB were found in the control group. There were no changes in either V(E) or the ventilatory equivalent for oxygen during maximal and submaximal exercise at sea level throughout the experimental period in either group. These results suggest that the changes in resting hypoxic and peripheral hypercapnic chemosensitivities following short-term intermittent hypoxia have little effect on exercise ventilation at sea level.