Section D — Coach Move — Exercise Physiology and Medicine
This section covers the Bachelor's chapter on Exercise Physiology and Medicine, Lessons 1 through 5: Skeletal Muscle Physiology and Molecular Adaptation, Cardiovascular Adaptation and Exercise Cardiology, Exercise Neuroscience and Cognition, RED-S and Exercise Immunology and the Athlete as Patient, and Research Methods in Exercise Science. All material is already in the chapter — no new content.
Part A — Vocabulary (20 points, 2 points each)
Select the single best answer for each question.
1. The sliding filament theory (Huxley/Niedergerke and Huxley/Hanson 1954 Nature) established:
A) That muscles contract by filaments shortening B) That thin and thick filaments slide past each other during contraction rather than shortening, producing the cross-bridge cycle that drives muscle force production C) That muscle is an electrical phenomenon D) An obsolete theory
2. The Holloszy 1967 Journal of Biological Chemistry paper established:
A) Resistance training adaptation B) Mitochondrial biogenesis as the cellular substrate of endurance training adaptation — endurance-trained rats showed substantially elevated mitochondrial content and oxidative enzyme activity; founding paper of molecular exercise physiology C) The first VO2 max measurement D) Heart rate training zones
3. PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha) is:
A) A muscle contractile protein B) The master transcriptional coactivator of mitochondrial biogenesis — phosphorylated by AMPK, deacetylated by SIRT1, transcriptionally upregulated by exercise; coactivates NRF1, NRF2, ERRα, TFAM for coordinated mitochondrial gene expression C) A signaling lipid D) A neurotransmitter
4. The AMPK-mTOR antagonism at TSC1/TSC2 refers to:
A) Direct interaction between AMPK and mTOR B) AMPK-driven phosphorylation of TSC2 activates it as a GAP for Rheb, hydrolyzing Rheb-GTP to Rheb-GDP and inhibiting mTORC1 — the molecular basis of concurrent training interference where endurance-induced AMPK can attenuate resistance-induced mTORC1 activation C) Two independent pathways D) An obsolete framework
5. Eccentric vs concentric cardiac hypertrophy refers to:
A) Two types of cardiac arrhythmia B) Eccentric (increased chamber volume with proportionate wall thickening; sarcomeres added in series; endurance training adaptation) versus concentric (wall thickening without proportionate chamber dilation; sarcomeres added in parallel; resistance training and pressure-overload pathology) C) Two types of valve disease D) Atrial vs ventricular hypertrophy
6. Hypertrophic Cardiomyopathy (HCM) is:
A) The physiological cardiac adaptation to training B) An inherited cardiomyopathy with myocardial hypertrophy not explained by loading conditions (typically sarcomeric protein mutations); principal cause of SCD in young athletes in U.S. registries C) An acquired condition from overtraining D) A type of valvular disease
7. Lactate threshold is:
A) The exercise intensity at which lactate is first produced B) The exercise intensity at which blood lactate begins rising above resting baseline — a trainable physiological boundary marking transition in glycolytic-oxidative balance; influences submaximal performance independently of VO2 max C) Maximum lactate concentration D) An obsolete metric
8. Loucks energy availability is:
A) Total daily caloric intake B) Dietary intake minus exercise energy expenditure, normalized to fat-free mass (kcal/kg FFM/day); Loucks 2003 controlled-feeding work showed substantial endocrine disruption below ~30 kcal/kg FFM/day in healthy female athletes C) Resting metabolic rate D) An obsolete concept
9. RED-S (Relative Energy Deficiency in Sport) is:
A) An obsolete athletic concept B) The 2014/2018 IOC framework extending the original female athlete triad (low energy availability, menstrual dysfunction, low BMD) to a broader syndrome affecting multiple body systems and all genders — with cardiovascular, gastrointestinal, immunological, hematological, psychological, growth, and metabolic consequences alongside performance impairment C) A specific genetic disorder D) A drug class
10. The Roberts 2015 J Physiology paper established:
A) That CWI is universally beneficial for athletes B) That post-exercise CWI attenuates the resistance-exercise-induced anabolic signaling cascade (reduced satellite cell activation, attenuated mTORC1 phosphorylation, reduced inflammatory cytokine signaling) and produces measurable attenuation of long-term strength and hypertrophy gains over 12 weeks vs active recovery C) That CWI causes harm D) That CWI is irrelevant to recovery
Part B — Concept Comprehension (20 points, 2 points each)
Select the single best answer for each question.
11. The Schoenfeld three-factor hypertrophy framework identifies:
A) Three exercises that build muscle B) Mechanical tension (primary driver in current meta-analyses), metabolic stress, and muscle damage as three contributors to hypertrophy — with subsequent meta-analyses reducing the relative emphasis on damage as independent contributor C) Three types of muscle fibers D) Three training schedules
12. The AMPK / PGC-1α / SIRT1 endurance cascade involves:
A) Direct ATP synthesis B) Endurance stimulus → AMPK activation (sensing elevated AMP/ATP) → PGC-1α phosphorylation; SIRT1 deacetylation supporting PGC-1α activity; PGC-1α coactivates NRF1/2/ERRα/TFAM driving nuclear and mitochondrial gene expression for biogenesis C) A G-protein-coupled receptor cascade D) A pathway only in cardiac muscle
13. The Fick equation (VO2 = Q × a-vO2 difference) decomposes VO2 max into:
A) Central and peripheral components, with plasma volume expansion as principal early training adaptation supporting stroke volume; trained mitochondrial density and capillary density as principal peripheral adaptations supporting oxygen extraction B) Only central components C) Only peripheral components D) An obsolete framework
14. The athlete's heart vs HCM clinical differential (Maron, Pelliccia work) includes:
A) Only ECG features B) Multiple features distinguishing physiological adaptation from pathological hypertrophy: wall thickness magnitude and pattern, chamber dimensions, diastolic function, ECG morphology, family history, genetic testing, regression with detraining — supporting careful evaluation rather than presumptive labeling C) Only echocardiographic features D) A single criterion
15. Sudden cardiac death in young athletes principal conditions include:
A) Acute myocardial infarction primarily B) HCM, arrhythmogenic right ventricular cardiomyopathy (ARVC), anomalous coronary arteries (often catastrophically clinically silent before fatal event), and inherited channelopathies (Long QT, Brugada, CPVT) — rare in absolute terms but real, identifiable in advance with appropriate evaluation in most cases C) Coronary spasm only D) Always genetic
16. The Erickson et al. 2011 PNAS paper on exercise and aging hippocampus reported:
A) No effect of exercise B) Older adults randomized to a year of moderate aerobic exercise showed approximately 2% increase in hippocampal volume versus expected 1.4% age-related decline in stretching control; serum BDNF rose in aerobic group and correlated with volume change; memory performance correlated with hippocampal volume change C) Only effects in young adults D) Only effects with very high-intensity training
17. The Schuch et al. 2016 vs Cooney et al. 2013 meta-analyses on exercise and depression reflect:
A) Definitive proof exercise treats depression B) Two methodologically different syntheses reaching somewhat different conclusions on effect-size magnitude — Schuch (after adjusting for publication bias) finding moderate effects, Cooney finding more modest effects with substantial heterogeneity — both supporting exercise as clinically meaningful adjunctive intervention but neither establishing it as definitive primary treatment C) That exercise has no effect on depression D) Identical methodology
18. The PROT-AGE recommendations (Bauer et al. 2013) propose:
A) That protein is unimportant for older adults B) Approximately 1.0-1.2 g/kg/day protein for healthy older adults and higher (1.2-1.5+ g/kg/day) for those with acute or chronic illness — substantially above the 0.8 g/kg/day RDA derived from young-adult nitrogen balance studies, reflecting anabolic resistance in older muscle C) That older adults should reduce protein intake D) That protein is harmful in older adults
19. Anabolic-androgenic steroid (AAS) effects and harms (Bhasin 1996, Pope 2014 Endocrine Society statement) include:
A) No demonstrable effects B) Substantial increases in muscle mass and strength beyond what training alone achieves, with documented harms including dyslipidemia (HDL decrease, LDL increase), left ventricular pathological hypertrophy, HPG-axis suppression with infertility and testicular atrophy, hepatotoxicity (oral 17α-alkylated), mood and psychiatric effects, dependence and withdrawal phenomena C) Only effects in elite athletes D) Safe for non-medical use
20. The Lion's integrator position at Bachelor's depth (Active Output) is grounded in:
A) Abstract metaphor B) The visible kinetic signal of integrated capacity from substrate (Food: mTORC1-driven myofibrillar synthesis), internal environment (Water: electrolytes and plasma volume), synchronizer (Light: circadian organization), consolidation (Sleep: recovery and protein synthesis), receiver (Brain: motor planning and motivation), interface (Breath), system probe (Cold), and adaptive load (Hot) C) Same as receiver D) Same as substrate
Part C — Application (30 points, 6 points each)
Write 4-6 complete sentences with specific molecular and mechanistic detail for each question.
21. mTORC1 cross-coach integration with Food Bachelor's. Walk the mTORC1 cascade from the mechanical-load arm in skeletal muscle (mechanical stretch → local IGF-1 release → IGF-1/insulin receptor → IRS-1 → PI3K → PIP₃ → PDK1 → Akt → TSC1/TSC2 inhibition → Rheb-GTP → mTORC1 → S6K1/4E-BP1). Cross-reference Food Bachelor's Lesson 1 — the nutrition-signaling arm via Sestrin2/GATOR/Rag. Why does the AND-gate convergence at mTORC1 at the lysosomal surface make biological sense — what is the integrated signal both arms must represent for protein synthesis to be appropriate?
22. Concurrent training interference at molecular depth. Walk the AMPK-mTORC1 antagonism at TSC1/TSC2. Why does endurance training in close temporal proximity to resistance training risk attenuating hypertrophy adaptation? Apply the goal-context decision framework (temporal separation, modality and intensity, population, training goal) to articulate when concurrent training interference matters and when it doesn't.
23. Cardiac safety surface at clinical depth. A 20-year-old college athlete experiences syncope during a running practice on a hot day. Apply the chapter's framework for sudden cardiac death evaluation: identify the principal conditions (HCM, ARVC, anomalous coronary, channelopathies including LQT1), the diagnostic pathway (history, family history, ECG, possibly echocardiogram and genetic testing), and the appropriate restriction-of-activity framing pending evaluation. Apply the descriptive-not-diagnostic framing.
24. Safety recognition (RED-S at clinical depth). A teammate in a weight-class sport has been training intensely with a substantial caloric deficit, has missed several menstrual periods, and is recovering poorly from training sessions. Walk through the chapter's RED-S framework — the Loucks energy availability concept, the IOC 2014/2018 expansion from female athlete triad to RED-S, the systemic consequences (reproductive, bone, cardiovascular, GI, immune, mood, performance). Name the appropriate resources and identify the older NEDA helpline that you should not cite.
25. Methodological consciousness (PED surface and the conditioning industry). The chapter acknowledges the AAS/PED surface descriptively. Walk through Bhasin 1996 and Pope 2014 Endocrine Society findings on AAS effects and harms. Articulate the gap between the research literature and the conditioning industry / social media framing of these compounds. Apply the five-point framework to a popular fitness claim of your choosing (effects, dose-response, replication, mechanism, translation).
Continue to Section E — Coach Cold.