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Interaction between exercise and air pollution.
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I can't let #greatsupervisor week @UBC pass without mentioning @UBCKin's @EnvPhysioLab. I can't thank Dr. Koehle enough!
Graduate Student Supervision
Doctoral Student Supervision (Jan 2008 - Nov 2019)
Endurance athletes competing at altitude experience a significant decrement in performance as a result of the reduced partial pressure of oxygen. There is significant inter-individual variability in how altitude affects these athletes and the mechanism through which this decrement occurs. The ability to recognize one’s personal response to hypoxia and employ strategies (i.e. acclimatization) to mitigate this response is extremely useful to competitive athletes. For my dissertation, I attempted to identify some of the mechanisms that are responsible for the inter-individual variation in exercise performance at altitude. I conducted (i) an initial study on “fly-in fly-out” acclimatization to prepare for competition at altitude; (ii) a study comparing onset of intrapulmonary arteriovenous anastomoses (IPAVA) at rest with the decrement in exercise performance at altitude and the effects of the pulmonary vasodilator sildenafil on IPAVA recruitment; (iii) a mock competition study investigating the effects of sildenafil on exercise performance at altitude; and (iv) a meta-analysis of the effects of sildenafil on exercise performance at altitude. The most important findings of my dissertation are that (i) a 12-hour overnight exposure to hypoxia does not give any acclimatization benefit nor does it have any detrimental effect on a maximal exercise test; (ii) sildenafil does not affect IPAVA recruitment in hypoxia, nor does IPAVA onset appear related to exercise performance in hypoxia; (iii) sildenafil does not improve exercise performance in a 16.1 km cycling time-trial at a simulated altitude of 3,000 m; (iv) the decrement in exercise performance at altitude appears to be closely related to oxygen saturation; and (v) while sildenafil does appear to reduce pulmonary artery pressure, and increase cardiac output and oxygen saturation, it does not reliably improve performance. This dissertation demonstrates the wide variation in the decrement in exercise performance due to hypoxia, examining several of the predictors and moderators of exercise performance.
No abstract available.
No abstract available.
High-altitude (and simulated high-altitude) environments can be extraordinarily stressful for low-altitude organisms because of the reduced oxygen availability (i.e. hypoxia). Humans, who live primarily at low altitude, can adjust physiologically (i.e., acclimatise or acclimate) to hypoxic environments; however, the human acclimatisation response to hypoxia is highly variable, evident from the differential susceptibility to acute altitude illnesses, such as acute mountain sickness (AMS). For my dissertation, I attempted to identify some of the physiological, genetic, and epidemiological variables that could explain the variation in hypoxia tolerance. I conducted (i) two studies using a normobaric hypoxia chamber at the University of British Columbia; (ii) two field studies in a mountainous region of the Nepalese Himalaya; and (iii) two meta-anaylyses. The most important findings of my dissertation are that (i) oxygen saturation (SPO₂) and heart rate (HR) were not strong markers of AMS susceptibility in laboratory or field settings; (ii) a low fraction of exhaled nitric oxide (FENO) was associated with increased susceptibility to AMS in the laboratory but not in the field; (iii) physiological responses (FENO, SPO₂, HR, blood pressure) to hypoxia were repeatable on two normobaric hypoxia exposures; (iv) AMS severity was lower on the second of two identical normobaric hypoxia exposures (but headache severity was similar); (v) in a large Nepalese sample, age, sex, ascent rate, and preventative strategies were associated with AMS susceptibility; (vi) the severity of AMS was similar in brothers; (vii) there were biogeographical differences in AMS susceptibility in the Nepalese sample; (viii) polymorphisms of the FAM149A gene were associated with AMS severity; (ix) AMS history was a poor predictor of future AMS outcomes; and (x) sleep quality was weakly related to other AMS symptoms. In conclusion, this dissertation demonstates that the measured physiological variables (FENO, SPO₂, HR, blood pressure) were not associated with AMS status, that a genetic basis to the variation in AMS susceptibility is likely, and that the Lake Louise Score definition of AMS should be amended. Our understanding of acute altitude tolerance in humans may be aided by the redefinition of AMS.
Master's Student Supervision (2010 - 2018)
Athlete monitoring provides valuable insight into the balance of an athlete’s stress and adaptation from training. Many methods exist to quantify athletes’ allostatic state, with a physical performance measure a primary link to sport performance. However, little research has focused on a critical aspect of field sport performance, sprinting. Therefore, the purpose of this thesis was to investigate the utility of sprint monitoring using in-depth kinematic analysis. Training load was measured daily, as the product of session duration and rating of perceived exertion, in 32 adolescent female soccer players, comprising a U-15 and U-18 team. Measures of 7-day and 28-day cumulative training loads and 7-day to 28-day exponentially weighted moving average (EWMA) and rolling average (RA) acute to chronic workload ratios (ACWR) were calculated. Players performed a countermovement jump (CMJ) on a contact mat and a 30 m sprint bi-weekly, and completed a daily wellness questionnaire to assess training load response over 14 weeks. From the 30 m sprint, 10 and 30 m times were measured using timing gates, and maximal acceleration, maximal velocity, and time to maximal velocity were measured using a radar gun. Linear mixed models were used to assess the influence of training load on CMJ, 30 m sprint performance variables, and athlete wellness. Cumulative training load over 7 days had a likely small positive effect on 30 m sprint time (d = 0.14; 90% CL: -0.01 to 0.28), while 28-day cumulative training load had a likely small positive effect on 30 m sprint time (d = 0.14; 0.00 to 0.28), a very likely small negative effect on maximal sprint velocity (d = -0.19; -0.03 to -0.35), and a likely moderate negative effect on athlete wellness (d = -0.35; -0.02 to -0.68). EWMA and RA ACWRs had possibly small (d = 0.18; -0.14 to 0.49) and likely moderate (d = 0.33; 0.00 to 0.66) positive effects on wellness. All other relationships were unclear. Monitoring sprint performance should be considered to evaluate response to training loads, with sprint time indicative of acute and chronic loads, while maximal sprint velocity and athlete wellness were more suggestive of chronic loads.
The purpose of this study was to investigate the efficacy of a 14-day, two-phase, field-based heat acclimatization (HA) training camp in international female soccer players. Sixteen outfield players engaged in (i) baseline absolute Plasma volume (PV) testing in Vancouver, Canada (~15˚C; 72.0% relative humidity: RH) 16 days prior to the start of the camp, (ii) Phase 1: 7 days of pre-HA (22.1±3.3˚C; 44.8±9.4%RH), (iii) Phase 2: 6 days of HA (34.5±1.2˚C; 53.2±4.3%RH), and (iv) 11 days of post-HA training (18.2±4.6˚C; 51.3±20.9%RH). Change in PV (%) from baseline was measured at the start of Phase 1, the end of Phase 1, and two days post-Phase 2. Core temperature (Tc), heart rate (HR), rate of perceived exertion (RPE), and Global Positioning System (GPS) derived metrics were recorded during all sessions. The physiological change during 5’-1’ submaximal running (12km/h) was observed pre and post Phase 1 and 2, two days post Phase 2 (2dayP), and eleven days post Phase 2 (11dayP) using HR during exercise (HRex) and recovery (HRR), as well as RPE. GPS metrics, HRR, and HRex during a four-a-side soccer game (4v4SSG) were used to observe physical performance in the heat pre and post Phase 2. All data were analyzed using magnitude-based inference statistics. PV increased by 7.4±3.6% (Standardized effect; SE=0.63) from the start of Phase 1 to the end of Phase 2, and this occurred primarily in Phase 1 (SE=0.64). 5’-1’ submaximal running improved over Phase 2 in hot conditions (HRex; SE= -0.49, HRR; SE=0.53). The greatest improvement in submaximal running in temperate conditions was delayed as the largest change from Phase 1 in HRex (SE= -0.42) and HRR (SE= 0.37) occurred 11dayP. The 4v4SSG revealed a moderate reduction in HRex (-3.5bpm), a large increase in HRR (5.7%), and a moderate increase in inertial explosive movements (20%) from pre to post Phase 2. Field-based HA can induce physiological change beneficial to soccer performance in temperate and hot conditions and the 5’-1’ submaximal running test may be used to effectively monitor submaximal HR responses that may have been induced by HA up to two-weeks out of the heat.
To our knowledge, no study has used an assessment of ataxia and a finger-tapping task on a mobile device to monitor acclimatization to hypoxia. This research evaluated the utility of this tool in assessing human acclimatization to hypoxia while monitoring the development of acute mountain sickness (AMS). This study used a single-blinded repeated-measures randomized crossover design. Subjects experienced a familiarization trial at a simulated altitude of 2000m, a high altitude simulating 4200m and a sham condition simulating 250m. Measurements of AMS, pulse oxygen saturation and performance of the finger-tapping task were completed immediately prior to, and 5 minutes, 4 hours, and 12 hours following entrance to the chamber. Fifteen healthy male and female subjects were recruited form the Vancouver area. Subjects were between the ages of 19 and 25 years old. Subjects had not traveled to an altitude of 3000m or higher in the 3 months prior to testing. Subjects were excluded if they had any cardiovascular or pulmonary conditions. A repeated-measures ANOVA was performed to analyze if significant results were found for reaction time and accuracy of the finger-tapping task. Accuracy of the finger-tapping task worsened over the exposure to hypoxia, however, error rate and response time were not affected based on this simulated altitude alone. All other measures, including symptom questionnaires and pulse oxygen saturation suggest that these subjects had normal responses to altitude. Based on these findings, it appears that these finger-tapping tasks that focus on measures may be useful while monitoring acclimatization to hypoxia.
No abstract available.
Running-related injuries (RRIs) have been attributed to a number of factors, but there is no consensus in the current literature as to whether sex is a risk factor for RRIs, or if risk factors for running-related pain differ by sex. It has been suggested that due to differences in anatomy and biomechanics, males and females have their own RRI risk profiles; several variables may need to be taken into consideration when assessing sex as a risk factor for RRIs and running-related pain.Purpose: The proposed study represented the first two phases of a three-tiered epidemiological project. The purpose of Phase I was to determine whether there were significant differences in site-specific running-related injuries/pain between males and females training for a 10-km race; a statistical model was then created in the second phase to determine what explains running-related pain in the lower extremity by sex, for runners preparing for a 10-km race.Methods: 114 recreational runners (46 males [37.9 ± 9.8 years; 75.46 ± 9.55 kg; 1.75 ± 0.08 m] and 68 females [32.60 ± 8.70 years; 63.47 ± 9.96 kg; 1.66 ± 0.06 m]) took part in a prospective cohort design of a gradual 12-week training program, and a comprehensive baseline assessment was recorded for each participant. Weekly online surveys were administered to monitor whether subjects experienced an RRI. The Visual Analogue Scale (VAS) was administered to record pain scores at 11 relevant anatomical locations in the lower limb and the whole body, at baseline and during Weeks 4, 8, and 12 of the program. Foot and Ankle Disability Index (FADI) pain scores were also measured at these time points.Results: Sex was not a significant factor in the onset of location-specific, running-related pain in the VAS sites, but significant main effects of sex were found for the FADI. Males and females had different explanatory variables for each of the VAS and FADI sites.Conclusions: The causes of running-related pain in the individual anatomical regions varied by sex, which suggests that running-related pain may be decreased by addressing sex-specific risk factors.
Kettlebell lifting continues to gain popularity as a strength and conditioning training tool and as a sport in and of itself (Girevoy Sport). Although the swing to chest-level and several multi-movement protocols have been analyzed, little research has attempted to quantify the aerobic stimulus of individual kettlebell movements, which would best inform kettlebell-related exercise prescription. The purpose of this study was to quantify the cardiopulmonary demand, assessed by oxygen consumption (V̇O₂) and heart rate (HR), of continuous high-intensity kettlebell snatches under conditions that consider Girevoy Sport, and to compare this demand to a more traditional graded rowing exercise test. Ten male participants (age = 28.4 ± 4.6 years, height = 185 ± 7 cm, body mass = 95.1 ± 14.9 kg) completed (1) a graded rowing exercise test to determine maximal oxygen consumption (V̇O₂max) and maximal heart rate (HRmax) and (2) a graded kettlebell snatch exercise test with a 16-kg kettlebell to determine peak oxygen consumption (V̇O₂peak) and peak heart rate (HRpeak) during this activity. Subjects achieved a V̇O₂max of 45.7 ± 6.9 ml·kg-¹·min-¹ and an HRmax of 177 ± 6.9 beats per minute (bpm). The kettlebell snatch test produced a V̇O₂peak of 37.3 ± 5.2 ml·kg-¹·min-¹ (82.1 ± 7.4% V̇O₂max) and a heart rate of 173 ± 8 beats per minute (97.3 ± 4.8% HRmax). These findings suggest that continuous high-intensity kettlebell snatches with 16-kg are likely provide an adequate aerobic stimulus to improve cardiorespiratory fitness in those whose V̇O₂max is ≤ 51 ml·kg-¹·min-¹ and those who are moderately trained and lower, according to recommendations from the American College of Sports Medicine.
We examined the control of breathing, cardio-respiratory effects and the prevalence of acute mountain sickness (AMS) in humans exposed to hypobaric hypoxia (HH), normobaric hypoxia (NH), and under two control conditions (hypobaric normoxia and normobaric normoxia). Subjects (n = 11) were familiarised with all tests prior to their first exposures. The order of conditions was randomized, each exposure lasted for 6 hours, and consecutive exposures were separated by a one-week washout period. Prior to and following exposures, subjects underwent hyperoxic and hypoxic Duffin rebreathing tests, measuring CO₂ threshold and sensitivity, and a hypoxic ventilatory response test (HVR), measuring sensitivity to O₂. Inside the environmental chamber, minute ventilation (VE), tidal volume (VT), frequency of breathing (fB), blood oxygenation (SPO₂), heart rate (HR) and blood pressure (BP) were measured at 5min, 30min and hourly until exit. Symptoms of AMS were evaluated hourly using the Lake Louise score (LLS). Both the hyperoxic and hypoxic CO₂ thresholds were lowered after HH and NH during the Duffin rebreathing test. Hypoxic sensitivity in the Duffin rebreathing test was only increased after HH exposure. No changes occurred in the HVR after any of the four exposures. Ventilatory parameters, SPO₂ and HR were higher in the hypoxic exposures as opposed to the normoxic exposures. No major differences were observed for VE or any other cardio-respiratory variables between NH than HH. The LLS was greater in AMS-susceptible than in AMS-resistant subjects, but LLS was similar in HH and NH. We conclude that 6 hours of hypoxic exposure is sufficient to lower the peripheral and central CO₂ threshold, but it is too short in duration to induce differences in cardio-respiratory variables between HH and NH or to create differences in AMS severity.
Introduction: High altitude pulmonary edema (HAPE) is caused by hypoxic vasoconstriction, leading to increased pulmonary artery pressure (PPA). Increased PPA results in extravasation of fluid from the pulmonary capillaries to the interstitial space and inhibition of gas exchange. Immersion pulmonary edema (IPE) is likely the result of increased hydrostatic pressure due to water immersion combined with cold and physical exertion, further elevating PPA. During maximal exercise, some humans develop pulmonary edema independent of hypoxia or immersion; this is a possible cause of exercise-induced arterial hypoxemia (EIAH). Purpose: The purpose of this study was to 1) investigate the common mechanisms that are responsible for the development of HAPE, IPE, and EIAH; and 2) investigate the factors that determine an individual’s susceptibility to HAPE/IPE. Hypotheses: We hypothesize that 1) individuals susceptible to HAPE/IPE will develop increased extravascular lung water (EVLW) following exercise; and 2) these changes will not occur in HAPE/IPE-resistant controls. Methods: This study included 9 healthy fit participants who previously experienced HAPE or IPE. Participants performed a 45-minute maximal exercise task on a cycle ergometer. A matched control group of 9 participants with experience at altitude or immersion and no history of HAPE/IPE also performed the task. Diffusion capacity of CO (DLco) was measured before and after exercise. Computed tomography was used to confirm EVLW following exercise. Results: Both groups showed a significant reduction in lung density post-exercise (p=0.013). Participants susceptible to HAPE/IPE had a significantly lower density compared to resistant participants (p=0.037). DLco decreased significantly after exercise (p