Novel insights on caffeine supplementation, CYP1A2 genotype, physiological responses and exercise performance.

Caffeine is a popular ergogenic aid due to its primary physiological effects that occur through antagonism of adenosine receptors in the central nervous system. This leads to a cascade of physiological reactions which increases focus and volition, and reduces perception of effort and pain, contributing to improved exercise performance. Substantial variability in the physiological and performance response to acute caffeine consumption is apparent, and a growing number of studies are implicating a single-nucleotide polymorphism in the CYP1A2 gene, responsible for caffeine metabolism, as a key factor that influences the acute responses to caffeine ingestion. However, existing literature regarding the influence of this polymorphism on the ergogenic effects of caffeine is controversial. Fast caffeine metabolisers (AA homozygotes) appear most likely to benefit from caffeine supplementation, although over half of studies showed no differences in the responses to caffeine between CYP1A2 genotypes, while others even showed either a possible advantage or disadvantage for C-allele carriers. Contrasting data are limited by weak study designs and small samples sizes, which did not allow separation of C-allele carriers into their sub-groups (AC and CC), and insufficient mechanistic evidence to elucidate findings. Mixed results prevent practical recommendations based upon genotype while genetic testing for CYP1A2 is also currently unwarranted. More mechanistic and applied research is required to elucidate how the CYP1A2 polymorphism might alter caffeine's ergogenic effect and the magnitude thereof, and whether CYP1A2 genotyping prior to caffeine supplementation is necessary.

The relationship between fat-free mass index and pulmonary hyperinflation in COPD patients.

BACKGROUND AND OBJECTIVE: Reduced fat-free mass (FFM), a common finding in chronic obstructive pulmonary disease (COPD), may indirectly impact peak exercise capacity through a greater level of pulmonary hyperinflation. We aimed to investigate if FFM index (FFM/squared height) impacts exercise induced dynamic hyperinflation in COPD patients. METHODS: Fifty-four patients with moderate-to-very severe COPD performed a symptom limited incremental cardiopulmonary exercise tests with serial measurements of inspiratory capacity (IC). FFM was measured by whole-body bioelectrical impedance. RESULTS: Patients were 66.7 ± 7.7 years old with mean forced expiratory volume in 1 s (FEV1) of 1.08 ± 0.41 L (42 ± 15% of predicted). Peak exercise IC was significantly (P < 0.05) correlated with IC at rest (r = 0.78), FEV1(r = 0.66), FVC (r = 0.59), FFM (r = 0.38) and FFM index (r = 0.29). However, only FEV1 and rest IC predict peak IC (r = 0.86; P < 0.01) in a multivariate linear regression analysis. CONCLUSIONS: FFM index was weakly associated with peak exercise IC in COPD patients. However, it ceased to be an independent predictor when corrected for expiratory airflow limitation (FEV1) and lung hyperinflation at rest (rest IC).

Effects of Expiratory Positive Airway Pressure on Exercise Tolerance, Dynamic Hyperinflation, and Dyspnea in COPD.

INTRODUCTION: The application of expiratory positive airway pressure (EPAP) in patients with COPD during exercise may reduce dynamic hyperinflation, while, on the other hand, it can increase the resistive work of breathing. Therefore, we evaluated the effects of 2 intensities of EPAP during exercise on tolerance, dynamic hyperinflation, and dyspnea in subjects with moderate to very severe COPD. METHODS: We performed a cross-sectional, experimental, 4-visit study. In visit 1, subjects performed symptom-limited cycling incremental cardiopulmonary exercise test (CPET). In visits 2-4, at least 48 h apart, in a randomized order, subjects performed constant CPET without EPAP, EPAP with 5 cm H2O (EPAP5), or EPAP with 10 cm H2O (EPAP10). RESULTS: The study included 15 non-hypoxemic subjects ranging from moderate to very severe COPD (mean FEV1 = 35 ± 11% predicted). Increasing intensities of EPAP during constant CPET tended to cause progressive reduction in exercise tolerance (P = .11). Of note, 10 of 15 subjects demonstrated significantly shorter average exercise duration with EPAP10 compared to the test without EPAP (-151 ± 105 s, P = .03 or -41 ± 26%). Minute ventilation increment was constrained by EPAP, secondary to a limited increase in tidal volume (P = .01). Finally, dyspnea sensation and serial measurements of inspiratory capacity during exercise were similar when comparing the three interventions at isotime and at end-constant CPETs. CONCLUSIONS: The application of EPAP5 or EPAP10 during exercise tended to cause a progressive reduction in exercise tolerance in subjects with COPD without improvement in dyspnea or dynamic hyperinflation at equivalent exercise duration.

Inspiratory loading and limb blood flow in COPD: The modulating effects of resting lung hyperinflation.

Inspiratory resistive loading (IRL) may have deleterious cardiocirculatory effects leading to poor peripheral perfusion in severely-hyperinflated patients with COPD. Nineteen patients (13 severely-hyperinflated with inspiratory capacity/total lung capacity ratio≤0.28) underwent calf blood flow (CBF) measurements by venous occlusion plethysmography at rest and during IRL at 60% maximal inspiratory pressure. Severely-hyperinflated patients had lower resting CBF and greater calf vascular resistance (CVR) than moderately-hyperinflated patients (p<0.05). All severely-hyperinflated patients had markedly reduced CBF (p=0.01). Opposite to our main hypothesis, however, IRL did not further reduce CBF in these patients (p>0.05). Conversely, it significantly decreased CBF and increased CVR in moderately-hyperinflated patients; in fact, end-trial CBF and CVR did not differ between the groups (p>0.05). In conclusion, marked impairments in resting appendicular blood flow in severely-hyperinflated patients with COPD were seen only after acute IRL in less hyperinflated patients. These findings set the stage for studies investigating the effects of lung deflation on peripheral hemodynamics in patients with severe hyperinflation.